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🚨 “How the Hell Is Leronlimab Doing This?” — MGK's Latest Post, Simplified 🚨
Let’s break down what the science nerd (MGK_2) just said in a way that actually makes sense.

What we’re talking about is metastatic triple-negative breast cancer (mTNBC) — aka the most aggressive, hardest-to-treat form of breast cancer, and stage 4, meaning the cancer has spread to other organs like the brain, lungs, or liver.

🧬 Most Cancer Drugs Just Slow It Down.
Leronlimab might actually be shutting it down. Here’s how:

🧠 What Is Leronlimab Even Doing?
Cancer spreads by breaking out of the original tumor and invading the rest of the body — it’s like a fire jumping houses. The tools it uses to do this are special chemical pathways. One of them involves a receptor called CCR5.

Leronlimab is an antibody that blocks CCR5.

That’s like boarding up the fire exits, stopping the cancer from escaping and spreading.

🧪 What Did MGK’s Post Say (But 50x Simpler)?
Here’s the TL;DR of what he posted, without the 10,000-word medical jargon:

✅ Leronlimab blocks the pathway (CCR5) that cancer cells use to:
Spread through the bloodstream or lymph system

Invade other organs

Avoid detection from the immune system

Repair themselves after chemo or radiation

Live forever (immortal cancer cells)

🧨 So when Leronlimab hits them, a few things happen:
They stop moving (less metastasis)

They become easier to kill with chemo

They don’t grow back as easily

The immune system has a better shot at recognizing and destroying them

🧪 Mouse Data Was Insane (Yes, Mice — but Still Important)
Leronlimab was tested in mice with human breast cancer cells injected into them (they use special immune-deficient mice so the human cancer doesn’t get rejected).

What happened?

Leronlimab cut the spread of breast cancer by 98–99.6%.
That’s basically “the cancer tried to spread… and failed.”

In plain speak: it not only stopped the fire — it flooded the house.

🔬 And What About in Humans?
Now that we’ve seen the animal data, let’s connect it to what we know from CytoDyn’s human trials:

30 patients with stage 4 mTNBC

Most had failed other treatments

Many had cancer in their brain, liver, and lungs

Small group now alive 36+ months later and cancer-free

MGK’s post helps explain how this may be happening — by cutting off the cancer’s ability to metastasize and survive.

🧠 Coolest Analogy MGK Used (And He Didn’t Even Know It)
"Think of your body like a car.
If the gas pedal (cancer growth) is stuck AND the brakes (tumor suppressors) are broken… the car speeds up until it crashes (cancer).
Leronlimab may be helping slam the brakes."

That’s what we’re looking at here — not just a drug that slows cancer, but one that may be restoring balance to the system.

💥 TL;DR for Non-Doctors
Cancer spreads using CCR5. Leronlimab blocks it.

Stops invasion. Makes chemo work better.

Massive impact on metastasis.

In mice, cut lung tumors by 98%.

In humans? Early signs say it may be doing the impossible.

MGK’s post was dense, but the message is this: Leronlimab isn’t just another drug — it’s a whole new way to fight cancer.

And guess what?

We get to see real long-term survival data — in actual humans — on May 15 at ESMO.

So yeah… 25¢ today might be the deal of the decade.

Let the countdown begin. 🔥

MGK_2

Neoplasm & Immunity
Neoplasm is an abnormal mass; an uncontrolled and uncoordinated persistent growth of tissue, even when the stimulation for growth is gone. The growth or proliferation of the tumor is uncontrolled.

Neoplastic malignant cells are not well differentiated. The tumor cell is usually only modestly comparable to a normal cell. Anaplastic tumors have no differentiation and have tremendous variation between individual cells of the tumor.

A cancerous and / or malignant tumor ends in -sarcoma or -carcinoma. Examples include: Fibrosarcoma. Chondrosarcoma. Adenocarcinoma. Squamous Cell Carcinoma, Renal Cell Carcinoma.

mTNBC (metastatic Triple-Negative Breast Cancer) is a carcinoma, not a sarcoma.

Its official name is metastatic Triple-Negative Breast Cancer (mTNBC). It is a subtype of invasive ductal carcinoma (IDC) which lacks estrogen receptors (ER), progesterone receptors (PR), and HER2 expression. Because of this, it does not respond to hormonal or HER2-targeted therapies, making treatment more challenging.

The key difference between carcinoma and sarcoma lies in the type of tissue from which they originate:

Carcinoma – A cancer that arises from epithelial cells, which line the surfaces of organs, glands, and body cavities.

Common locations: Breast, lung, prostate, colon, pancreas, skin (e.g., basal cell carcinoma, squamous cell carcinoma).

More common than sarcomas.

Examples: Triple-Negative Breast Cancer (TNBC), lung adenocarcinoma, prostate carcinoma.

Sarcoma – A cancer that originates in mesenchymal cells, which form connective tissues such as bones, muscles, fat, cartilage, and blood vessels.

Less common but often more aggressive.

Examples: Osteosarcoma (bone cancer), Liposarcoma (fat tissue cancer), Rhabdomyosarcoma (muscle cancer).

So, mTNBC is a carcinoma because it originates from the epithelial cells in the breast ducts. Sarcomas, on the other hand, arise from the structural and connective tissues of the body.

Malignant tumors produce proteolytic enzymes that break down surrounding structures, such as vein and lymphatics, so as to invade those structures. Some structures try to resist metastatic invasion such as elastin, collagen, cartilage. Arteries are more resistant to metastatic invasion because of the elastin. But not veins. Not lymphatics and not peri-neuro spaces.

Metastasis is the spread from the tumor's primary site to somewhere else, distant and not continuous. Metastasis does not occur in benign tumors. Metastasis occurs through the body's passages. Respiratory tracts, Gastro-Intestinal Tract, Urinary Tract. A malignant tumor can use these natural passages to spread. A tumor of the lung can spread to another site in the lungs via the respiratory tract.

A malignant tumor can spread through natural body cavities. Pericardial cavity. The pleural cavity. The peritoneal cavity. There are spaces/cavities in the spinal cord. Subarachnoid space. The malignant tumor can detach from its primary site and enter these body cavities and spread. A tumor can go from the stomach to the ovary by entering the peritoneal cavity.

A tumor can use lymphatics to spread. Usually carcinomas spread via lymphatics. However, sarcomas can also spread via lymphatics. It is more common for carcinomas to use lymphatics to spread. Sarcoma usually spreads through the vein, not through the artery because of the high amount of elastic tissue in the artery.

The hallmark of a malignant tumor is anaplasia, invasion and metastasis. If the cells have not yet invaded the basement membrane, the tumor is not yet at least malignant. It may just be hypertrophied, swollen, indurated or enlarged. If the basement membrane of the organ tissue has been disrupted by the tumor, then it is Grade IV, malignancy because it has invaded another tissue.

The question then is how does leronlimab cure this? How does leronlimab prevent the cells of the body from becoming anaplastic? To becoming non-differentiated? To becoming immortal? To becoming unlimited in their replication? How does leronlimab make it no longer possible for the tumor to invade other tissues? How does it prevent future metastasis?

What lies at the heart of of Carcinogenesis? or What is the most important thing that is responsible for the development of cancer? A Non-Lethal Mutation lies at the heart of carcinogenesis. Inside the cell, you have a nucleus. Inside the nucleus, you have chromosomes. Inside every chromosome, you have the helical structured DNA. Inside these DNAs, we have genes. Genes are part of DNA. Genes are known as the unit of heredity. Genes are units of DNA that can encode a particular protein or an RNA molecule. That's about the extent of where I'll go with that definition of a Gene.

A mutation is a permanent hereditable change in the base sequence of the DNA of an organism. This mutation alters the Gene as well, because that mutation is also passed down to the daughter cell. So then a Non-Lethal Mutation does not cause the cell to die. If it were lethal, the cell would die and that would prevent any cancer from developing. If the cell dies, then there is no cancer. But if the mutation does not kill the cell, then that mutation could possibly lead to cancer, but for cancer to become more likely, the Proto-Oncogene and the Tumor Suppressor Gene should also be altered in that mutation to make cancer more probable.

If the Proto-Oncogene and the Tumor Suppressor Gene are mutated, then, there is a high possibility of cancer. The Proto-Oncogene encodes protein which regulates the rate of proliferation/growth and cell differentiation of the cell. The Proto-Oncogene is necessary for the normal growth and differentiation of our cells. When it mutates, it is called an Oncogene for a cancer Gene and that mutation can result in cancer development as a result of the mutated Proto-Oncogene.

Tumor Suppressor Genes are the opposite of Proto-Oncogenes. Tumor Suppressor Genes inhibit cell proliferation and tumor development. When this Gene mutates, the Tumor Suppressor Gene has diminished function and the tumor no longer is suppressed.

The best analogy is to use the analogy of a speeding car. If you're on the highway and you want to speed up, you press on the (Gas Pedal = Proto-Oncogene). If you want to slow down, you remove your foot from the Gas Pedal but unfortunately, the car doesn't slow down. Something is wrong. Your Gas Pedal is stuck. The Proto-Oncogene is like your stuck Gas Pedal. So, how do you slow the car down? You need to press on the (Brake = Tumor Suppressor Gene). Well, by doing so, the car hasn't slowed. The (Brakes are Defective because the Tumor Suppressor Gene has mutated), and you're driving fast. As we all know, the outcome is not good. (Crash = Cancer). If there is both a mutation to the Proto-Oncogene and also another mutation of the Tumor Suppressor Gene as well, then the car can't slow down and cancer is likely to form. Does leronlimab prevent these mutations from happening again in the future following a full blown treatment?

Other genes which could lead to cancer are genes that regulate apoptosis and genes that regulate DNA repair. If these genes mutate, then, cancer could form. Apoptosis is a pathway of programmed cell death, where the cells commit suicide. Apoptosis is a better alternative than continued living when the cell is so damaged that the DNA can no longer be repaired and when the risk of Gene mutation is great.

If the genes which regulate DNA repair are damaged, then that would result in decreased cellular DNA repair. So, now, in this scenario, the Proto-Oncogene and the Tumor Suppressor Genes get damaged, but they won't get repaired, and the result of that is a speeding car that can't stop = bad result = crash or the development of cancer in the long run. Tumor cells have impaired DNA repair capacity.

These malignant tumor cells also have unlimited replicative capability. This happens by maintenance of the length and function of the telomere. This makes these cells immortal.

Sustained angiogenesis, formation of new blood vessels. These cells need nutrients, blood supply. They induce angiogenesis via VEGF. Vascular Endothelial Growth Factor.

The cells have the ability to invade and metastasize.

So, let's take a look at how a Normal Cell transforms into a malignant tumor. It has to sustain some sort of DNA damage. Exposure to some DNA damaging agent causing Gene damage. That could be of chemical, viral or some radiation etiology. Exposure of these cells to such an insult could lead to such a mutation. Those insults could cause a mutation in the Gene DNA. If DNA Repair is intact, and if the damage is not that severe, then the cell possibly can restore itself back to normal. If DNA Repair is compromised, the cell possibly may not repair itself, or if the DNA simply is not repaired, then a mutation in the Genome of the cell may be incurred. This is a result of failure of Gene used for DNA repair. This could be a result in the Failure of the Gene that is used to Repair DNA or failure in the Gene used for Apoptosis. If the mutation which results causes a change to both the Tumor Suppressor Gene and to the Proto-Oncogene, that would lead to Unregulated Cell Proliferation. The mutation could also cause Apoptosis to turn off. In both of these scenarios, with Apoptosis turned off and with Unregulated Cell Proliferation, the Tumor grows and can't stop growing; expansion of the tumor cells. Eventually, the growing Tumor requires a collateral circulation for survival. This leads to Angiogenesis or the development of a collateral blood supply. The Tumor tries to evade the immune system. It develops a means by which to protect itself and to avoid immune detection, an escape from immunity. As the Tumor continues to grow, the malignant potential of the Tumor increases. Its aggressiveness increases. More mutations occur. Eventually, it breaks the basement membrane and eventually becomes malignant. Becoming malignant means invading another tissue. Metastasizing. The more mutations, the less likely to respond to therapy. The less antigenic the mutation is, the more likely it is to avoid immune detection and the more likely it is to survive. The more antigenic the mutation is, the less likely it is to avoid immune detection and the less likely it is to survive. Therefore, the mutations that avoid immune detection survive.

The question is how does formal treatment with leronlimab prevent any of that from happening again? How does it prevent it from happening for over 36 months when it was happening 3 years earlier to a great extent?

Let's keep all this in mind and let's go through this recently modified publication about CytoDyn's mTNBC trial performed over 3 years ago. The article was recently revised/modified on November 9, 2024: Leronlimab, a humanized monoclonal antibody to CCR5, blocks breast cancer cellular metastasis and enhances cell death induced by DNA damaging chemotherapy.

"Background: Triple-negative breast cancer (BCa) (TNBC) is a deadly form of human BCa with limited treatment options and poor prognosis. In our prior analysis of over 2200 breast cancer samples, the G protein-coupled receptor CCR5 was expressed in >?95% of TNBC samples. A humanized monoclonal antibody to CCR5 (leronlimab), used in the treatment of HIV-infected patients, has shown minimal side effects in large patient populations.

Methods: A humanized monoclonal antibody to CCR5, leronlimab, was used for the first time in tissue culture and in mice to determine binding characteristics to human breast cancer cells, intracellular signaling, and impact on (i) metastasis prevention and (ii) impact on established metastasis.

Results: Herein, leronlimab was shown to bind CCR5 in multiple breast cancer cell lines. Binding of leronlimab to CCR5 reduced ligand-induced Ca+?2 signaling, invasion of TNBC into Matrigel, and transwell migration. Leronlimab enhanced the BCa cell killing of the BCa chemotherapy reagent, doxorubicin. In xenografts conducted with Nu/Nu mice, leronlimab reduced lung metastasis of the TNBC cell line, MB-MDA-231, by >?98% at 6?weeks*.* Treatment with leronlimab reduced the metastatic tumor burden of established TNBC lung metastasis.

Conclusions: The safety profile of leronlimab, together with strong preclinical evidence to both prevent and reduce established breast cancer metastasis herein, suggests studies of clinical efficacy may be warranted."
...

The above was revised November 9, 2024 and summarized the Research herein: Leronlimab, a humanized monoclonal antibody to CCR5, blocks breast cancer cellular metastasis and enhances cell death induced by DNA damaging chemotherapy

*"*Leronlimab blocks CCR5-mediated invasion of human breast cancer cells into the extracellular matrix

The ability of breast cancer cells to invade extracellular matrix is distinguishable from but an important step in tumor metastasis*. To test the ability of leronlimab to block* cell invasion in 3D Matrigel invasion assay, MDA-MB-231 cells were used. CCL5 was used as a chemoattractant to induce invasion*. The small-molecule inhibitor of CCR5, vicriviroc, was used as a form of positive control. Leronlimab reduced CCL5-induced MDA-MB-231 breast cancer cell invasion with similar efficacy as vicriviroc (Fig.* 4a, b) (855?±?8.7, N?=?8 for control vs. 520?±?9.1?µM distance traveled, N?=?9 for leronlimab, P?<?0.001). We also tested the effects of different doses of leronlimab on breast cancer cell invasion, and the results showed that both 175 and 350?mg/ml of leronlimab can effectively block MDA-MB-231 cell invasion (Fig. 4c, d). Thus, the pro-invasive effect of CCR5 can be abrogated by a humanized monoclonal antibody to CCR5."

...
*"*Leronlimab prevents breast cancer cell metastasis in a mouse lung metastasis model

Leronlimab blocks breast cancer metastasis in vivo. In view of the finding that CCR5 inhibition by leronlimab reduced calcium signaling and cell invasion*, we determined the in vivo effect of leronlimab on the formation of lung metastasis. As a form of control, maraviroc was deployed as previously described. We used MDA-MB-231 cells transduced with the Luc2-eGFP lentiviral vector (MDA.pFULG cells) as an experimental metastasis model. The codons within the Luc2 gene in this vector have been optimized for the expression in mammalian cells, and therefore, mammalian cells expressing this reporter are 10 to 100 times brighter than the unmodified Luc gene. After injection of MDA. pFULG cells into the tail vein of mice, noninvasive BLI enabled the early detection of breast cancer metastasis. Weekly BLI was conducted for 8?weeks, and the radiance antemortem was used as a surrogate measurement of tumor burden. The dose of leronlimab was based on the bioequivalent dose shown to be safe in patients with HIV (700?mg) and the dose previously used to treat GvHD in mice.* Mice treated with leronlimab (2?mg/mouse) or maraviroc (8?mg/kg twice daily) showed a significant reduction in the volume of pulmonary metastases compared with vehicle-treated mice at 8?weeks (Fig. 5a, b, 860?×?106 (n?=?22 mice) vs. 3.7?×?106 photons/s/cm2/sr (n?=?6 mice) for leronlimab, vs. 0.4x ×?106 (N?=?7) for maraviroc). Leronlimab reduced lung metastatic burden >?98% at 8?weeks (99.6%). Collectively, these results provide evidence that the CCR5 antagonist leronlimab reduces the formation of lung metastasis in a murine xenograft model*."*

r/Livimmune - Figure 5
Figure 5
"We conducted a histological analysis of the lung metastases from the mice post-mortem. In order to determine the relative area of the lung occupied by metastasis at death in the mice that were either treated with leronlimab or unreated, the mice were euthanized and the lungs analyzed after paraffin embedding. Longitudinal sections (4 µm) of the entire lung were obtained every 100?µm and stained with hematoxylin and eosin. Each section was evaluated to identify lesions and to differentiate lesions from other space-occupying alterations including consolidation and inflammation. The region of lung metastasis for each animal was quantified in a blinded fashion using Fiji ImageJ, and the mean data were compared as mean?±?SEM for N?=?5 separate mice (Supplemental Figure 5 (see Additional file 1)). These studies showed that the mean tumor size was significantly reduced in the leronlimab-treated mice*."*

...

*"*Leronlimab enhances cell killing by DNA damage-inducing chemotherapy agents used for breast cancer treatment

Because CCR5 has been shown to activate DNA repair pathways*, we investigated the potential for* leronlimab to sensitize breast cancer cells to DNA-damaging agents*. To test this hypothesis, we treated MDA-MB-231 cells with* doxorubicin, a topoisomerase II inhibitor that induces DNA damage, together with either leronlimab (Fig. 6a) or maraviroc (Fig. 6b)."

r/Livimmune - Figure 6
Figure 6
"Leronlimab enhances the cell death induced by doxorubicin, a DNA damage-inducing chemotherapy agent. a MDA-MB-231 cells were treated with 10?µg/ml of leronlimab combined with different dose of doxorubicin for 3?days. The MTT assay was used to determine the relative cell number. The relative absorbance is shown as a fraction of the untreated control. The normalization of leronlimab-treated cells was to leronlimab with no doxorubicin. In b, the cells were treated with maraviroc (100?mM) combined with different doses of doxorubicin, used as a positive control. Data are shown as mean?±?SEM for N?=?8"

...

"The rationale for the current studies includes evidence that CCR5 may participate in the metastatic progression of breast cancer. In the current studies, we show that the humanized monoclonal antibody leronlimab efficiently blocks ligand-induced Ca2+ signaling, cellular invasion, and tumor metastasis*. Prior findings had shown that CCR5 small-molecule antagonists (maraviroc and vicriviroc) block metastasis of human breast cancer xenografts (MDA-MB-231 cells). The current studies extend these findings by demonstrating the humanized monoclonal antibody to CCR5,* leronlimab, efficiently bound CCR5 expressed on human breast cancer cells, blocked ligand-induced Ca2+ signaling, and inhibited Matrigel invasion of breast cancer cells. Furthermore, leronlimab reduced tumor metastasis in immune-deficient mice. In a subset of mice with established TNBC lung metastasis, leronlimab reduced the metastatic tumor burden and increased overall survival*. As leronlimab has been well tolerated in the HIV patient population without significant drug-related adverse events, the current studies suggest leronlimab may have clinical application."*

...

"The current studies extend prior studies demonstrating the importance of CCR5 in breast tumor metastasis prevention and by showing for the first time a reduction in the volume of established metastasis with life extension. The requirement for CCR5 in oncogene-induced cellular proliferation was supported by transgenic studies in which MMTV-PyMT-induced mammary tumors were reduced in CCR5-/- mice. Multiple CCR5-mediated pathways may contribute to tumor progression including MDSC, vascularity, and lymphangiogenesis*. CCR5 siRNA did not reduce the metastatic phenotype of MDA-MB-231 cells in the absence of additional MDSC, endothelial cells produce CCL5, and augmented breast cancer metastasis in another study. In addition,* CCR5 inhibitors also reduced lymphangiogenesis in triple-negative breast cancer (TNBC) cell line xenografts*. Other approaches to restrain tumor metastasis via CCR5 inhibition include targeting CCL5 in the bone marrow via nanoparticle-delivered expression silencing, in combination with maraviroc, which augmented anti-tumor immunity.*
...

A substantial number of studies have provided evidence in other systems that CCR5 participates in the important anti-tumor immune response. In the current studies, leronlimab restrained the development of tumor metastasis in murine xenografts in Nu/Nu mice which lack functional T cells. The nude mouse (nu or Hfh11nu or Foxn1nu) lack a thymus due to a mutation in the FOXN1 gene. The absence of a thymus means that there is no production of T cells; therefore, they are unable to activate the different types of immune responses (adaptive) during the implantation of cancer cells. These mice lack antibody formation, cell-mediated immune responses, and delayed-type hypersensitivity responses but produce NK cells, resulting in a reduced capability of killing virus-infected or malignant cells. Our studies suggest therefore that T cell participation is not necessary for the anti-tumor function of leronlimab observed in the current studies but do not exclude a potential role for NK cells which express CCR5*. Furthermore, as leronlimab is a humanized antibody that does not bind murine cells, it is most likely* the effect seen with leronlimab is mediated directly on the human breast cancer cells, rather the local murine tumor environment. That said, evidence supports a model in which additional immune functions are regulated by CCR5 and T cells in other settings. CCL5 recruits CCR5-expressing TAMs. T cells participate in the anti-tumor immune responses, in part through CCR5-dependent regulation of macrophage differentiation. The recruitment of immune cells, including tumor-infiltrating lymphocytes (TILs), MDSCs, tumor-associated macrophages (TAMs), innate lymphoid cells (ILCs), Tregs, mesenchymal stem cells (MSCs), and immature dendritic cells (DCs), contributes to tumor-induced immunosuppression. Many of these cell types express CCR5 and/or produce ligands for CCR5. Prior studies showed the small molecule CCR5 inhibitor maraviroc reduced MDSC-induced colon cancer metastasis. In the phase 1 pilot MARACON study, patients with advanced-stage metastatic colorectal cancer that were refractory to current therapies were treated with maraviroc. CCR5 inhibition correlated with reduced proliferation and an anti-tumoral macrophage polarized M1 morphology, although more complex interactions occur with PD-1- and CTLA-4-positive cells surrounding tumors with patchy CCR5 expression.
...

It is likely that CCR5 plays a broader role in governing cancer metastasis as maraviroc and vicriviroc reduced prostate cancer cell metastasis to the bones, brain, and viscera in immune-competent mice and reduced metastasis or cellular migration in glioblastoma and a variety of other malignancies. Prior studies had shown that CCR5 induces cancer cell homing to metastatic sites, augments the pro-inflammatory pro-metastatic immune phenotype, and enhances DNA repair, providing aberrant cell survival and resistance to DNA-damaging agents. The current studies, showing a reduction in the volume of established breast cancer metastasis with life extension, provide support for a controlled clinical intervention study using leronlimab in patients with TNBC.

Conclusion

Our studies show that the humanized monoclonal antibody, leronlimab, directed to the G protein-coupled receptor, CCR5, can both prevent breast cancer metastasis and reduce established metastasis. As CCR5 is expressed on the surface of breast cancer cells and leronlimab reduced CCR5-dependent cell-autonomous functions, including calcium signaling and cellular invasion, the impact of leronlimab in this case is likely mediated via a direct effect on the breast cancer cells. The studies were conducted in immune-deficient Nu/Nu mice, suggesting certain immune functions are not necessary for the action of leronlimab on TNBC metastasis in vivo. Leronlimab is administered as a weekly subcutaneous injection and has been used in more than 800 patients with HIV, without serious adverse events related to the drug. Together these findings suggest additional clinical studies of leronlimab in metastatic human breast cancer are warranted."

Tiny-Ad-8280

🚨 25¢ Stock. Stage 4 Cancer. 36+ Months Cancer-Free. Do the Math. 🚨
Let me tell you a story that shouldn’t be real — but is.

A story about terminal cancer patients who were supposed to be dead by now…
But instead, they’re alive. And cancer-free.

The company? CytoDyn ($CYDY) — a tiny biotech stock trading at just 25 cents.
The drug? Leronlimab.
And the data it’s about to present on May 15th at Europe’s biggest cancer conference (ESMO) might change everything.

Here’s what every investor — and every human — should know:

🧬 First, What Is Stage 4 mTNBC?
Let’s break that down:

Stage 4 = metastatic cancer — it’s spread from the breast to other organs like the brain, lungs, or liver.

mTNBC = metastatic triple-negative breast cancer — the most aggressive, deadliest form. It doesn’t respond to hormone therapy or HER2-targeted drugs. There’s no known cure.

Once you reach stage 4 mTNBC, the median survival is less than 12 months.
Let’s be real: Most patients don’t live a year.

🧪 Then Came Leronlimab
CytoDyn ran a small trial with 30 patients who already failed other treatments.
Many had cancer in their brain, liver, and lungs. They were out of options.

Here’s what happened:

All 30 patients (mixed doses):

Median overall survival (OS): 6.6 months

Median progression-free survival (PFS): 3.8 months

🧠 PFS = how long the cancer stays stable before it gets worse.
OS = how long people stay alive.

But then they zoomed in on 19 patients who got higher doses (525–700mg):

Median OS jumped to 12+ months

Median PFS rose to 6.1 months

❗️12+ means they were still alive at the time — they couldn’t even finish calculating it.

💥 The Bombshell: 36+ Months Cancer-Free
Fast forward to 2025.

CytoDyn got follow-up records after resolving a dispute with their old CRO (Amarex). What they found?

“A small group of patients… survived more than 36 months after receiving Leronlimab… and currently identify as having no evidence of ongoing disease.”

Read that again.

These were terminal cancer patients — not just surviving, but alive three years later with zero signs of cancer.

Not "slowed down." Not "in remission."

🎯 Cancer. Free.

🤔 What’s a “Functional Cure”?
It means the patient isn’t just surviving — they’re living a normal life, no signs of cancer, no progression.

In stage 4 mTNBC, that’s never been done before.

This isn’t about managing cancer. It’s about potentially beating it.

🥊 How Does It Compare to Trodelvy?
Trodelvy is another mTNBC drug.
Gilead bought it for $21 billion in 2020 after it showed:

Median OS: 11.8 months

PFS: 4.8 months

That was considered a major success — and it should’ve been.

But Leronlimab?

Has patients alive 36+ months

With no signs of disease

And median OS still growing

It’s not just a different league — it’s a different universe.

🧠 Why May 15th Matters
That’s when the world sees this data.
At ESMO Breast Cancer 2025 in Munich.

Dr. Richard Pestell — world-class oncologist (ex-J&J and Pfizer) — is presenting it.

And yeah, it’s a “poster” presentation.
But so was Trodelvy’s first public showing.

👉 Poster sessions are where Big Pharma scouts its next buyout.

💡 TL;DR — Send This to Your Group Chat
Stage 4 mTNBC = death sentence. Median survival is <12 months.

Leronlimab = 36+ month survival. Cancer-free. Possibly a functional cure.

Trodelvy got a $21B deal with 12-month survival.

Leronlimab’s median OS can’t even be calculated yet… because patients are still alive.

This gets revealed to the world on May 15th.

The stock? Still trading for just $0.25.

🔥 Final Thought
If this data holds up, it’s not just the biotech story of the decade…

💣 It might be one of the biggest medical breakthroughs in human history.

Because for the first time ever, we might be seeing a drug that functionally cures terminal cancer.

And it’s hidden inside a penny stock almost nobody is watching.

May 15th will tell the world.
Until then… do your homework.

https://journals.asm.org/doi/10.1128/jvi.02018-24

Addition of a short HIV-1 fusion-inhibitory peptide to PRO 140 antibody dramatically increases its antiviral breadth and potency

LOL. It is coming though.

Tiny-Ad-8280

🚨 The ESMO Poster Drop Is Real — But What Does It Mean for CYDY? Deal? Delay? Let’s Set the Record Straight. 🚨
We’re 7 weeks out from one of the most pivotal events in CytoDyn’s history — the ESMO Breast Cancer Conference (May 15) — and the company just locked in poster #369P, confirming that Dr. Richard Pestell will present data showing long-term survival in mTNBC patients treated with Leronlimab.

Sounds like a big deal… but people are confused. Is this just another “meh” biotech event? Or is something bigger brewing?

Let’s break it down — clearly, factually, and with all the details to avoid speculation and Reddit rumors.

🧠 What’s Being Presented?
The abstract title says it all:

Improved Long-Term Survival in Patients with Metastatic Triple-Negative Breast Cancer Following CCR5 Antagonism: A Case Series

We already know from the March Shareholder Letter that these are stage 4 mTNBC patients who had failed prior treatments, and some of them are now alive 36+ months later, cancer-free.

That’s radical, given the median survival in this population is around 12 months with the best drugs out there (e.g., Trodelvy).

This isn’t about tumor shrinkage. This is about people still alive — and NED (no evidence of disease) — three years later.

🧬 Why Haven’t They Released the Mechanism of Action (MOA) Yet?
Because ESMO rules prohibit full public disclosure of new clinical data before the abstract is officially presented.

That includes:

Final survival stats

Scientific interpretation

MOA explanations (like why Leronlimab works the way it does)

If they disclose too much, they risk getting disqualified from the conference. These are standard practices at major conferences like ESMO and ASCO — not a CYDY issue.

So yes — they’re holding the biggest cards (MOA + full survival data) until May 15.

💰 Why People Are Whispering About a Deal Before ESMO
Let’s be clear: there’s no public evidence of a deal in place.

But here’s why some believe a pre-ESMO deal is possible (though not guaranteed):

CYDY hasn’t raised money since releasing the survival data in February. That’s unusual for a small biotech. Most would raise ASAP on any good news to extend runway. That they haven’t may suggest they’re expecting non-dilutive capital (i.e., a partner or license deal).

They just formed an Oncology Advisory Board. That’s a classic move companies make when preparing for deeper clinical strategy — or partnership alignment. You don’t do that for fun.

Quote from the March Shareholder Letter:

“We believe leronlimab has already established the potential for tremendous value in the clinic, and in the coming months we look forward to sharing the basis for that conclusion.”

That’s not a throwaway line. That’s teeing something up.

Again — none of this confirms a deal before May 15. But it explains why some investors are speculating that things could happen before the data goes public and Big Pharma competition gets a chance to react.

Because once that data drops? It’s public. And if it’s as good as we think, the bidding war starts.

🧠 Reminder: This Is Exactly How Trodelvy’s $21B Journey Started
In 2018, Immunomedics dropped mTNBC survival data at ASCO (just like this).

It was also a poster.

Gilead came in 2020 with a $21 billion acquisition.

Leronlimab could be showing even better survival than Trodelvy’s 12 months. If true, this is the kind of data that moves mountains.

🧾 TL;DR (for the scrollers)
Leronlimab’s cancer data is going public at ESMO May 15

Poster is confirmed and presented by Dr. Pestell — a heavyweight oncologist

mTNBC patients: stage 4, treatment-failed — now alive 3+ years and cancer-free

MOA being held back for ESMO due to strict abstract rules (not secrecy)

They haven’t raised cash = maybe expecting upfront money from partner?

Oncology Advisory Board formed = prepping for scale

Reminder: Trodelvy started the exact same way (poster ? $21B exit)

This isn’t hype — this is what real biotech inflection points look like.

May 15 is the day the world finds out. But don’t be shocked if Big Pharma moves before then.

Strap in. 🚀

MGK_2

This Mechanism Screams Succumb No More
Greetings to All of You. Welcome here.

I suspect this post becomes a study, but I'll try to keep it intriguing.

Way back, I did a bit of analysis on CytoDyn's mTNBC Clinical Trial. Here are some of these posts:

Points taken off latest PR on TNBC

Improved Comparison of the previous PR on 7/19 and The Compassionate Use Study of LL in BC

My thoughts on the possibility of BTD for LL on mTNBC

Understanding the Significance of 3,600% Improvement in Overall Survival

In Preparation for the Coming Results on mTNBC

I want to try to get to the heart of the matter, as to why some patients who were treated with leronlimab for mTNBC ended up having extended Overall Survivability exceeding 36 months and going on 4 years now with no evidence of any existing tumor or metastasis.

It would be helpful to understand what in fact is happening and I know this information is forth coming as Dr. J said, but maybe we could try to figure out the general means by which this potentially happens for our own benefit. Here are some statements by which Dr. Lalezari has expressed CytoDyn's forthcoming disclosure of their newly understood Mechanism of Action:

"Looking ahead, we are excited to share more about the clarity forming around the putative mechanism of action of leronlimab in solid tumors...

...This is no longer a platform drug in search of an indication; we now have compelling data to support a role for leronlimab in solid-tumor oncology and are executing on that vision.

...The exciting survival outcomes announced in February 2025 provide early clinical evidence of leronlimab’s potential impact across the field of solid-tumor oncology. As previously announced, we’ve submitted our findings as an abstract to the European Society for Medical Oncology meeting in Munich, Germany in May 2025. We are eager to share additional insights into the apparent mechanism behind the survival outcomes and will do so once appropriate and in compliance with pre-conference publication and announcement allowances. In the meantime, CytoDyn has initiated a follow-up protocol so we can continue to monitor the surviving patients into the future.

...In concert with the observation of prolonged survival in patients with mTNBC described above, CytoDyn remains focused on expeditiously resuming our clinical development in this indication. Two previously announced preclinical studies in TNBC that will identify treatment strategies to optimize the design of future studies are now underway. A third study has begun to further examine the apparent mechanism behind the observed increase in survival as compared to existing treatment paths. In the meantime, we will continue discussions with KOLs about the possibility of initiating a follow-up study in patients with mTNBC on an abbreviated timeline, based on currently available data."

Getting to the root of what leronlimab actually is, it is a monoclonal antibody specifically designed to block CCR5, primarily & initially designed to prevent HIV from entering the CD4 T-Lymphocyte thereby preventing HIV replication. The unforeseen outcomes of blocking CCR5 turned out to result in many more positive purposes and indications which were never planned for. Now, it seems to be the case that some of these unintended effects of using leronlimab leads to a prolonged overall survival time which follows treatment of mTNBC. The same prolonged OS could also be another similar unintended but welcome consequence of leronlimab in the treatment of any/all metastatic tumors that depend upon CCR5 to metastasize.

Now, it could be ascertained, that many of the patients under treatment with leronlimab for their mTNBC, could also have that same extended Overall Survivability OS. What is interesting is that these patients, almost immediately upon the initiation of treatment with leronlimab, begin to feel much better right away. Although their tumors exist at the outset of treatment, possibly even raging, the patients themselves begin to feel better, rapidly improving; they recognize the near immediate subsidence of their tumor's disseminating rage. So that encourages them to be compliant and continue taking their leronlimab treatment as scheduled. Over time, their symptoms do dissipate as does the magnitude and quantity of their tumors. Their tumors shrink in size and reduce in number while they themselves feel stronger and improved to the point of approaching normalcy. What is now understood is that after their treatment period has been completed, their tumors do not return. Why not? That is the point of this.

Why do these leronlimab treated tumors not return? Patients or family members of the patients that take the medication do immediately recognize upon the initial dose of the medication, that the medication is quite readily working by their quickened response and improvement of symptoms. They form an inherent notion that the medication is doing what it has been intended to do. They know this assuredly when subsequent CTs or MRIs radiographically, (Our Friend is Still Alive), depict that tumor quantity and magnitude have diminished. When blood serum labs are drawn and their CTCs and CAMLs have dropped to zero, they know assuredly that their cancer is dying, no longer spreading, and that their tumors are vanishing.

Was Dr. Chris Recknor onto some other Mechanism of Action that Screamed Succumb No More when he discussed in the 6/30/2022 Conference Call how the CCR5 blockade leronlimab has other profound effects upon other chemokines and could thereby lead to other unknown but wanted effects?:

"28:30 Chris Recknor: These chemokines act as a beacon to attract other cells in the area. The difference is really big because we thought we just worked on CCR5, but we are also working on CCL2, 3, 11 and 18. In NASH studies, we can see correlation b/w CCL3 which is Macrophage Inflammatory Protein Alpha 1 levels and they increase in severity of NASH on biopsies. So patients in full blown NASH, show highest levels of CCL3, but leronlimab reduced CCL3 with 350mg compared to placebo from baseline from week 14. CCL2 is another one that moves monocytes, called Monocyte Chem-Attratic Protein and is a key biomarker associated with NASH. Leronlimab reduced mean CCL2 from baseline to week 14 in 350mg group compared to placebo.

Now when dr. Chung was talking about HIV and NASH, this has great application, because CCL2 applied to the treatment of the HIV patients is important because lower CCL2 levels correlate with less viral replication in effect to macrophages, less rapid feeding, of the latent HIV reservoir and less chance HIV central nervous system invasion. The ability to reduce CCL2 may have application to HIV and NASH and may really position leronlimab very effectively now to outpatients.

One other key biomarker is molecule Vascular Cell Adhesion Molecule VCAM is very important because VCAM allow immune cells to migrate through blood vessel walls. We did not know that leronlimab reduces VCAM until NASH, but now we have now observed a reduction from mean change to baseline in week 14 for the NASH 350 mg for VCAM and this is important because it has application to other inflammatory markers that are reduced. So further trials need to be conducted with larger numbers, but the exploratory biomarker analysis may be very relevant for informing about future research in other disease states including cancer. Dr. Kelly can you provide an update in oncology."

and immediately thereafter, Scott Kelly chimes in:

"32:20 Dr. Scott Kelly: Yes, Chris Recknor left with a perfect thing about VCAM b/c we do believe VCAM is important for oncology in leronlimab. What we are doing now, we are currently evaluating opportunities KOM Smithing ford, in mTNBC program for leronlimab in combo with a current SOC as well as colon cancer trial, we have animal and human data for mTNBC as well as animal data on the effects of leronlimab on colon cancer."
...
"36:07 Dr. Scott Kelly: We are very encouraged by the fact of leronlimab on the biomarkers and NASH. Many of these same biomarkers are supported by the literature to be important in our oncology program including CCL2, CCL5, CCL18, VCAM and VEGF. Some of these biomarkers also correlate with the potential to decrease metastasis, control the tumor microenvironment and correlate with antifibrosis"

Told ya this would be a study.

Remember, though all of this is only appreciated through the analysis of lab work on a patient, thereby drawing test tubes of blood and then analyzing, the phenotypic outcome of all of this is actually physically expressed in the improvement of these patient's symptoms, by their return to normalcy, which we can readily and immediately appreciate. But for purposes of Scientific Analysis and Comparison, these Biomarkers and Surrogates are used to understand how well the patient is doing, simply by knowing the value of the laboratory results.

CytoDyn Announces Preliminary Results from 30 mTNBC Patients Treated with Leronlimab. Decreases in CAMLs after 4 Doses of Leronlimab were Identified in Over 70% of Patients and were Associated with a 450% Significant Increase in Overall Survival at 12-Month Analysis

CytoDyn Announces Preliminary Results from 30 mTNBC Patients Treated with Leronlimab. Decreases in CAMLs after 4 Doses of Leronlimab were Identified in Over 70% of Patients and were Associated with a 450% Significant Increase in Overall Survival at 12-Month Analysis

July 19, 2021 06:00 ET | Source: CytoDyn Inc.

VANCOUVER, Washington, July 19, 2021 (GLOBE NEWSWIRE) -- CytoDyn Inc. (OTCQB: CYDY) ("CytoDyn" or the "Company"), a late-stage biotechnology company developing leronlimab, a CCR5 antagonist with the potential for multiple therapeutic indications, announced today strong preliminary results from its Phase 1b/2 trials and compassionate use with a total of 30 metastatic triple-negative breast cancer (mTNBC) patients. Patients in Phase 1b/2 were treated with leronlimab in combination with carboplatin.

Key findings from the interim 12-month analysis include the following:

72% of patients had a decrease in CAMLs (cancer-associated macrophage-like cells) ~30 days after induction of leronlimab

The decrease in CAMLs was associated with:

A ~300% increase in mean progression-free survival (mPFS)

A significant ~450% increase in overall survival (OS) at 12 months

High CCR5 in tumor tissue biopsies may help to stratify patients likely to progress on leronlimab

Decreases in CAMLs and CTCs (circulating tumor cells) appear to be related to slower progression and lower mortality

CAMLs appear to identify populations that are responding to leronlimab

Daniel Adams, Director of Clinical Research & Development, Creatv MicroTech, Inc., stated, “While these are only interim results at the 12-month point, our ability to rapidly monitor and identify patients that appear to respond to leronlimab using a single tube of blood is quite an encouraging finding. The fact that greater than 70% of patients saw positive changes in circulating tumor cells after a single dose of leronlimab was made even more informative by their dramatic increases in both progression-free survival and overall survival. The fact that a large group of patients taking leronlimab had an mPFS of approximately 6 months is well beyond that experienced with current treatment options available to these women, who typically have mPFS of approximately 2 months. This result is even more amazing as these women did not even reach mOS in 12 months, considering the typical mOS in this population is only 6 to 7 months.”

Scott Kelly, M.D., CytoDyn’s Chief Medical Officer and Chairman of the Board, commented, “We are very excited about these preliminary results and are eager to discuss the next regulatory steps based on this data. Based on leronlimab’s mechanism of action, we believe these results may provide tangible hope for patients suffering from mTNBC, and potentially other forms of cancer. As we have said previously, we believe CytoDyn will evolve into an oncology-focused company as well as other potential indications.”

So, all of this is not just fantasy or theoretical for that matter, but rather, it is 100% real and the data shall be presented at ESMO in mid-May. But, on the topic of reality, I see the need to ask whether it is actually real or not to actually expect that many of those who are treated with leronlimab for mTNBC or for that matter, any CCR5 dependent tumor, to actually expect an OS of 36 months or more? Is it also a reality that this theory be applied to any other CCR5 dependent cancer under treated by leronlimab? As we have already reviewed, that with this particular test, we can know who responds well and who doesn't respond well to treatment of mTNBC with leronlimab.

"CytoDyn now has verified a testing method to assess within the 1st Treatment Cycle, (28 days), whether or not the current method of treatment would be successful in improving the patient's progression free survival and overall survivability or if the current method of treatment would result in a worsened progression free survival and a worsened overall survivability.

If you have a decrease in CTCs in the 1st 28 days, the patient would benefit from current treatment.

If you have an increase in either CTCs or CAMLs, the patient would not benefit from current treatment.

[If CTCs and CAMLs are both 0 for (2) months in a row, treatment may be stopped as the patient is likely cured.

If evidence of the cancer returns, another round of full blown treatment should immediately be initiated]."

We already know that for leronlimab to work, there must be some CCR5 dependency of the tumor, which means, that the specific tumor in question, depends upon the presence of some quantity of CCR5. This means that, if CCR5 were not present, then the tumor itself would also not be present. Either the tumor or the surrounding microenvironment is mandatory to possess some quantity of CCR5 for the tumor to proliferate. Without that presence of CCR5, leronlimab would accomplish nothing in such a milieu. However, given that some quantity of CCR5 is present with in the tissues of the tumor or tumor microenvironment, then leronlimab has the potential to deliver the stated results of 36 month and growing OS. But why? or How does it do this if it is not present and not being administered?

Leronlimab delivers this killing blow to the tumor of course, when it is being administered to treat the patient. However, when the treatment period is over and done with, leronlimab then, is no longer being administered. So then, during the time period which follows the treatment period, is leronlimab still doing anything of note? Considering these recent findings of 36 months and growing of Overall Survivability, the question posed is a valid. Is leronlimab still at work or has leronlimab induced some permanent changes or only long lasting changes which make it impossible or less likely for that specific tumor to proliferate in that patient's body? I think we shall soon learn what CytoDyn definitively believes or understands to be true, possibly even prior to the start of ESMO in mid-May, but I lay out below, some hypotheses I make.

One consideration might be that it is almost as if during the treatment period, leronlimab somehow, in a sense, places a lock and key over the CCR5 receptor. That over the course of treatment with leronlimab, the CCR5 receptor becomes somehow transformed and no longer remains capable of enabling the tumor to proliferate; or that the tumor no longer remains sensitized towards CCL5 RANTES; or that the CCR5 receptors no longer remain sensitized to the CCL5 RANTES ligand.

Or what if, because of leronlimab's effect on the tumor, the tumor somehow mutates and starts producing a mutated form of RANTES, CCL5, in an attempt to get around leronlimab's thwarting effects. Such that RANTES itself might have a higher affinity for CCR5 than leronlimab itself, however, with the tumor creating that mutation in response to treatment with leronlimab, RANTES itself becomes deformed and now no longer even attaches to CCR5?

If any of this were to possibly happen, then, the same, extended Overall Survivability would result with no evidence of disease progression.

What if dormant cells of the tumor actually wake up 4 years or 48 months later, and attempt a comeback, a return of power, now using a less sensitized or de-sensitized version of CCR5 or a deformed or transformed CCL5 RANTES, its comeback would only be a weakened incursion. In addition, the patient's own immune response would be highly sensitized and attuned against any return of that specific tumor because of the memory it established from the initial tumor. The killer T-Cells would hone in on and quickly shut down any return of those specific tumor cells attempting to return. That is because 4 years earlier, when the tumor was originally raging, and when leronlimab was initially administered, leronlimab had permitted, allowed, enabled and enhanced the full flawless functioning and deployment of the patient's immune system even though their symptoms had seemingly improved. The weaponry specifically developed against this tumor were all being created for future use. Over the course of the initial treatment period, the patient developed an unassailable Immunity against that specific tumor such that any subsequent revitalization of the dormant tumor cells or even return of any new identical tumor cells which follow the tumor's initial eradication, would be immediately shut down by a vicious onslaught which is conducted by the totality of only those specifically manufactured immune defenses meant only for this purpose.

The following details what happens without leronlimab treatment and could explain why the current SOC Trodelvy does not have a 36 - 48 month OS.

"After breast cancer treatment, dormant tumor cells continue to lay in wait in some patients. These so-called “sleeper cells,” also referred to as minimal residual disease (MRD), can reactivate years or even decades later. Once the cells begin to expand and circulate in the bloodstream, it can lead to the spread of metastatic breast cancer. Patients who have MRD are more likely to experience breast cancer recurrence and have decreased overall survival."

Another possibility could be that leronlimab immediately induces an inherent change within a protein or a cell or within a group of proteins and/or cells in the immune system of every patient with CCR5 within their tumor microenvironment. As soon as leronlimab is given, that immune system change is immediately made leading to the improvement in symptoms and over time, that change is strengthened, reinforced and perfected such that by the end of the treatment period, the tumor is no longer able to proliferate whatsoever and is then quickly resorbed by the body.

However, should the tumor somehow break free of its resistance, or is somehow permitted and escapes so as to come forth in the body, then, the body's own defenses which were originally developed from the initial leronlimab treatment period would begin to battle against the tumor. But, given the fact that the tumor in fact had the capacity to overcome the body's own defenses to somehow arise again, then the body's own defenses would then be insufficient against the tumor and to stop the tumor from proliferating, would require another treatment round of leronlimab dosing to again suppress the tumor once and for all from proliferating. This type of tumor that can somehow, overtime, return back again, is of very virulent disease, and is unwilling to conform to just one round of this defense.

However, with a second treatment round of leronlimab, the tumor would again be shut down and this time for good, never to return. All of this is visual. All of this happens before our eyes, as we watch the tumors melt and shrink away, but it happens over an extended period of time and it is not yet understood exactly how or why, but that day is coming to know the how and the why of it.

Or Is the Placebo Effect at work? Knowing that you've been treated with leronlimab for some time, do you simply believe yourself cured placing you at the epitome of health? And by believing, do you simply will yourself into feeling good and into being cancer free by willing your own Immune defenses to be ready, willing and activated to fight on your behalf?

"Creatv have the software which count CTC circulating Tumor Cells or Metastasis. [I would think that at ESMO they will be touting their software while discussing these Overall Survivability results of 36-48 months.] [Remember mTNBC metastasizes to the brain.] Leronlimab obliterate tumors period. Leronlimab knocks out VEGF, angiogenesis and prevents metastasis, dries up tumors and blood vessels. Leronlimab crosses the BBB, so it dries up tumors in the brain too. MD Anderson knows.]

---

this is amazing from the 10-k, page 7-8.

One patient was administered leronlimab with stage 4 HER2+ breast cancer with metastasis to liver, lung, and brain. The patient received her first dose in November 2019 and remained on study drug until spring 2022
Brain Metastasis. Liver, Lung metastasis. No PD1 or PDL1 inhibitor at all. She was on Leronlimab nearly 30 months. 2.5 years on Leronlimab with Brain mets.

30 month overall survivability for this patient. If that's when she died.

·From the FB page:
In my humble opinion something big is coming In cancer.
1. They put together an oncology board out of the blue.
2. The letter started with cancer & ended with “This is no longer a platform drug in search of an indication; we now have compelling data to support a role for leronlimab in solid-tumor oncology & are executing on that vision”.
3 “ leronlimab could play a significant role as a paradigm-shifting therapeutic in oncology”
4 “This is only the beginning of the Company’s 2025 oncology story”
5 “the developments in oncology have set the stage for 2025 to be a benchmark year for CytoDyn”
6 They are excited to share the results but can’t until after the ESMO conference.
7 They set up a new protocol to continue monitoring the survival patients
8 They began 2 preclinical’s in cancer & more importantly added a 3rd to “ further examine the apparent mechanism behind the observed increase in survival as compared to existing treatment paths”
9. Max’s post was all about mTNBC & not his HIV specialty
Buckle up!!

Lab_Monkey_

Leronlimab Treatment for Multidrug-Resistant HIV-1 (OPTIMIZE): a Randomized, Double-Blind, Placebo-Controlled Trial
This JAIDS article was just posted on the Publications page of the Cytodyn website. As has been stated before, the cadence of the release of information, and the delay of release in relation to the published date is very interesting. They are definitely a step ahead of the public sphere of knowledge.

Conclusions:
Leronlimab resulted in significantly reduced plasma HIV-1 within one week after addition to failing ART. After 24 weeks combined with an OBT, most participants had plasma HIV-1 RNA levels <50 copies per mL plasma, suggesting utility of leronlimab as a component of salvage therapy.

Yang, Otto O. MDd; Lalezari, Jacob P. MDf,g; Sacha, Jonah B. PhDh; Hansen, Scott G. PhDh; Meidling, Joseph MBAg; etal.

MGK_2

Advancement Forward, Behind The Scenes
Greetings Folks

Let's try to see a bigger picture. I speculate here based on what we know.

We've said this would take time. We've said that it is down the road a ways, that this could take a little while yet. This post may also confirm that understanding, I believe.

Here is a refresher of where I'm going, only, disregard the possibility that the 250 million shares were institutionally owned.

We have discussed in recent weeks, the potential of a collaboration, and I explained and reasoned why and how this collaboration could exist. The GF component is primarily tied to HIV. I have also indicated that the ViiV component would also be tied to HIV. But the GSK component could have multiple ties. That to HIV, Oncology, MASH, Alzheimer's, virtually everything that CytoDyn is pursuing.

"Our Strategy

We are a focused biopharma company. We prevent and treat disease with specialty medicines, vaccines and general medicines. We focus on the science of the immune system and advanced technologies, investing in four core therapeutic areas - respiratory, immunology and inflammation; oncology; HIV and infectious diseases – to impact health at scale. Our Ahead Together strategy means intervening early to prevent and change the course of disease, helping to protect people and support healthcare systems."

We have also made strong arguments considering Novo Nordisk as a possible licensee of Livimmune for the combination of Ozempic with Leronlimab targeting MASH and liver fibrosis. Eli Lilly is another one on the list for that same indication, but with the combination of Mounjaro and Leronlimab for MASH and liver fibrosis. I've discussed also in the past another possibility of Madrigal licensing Livimmune with the combination of Rezdiffra and Leronlimab for MASH and liver fibrosis.

But, let's take a look at some Parallel plays that could be happening behind the scenes. We know GSK is running a Pulmonary Fibrosis Pilot Trial at Boston University.

Essentially, as a result of the findings of the most recent murine study which are stated here:

"The third study, concluded in January 2025, [resulting in a p-value across all 3 studies < 0.01] evaluated reversal of liver fibrosis in mice who received carbon tetrachloride, a liver fibrosis-inducing agent, from birth to sacrifice at day 35.

“The management of patients with advanced liver fibrosis due to a variety of etiologies is an area of enormous unmet need in the field of hepatology. The results of these three preclinical studies support both the biologic activity and potential clinical benefit of leronlimab’s ability to bind to CCR5 receptors on hepatic stellate cells, leading to a reversal of established liver fibrosis,” said Melissa Palmer, MD FAASLD, the Company’s Lead Consultant in Hepatology."

we can therefore make the assumption that the Pulmonary Fibrosis Pilot trial is now Ongoing. I really love this trenddetector!! GSK teams up with the Center for Regenerative Medicine (CReM) at Boston University and Boston Medical Center. This Pilot Trial was contingent upon the determination of the fact that leronlimab certainly is capable of removing fibrosis regardless of its etiology, p-value < 0.01.

"London-based GSK is crossing the pond to form a new lung disease research collaboration with Boston scientists. The Big Pharma is joining forces with researchers from the Center for Regenerative Medicine (CReM) at Boston University and Boston Medical Center to develop new models for lung diseases like pulmonary fibrosis..."

So, if GSK is probably pursuing this promised Pulmonary Fibrosis Pilot Trial at Boston University at their own center, Boston Medical Center,

"As a side note, we have been contacted by colleagues at a major academic institution who indicated that, if the liver fibrosis reversal results are confirmed in the follow-up studies, they would be interested in funding a pilot study of leronlimab in the treatment of patients with pulmonary fibrosis at their own center."

Then, it would seem that the indication of fibrosis of any etiology may be divisible or separateable. Meaning that leronlimab may be licensed by various companies for the indication of fibrosis, but for Indications that would be separated based on organ type. Therefore, Pulmonary Fibrosis would be considered a separate indication from Liver Fibrosis which would be a different indication from Cardiac Fibrosis which would be a different indication from Kidney Fibrosis and a different indication from Pancreatic Fibrosis. Etc...

So, if GSK is not pursuing MASH, then, we can consider either Novo Nordisk, Eli Lilly or Madrigal for a licensing agreement with leronlimab to act as the anti-fibrotic in that combination treatment for MASH.

Let's go back to GSK. Not for MASH, but rather for MSS mCRC. I have to ask the question. Why has there been no discussion on the current progress of the Phase 2 Clinical Trial? At least nothing to speak of really? If there are delays, there has been no mention of them, or of any progress for that matter. I read an interesting post by Jake at Investor's Hangout, where he says:

"...CYDY management would much prefer to avoid the time and expense of building out a go it alone in-house drug development structure in favor of having a BP partnership/eventual BO doing that heavy lifting. In that vein, the fact that these 2 jobs remain open is consistent with the premise that an oncology partnership is on the near horizon."

So, what Jake is suggesting is certainly a possibility and if these (2) jobs he is referring to are not yet filled, though they certainly are necessary for the MSS mCRC Clinical Trial to proceed, could it be that CytoDyn's real intention all along was to proceed forward in this MSS mCRC Clinical Trial in a partnership with a large BP and not all alone? Yes, Very possible.

Could that explain the delay in hearing from CytoDyn? Maybe the NDA requires that enrollment be completed before making any announcement? Regardless, CytoDyn's number one Priority is MSS mCRC.

From Fulfillment:

"When Dr. Lalezari took his seat as CEO in December 2023, insufficient time had passed since Bevacizumab's maker's approval in the summer of 2023 to determine whether or not they would be interested in the proposed MSS mCRC combination trial, but in May of 2024, CytoDyn had worked out plans with Bevacizumab's maker to make this trial the #1 Priority. Now, based on leronlimab's MOA, we know the outcome really and how this should pan out. So, like AffectionateAd3095 says, Let's Move Forward and Get This Party Started. In a word, Fulfillment. This 1st contract gets the ball rolling which carries with it too much momentum to ever be able to bring it to a stop again."

So, if MSS mCRC is Priority #1, we can conclude that the likely partnership in MSS mCRC would be with GSK.

From A Panoramic View:

"...so if it were to be done in conjunction with another PD-1 blockade, then GSK could also be in the picture considering their 100% effective performance in mCRC with their dolstarlimab or Jemperli.

This dolstarlimab GSK study was performed only in patients with a certain genetic defect which thereby eliminated 96% of patients with mCRC from even being eligible for their very limited and specific patient population trial:

"all of the tumors had a gene mutation that prohibited cells from repairing DNA damage. These mutations are found in 4% of cancer patients. Pembrolizumab, a Merck checkpoint inhibitor, was given to patients in that experiment for up to two years. In around one-third to one-half of the patients, tumors shrunk or stabilized, and they survived longer. Tumors eliminated in 10% of those who took part in the study. The experiment needs to be duplicated in a much larger study, according to the researchers, who point out that the current study only looked at individuals with a unique genetic signature in their tumors."

Maybe, if GSK wanted to partner, leronlimab would make it possible for Jemperli to treat even those without that unique genetic signature. Leronlimab potentially could allow GSK's PD-1 blockade Jemperli to expand its reach in mCRC from only 4% of the MSS mCRC patient population who do have that genetic mutation to 100% of the MSS type mCRC tumors.

The point of all this is to show that something is happening behind the scenes in regards to MSS mCRC. In the past few months, I have shown that much has been happening behind the scenes in regards to HIV Cure, MASH and Fibrosis. I have been discussing HIV Cure, MASH and Fibrosis, but hardly any mention or discussion of MSS mCRC. Well this unexpected delay during the enrollment phase of the MSS mCRC Clinical Trial could be due to an NDA collaboration in this very trial.

We have said on many occasions that G is CytoDyn's arch rival. We have said that CytoDyn is darn close to an HIV Cure. That would be a devastating blow to G when CytoDyn makes that declaration themselves. We have said that 4 years of no evidence of cancer return is equal to a Cure. When CytoDyn proves this scientifically, that too would be a horrific blow to G's cancer treatment medication which they are intending for many types of cancers, not just mTNBC. Leronlimab's capacity against Fibrosis would not so much affect G at the moment, but in time, would minimize the need for G's drugs.

A Cure to HIV is very close. A Cure of mTNBC seems plausible. Certainly, an OS of 24 months is quite doable and that is a double of G's current 12.1 month OS. It already seems as if CytoDyn has a partner in HIV. I've explained that many times. The GF has already awarded Jonah Sacha nearly a million dollars for his work on the HIV Reservoir. How many more grants like that one are coming down the road? There is more work to do regarding Triple Therapy and more work regarding the Placenta LS Mutations. LATCH is happening this year in (2) Clinical Trials. These advancements have the potential to utterly demoralize G. But all of this is very much still ongoing. Considering Max Lataillade, that partnership could very likely expand and morph into a collaboration between The GF, ViiV and GSK together with CytoDyn. We know GSK is pursuing Pulmonary Fibrosis at Boston University, precisely at the same time that CytoDyn was promised a Pilot Trial in patients at their own medical center, possibly Boston Medical Center.

In accordance with Jake's post, Given the delay in communications, I'm considering the possibility that an NDA could exist in regards to the MSS mCRC Clinical Trial that is currently ongoing. How helpful would that be if GSK were to partner somehow in this MSS mCRC Clinical Trial. Whether it is with Jemperli or not, their hand in the MSS mCRC Clinical Trial would be invaluable to CytoDyn. Their help would greatly subdue G's influence upon the outcome of this trial.

I don't believe GSK would bring Jemperli into this Clinical Trial because the protocol for this Clinical Trial has already been approved by the FDA having leronlimab in combination with trifluridine plus tipiracil (TAS-102) and bevacizumab in patients with CCR5+, MSS, relapsed or refractory mCRC. To include Jemperli, would greatly slow things down. If they wanted to include Jemperli, it could be done at a later point. Remember, in the mTNBC murine study, they are comparing leronlimab to Keytruda, which is Merck's PD-1 blockade, very similar to GSK's PD-1 blockade Jemperli. If they find strong evidence that leronlimab works synergistically with Keytruda, then, it very well may be synergistic with Jemperli as well.

"Based on these survival observations, the Company has initiated two pre-clinical studies in mTNBC that will evaluate possible treatment synergies between leronlimab, an antibody-drug complex treatment (sacituzumab govitecan), and an immune checkpoint inhibitor (pembrolizumab). The Company will also continue to perform follow-up testing on the group of mTNBC survivors who currently identify as having no evidence of ongoing disease."

So, with these 3 indications, and the (organizations who may be involved in order of likelihood):

HIV: (GF, ViiV, GSK)

Fibrosis: (GSK, Novo Nordisk, Eli Lilly, Madrigal)

MSS mCRC: (GSK, Merck)

If any of this in fact is true, how close are we to that moment of disclosure? Well, if the MSS mCRC Clinical Trial is to progress beyond enrollment, then that disclosure would need to be made soon. We have said many times that GSK shares much in common with CytoDyn and they too may have found a way to get involved in the ongoing Phase 2 Clinical Trial of MSS mCRC. The trial was not originally written to include GSK or their drug Jemperli, but given the recent re-testing of Keytruda in combination with leronlimab against mTNBC, it becomes a possibility that there is synergy between a CCR5 blockade and a PD-1 inhibitor and that would greatly interest GSK.

GSK is a possible collaborator with CytoDyn in all 3 indications above. G would be an antagonist to each of the 3 indications above. G has been successful in stealing away any advancement CytoDyn has made in any indication. There are ways GSK could get involved without getting directly involved. They could lend a hand in the trial in ways which are not that obvious and those 2 jobs may not be fulfilled because GSK may be the intended recipient. What would be the motive? To protect the trial. To thwart any attacks made against the trial. To insure that the trial is conducted fairly, because CytoDyn hardly has the resources to insure this happens aside from its CRO Syneos Health.

Seems to me, GSK is in on all 3 of these indications. Does GSK have a beef with G? I think they might. Leronlimab has the potential to annihilate and G fears that, so they do what they can with what they have to prevent this, regardless of ethics. If G bought out CytoDyn, they would shelve leronlimab. Know this. That would be equivalent to a nuclear bomb placed on leronlimab.

Maybe GSK doesn't partner up regarding MSS mCRC, but they only help out for some agreed upon reason. I think CytoDyn can rely upon GSK for an assist in the event it becomes necessary, especially if G were the reason for that need. Maybe GSK would agree to outbid G if there ever was an offer by G, who knows, just speculating.

CytoDyn does come out with the Cure to HIV. CytoDyn does come out with the Cure to mTNBC. Leronlimab becomes the only drug that substantially reduces the fibrotic scarring of any organ that develops fibrosis. CytoDyn completes the MSS mCRC Clinical Trial obtaining statistically significant efficacy of leronlimab against MSS mCRC. All of this pushes G into a corner, with no where to go.

If you were G, how do you recover from all of that? You don't. If a Cure to HIV is established, is there any need any more for scheduled on going forever treatments? The same question is posed for mTNBC? By eradicating fibrosis, the degree of disease is greatly diminished. Why then would any treatment be necessary once the fibrosis is gone? If the same results are obtained in MSS mCRC that were obtained in mTNBC, then we can expect great results in MSS mCRC. In all of this, CytoDyn requires an assist, a partner. I think GSK is poised or most aligned with CytoDyn's own objectives and may even be playing somewhat of a protective role thereby giving Dr. Lalezari the confidence to say:

"I believe our current strategy will result in significant value return to the Company and its shareholders and should give us the opportunity to do so on an abbreviated timeline. We are on good terms with the FDA, we have the funds required to pursue our key development objectives and we have the requisite expertise and associations to execute on our vision. Entering 2025, the Company is in control of its own destiny."

Think again who they have: Max Lataillade, Melissa Palmer and Richard Pestell. These are individuals of great experience. Friends with the Gates Fund and with Emma Walmsley, CEO of GSK. Are they just sitting on their laurels?

Nice day guys. Looking forward to a gap up soon and moving forward from there.

Not celebrating anything. Just acknowledging the obvious. Someday CYDY will be able to hold a gain. In the meantime use the downturns to accumulate for the long term and if you have the balls for it, swing trade. That really has been the only way to make money these last few years. Stocks are vehichles for making money. If you want to support the companies research write a check and donate to the cause directly.

Looking forward to the news on Tuesday.

"The ONLY achievement for a biotech is a drug BLA or NDA approval (NOT a Right to Try or some research hack, NOT butt monkeys)."

Ridiculously simplistic viewpoint IMO.

https://www.linkedin.com/pulse/leronlimab-breakthrough-immunotherapy-farbefirma-qi4if

Leronlimab: A Breakthrough in Immunotherapy

Farbe Firma Pvt. Ltd.Farbe Firma Pvt. Ltd.
Farbe Firma Pvt. Ltd.
Injectables | Lyophilized | Liposomes | Nanoparticle | NDDS | Peptides | Microspheres | Emulsion | Suspension | Depot
Published Jan 22, 2025
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Introduction

Leronlimab is a humanized monoclonal antibody designed to target the CCR5 receptor on T cells. This innovative therapy aims to harness the body's immune system to treat various conditions, including HIV infection, metastatic triple-negative breast cancer, and severe respiratory complications associated with COVID-19.

Mechanism of Action

Leronlimab works by binding to the CCR5 receptor, which is found on the surface of certain immune cells. By blocking this receptor, leronlimab helps to modulate the immune response, making it a valuable tool in the treatment of diseases driven by excessive immune activation.

Clinical Research and Efficacy

Clinical trials have shown promising results for leronlimab in the treatment of HIV infection and metastatic triple-negative breast cancer. In HIV patients, leronlimab has demonstrated significant viral load reduction and improved immune function when used in combination with standard antiretroviral therapies. In breast cancer patients, leronlimab has shown potential in improving overall survival and progression-free survival rates.

Side Effects and Considerations

Common side effects of leronlimab include diarrhea, headache, swollen lymph nodes, high blood pressure, and injection site reactions. These side effects are generally manageable but require close monitoring by healthcare providers. Patients receiving leronlimab should be monitored for signs of infection and other adverse reactions.

Conclusion

Leronlimab represents a significant advancement in immunotherapy, offering new hope for patients with HIV, metastatic triple-negative breast cancer, and severe respiratory complications associated with COVID-19. Its ability to modulate the immune response provides a targeted and effective treatment option for these conditions.

Yep, bad few days that is for sure. Congrats.

Those NDA's are difficult to get around!

Not sure if this older video was ever posted here but it is worth a watch for those interested in how leronlimab works in cancer:

https://s3.amazonaws.com/content.stockpr.com/cytodyn/db/205/3059/video_mp4/cyto.mp4

Fidelity:

McLean Capital Management resumes coverage for Cytodyn with NEUTRAL recommendation.
Investars Analyst Actions - public
3:12 PM ET Mar-11-2025
On March 11, 2025 McLean Capital Management resumed coverage for Cytodyn (CYDY.NaE) with a NEUTRAL recommendation.

From a couple days ago MGK_2:

Abrupt Turnaround
I liked u/Biotrends_USA recent post Collaboration With BP?, so this is my response.

Shareholders need to wait until the event we've been looking for begins; once it starts, it's over. The interaction, the trading of shares exceeds all rational expectation. How does that happen? Bidding War or Governmental Intervention.

Doesn't it seem as if a standstill is at hand? Neither side is giving up. Almost an unsolvable dilemma. Tremendous resistance remains in opposition against this molecule, but the promises that this molecule provides exceeds the resistance poised against it. The resistance wants to crush, destroy and demoralize, by stealing away investments and hope placed in the molecule.

There is no way CytoDyn partners together with the Puppet Master G. That particular company which heads up the short campaign against CytoDyn has got to be a pharmaceutical, so therefore, how could CytoDyn ever trust its chief nemesis, its arch rival? It certainly can not ever trust them, so then how could it partner up with them?

The SEC is supposed to intervene in order to prevent illegal market manipulation tactics. Even the stock brokerage houses which facilitate these illegal short trades are complicit. A new administration has come, but so far, no changes have been appreciated.

If these attacks ever do cease, then the parties could come to the table to work things out. I don't have any hope in this solution. How can the memories of what has happened be forgotten, which is necessary to arrive at a deal? If they can't be forgotten, how can a deal be arrived at? Though CytoDyn settled for a rather low settlement in Amarex, did they really have a choice? To get more would have cost more time and money and how much more could Amarex even pay?

Looking forward, how then can CytoDyn ensure to be fully protected from the onslaughts of G in a partnership deal with anybody? The only real evidence of a partnership deal is from the GF. If G is truly against anybody partnering with CytoDyn, then how do they feel about any current investment into CytoDyn or into leronlimab, even if that investment is given to OHSU? If that investment is put towards solutions which G wants domination over? How does G feel about any investment / grant made towards finding the Cure to HIV? Clearly, they are opposed, and CytoDyn is such a small target, with such great rewards if defeated, that they make a perfect target for big old G to rampage.

CytoDyn is too small to be supported and defended by many of the big names, though CytoDyn's potential pipeline is quite rich. It can not be denied that by some unknown means, CytoDyn has found a way to survive. Because of its main resource, otherwise known as leronlimab, through some of its specialty shareholders, as well as its myriad of shareholders, CytoDyn has found that amazing means to remain afloat, despite the constant barrage of fire which persists against it, yet, CytoDyn remains vigilant in putting up its own offensive and fighting back. CytoDyn has built up an arsenal of weaponry focused on their targets, aimed and honed square upon the Cure to HIV, treatment for MSS mCRC, mTNBC, GBM, Fibrosis, MASH, Alzheimer's Disease, Chronic Fatigue Syndrome and on and on.

How do they achieve this? There are some liquid reserves from a settlement with Amarex, but much of its current pipeline is being driven by unknown sponsors who are willing to run Pilot Trials in the various indications listed above, all of which incur zero cost to CytoDyn. CytoDyn's only responsibility is to provide the leronlimab for those unidentified sponsored Pilot Trials.

Lalezari has kept a very low profile. He certainly does not tempt G. He must make an occasional PR or two, but, he does not flaunt his findings. In fact, he may even be trying to suppress what he would otherwise, rather exaggerate. Lalezari purposely tries to minimize CytoDyn's vulnerability. By exploiting possibilities before they are quite ready, that would increase CytoDyn's vulnerability. Lalezari therefore does the opposite. He wants that vulnerability be kept to a minimum, so he remains tight lipped. Rather silent. Why does he do this? I think the answer lies in the answer to the following question. How can he trust G at all?

Whoever is manipulating the market against CytoDyn is the same entity as who ever turned Amarex against CytoDyn and is the same as whoever ran the ambulance chasers. It is that entity who is the Puppet Master and they are still out there continuing day in and day out in constant opposition against CytoDyn's advancement. This Puppet Master isn't going to give any amount, not even an inch. But neither is CytoDyn.

CytoDyn has an obligation to its shareholders and to its resource leronlimab. The SEC should intervene to keep it a fair playing field, but they, so far have failed, but they are now part of a new administration and hopefully, changes are soon to be appreciated soon. G is absolutely not in favor of any pro-leronlimab Big Pharmaceutical to come to CytoDyn's aid. Therefore, this particular partnership information remains under lock and key via NDA and CytoDyn hasn't let out a peep. G is dead set against any collaboration CytoDyn might make with any Big Pharma as they see any collaboration as a much stronger antagonist against their own goals and ambitions of HIV treatment. It is absolutely G's desire that CytoDyn never partners, thereby keeping CytoDyn small enough, without any substantial financial backing, in order to keep it at bay with the inability to ever put up a real fight. To ensure that CytoDyn never has a means by which to advance, or to substantially and drastically slow down and retard CytoDyn's advancement efforts to reach their goal that would really hit G where it counts, which is of course a leronlimab approval. This really is the battle here. A never ending circle till one comes out on top. For G, it is money very well spent to prevent a leronlimab approval, because they know what the cost to them would be if leronlimab were approved.

G can't give up their life blood. They have all sorts of HIV treatments, ART, HAART, long acting agents and they also have a treatment for mTNBC. Leronlimab is a direct competitor for these indications. G can not lose this part of their business, because, this is their entire business really. But leronlimab is a direct threat to all of that and G knows this. I don't think G is willing to give up even one, because if leronlimab received approval in just one indication, it receives indication in all, because by "off label use", leronlimab, with its clean safety profile, would be patient requested for everything and doctors would be willing to prescribe it, as it would in fact heal and patients would pay directly for the medication for the no side effects benefit.

So therefore, G remains persistent in hampering CytoDyn. But CytoDyn also continues on with its own goals and ambitions, albeit more slowly. Slowly, but surely, leronlimab shall be shown superior to G's current treatments. Little by little, it shall be made known, that leronlimab is the superior medication in all these indications. Bit by bit, these indications are again put back into CytoDyn's pipeline, as is currently being done in the mTNBC indication. Doesn't it feel good that the GF has CytoDyn's back when it comes to HIV. But as for mTNBC, who has CytoDyn's back? GSK? Merck? What about in Fibrosis? Madrigal? Novo Nordisk? Eli Lilly?

These are some threats to G, but these possibilities pose another reason why G should double down and could be why they are currently doubling down. CYDY went from $0.45 back to $0.25 in just 2 weeks. The problem at hand, the dilemma we face, is difficult. Almost unsolvable. Neither side is willing to compromise or to give even an inch.

With CytoDyn remaining on its own, without the aid of a partnership or buyout, this battle goes on forever. It is a slow downward spiral by attritional forces imposed by G, but G must remain prepared for a long drawn out war because CytoDyn has many sponsors to bring this drug to its fruition. As I said above, the fight appears to be at sort of a standstill, where a stalemate could be arrived at with minimal advancements made either way, yet the piss poor fighting continues on and on to no end. No answer to it exists except for...

The fact that NDAs do exist. The fact that CytoDyn has NDAs in place but they are keeping that information close to their vest. The information regarding partnerships and licensures. When this information is publicly released, it then leads to a bidding war. The bidding for this tiny company subsequently increases. Yes, this tiny company with zero income, with a large load of debt, and a compromised reputation, receives a bid over and above the value set in the NDA. Yes, it has become obvious, that CytoDyn has successfully and unceasingly worked to restore its reputation and has also branched out in multiple indications, proving its only resource to be effective in a variety of indications, making it extremely attractive to many Big Pharmaceuticals.

Yes, this tiny company actually draws a higher price than its value set in the NDA due to a bidding war. It is either this or Governmental Intervention that begins the Abrupt Turnaround for CytoDyn. These are my possible answers to the current unsolvable dilemma. A bidding war and/or Governmental Intervention fixes the problem. It strengthens CytoDyn so immensely and destroys G's counter opposition completely. This would allow CytoDyn to pursue its pipeline at a much more rapid pace.

A bidding war and/or Governmental Intervention immediately and within seconds dramatically increases share price. It makes it nearly impossible for shorts to try to cover. Gone are all the problems associated with the determination of how the treatments for these indications develop, because the courting entity has the know how and is capable of getting it done on their own.

I suspect that the winner of this bidding war is a large Big Pharmaceutical who is bigger than G, who can set the direction, and who can set the record straight. I see CytoDyn being bought up and then licensed out. The buying company would own CytoDyn, but wouldn't want to Trial each and every indication, so it therefore chooses to license out only the indications which it doesn't want.

At the close of the bidding war, that time period provides many a shareholder an opportunity to exit. Because, CytoDyn would then be owned and operated by another massive entity, larger than G, who acquires the majority of indications, but also chooses to license a few different indications out. These are my thoughts. Hopefully, you agree that this makes some sense.

The timing looks good. Definitely rapidly approaching. By either bidding war or Governmental Intervention, I see the current back and forth situation of strike after strike dissipating rapidly and coming to an end swiftly, as in one full swoop, resulting in the elimination of CytoDyn's opposition and the subsequent provision of all those things necessary so as to advance and develop leronlimab at a pace suitable for its various applications against human infirmity.

I think I share this hope with many here, so, this is just to affirm the reason why we wait. I hope this was helpful.

Sunday post:

MGK_2

Game Changing
Loyal to Truth. This post was inspired by My69z.

Referencing this PR on July 9, 2024: CytoDyn Announces Amarex Settlement,

"The material terms of the settlement are as follows: (i) Amarex will pay $12,000,000 to CytoDyn, $10,000,000 was paid upon execution of the agreement and the remainder to be paid within the next 12 months; (ii) the surety bond, valued at $6,500,000, will be released to CytoDyn in full; (iii) all sums Amarex had claimed as due and payable, aggregating to approximately $14,000,000, will be eliminated, with no payment required from CytoDyn; and (iv) a mutual release of claims, resolving all legal claims between the parties."

Did we actually believe that CytoDyn only settled for just $12 million cash, the release of the $6.5 million surety bond and the elimination of all liability claims totaling $14 million to constitute the entirety of the settlement, when we knew full well that this was only a drop in the bucket of what the punitive and compensatory damages were actually worth? We all knew Amarex caused significant harm to CytoDyn and if justice got its way, was easily worth in excess of 10x this combined $32.5 million.

CytoDyn settled at this low figure, possibly because Amarex likely didn't have the more appropriate funds and their own insurance company also probably was tapped out and limited at $10 million. The $2 million probably came directly from Amarex, which is due by July 2025, together with the elimination of any liability claim and the release of the surety bond, is what was agreed to.

The claims against Amarex were severe and CytoDyn won the arbitration, so the judgement went in CytoDyn's direction. Even though the size of this settlement is paltry, it still represents a decimating blow to the loser. CytoDyn's case was very strong, and if they had the means to extract more, they would have. There just wasn't anything left on the table to take so as to justify an increase in the size of the settlement.

Truth was spoken that day, just not by the magnitude of the judgement. But CytoDyn seemed satisfied. Some expected CytoDyn to crumble under the sheer weight of the costs of litigation. But CytoDyn knew they were wronged and had the proof, and therefore, they proceeded with their claim.

From the most recent Press Release, CytoDyn Announces Promising Survival Observations In mTNBC, and since the entire PR pertains to this discussion, I'll repeat it here in its totality:

"VANCOUVER, Washington, Feb. 24, 2025 (GLOBE NEWSWIRE) -- CytoDyn Inc. (OTCQB: CYDY) ("CytoDyn" or the "Company"), a biotechnology company developing leronlimab, a CCR5 antagonist with the potential for multiple therapeutic indications, today announced encouraging survival outcomes among a group of patients with metastatic triple-negative breast cancer (“mTNBC”) treated with leronlimab. Although mTNBC typically has a poor prognosis, observed survival rates at 12, 24, and 36 months after treatment with leronlimab compare favorably with reported life expectancy after treatment with currently approved therapies. In addition, the Company confirmed that a small group of patients who failed treatment after developing metastatic disease survived more than 36 months after receiving leronlimab, are alive today, and currently identify as having no evidence of ongoing disease.

Following the resolution of the Company’s dispute with its former CRO, CytoDyn obtained follow-up records from patients treated with leronlimab during the Company’s prior clinical trials in oncology. After confirming these patient outcomes, CytoDyn worked with consultants and key opinion leaders to summarize the findings and submit an abstract to the European Society for Medical Oncology (ESMO) Breast Cancer meeting taking place in Munich, Germany, from May 14 to 17, 2025.

“We are encouraged by the longer-term survival data to pursue this potentially paradigm-shifting therapeutic pathway for patients suffering from metastatic triple-negative breast cancer,” said Richard Pestell, MD, PhD, AO, the Company’s Lead Consultant in Preclinical and Clinical Oncology. “As a cancer therapeutic, leronlimab was well tolerated with remarkably infrequent treatment-related adverse events. These promising results suggest further studies with leronlimab are warranted to expand oncology treatment options and improve patient care.”

Dr. Jacob Lalezari, CEO of CytoDyn, added: “These provocative observations of improved survival in patients with mTNBC and prior treatment failure in the metastatic setting, including reported clearance of disease in a group of long-term survivors, provides early clinical evidence of leronlimab’s potential impact in the treatment of TNBC and other solid tumors. I expect the Company’s oncology efforts to accelerate in the coming months, with further announcements in both mTNBC and colorectal cancer.”

Based on these survival observations, the Company has initiated two pre-clinical studies in mTNBC that will evaluate possible treatment synergies between leronlimab, an antibody-drug complex treatment (sacituzumab govitecan), and an immune checkpoint inhibitor (pembrolizumab). The Company will also continue to perform follow-up testing on the group of mTNBC survivors who currently identify as having no evidence of ongoing disease."

With regard to mTNBC while discussing the Basket Trials, In the December 14, 2021 Conference Call, Nitya Ray spoke:

"27:60 Nitya Ray: The BTD application that is submitted is 28 patients from 3 different trials. And out of the 28, 6 had brain metastases. They are all mTNBC patients. So we have submitted all of the results, including all of the patients with brain metastases, now with the FDA and FDA is reviewing it and we are waiting for FDA to respond for BTD application and we expect to hear from them in about 2 weeks. 2-3 weeks. Our CTA application I believe was submitted on November 5. So by January 5, we should hear from FDA. and then we are going to discuss with FDA and see that forward with brain metastases. Now, these are not the only patients with brain metastases because these are mTNBC patients. But, we have other patients in the Basket Trial and not mTNBC, with brain metastases. And so we are very excited about what is happening with these patients. And so we are going to discuss this with the FDA and we do plan, after we receive the response from the FDA on the BTD application that is submitted, we are going to plan for perhaps another BTD just focusing on the brain metastases."

r/Livimmune - Game Changing
In expectation of the results of the mTNBC Clinical Trial, on September 5, 2022, I prepared the following: In Preparation For The Coming Results On mTNBC and wrote therein:

"Come 9/16/2022, we should be able to learn what the more refined PFS is for these 21 patients and what the more refined Overall Survivability is for these 21 patients. The study started 4/22/2019. By 7/19/21, the PFS was 8 months and the OS was 36 months. Since then, 13 months have passed. All in All, the patients were not very healthy. It was a combination of Compassionate Use, brain metastasis and patients had failed 2 other treatment protocols. Patients were treated differently, and may only have received up to 4 doses of leronlimab + carboplatin total while some other received much more, however, leronlimab may have been dosed even after PFS endpoint was reached and after the cancer had returned which may have extended OS. Hopefully, all of this is documented in the results of the trial. From the 7/19/21 PR, we currently had a PFS of 8 months and an OS of 36 months. Since November 2021, the PFS was recalculated to be 6.5 months and the OS became 12.5 months. 10 months have passed since then. Come 9/16/22, could the OS go to 20+ months?"

(How was CytoDyn able to put out in that PR a PFS of 8 months and an OS of 36 months if that period of time had not already passed? In short, they extrapolated.)

But the results of the mTNBC Clinical Trial were never released on the Estimated Study Completion of 9/16/2022. Why not? Knowing now what I didn't know then, I can say now that the data had to have been withheld. CytoDyn never said anything about why they didn't provide these crucial results, but that important data was due then, but it was never presented. Now, with the recent PR, it becomes clear that Amarex withheld the data, so CytoDyn had nothing with which to present. In fact, they had no presentation on 9/16/2022.

The settlement likely gave CytoDyn access to crucial clinical trial data which was previously unavailable to CytoDyn due to the dispute with Amarex. This is supported by the recent announcement of encouraging survival outcomes in metastatic triple-negative breast cancer (mTNBC) patients treated with leronlimab. Why would Amarex hide this data that was crucially important to all of humanity? In an effort to ruin CytoDyn's credibility? In an attempt to paint CytoDyn as duly incompetent? They no longer can claim that CytoDyn stopped payment, because they in fact lost the arbitration. Therefore, what is the truth here? Was there another reason they kept the information?

How much pressure was Amarex really under? Who were they in collusion with? Will this ever be uncovered and revealed? Could or Would the decision of the arbiter bring this information about? Yes, absolutely. What did Amarex need to do to avoid the decision of the arbiter? Settle.

Consider now the affected manuscripts. They probably do require tweaking. From the 12/14/2023 Webcast:

"00:33:19, Dr. Jacob Lalezari:

I've also recently reviewed the cancer data. And it is urgent that we get CD07 (mTNBC) published for that, again, provocative single benefit. So publications, are getting a protocol finalized, off hold, begin the process to implement, get these publications, including the NASH study, the long COVID study, submitted for peer review. I had talked to folks at NIH some years ago about our COVID data in the ICU population. They've been waiting to see the data in a peer reviewed format. And so that's a huge priority for me. And then at the same time, there's no reason why we cannot aggressively pursue partnerships to extend the research platform for leronlimab. And I will commit to that wherever that makes sense. So those are the significant events that, you know, I'll be looking for over the next, you know, two to six months."

r/Livimmune - Game Changing
From the 3/5/2024 Webcast:

"7:07: Turning now to the commitment to prioritize publications of our existing clinical data. I am pleased to announce that we are moving forward with the submission of (4) manuscripts in the coming weeks including (2) papers with 8 of 10 women with triple negative breast cancer. A paper in patients with multi-drug resistant HIV and a paper in patients with Mild to Moderate Covid-19.

7:40: The 1st publication will report on the observations that 8 of 10 women on the 3rd line therapies for triple negative breast cancer had either stable disease or a partial response after 6 months of combined treatment of leronlimab with a chemotherapy agent called carboplatin. This result compares favorably with historical controls.

8:09: The 2nd publication will report (2) further observations that suggests that leronlimab may have a role in the treatment of triple negative breast cancer. First, in the pooled analysis of 28 patients, there appeared to be a signal on the dose response. The patients on the higher 525mg dose of leronlimab, had a modestly increased progression free and overall survival compared to the 350mg dose.

Second, I think most provocatively, the pooled analysis showed that after receiving an initial dose of leronlimab, patients divided into one of two categories. About 25% of the patients had an increase in Circulating Tumor Cells, these are cells that are measured in the blood and can be referred to as CTCs. While about 75% of the patients had a decrease or absence of these CTCs in the weeks following the first dose of leronlimab.

9:17: That differentiation in CTC response in turn appeared to identify which patients subsequently responded to leronlimab with improved progression free and overall survival. Indeed, I believe the data on CTC response, is perhaps the most compelling part of the leronlimab story in triple negative breast cancer and could provide the basis for a screening test to identify which patients are most likely to respond from leronlimab in a follow up study.

I say all this to say, Why did Amarex keep data away from CytoDyn? Why was it part of the settlement to provide data to CytoDyn which had already been due them 3 years earlier? They claim they were withholding it because CytoDyn didn't pay, but since CytoDyn won the arbitration, their argument is null and void and that data rightfully belonged to CytoDyn all the while. Therefore, following the settlement, that data has been transferred to CytoDyn.

" In addition, the Company confirmed that a small group of patients who failed treatment after developing metastatic disease survived more than 36 months after receiving leronlimab, are alive today, and currently identify as having no evidence of ongoing disease.

Following the resolution of the Company’s dispute with its former CRO, CytoDyn obtained follow-up records from patients treated with leronlimab during the Company’s prior clinical trials in oncology. After confirming these patient outcomes, CytoDyn worked with consultants and key opinion leaders to summarize the findings and submit an abstract to the European Society for Medical Oncology (ESMO) Breast Cancer meeting taking place in Munich, Germany, from May 14 to 17, 2025.

“We are encouraged by the longer-term survival data to pursue this potentially paradigm-shifting therapeutic pathway for patients suffering from metastatic triple-negative breast cancer,” said Richard Pestell, MD, PhD, AO, the Company’s Lead Consultant in Preclinical and Clinical Oncology."

The survival data for mTNBC patients is indeed remarkable. Some patients who had failed prior treatments for metastatic disease survived beyond 36 months, are currently alive, and show no evidence of active disease. This outcome is particularly significant given the aggressive nature of mTNBC and limited treatment options available.

Was there something behind that data they wanted to keep from CytoDyn? What did that data show? This is what I'm thinking. The fact that leronlimab eradicates metastatic disease to the brain? The fact that OS could not be definitively stated because patients were still alive? The fact that Circulating Tumor Cells essentially vanished after treatment with leronlimab?

What about the Basket Trial of various tumor types? Recall what Nitya Ray was saying. He wanted to gain BTD on metastatic Brain tumors. There were other tumors in that Basket Trial which could potentially reveal additional positive data. CytoDyn's access to the follow-up records of patients previously treated with leronlimab in oncology trials such as the Basket Trial could lead to even more discoveries across various cancer types

The mTNBC results I was looking for in September of 2022 should soon be revealed at ESMO in May of 2025. Shouldn't these all inclusive results also be incorporated in the (2) mTNBC manuscripts planned for publication as well?

Amarex agreed to provide this missing data which they sat on for years which they knew rightfully belonged to CytoDyn. But, they used the data similar to how hostages are used to negotiate with. As a means to augment the settlement agreement, which they knew fell far short of what it rightfully should have been, then they agreed to provide that data. But the value of this lost and forgotten data could become much more valuable than the one time payment. So that could be why CytoDyn agreed to the terms of the settlement agreement.

Certainly, this is not a fair resolution, but do CytoDyn shareholders have a choice? Not really. We hold and hope for the best. But, if what has been seen thus far holds true going forward, leronlimab becomes the treatment / cure for mTNBC plain and simple. 4 years of OS with no sign of ongoing disease = Cure.

At the time of settlement, they may not have realized that the return of the data which rightfully belonged to CytoDyn was worth far more than the $32.5 million in cash, eliminated liability and returned surety bond.

What else can we expect to come forth from this lost data? Actual OS of mTNBC patients to exceed even what was calculated through extrapolation? 36 months going on 48 months. Cure of mTNBC? The fact that leronlimab eradicates metastatic Brain tumors as Nitya Ray pointed out. How the addition of leronlimab augmented the beneficial effects of the chemotherapy carboplatin while attenuating its inflammatory side effects? Could the data show that there is a means by which we can know which patients respond to leronlimab and which patients will not? Abstract Changes In Circulating Tumor Cells

Is this why CytoDyn accepted the settlement agreement? Because the potential value of the data far exceeds the temporary monetary benefit? And why did Amarex agree to providing this data? Because they knew they could keep the monetary value of the settlement lower by providing the withheld (hostage) data and they didn't want this decision to go to the arbiter because they knew that if the decision was left to the arbiter, then their monetary payments would have put them into bankruptcy.

Why would Amarex withhold data on mTNBC? Life saving data, that could prolong the lives of patients suffering with the disease, and data that could cure patients of that disease? Why was it buried, left for dead? Would Amarex even have an answer? or would their finger be pointed at their Master? The arbiter would have been ruthless, CytoDyn remains cool and composed knowing that Truth is in its hands. CytoDyn has been in a war for so long, they knew the coming data would be well worth the compromised settlement. They knew the data had what it takes to get this mTNBC Clinical Trial back into ESMO, back in front of potential partners in the effort to cure this horrible disease.

This was a massive CytoDyn win against its own CRO parasite that shall be utilized to improve and preserve the lives of patients with mTNBC. CytoDyn finished those who directly attempted to play games with the truth, those who directly manipulated data to serve their own agenda, who attempted to silence them, by withholding their results. All of that has ended and their data shall be seen at ESMO in May. The first step to clearing sickness and disease is to eradicate the cause and that is what CytoDyn did in that settlement. It has cleared itself of its once CRO parasite which acted as a proxy of G.

CytoDyn has been on a Rampage ever since, clearing out its internal enemies and cleaning itself up for the work ahead which it is now in preparation and is undergoing. A Rampage that causes it to become the center of attention in that coming Bidding War. All of this means is that patience is required. That means, we are to live life. Have a really nice Sunday.

I don't see much discussion about Dr NP on here or anywhere else for that matter. Tom was providing a link. If people want to follow it that is up to them.

What is ironic is two of the posts since Tom posted the link are from YOU!

Thanks for posting. When is the sentencing?

Designer_Anteater_18

What if's answered by AI
If Cytodyn cures HIV, what big pharma companies would it negatively impact the most?

ChatGPT said:
If CytoDyn's leronlimab successfully cures or significantly improves HIV treatment, it would pose a major threat to several Big Pharma companies that dominate the HIV/AIDS market. The biggest losers would be:

1. Gilead Sciences (GILD) – HIV Market Leader
Gilead dominates the HIV treatment market, with blockbuster antiretroviral therapies (ARTs) like Biktarvy, Descovy, Truvada, and Genvoya.

Their HIV franchise brings in ~$17B+ annually, accounting for a huge portion of their revenue.

If leronlimab cures HIV or provides a superior treatment with fewer side effects, Gilead could lose billions in recurring revenue.

2. Viiv Healthcare (GSK, Pfizer, Shionogi Joint Venture)
Viiv, controlled by GlaxoSmithKline (GSK), owns Tivicay, Dovato, and Juluca—key integrase inhibitors for HIV.

They generate over $5B annually in HIV drug sales.

Leronlimab could disrupt GSK’s long-term HIV pipeline, forcing them to shift strategies or partner with CytoDyn.

3. Merck (MRK) – Integrase Inhibitors
Merck sells Isentress (raltegravir), one of the first integrase inhibitors used in HIV treatment.

While its HIV portfolio is smaller than Gilead’s or Viiv’s, a cure would make its existing therapies obsolete.

4. Johnson & Johnson (J&J) – Long-Acting HIV Drugs
J&J’s Janssen unit sells Cabenuva, a long-acting injectable for HIV treatment.

If leronlimab eliminates HIV, long-acting therapies like Cabenuva could become unnecessary, hitting J&J’s revenue stream.

5. AbbVie (ABBV) – HIV Drug Components
AbbVie produces Norvir (ritonavir), a key booster drug in many HIV regimens.

A cure would reduce demand for protease inhibitors, impacting sales of Norvir and related drugs.

Big Picture: Billions at Stake
A cure for HIV would eliminate the need for lifelong treatments, which is exactly how Big Pharma profits. The total HIV market is worth over $30 billion annually, and companies like Gilead, Viiv (GSK), and Merck heavily rely on recurring revenues from ARTs.

If CytoDyn succeeds, expect major resistance from these companies, including potential buyouts, smear campaigns, or regulatory hurdles. This is why a grassroots movement and retail investor backing (like the GameStop model) could be critical in countering Big Pharma’s influence and ensuring leronlimab reaches the market.

You said:
If Cytodyn cures mTNBC what big pharma companies would most negatively affected?

ChatGPT said:
If CytoDyn's leronlimab successfully cures or significantly improves treatment for metastatic triple-negative breast cancer (mTNBC), it would disrupt the oncology market, particularly hurting Big Pharma companies that rely on expensive, recurring cancer treatments. The biggest losers would be:

1. Gilead Sciences (GILD) – Trodelvy (mTNBC Blockbuster)
Gilead's Trodelvy (sacituzumab govitecan) is a key drug for mTNBC treatment, bringing in $1B+ annually, with expectations to surpass $5B in peak sales.

If leronlimab outperforms Trodelvy or works without severe side effects, Gilead’s mTNBC revenue could collapse.

Trodelvy is also expanding to other cancers, so a broader application of leronlimab could be even more damaging to Gilead.

2. Merck (MRK) – Keytruda (mTNBC & Other Cancers)
Keytruda (pembrolizumab) is Merck’s blockbuster immunotherapy, generating over $25B per year, with mTNBC as one of its key approved indications.

If leronlimab replaces Keytruda as a more effective, safer alternative, Merck would lose billions across multiple cancer types.

3. Roche (RHHBY) – Tecentriq (mTNBC Immunotherapy)
Tecentriq (atezolizumab) was previously approved for mTNBC but was withdrawn in the U.S. in 2021 due to disappointing results.

Roche still uses Tecentriq in other cancers, and if leronlimab succeeds, it could set a new oncology standard, reducing Roche’s immunotherapy sales.

4. Pfizer (PFE) & Seagen – Antibody-Drug Conjugates (ADCs)
Pfizer’s recent acquisition of Seagen for $43B was a massive bet on ADC cancer treatments, including for mTNBC.

If leronlimab proves superior, Pfizer’s investment in ADC-based breast cancer therapies could backfire, making Seagen’s portfolio less valuable.

5. AstraZeneca (AZN) – Enhertu & Imfinzi
Enhertu (trastuzumab deruxtecan), an ADC developed with Daiichi Sankyo, is expanding into breast cancers, including TNBC.

Imfinzi (durvalumab) is another immunotherapy that could be disrupted if leronlimab proves more effective.

AstraZeneca would lose market share if leronlimab becomes the preferred TNBC treatment.

Why This Matters: Cancer is a Cash Cow for Big Pharma
mTNBC is one of the deadliest and hardest-to-treat cancers, meaning current treatments are expensive, recurring, and highly profitable.

If leronlimab significantly outperforms existing therapies or even cures mTNBC, it could shatter the high-revenue cancer treatment model.

Big Pharma thrives on long-term cancer treatment regimens—a cure would be financially devastating for these companies.

The Big Pharma Playbook: Expect Resistance
If CytoDyn proves leronlimab works for mTNBC, expect Big Pharma to fight back:

Regulatory roadblocks (e.g., slow FDA approvals, added trial requirements)

Smear campaigns to question efficacy or safety

Stock manipulation (short-selling, misinformation)

Acquisition attempts (to shelve or control leronlimab’s release)

This is why a retail investor movement and grassroots campaign could be critical to ensuring leronlimab reaches patients.

You said:
Is there path to regulatory approval for any of leronlimab's indications, would it be possible to partner or license leronlimab for individual indications?

ChatGPT said:
Yes, there is a clear path to regulatory approval for leronlimab in multiple indications, and partnering or licensing leronlimab for individual indications is absolutely possible—and even likely.

1. Regulatory Path to Approval for Leronlimab
CytoDyn has already completed multiple clinical trials and has an open Investigational New Drug (IND) application with the FDA. The main regulatory hurdles involve completing the necessary Phase II/III trials and securing partnerships or funding to do so efficiently.

Current Status by Indication:
Cancer (Oncology) – mTNBC & CRC

CytoDyn received FDA clearance for a Phase II trial in metastatic colorectal cancer (mCRC), which is now being managed by Syneos Health (CRO).

mTNBC data from past trials showed strong survival benefits; if further studies confirm this, it could lead to FDA Breakthrough Therapy or Fast Track designation.

If a Big Pharma partner steps in (e.g., Merck, GSK, or Absci), approval could be expedited.

NASH (Non-Alcoholic Steatohepatitis)

The murine (mouse) study data showed that high-dose leronlimab outperformed Madrigal’s FDA-approved Resmetirom.

A partnership in NASH (potentially with Madrigal or Merck) could allow CytoDyn to skip early-phase trials and move directly to human clinical testing.

Given the huge market opportunity (NASH could be a $30B+ market), this is a prime target for partnership/licensing.

HIV

Leronlimab previously completed a Phase III trial for HIV and received FDA Refuse to File (RTF) due to CMC issues, not efficacy.

If CytoDyn resolves manufacturing concerns and secures a licensing or co-development deal (e.g., with Viiv, GSK, or a Gates Foundation-backed entity), HIV approval could be revived.

A conditional approval or Fast Track designation could be possible for special populations (e.g., multi-drug-resistant HIV patients).

COVID-19 & Long COVID

Past trials showed efficacy in COVID-19 (especially in severe cases), but due to the shifting regulatory landscape, this indication is on hold.

However, Long COVID is still an open opportunity, and new studies could be launched under an Emergency Use Authorization (EUA) pathway if a new outbreak or strong data emerges.

2. Can CytoDyn License or Partner Leronlimab by Indication?
Yes, it is entirely possible to license or partner leronlimab for individual indications—and this is likely the best strategy for CytoDyn given its financial constraints.

Why Licensing Partnerships Make Sense:
Big Pharma prefers targeted, single-indication deals rather than acquiring an entire company.

CytoDyn lacks cash flow, so partnering allows them to get upfront cash and milestone payments without dilution.

Multiple partnerships could exist simultaneously, e.g.:

A cancer partnership (e.g., with Merck for mTNBC/CRC)

A NASH partnership (e.g., with Madrigal or GSK)

An HIV licensing deal (e.g., with Viiv/GSK or a Gates Foundation-backed initiative)

Potential Partner Scenarios:
Indication Potential Partners
mTNBC & CRC Merck, Gilead, Pfizer, AstraZeneca, Roche
NASH Madrigal, Merck, Novo Nordisk, GSK
HIV Viiv Healthcare (GSK/Pfizer), Merck, Gilead, Gates Foundation-backed orgs
Long COVID NIH, Government Grants, Big Pharma with interest in immune modulation
Conclusion: Path Forward
Regulatory approval is achievable—especially in oncology and NASH, where CytoDyn is already advancing.

Leronlimab could be licensed per indication, allowing CytoDyn to retain ownership while leveraging Big Pharma’s resources.

The biggest challenge is securing funding or partnerships—but the right deal could unlock billions in value.

If a grassroots movement and retail investor backing can raise awareness, it might force Big Pharma’s hand to accelerate partnerships or pursue acquisitions.

I'm going to be deleting posts about who is or isn't black ops from here on out. This board is about CYDY. Either stay on topic or don't post.

A string of fascinating messages and replies you might enjoy:

: Katangolo
Dr. J and the Team have been keeping their cards close to the vest. This started before he came on board when we were handcuffed with the FDA hold. We had proactiv videos, YouTube interviews, etc; it all looked like a circus roadshow.

The powers that be didn’t like this for obvious reasons and the pendulum swung back viciously, giving us almost no communication during the Hold. CA Comes in and tells us the pendulum is swinging back and the team tells us we will be pleased with their new approach to communication with shareholders. So we then get quarterly calls and press releases.

Jay comes in with his quarterly letter to shareholders. Not much in terms of conference calls, and Q&A session sessions that we were used to for years. Basically we are told you can submit questions, but nothing’s really ever answered, and there are no direct communications with shareholders outside of the shareholder letters and press releases.

This is frustrating to many out there, but I’m OK with it because I think they have an endgame in mind. Our new PR firm seems to me to be brilliantly, rolling things out in a cadence that leads to the endgame and those with diamond hands, a steel gut and patience can manage this without the fret that other shareholders are experiencing right now.

The approach I see the company taking is - give us a few hints at the direction they are going and they don’t tell us when they begin the studies or the endeavors that they are hinting at but instead let the results happen first, and then inform us. They did this with glioblastoma, they did this with the mash trials, they did this with SMC labs., and they’re doing this with the work that Max, Richard, and Melissa are doing.

Do we think they are not working? Absolutely not. We’re getting breadcrumbs about what they are doing and we are, like I’ve said for a while, putting pieces of a puzzle together. Collecting the breadcrumbs. The real problem, which is actually a gift, are the NDA’s, which are in place. We’ve been told since the times of Scott Kelly that multiple NDA’s are in place. And subsequent levels of leadership have also told us NDA’s are in place.

I believe we are in a silent period now because of those NDA’s. If the suppositions above that I am positing are true, the company can’t say anything to begin with and their m.o. has them with a results first, then inform (shareholders) later, approach.

So back to the question about what is actually going on right now. This has me thinking that the trials with Trodelvy and Keytruda are underway if not finished. Glioblastoma as well. The same possibilities strongly lead me to believe this is the case with fibromyalgia, Alzheimer’s, pulmonary fibrosis possibly HIV and inflammation although my gut says this has been shelved, CRC & mTNBC. Jonah is working hard on an HIV cure and we are getting strong clues that BMGF is involved in probably making moves behind the scenes.

So yes, this is frustrating from a shareholder perspective (or is it?) because we want to know what’s going on and we would like to share price to go up. Come back to the concept of the NDA‘s, which hamstrings the company from telling us anything but allows them to be sitting at a table negotiating with all of the big Pharma, who are salivating over the very real possibility that, through a negotiation, they can get access to controlling and developing this molecule for the indications they are interested in. Hopefully one company wins it all and doesn’t piecemeal the indications but we don’t lose at all if for example, BMFG gets HIV and someone else gets fibrosis, etc.

These negotiations take time. We have a lot of evidence that negotiations are going on right now. Silence is certainly a big clue. So Jay drops a few press releases to keep us happy and let us know what they have been working on and shareholder letters give us clues as to what they actually are working on.

It’s an honor for me to be a part of this group of people; these Internet sleuths, made up of lawyers, researchers, lay people who are investors, doctors, engineers, and beyond. Collectively, we put our pieces out there for each other to digest and synthesize a story that’s becoming more beautiful each day. It helps filling the gaps of the silence we sit with.

But that silence is leading us to what I believe will be the promised land. Patience leads to Patients.

All IMHO and certainly not financial advice. Just hope.

GLTAL



sherlock57
Re: Katangolo #150780
Kat--Appreciate your post on the "radio silence." Like you, I think our patience will be amply rewarded. But I suspect the extended nature of the negotiations probably have a lot to do with the uniqueness of the mab itself--the various indications it can address, the difference in price-point for life-saving drugs (think cancer) versus more maintenance kind of uses (say HIV or AD). And hanging over any potential deal out there, for any of the indications, is the long-acting version under development. What Pharma Co would sign a deal for weekly leronlimab when a longer-acting version is just a few years away?

I also don't think Jacob Lalezari is a "normal" CEO--in other words, he's not just in it for the money. So I think "the vision thing" should be part of the discussion--how does Dr Lalezari want to develop the drug? I don't know how it plays out, but he is the current Vice President of the Board and founding member of NP2, a non-profit Pharma Co whose mission is to reduce the price of generic cancer drugs whose prices have skyrocketed in recent years. I don't think he is going to let his role at NP2 interfere with his fiduciary responsibility to shareholders--I hope not! But I think his humanity will guide--is guiding--some of the decisions that lie ahead.

I can't think of any other drug out there, when it is approved, that can be used for multiple life-saving indications as well as multiple chronic indications. How does one go about pricing leronlimab for a cancer cure--as the recent press release on mTNBC suggests--when it will also be used weekly for inflammation-related indications? Can you price the same drug differently for different indications? If it's priced like a cancer drug, any off-label use would be prohibitive. So I suspect any Big Pharma out there would have to consider these kind of issues when negotiating with Cytodyn. And that's why I'm fine being patient. And I love all this preclinical work and the upcoming clinical trials--we need more hard evidence about leronlimab's MOA and utility in various indications. Even if it takes longer than we might hope.

Personally, I'd like to see Cytodyn partner with someone for one of the inflammation-related indications. (Pick one! Several to choose...). That, along with Gates Foundation money for the HIV cure, would give us enough cash to aggressively go after the cancer indications. And then hand off leronlimab to NP2 when the weekly version of leronlimab goes generic. And we keep the long-acting version for ourselves. And any gene-therapy applications too.

Hey, I'm not a medical professional, or a lawyer or a Wall Street guy. I did go to art school, though, and I'm well-trained to think big, and think creatively. Kat's post was quite thoughtful and detailed, and inspired me to riff off on the above-related concerns, which have been rambling around in my noggin a while now. I'd love to hear any responses from doctors and lawyers and people in the business. And one final thought--when I think about Dr Lalezari, the old saw about TR comes to mind--Speak softly but carry a big stick. To any Cytodyn stockholder, I'd say Lalezari should "Speak softly, and carry a laptop full of unimpeachable data." Not quite as poetic, but appropriate to our situation.

At the risk of sounding like Colombo--you know, "Just one more thing"... I'd like to express my gratitude to the Board and the mods. I feel like I could sit down with any of you here and have a good, reasonable conversation. And remain civil throughout. Can't say that about any other stock message board! Thanks everyone.


Respert24
Re: sherlock57 #150813
Good post, Sherlock57. I wanted to give some thoughts around a few of your points because I see it a little differently.

"And hanging over any potential deal out there, for any of the indications, is the long-acting version under development. What Pharma Co would sign a deal for weekly leronlimab when a longer-acting version is just a few years away?"

I believe the main thing hanging over our heads was lack of robust data, along with, and stymied by, the remnants of what was once an active, well trafficked circus. The tent didn't come fully down until recently, and the bearded lady just finally stopped swinging by to shave in the executive bathroom. The cleanup has been a priority behind the scenes, and as we just witnessed with the mTNBC follow up we were all annoyed nobody seemed to think of doing, there's much more to the Leronlimab story that needs to be told. A guy in a top hat holding a CYDY coffee mug ultimately wasn't going to get the job done, well intentioned or not.

The original plan was to provide just enough compelling signals in a variety of indications to boost the buyout price. It actually came very close to working, but for those pesky kids*.

*the FDA, Amarex, Gilead-stocked DSMB decisions, and more!

The plan now is not much different, except that the data will be more of the unassailable variety and nobody is hawking peanuts or hot dogs. Not to mention the quantity of such data, which together will help dictate any current partnership and/or future buyout with more precision.

That's where the preclinicals are helping our cause. They're inexpensive, all things being equal, and fairly quick too. They help clarify Leronlimab's dosing and potential capabilities in each indication we're trying to grow. Which is necessary to bolster the often-muddied-but-always-compelling sparks of human data we have across all indications.

As for the worry that a long-acting LL being close to reality is dragging out the talks, I'd argue it's not going to get in the way of any current licensing or partnership deal. If anything, it just makes CYDY and LL more valuable. It'll allow whoever owns the drug to extend patent life and broaden LL's market.

The ways and conditions in which Leronlimab will be impactful will be worthy of infomercial-worthy ads. It slices, it dices, it juliennes!

There'll eventually be a variety of ways in which LL is dosed to ensure the right amount of Leron is humping (medical term) the appropriate number of CCR5 receptors for the correct amount of time, and no more or less. So basically, long acting is like, the 10th trick our little pony has in its future. By then, of course, it wont' be a pony any longer but the Secretariat of platform drugs.

Big pharma wants LL for Mash, fibrosis, and/or oncology right this second. The sooner they get it, the less it will cost them on both the front and back end. Because if they wait too long to lock in fibrosis, there's going to be advancements in crc and mtnbc initiatives. Alzheimer's capability will become clear. Glio potential starts to grow fast like, well, a glioblastoma tumor. The price to play goes up substantially every time new data advances one of our indications.

Which brings me to something I've been saying behind the scenes with people. It probably won't be a very long time from the start of a partnership to the offer of a buyout.

Because if you license an indication the traditional way, with the intent to see it through a phase 2 or 3, or through approval, at which point you intend to buy out Cytodyn, that's going to take at least a year on the very aggressive side of things. But more likely a few years. They need to get a trial or trials rolling, see them through, and spend months analyzing the data. By that time there's a possibility (just throwing out hypothetical and hopeful scenarios here) that maybe we learn that the DSMB in the crc trial recommends stopping the trial and giving everyone in it LL based on early success. Or LL helps cure an HIV paitent. The Bill and Melinda Gates Foundation collaborates on HIV and Alzheimer's and we get preliminary data in humans that shows LL slows or delays mental decline.

My point is that each of the fires Jay and the team have going are building in real time. Merck could come in and snag fibrosis and Mash with a killer licensing deal, but long before we get to the traditional buyout period for licensing deals (advancing the drug through phase 2/3 successfully, or winning approval) there's bound to be one or more fires for giant indications like oncology raging damn near out of control.

We're on the cusp of so many huge advances and how it all plays out is anyone's guess. Which puts us in control of our own destiny, just like Jay said. But I think he meant it in terms of having the leverage of multiple, major indications advancing successfully in real time. We don't have to go to anyone, they need to come to us.

So that's why I think we get a strong licensing deal very soon from a company capable of buying us out one day, and that "one day" comes quicker than what traditionally happens. Get in the catbird seat and be in position to buy Cytodyn while three huge indications are just potential versus later when one or two are mere steps from approval and you have to add a zero on the end of your offer to get it through.

You also wrote:

"Personally, I'd like to see Cytodyn partner with someone for one of the inflammation-related indications. (Pick one! Several to choose...). That, along with Gates Foundation money for the HIV cure, would give us enough cash to aggressively go after the cancer indications. And then hand off leronlimab to NP2 when the weekly version of leronlimab goes generic. And we keep the long-acting version for ourselves. And any gene-therapy applications too."

The problem with keeping something for our onesies, is that Cytodyn is not in a position to build out a proper go-to-market team. Nor do they seem to want to. You need a LOT of people to go from four employees and a slew of consultants to running your own regulatory, marketing, and sales teams. The vast majority of small biotech companies take the buyout for that reason. It's truly a job for the big boys, and we'll have a big boy already eyeballing the whole shebang.

But I like your thinking on the GF involvement, and I too think it will play out that way. We're going to have them involved for probably HIV and Alzheimer's (my best guess) and a big pharma partner for fibrosis/Mash. This combo allows us to get all of our initiatives advancing forward as fast and reliably as possible. Money won't be a problem.

But we differ in that I believe somewhere along the line the Merck/Gilead/GSK team is going to have to offer a truckload to buy the whole thing before it's so far along they literally can't afford it.

I don't see our eventual buyout floor being anything less than the $21 billion Gilead paid for Immunomedics, as long as things advance even partially like we all hope. It'll be super interesting to see how this all plays out, who gets in for how much "now", and what that means for the timing and price of a buyout offer down the road. But make no mistake, we're in the negotiating period for the partnerships right this second and could/should hear something at virtually any moment.

Niknak1. the moderators have no control over your request. Please contact Ihub directly and state your case.

https://onco-this-week.com/promising-survival-observations-in-mtnbc-patients-treated-with-leronlimab-announced/

March 4, 2025
Trial Results
TNBC

Dr. Jacob Lalezari, CEO of CytoDyn, added: “These provocative observations of improved survival in patients with mTNBC and prior treatment failure in the metastatic setting, including reported clearance of disease in a group of long-term survivors, provides early clinical evidence of leronlimab’s potential impact in the treatment of TNBC and other solid tumors. I expect the Company’s oncology efforts to accelerate in the coming months, with further announcements in both mTNBC and colorectal cancer.”

Read the full story on "Promising Survival Observations in mTNBC Patients Treated with Leronlimab Announced"

Nice BUILDGOODTHINGS!

A years woth of info here:

https://www.reddit.com/r/Livimmune/comments/1j3p4jf/cytodyn_science_news_since_early_2024_by_disease/


What a summary!!

What is the status of that suit?

Posted By: Katangolo
amFAR just posted this on the website. AI? A question about an HIV cure? A question about cancer cure?

Coincidence? At the very least interesting…

https://www.amfar.org/news/can-ai-help-piece-...r-and-hiv/


Can AI Help Piece Together the Puzzle of Cancer—and HIV?
Cracking the omics code

By Andrea Gramatica, PhD
February 28, 2025
In biology, omics refers to the comprehensive study of the molecules that make up cells and organisms. This includes genomics, for example, which focuses on the entire set of genes, or proteomics, which studies all proteins. These layers of information work together to determine how cells function, interact, and respond to their environment. Understanding omics data is crucial for medical research because it provides a holistic view of biological processes and helps scientists identify disease markers, predict treatment responses, and uncover hidden mechanisms of various conditions.


Towards precision medicine
New technologies now allow scientists to study patients in much greater detail by analyzing their omics data (genes, proteins, and other biological markers). This wealth of data has been instrumental in guiding the development of tailored treatments, marking a shift towards precision medicine—therapies designed to optimize outcomes for particular groups of patients.

A major hurdle in medical research is dealing with incomplete datasets: Genetic, protein, and molecular data often come in fragments, making it difficult to draw solid conclusions. Imagine trying to complete a puzzle with missing pieces; without them, the full picture remains unclear. Scientists face a similar challenge when studying diseases.

Expert puzzle solver
A new study led by Dr. Bo Wang and colleagues at the University of Toronto, Canada, published in Nature Machine Intelligence introduces Integrate Any Omics (IntegrAO), an AI-driven tool designed to integrate fragmented biological datasets in cancer research for more precise classification. By acting like an expert puzzle solver, IntegrAO stitches together different pieces of information, ensuring no valuable data is left behind.

This technology could be a game-changer in HIV research. Over the past 40 years, numerous clinical trials and laboratory studies have been conducted on blood and tissue samples from people living with HIV at different stages of infection, in varied settings, and under diverse treatment regimens. These studies have generated enormous amounts of omics data (spanning genomics, transcriptomics, proteomics, and epigenomics), providing a deep pool of biological information. However, much of this data was collected long before AI-powered tools were available and is not structured for seamless computational analysis. As a result, the sheer volume and complexity of the data remain an untapped resource for advancing HIV therapeutics.

Patterns revealed
The type of approach described in Dr. Wang’s study presents an opportunity to change this. By integrating and harmonizing these fragmented datasets, the model could reveal patterns that were previously inaccessible, uncovering new therapeutic targets and potential pathways to a cure.

As AI-driven tools like IntegrAO continue to evolve, they offer hope for a future where science and technology work hand in hand to deliver more effective, personalized treatments for HIV, cancer, and beyond. This is the dawn of a new era in precision medicine, one where AI helps bridge the gap between big data and real-world patient care, bringing us closer to solving some of the most complex medical mysteries of our time.

Dr. Gramatica is an amfAR vice president and director of research.

"One example: the current CEO of Cytodyn was CMO under Nader Pourhassan the Frauder, and was fine with all his actions."

That is a false statement. It is a matter of public record how Dr JL felt about Nader. Stop trying to make it look like he was complicit with Nader's actions. It looks bad on you and may very well be libelous.

Jake2212 does't post a lot but when he does it is always worth a read:

Posted By: Jake2212
Is Gilead seriously in play to invest in LL for breast cancer? Some may recall my post shortly after last Monday's TNBC PR in which I opined that Dr Jay clearly has a good reason to invest the time and money to conduct another preclinical study for LL in mTNBC, this time with SMC Labs. I assumed then that CYDY's main focus would be on the Keytruda arm, but noted parenthetically that, because we don't know what we don't know, perhaps the Trodelvy arm might actually be the main focus.

Well, faced with the necessity to muddle through another weekend without football games to watch, I revisited the March, 2023, BioSpace article in which Cyrus had waxed eloquent about the ongoing MD Anderson mouse study involving LL and Keytruda, with his expectation of synergistic results. But no results were ever announced. Unless the study was never completed, I would think that both CYDY and MRK were furnished with the results, suggesting to me that either CYDY or MRK may have invoked a NDA to bury the results. That outcome would have been consistent with ohm's prediction that Keytruda would add nothing to LL. Therefore, no synergistic effect.

So why repeat the LL/Keytruda mouse study 2 years later? Well. unless CYDY believes that the SMC Labs mice are considerably more humanized than the MD Anderson mice, the reason escapes me.

On the other hand, Gilead's Trodelvy, the other leading FDA approved treatment for mTNBC, wasn't involved in the aforementioned MD Anderson study, but was the drug that the FDA cited to deny LL breakthrough designation status when CYDY announced LL's mTNBC phase 2 clinical trial results in August and November, 2021. Back then, LL produced a OS (overall survival) endpoint that although only slightly better than Trodelvy's, was still ongoing because more than half of the 26 women from the trial were still alive.

From last Monday's PR we now know that LL's OS was ultimately many months beyond Trodelvy's. The exact difference will undoubtedly be announced at or before the upcoming conference in Munich. Also, bear in mind that 9 of the 26 women in the trial received only 350 mg doses of LL, and only 3 received the maximum 700 mg doses. Given that the 350 mg doses would not have fully covered the CCR5 cells (thank you ohm), it may well be that the final Leronlimab OS data for the other 17 women (if over half are now deceased) will be particularly provocative compared to Trodelvy.

As I now ponder the above info, it seems much more reasonable to intuit that the LL/Trodelvy arm will be the main focus of attention for both CYDY and Gilead. According to Gilead's recently released annual report, Trodelvy produced revenue of 1.3B in 2024, all of it treating breast cancer. In Merck's annual report, I was not able to isolate Keytruda's breast cancer revenue, but I believe it would compare favorably to or exceed Trodelvy's.

MRK's sp has declined about 30% in the last 12 months, while GILD's sp has increased 70% since last June. GILD had 10B in cash at the end of 2024. And ohm has stated in a recent post that he would not be surprised if LL and Trodelvy were to produce a synergistic effect. If that proves to be true, or even if it doesn't, obtaining the use or ownership of a breast cancer drug arguably far superior to Keytruda or Trodelvy would likely translate to billions in new revenues for GILD, and that's without considering the rest of ohm's list.

Admittedly, however, MRK should also be actively engaged with CYDY concerning LL. With a faltering sp, stagnant revenues, and a Keytruda patent cliff now 2 years closer, MRK has good reason to reconsider LL in light of the newly revised Leronlimab OS that has probably already been communicated to MRK by CYDY. Because, if MRK is no longer interested in CYDY/LL, why is Keytruda still being included in the current mouse trial? And what could be better than 2 BP heavyweights being focused on the major impact that using or owning LL could have for them.

Seems very interesting to me. But bear in mind that I don't know what I don't know. And that's always problematic.


MGK_2 responded:

MGK_2
Re: Jake2212 #150709
I put together this analysis on the human mTNBC trial as depicted in this
CytoDyn Announces Preliminary Results from 30 mTNBC Patients Treated with Leronlimab. Decreases in CAMLs after 4 Doses of Leronlimab were Identified in Over 70% of Patients and were Associated with a 450% Significant Increase in Overall Survival at 12-Month Analysis

I go into an analysis of it In Preparation for the Coming Results on mTNBC

Improved Comparison of the previous PR on 7/19 and The Compassionate Use Study of LL in BC

Here is an excerpt:
Quote:
"In standard of care, the majority of TNBC patients do not make it beyond 6-7 months. In the 7/19 PR, all 21 out of the 29 patients who actually responded to the Leronlimab treatment as seen by increases in CAML and / or CTC, remained alive at the 12 month point of analysis. 21 of 29 remained alive at 12 months with a series of (4) 700mg Leronlimab injections with carboplatin, where if they were to have received Standard of Care, they would have died by the 6-7 months point. In the latest PR on Compassionate Use Study of LL in BC, the numbers, claimed are 570-980% increase in Overall Survivability, (OS); this translates into 34 to 59 months of life with scheduled, continuous weekly 350mg Leronlimab injections. That's 3 to 5 years of life with continuous weekly Leronlimab injections."


I put together this post at about that time to determine how they extrapolated to get 4 year OS

Example using Spreadsheet to Estimate Overall Survivability using available Trial Data for future prediction

Here is an excerpt:

Quote:
The Press Release gave a range from 34-59 months as Overall Survivability. The mid point of that is at 48 months or at 4 years. On my hypothetical data example of this study, we have at 48 months: the likelihood of surviving is 46.2%. But 95% confidence interval requires adding and subtracting 17.37% which gives us a Range of 28.83 - 63.57%. 50% is within this Range. So this data set could qualify to be comparable with the actual since this Range include 50% at the same 3 month time interval of 48 months.

Now, in my hypothetical data set presented here, the Overall Survivability occurs at the 3 month time interval of 42 months, since Survivability is 49.6%, (closest to 50%). Here the 95% Confidence Intervals are: 17.5% giving a range of likely survivorship from 32.1 - 67.1%. Since 67% occurs at 24 months and since 32% occurs at nearly 57 months, we have a Range of 24 - 57 months, which is somewhat similar to the results of the Press Release, (34-59) months .


Lastly, previously put together thoughts on BTD
BTD for LL on mTNBC

Here is an excerpt:

Quote:
In contrast, our Compassionate Use Study reveals an overall survivability of 34-59 months, or 3-5 years . This was determined by use of statistical analysis and extrapolating a death rate to determine time at which 50% of original 30 patients would likely be dead by, and that came out to time range.

The FDA recommended withdrawal due to the current landscape of medications for treating mTNBC. Certainly, the FDA is aware of this most recent LL study and how it utterly blows the doors off the outcome from Atezolizumab with Paclitaxel. We just may have been the reason why the FDA made this recommendation.

With regard to BTD, break through therapy designation, I believe Leronlimab is the best drug for mTNBC out there right now. No one can touch our PFS or OS. We double the stand alone Standard of Care Paclitaxel for PD-L1 BC in PFS and OS. We have no side effects stand alone , but in this Compassionate Use Study of Leronlimab in Breast Cancer, LL was combined according to each Treating Physician's Choice with any one single-agent chemotherapy drug administrated according to local practice: eribulin, gemcitabine, capecitabine, paclitaxel, nab-paclitaxel, vinorelbine, ixabepilone, or carboplatin. Side effects of chemotherapy produce considerable morbidity.

I feel momentum growing, excitement is in the air and confidence building with CYDY investors. Thanks for your contributions to this board.

Some nice reading on a lazy Sunday afternoon:

MGK_2

Looking Forward
Welcome Here Folks.

As for me, being honest with myself, I'm not that good at compliments. Many thanks for all your kind words. Let's remember, although it may seem so, I'm not writing for anybody's benefit, really, except for mine. I write as I see fit to document this investment and this particular modality works best for me. One of the best aspects of Reddit is that it is searchable, so that particularly helps me to find things written days, weeks, months or even years ago.

I'm just like all of you, with no inside connections, but I try to make sense of what happens throughout the week and I put it down in writing. I've stayed focused, because, like many of you, I too have a significant portion invested in CytoDyn. This is not a pulpit. I'm in the pew with all of you. As far as teaching, I don't mind. If I can, I put out some posts which educate, but I have to feel it in order to do it.

For instance, yesterday's post, Comparing And Contrasting Murine 1 mTNBC To Murine 2 mTNBC, had a bit of my own thought mixed in there. This paragraph was the brunt of that post:

"This is like a conflict posed to the company. If the combination does well on the first study, do you repeat it again on the second to confirm? If the combination does poorly on the first study, do you repeat it again to make sure? I think in such situations, common sense is used. If the finding is that the combination drug does well is so profound, or if it is only borderline good, then I say that they would decide to repeat the study to confirm the finding one way or the other. If the finding is that the combination did poorly is profound, then, they would decide not to repeat the study. If the initial finding was a borderline poor result, then the decision would be to repeat the study to validate. So with this understanding, and since they are repeating the study, I can rule out that the initial murine study was not profoundly poor using the combination of (leronlimab + Keytruda). Therefore the outcome was either borderline good or bad or profoundly good that the combination drug exceeds monotherapy. It is possible, that the anti-inflammatory effects of leronlimab do in fact improve Keytruda's capacity to destroy the mTNBC tumors."

This was all my own reasoning. We do know for sure that CytoDyn is repeating (or has already repeated) the Murine mTNBC study, but whether or not the Murine 1 mTNBC study showed statistically significant benefit of the combination (leronlimab + Keytruda) over either drug alone, can not be definitively known, at least not from that reasoning. All I was saying was that the combination, more than likely, was not unequivocally worse than Keytruda monotherapy. If that were the case, then why repeat the study? I said that if the results of Murine 1 had showed that the combination was unequivocally superior to Keytruda monotherapy, or even if the results were equivocal, then the study would likely be repeated. These were all my stipulations and I reasoned out my thinking to explain why I made certain conclusions.

It is my firm belief that the leadership at CytoDyn are rational and do think and act rationally. Seems to me that things are in fact panning out for CytoDyn, and that affirms my trust in it's leadership. Otherwise, why would I spend so much time documenting something, if I thought it was doomed to failure? Certainly, I don't believe that, but rather believe in its future success. I hope that comes through in these posts.

CytoDyn is repeating the Murine mTNBC study in combination with Keytruda and in combination with Trodelvy. Here is a ChatGPT comparison of these 2 FDA Approved mTNBC medications:

Comparison of Keytruda vs. Trodelvy in Metastatic Triple-Negative Breast Cancer (mTNBC)
Parameter Keytruda (Pembrolizumab) + Chemo Trodelvy (Sacituzumab Govitecan)
Mechanism of Action Anti-PD-1 immune checkpoint inhibitor Antibody-drug conjugate targeting Trop-2
FDA-Approved Patient Population ~25–40% of mTNBC patients (PD-L1 CPS ≥10) All mTNBC≥2 prior therapies patients after
Median Overall Survival (OS) 23.0 months (PD-L1 CPS ≥10) vs. 16.1 months (chemo alone) 11.8 months vs. 6.9 months (chemo alone)
Median Progression-Free Survival (PFS) 9.7 months vs. 5.6 months (chemo alone) 4.8 months vs. 1.7 months (chemo alone)
Treatment Line 1st-line treatment in PD-L1+ patients 2nd-line or later treatment after prior therapies
Key Benefit Significant OS benefit in PD-L1+ patients Effective in broader mTNBC population
Common Side Effects Immune-related (colitis, pneumonitis, thyroid issues) Neutropenia, diarrhea, fatigue
Key Takeaways
Keytruda is used earlier (1st-line) in PD-L1-positive (CPS ≥10) mTNBC patients (~25–40%), offering a longer OS (23 months) and PFS (9.7 months) compared to chemo.

Trodelvy is used later (2nd-line or beyond) in all mTNBC patients, providing an OS of 11.8 months and PFS of 4.8 months, but still a significant benefit for those who progress after prior treatments.

Conclusion:

If PD-L1 CPS ≥10 ? Keytruda + chemo is the preferred first-line treatment.

If PD-L1 CPS <10 or after progression ? Trodelvy is a strong option in later-line treatment.

where CPS stands for Combined Positive Score. It is a scoring system used to measure PD-L1 expression in tumors.

How CPS is Calculated:
CPS=[(Number of PD-L1 positive cells (tumor cells, lymphocytes, macrophages)) / (Total number of viable tumor cells)] ×100

The higher the CPS, the more PD-L1 expression, which indicates a greater likelihood of response to immune checkpoint inhibitors like Keytruda (pembrolizumab).

In mTNBC, a CPS ≥10 is the threshold for Keytruda approval in combination with chemotherapy.

Murine 2 mTNBC study aims to combine leronlimab with each of these FDA approved medications to determine whether or not the combination product provides a statistically significant benefit over monotherapy of each drug. It also aims to compare and contrast leronlimab monotherapy against both of these monotherapies as well as against the combination therapies. My thoughts were that CytoDyn wouldn't be doing this repeat study unless they initially saw from Murine 1 mTNBC, that the combination with Keytruda was either borderline with or had exceeded Keytruda monotherapy. The combination with Trodelvy is being done as an experiment as this is the first Murine study for Trodelvy against leronlimab. The expectation for Trodelvy is that it too proves to be better in combination than as monotherapy because of the 2 distinct mechanisms of action between Trodelvy and leronlimab.

In addition, CytoDyn has confirmation from its human phase 2 trial that some patients yet remain alive, and having no signs of disease, over the 36 months following administration of leronlimab. That means leronlimab's OS exceeds 36 months for these patients. By the time ESMO comes around in May of this year, these patients would be living for over 48 months, since their last leronlimab treatment. That would make leronlimab's OS = 48 months for these patients. In my book, that would be Cured...

"After confirming these patient outcomes, CytoDyn worked with consultants and key opinion leaders to summarize the findings and submit an abstract to the European Society for Medical Oncology (ESMO) Breast Cancer meeting taking place in Munich, Germany, from May 14 to 17, 2025."

Comparing leronlimab's assumed OS of 48 months in these patients with Keytruda's current OS of 23 months, (from table above), that would be a double or more. We might ask a question, Why is Keytruda's OS more than double Trodelvy's OS? (I just said, leronlimab's monotherapy OS = 48 months in May of 2025 is more than double Keytruda's OS. Why? Because leronlimab treats all MSS Type Tumors via CCR5 blockade.) From table above, Keytruda is only indicated to treat (PD-1+ with CPS >10) Tumors. This represents only 25-40% of all mTNBC tumors. (See the chart above.) In contrast, Trodelvy is indicated for all mTNBC Tumors, (regardless of PD1 and regardless of MSS or MSI Type), but requires at least 2 prior treatments for authorization. These PD-1+ Tumors, though they are mTNBC, they are in fact a fractional part of the 5% MSI Type Tumors and not a part of the 95% more typical MSS Type Tumors. So Keytruda really is just treating another MSI-H Type Tumor and that is why the OS for Keytruda is so high at 23 months. It is as if it is treating HR+ or HER2- Breast Cancer. Where as leronlimab's OS could be found to exceed twice Keytruda's OS and 4 times Trodelvy's, while leronlimab treats the more difficult MSS tumors.

What else would leronlimab add to Keytruda's list of deficiencies? The combination of (leronlimab + Keytruda) MOA could become CCR5 blockade + PD-L1 blockade, which could be superfluous. The FDA could approve All of mTNBC to the combination (leronlimab + Keytruda). The OS could likely exceed 30 months on average. PFS could exceed 20 months.

So, the hope of all this repeat Murine mTNBC study is to determine if leronlimab could provide in combination with the above medications, extended benefits for patients and an extended catchment basin for at least one of these medications, (preferably Keytruda), due to the augmentative effects added by leronlimab.

Merck has a close eye, watching the outcome of this Murine 2 mTNBC study and who knows, this study could already be complete. An excerpt from Undeniable Indisputable And Unequivocal:

"Merck would love to have the 85% that Keytruda leaves on the table, wouldn't they? Look at what they've built with only the 15% their blockbuster treats. Now, with the thousands of tests and trials to expand the use of Keytruda, it becomes obvious that they are desperately seeking a way to treat all the rest."

Like for instance mCRC. But that could really bring in a counter offer from GSK with their Jemperli.

"Our protocol built on the published pre-clinical work of Dr. Dan Linder at the Cleveland Clinic, who demonstrated that leronlimab inhibited metastasis in a humanized Mouse model of colon cancer. As well as the unpublished, clinical observation that four of six patients with colon cancer in our prior basket trial, had either stable, or partially responsive disease up to 11 months after starting leronlimab."

Cyrus Arman describes the mCRC patients in the Basket Trial.

r/Livimmune - 4 of 6 with Stable Disease: No Progression of Disease with Leronlimab
4 of 6 with Stable Disease: No Progression of Disease with Leronlimab
"55:22: So, when we look again at their tumor growth through the spyre grams and through the waterfall plots, that we only had 6 patients here. But as you can see, all of them remain within the stable disease and many actually achieve partial responses over the course of the short study. And one of them actually had no measurable lesions on the PET scan at follow-up. And the remainder saw either stable disease or partial responses."

As you might already sense, as I have recently also realized, that CytoDyn is way ahead of their Press Releases and are doing things way before they even tell us anything about what they are doing. Probably has something to do with their new Press Release company, Gagnier Communications.

So if the Press Releases are behind and Merck with a watchful eye... Who owns those 250,000,000 Institutional Shares again? We know that Merck is absolutely keen about finding a way to extend their patent on Keytruda which is soon to go South in 2028 unless something soon is discovered. If the study is already done and Results are already Resulted, and if the combination (leronlimab + Keytruda) has statistically significant improvement over Keytruda monotherapy... who owns those shares??

As we already know, CytoDyn has much going on in the HIV front. The HIV Cure has taken center stage. With the Patenting of AAV technology and the recent discoveries of both Triple Therapy and LS Mutations which enable leronlimab to cross the placenta, Jonah Sacha is drawing ever so close to an HIV Cure. This has not been unnoticed by Bill Gates at the GF who recently awarded Jonah Sacha another $966,600 towards research on the HIV Reservoir. What happens when the GF actually makes an investment into a partnership which includes CytoDyn? Or is this where those 250 M Institutional Shares went?

We talked in the past about moving from Phase 2 to Phase 3 requiring an investment of some sort coming from Big Pharma, or maybe even from the GF. I think it was that Phase 1 to Phase 2 required the lifting of the clinical hold. Now, CytoDyn is in Phase 2, but to get to Phase 3, a large investment is required. If the 22% Institutional Ownership is in fact real, then we are already in Phase 3.

Seems to me, if u/Upwithstock is correct, then, by 60 days post 1/14/25, (the date when CytoDyn filed form 424B, which would be the date when the 13D entity would have declared to buy 5% of the company), which would be March 14, 2025, by 3/14/25, CytoDyn might officially be in Phase 3 when it could officially be declared by. From the discussion above, the entity could be the GF. It could be Merck. I've said over and over, I think it's GSK because of so many commonalities it shares with CytoDyn. We've spoken about Novo Nordisk too. Hell, it could be G because of both CytoDyn's proximity to the HIV Cure and even to the mTNBC Cure.

CytoDyn is unrelenting as far as the pressure it is applying to Big Pharma on so many fronts. Hell in HIV, CytoDyn is pushing Cure. In mTNBC, CytoDyn is pushing Cure. In Fibrosis, the removal of. A whole new world abides beyond the curtain in long acting leronlimab. And that curtain is about to open. It goes on an on. In addition, CytoDyn is gaining favor with some big players such as the Gates Fund. The Gates Fund is gaining the favor of the new DJT administration. I definitely see the favor of a GSK and a ViiV if they prove not to become partners, both still want an HIV Cure. I definitely see a Novo Nordisk or an Eli Lilly interested at least in a licensing deal or even Madrigal at some point wanting a licensing deal. Alzheimer's Disease is on the way and so is Chronic Fatigue Syndrome. Unrelenting and Unstoppable.

The only way CytoDyn stops is via Buy-Out. Otherwise, CytoDyn doesn't sleep. It goes back to war. It is done resting. It did that for 2 long years getting the hold lifted. We are in the game, and can not be knocked out, unless of course, a buying company buys and then shelves leronlimab. May it never be, but that is a possibility, unless of course, we vet/examine the buyer extensively. Since it is Dr. Lalezari's purpose to place this company in the hands of someone who absolutely gets leronlimab FDA approved, therefore, I leave this determination, as to who to sell to, in his hands.

If there is any inkling of proof that G is behind the short selling or behind the market makers or behind what Amarex did, then in no way should they be the buyers. In no way should they have over 5% control either, especially not at $0.15 / share. Or are these Institutional Shares reserved for purchase at a somewhat higher price? Even if they are bought at $1/share, I don't believe G's intentions or end game would be shared by Dr. Lalezari. Let's see what happens here. Intentions of the buyer are very important.

CytoDyn is not going to abandon its game because of a 22% interest which may not be aligned. But, I don't believe Dr. Lalezari would permit such an interest at 22% had it not been aligned with his overall game plan. CytoDyn has been on this same trajectory ever since Dr. Lalezari came on board and this is the trajectory we remain on. We are getting somewhere, and shall not be derailed.

Again, we need to wait and see. Time is approaching. 3/14/25? Don't really know, but sure does seem very close.

MGK_2

Comparing and Contrasting Murine 1 mTNBC to Murine 2 mTNBC
Just wanted to extrapolate a bit to compare and contrast the prior MD Anderson Cancer Center murine 1 study in metastatic Triple Negative Breast Cancer with the current murine 2 study in metastatic Triple Negative Breast Cancer. (mTNBC)

Here is the Time Line History:

In October 2021, This BioSpace copy of CytoDyn's Press Release CytoDyn Announces Study To Evaluate Potential Synergistic Effects Of Leronlimab With Immune Checkpoint Blockade ICB, lays out murine 1 mTNBC study. CytoDyn

"today announced a study for treating triple-negative breast cancer (TNBC) with leronlimab in a humanized TNBC xenograft model. This investigator-initiated study is being led by Jangsoon Lee, Ph.D., assistant professor of Breast Medical Oncology Research at The University of Texas MD Anderson Cancer Center*.*

The study is intended to determine the potential synergistic therapeutic efficacy of leronlimab in combination with immune checkpoint blockade (ICB) to attempt to raise the standard of care for breast cancer patients.
...
We are also very grateful to Dr. Scott Kelly for arranging for this study to be conducted by Dr. Jangsoon Lee, assistant professor of Breast Medical Oncology Research at The University of Texas MD Anderson Cancer Center*.”"*

This raised the question, "Which Immune Checkpoint Blockade (ICB) was being tested in combination with leronlimab?"

The following gives an idea of how much time would be necessary for the result. 6 weeks of mouse time is equivalent to 6 years of human life. Therefore, not even a few months would be necessary to determine the approximate effectiveness of an ICB combined with Leronlimab in the treatment of mTNBC. Let's say that leronlimab has an overall survivability (OS) of about 13 months and a progression free survival (PFS) of about 6 months for mTNBC. Let's triple that for HR+ and HER2- type breast cancers where OS = 36 months and PFS = 18 months. Therefore, if 6 mice weeks = 6 human years, then 3 mice weeks = 3 human years. So therefore, the results of the effectiveness of this combination of medications should not take long at all. If the combination medication was very effective, even allowing these mice to survive for just 4 weeks, or 5 weeks after being inoculated with the cancer tumors, then we can know that the combination is very effective in MSS tumor types. MSS being Microsatellite stable, which are a type of tumor which are very difficult to treat, but 85% of breast cancer is MSS. Keytruda alone is only indicated currently to treat MSI or Microsatellite Instability. But, Keytruda + leronlimab could become indicated to treat the MSS tumor population or about 2,000% more than what it currently treats in breast cancer alone. If it is found that leronlimab allows some of its mTNBC patients to remain alive for 4 years after treatment, they would be considered Cured. mTNBC patients usually don't live beyond 1 year following diagnosis. HR2+ and HER2- patients could live 3 years post diagnosis, but not mTNBC patients.

Now, the results of this study were never publicly released because the data was owned by MD Anderson. Scott Kelly originally set the trial up with MD Anderson in partnership with CytoDyn. The data was only disclosed to CytoDyn, but the hard data & Results were not given to CytoDyn. They were only shown the results. If they wanted the hard results to work with the data, they would need to purchase it from MD Anderson and that was not done because of costs. But they saw what they needed to see.

They wanted to determine whether there was any benefit to combining leronlimab with a check point inhibitor, PD-1 blockade, and they had a look at the data and got an answer, but never said one way or the other what they found.

Continuing on with the time line, 18 months after murine 1 mTNBC started, in March of 2023, in the BioSpace Article Embattled CytoDyn Sets New Course Towards NASH, Tough Tumors, Cyrus Arman related,

"Along with NASH, CytoDyn will focus primarily on oncology*. Here, the company* will target colorectal cancer and hormone receptor-positive, HER2-negative breast cancer.

These are both areas where checkpoint inhibitors have failed to show efficacy when added to a standard-of-care backbone, Arman said, adding that leronlimab has shown positive signals in both.

“From a mechanistic standpoint, we believe we could get a synergistic effect with a checkpoint inhibitor,” he said.

Leronlimab is currently being trialed in combination with Keytruda (pembrolizumab) in a breast cancer xenograft model in partnership with MD Anderson Cancer Center.

Arman said CytoDyn expects to observe an enhanced anti-tumor effect from the combination and identify immunological biomarkers.

In terms of future partnerships, Arman isn’t concerned that CytoDyn’s history will have a negative effect.

“I think that most companies are data-first,” he said. “If we come and we show the data that we have…I think they’ll see, here’s an organization that has transformed from what it used to be.”"

Cyrus let us know, that the Immune Checkpoint Inhibitor was with Merck's Keytruda, pembrolizumab. "Arman said CytoDyn expects to observe an enhanced anti-tumor effect from the combination and identify immunological biomarkers." But Cyrus said this 18 months after the study began. Does that make any sense? By that time, the study had already concluded. CytoDyn had already been shown the results. CytoDyn already knew whether or not there was an improvement over leronlimab monotherapy by combining leronlimab with Keytruda against mTNBC. Nevertheless, Cyrus made the statement and he was comfortable making this statement in the BioSpace Article 18 months after the study began. CytoDyn was comfortable because the outcome of the study was likely favorable towards the combo treatment over leronlimab monotherapy."

Yet another 18 months of mTNBC hiatus passes, and then in the September 2024 Letter To Shareholders, mTNBC is reintroduced:

"In addition to CRC, CytoDyn is investigating the role for leronlimab in two other oncology indications via strategic and low-cost research and development opportunities*, and in collaboration with several reputable institutions. I am pleased to announce that CytoDyn is working with a team of experts to resume the exploration of* Triple-Negative Breast Cancer (“TNBC”), including colleagues from the University of Hawaii Cancer Center, MD Anderson Cancer Center, and the Pennsylvania Cancer and Regenerative Medicine Research Center*. We will be working with this team in the coming months to design and conduct a preclinical TNBC study that will aim to confirm the mechanism of action of leronlimab in oncology and address the question of* potential synergies with both antibody-drug conjugates and immune checkpoint inhibitors*. The Company intends to use this preclinical study to form the basis for a potential partnership and better inform the design of a follow-up clinical study in patients with metastatic TNBC."*

Then, close to Thanksgiving time of 2024, CytoCyn Appoints Richard Pestell MD, PHD As Lead Consultant In Oncology.

"He is currently the President of the Pennsylvania Cancer and Regenerative Medicine Research Center*, a part of the Baruch S. Blumberg Institute in Doylestown, Pennsylvania. Prior to this role, he spent a decade at Thomas Jefferson University in Philadelphia, Pennsylvania, serving as Director of the Sidney Kimmel Cancer Center, Chairman of the Department of Cancer Biology and Executive Vice President. Dr. Pestell’s work has been published in over 600 publications, and his research has been credited with well over 95,000 citations. He previously served as Vice Chairman of the Board, and* Chief Medical Officer (CMO), spearheading the Company’s successful effort to obtain Fast Track Designation from the FDA for the use of leronlimab in combination with carboplatin for the treatment of patients with CCR5-positive metastatic triple-negative breast cancer. In addition, Dr. Pestell was instrumental in designing and initiating CytoDyn’s Phase 1b/2 clinical trial in that indication*."*

Lastly on the Timeline, most recently, on February 24, 2025, CytoDyn released CytoDyn Announces Promising Survival Observations In mTNBC Patients Treated With Leronlimab. This Press Release discusses the Phase 1b/2 clinical trial that Dr. Pestell initiated referenced just above. The resulted data of that clinical trial were delayed due to the actions of CytoDyn's CRO at the time, Amarex. Over the past few years, CytoDyn worked to obtain this data and has the results.

"...today announced encouraging survival outcomes among a group of patients with metastatic triple-negative breast cancer (“mTNBC”) treated with leronlimab.

... In addition, the Company confirmed that a small group of patients who failed treatment after developing metastatic disease survived more than 36 months after receiving leronlimab, are alive today, and currently identify as having no evidence of ongoing disease*.*

... Following the resolution of the Company’s dispute with its former CRO, CytoDyn obtained follow-up records from patients treated with leronlimab during the Company’s prior clinical trials in oncology. After confirming these patient outcomes*, CytoDyn worked with consultants and key opinion leaders to summarize the findings and submit an abstract to the* European Society for Medical Oncology (ESMO) Breast Cancer meeting taking place in Munich, Germany, from May 14 to 17, 2025*.*

“We are encouraged by the longer-term survival data to pursue this potentially paradigm-shifting therapeutic pathway for patients suffering from metastatic triple-negative breast cancer,” said Richard Pestell, MD, PhD, AO, the Company’s Lead Consultant in Preclinical and Clinical Oncology. “As a cancer therapeutic, leronlimab was well tolerated with remarkably infrequent treatment-related adverse events. These promising results suggest further studies with leronlimab are warranted to expand oncology treatment options and improve patient care.”

Dr. Jacob Lalezari, CEO of CytoDyn, added: “These provocative observations of improved survival in patients with mTNBC and prior treatment failure in the metastatic setting, including reported clearance of disease in a group of long-term survivors, provides early clinical evidence of leronlimab’s potential impact in the treatment of TNBC and other solid tumors*. I expect the Company’s oncology efforts to accelerate in the coming months, with* further announcements in both mTNBC and colorectal cancer*.”*

Based on these survival observations, the Company has initiated two pre-clinical studies in mTNBC that will evaluate possible treatment synergies between leronlimab, an antibody-drug complex treatment (sacituzumab govitecan), and an immune checkpoint inhibitor (pembrolizumab). The Company will also continue to perform follow-up testing on the group of mTNBC survivors who currently identify as having no evidence of ongoing disease."

So, this last paragraph is where we are at right now. End of the History Time Line. Discussion.

Everything written in this most recent February 2025 Press Release was also known in the September 2024, Letter To Shareholders. They are way ahead of what they announce. In September, 2024, CytoDyn knew they would be doing murine studies again in mTNBC.

"We will be working with this team in the coming months to design and conduct a preclinical TNBC study that will aim to confirm the mechanism of action of leronlimab in oncology and address the question of potential synergies with both antibody-drug conjugates and immune checkpoint inhibitors*. The Company intends to use this preclinical study to form the basis for a potential partnership and better inform the design of a follow-up clinical study in patients with metastatic TNBC.*"

They knew back in September, 2024, that they would be combining leronlimab with both Gilead's Trodolvy (sacituzumab govitecan) and Merck's Keytruda (pembrolizumab). February 2025 PR was just a delayed release of knowledge which they already had back in September of 2024. They needed the time in between for Pestell to come on board, and his team of experts to get organized to take a look at the prior MD Anderson murine 1 study which was set up by Scott Kelly, and extract out of it, the pertinent information which would be useful and design and initiate an appropriate combination murine 2 study in mTNBC that would use leronlimab in combination with both Keytruda and Trodelvy.

My main question is, "Why did they choose to include another combination of leronlimab + Keytruda?" Remember, Cyrus Arman hinted that the results were good?

“From a mechanistic standpoint, we believe we could get a synergistic effect with a checkpoint inhibitor,” he said.

Leronlimab is currently being trialed in combination with Keytruda (pembrolizumab) in a breast cancer xenograft model in partnership with MD Anderson Cancer Center.

Arman said CytoDyn expects to observe an enhanced anti-tumor effect from the combination and identify immunological biomarkers."

This is like a conflict posed to the company. If the combination does well on the first study, do you repeat it again on the second to confirm? If the combination does poorly on the first study, do you repeat it again to make sure? I think in such situations, common sense is used. If the finding is that the combination drug does well is so profound, or if it is only borderline good, then I say that they would decide to repeat the study to confirm the finding one way or the other. If the finding is that the combination did poorly is profound, then, they would decide not to repeat the study. If the initial finding was a borderline poor result, then the decision would be to repeat the study to validate. So with this understanding, and since they are repeating the study, I can rule out that the initial murine study was not profoundly poor using the combination of (leronlimab + Keytruda). Therefore the outcome was either borderline good or bad or profoundly good that the combination drug exceeds monotherapy. It is possible, that the anti-inflammatory effects of leronlimab do in fact improve Keytruda's capacity to destroy the mTNBC tumors.

Considering the above paragraph, it is my suspicion that CytoDyn has chosen to repeat the combination of (leronlimab + Keytruda) in the new murine 2 studies with Richard Pestell against mTNBC because the initial MD Anderson murine 1 study probably did show that the combination of these two drugs was better than leronlimab alone against both MSS mTNBC. I tend to believe that if the original MD Anderson murine 1 study did not show any improvement what-so-ever of the combination of (leronlimab + Keytruda) over leronlimab monotherapy, then they would not have decided to confirm their findings by including Keytruda, in this second up coming study. There was enough good in the initial murine 1 study to warrant a repeat and confirmation of those good findings. Why validate a profoundly poor result by making the same mistake twice? Rather, the decision to validate the good is profoundly better.

If this conjecture proves to be the outcome of the 2nd murine mTNBC study, then this combination of (leronlimab + Keytruda) would give Merck the indication to treat 100% of MSS mTNBCs. Merck already has Keytruda's right to treat MSI mTNBC tumors. Right now, Keytruda alone may treat MSI type tumors, but not MSS type tumors. That is only 15% of all mTNBC tumors. But, if this combination is proven to be more effective than leronlimab alone, then 100% of mTNBC tumors become treatable by the combination drug. Chances of Merck offer just went up greatly.

As for Gilead's Trodelvy, sacituzumab govitecan, the combination of this antibody-drug conjugate with leronlimab, would be the 1st time this combination is being studied, but could very well be better than leronlimab alone by simply considering the fact that each drug has its own distinct mechanism of action and the combination could prove to exceed the monotherapy of either. Leronlimab's anti-inflammatory effects could bolster Trodelvy's capacity to fight the disease and make its contribution much greater that without leronlimab. If this becomes the outcome of this combination study, the possibility of getting an offer from Gilead greatly increases. Because, then, CytoDyn would have virtually (2) Cures in Indications Gilead already is in, HIV and mTNBC.

When we get to European Society for Medical Oncology (ESMO) Breast Cancer meeting taking place in Munich, Germany, from May 14 to 17, 2025*.* , these patients will already have been Breast Cancer Free for 48 months, in other words 4 years without BC = Cured. The Company will also continue to perform follow-up testing on the group of mTNBC survivors who currently identify as having no evidence of ongoing disease.

The implications that what Richard Pestell & CytoDyn are doing in conducting this confirmatory combination murine 2 study in mTNBC are huge. You don't repeat a study when initially, it's a total failure. We already know it is not a failure from the human trial, because as stated in the latest Press Release, some patients are still alive nearly 4 years after taking leronlimab, when most would have already died at most 1 year after contracting the disease. Remember, don't confuse mTNBC and HR+ or HER2- cancers. CytoDyn is expanding on what they already know from prior human trials and prior murine studies. More specific knowledge shall be gained, such that the next human clinical trial in mTNBC leads to leronlimab's approval. What a journey Folks!

Maybe this will help. Price performance od CYDY:
5-day 3.33%
10-day 40.91%
1-month 19.23%
3-month 158.33%
6-month 138.46%
YTD 181.82%
1-year 93.75%

Wonder which entity will be the first to want to trial the fibrosis indication using LL? GSK? GILD? PFE? MRK?

https://www.smccro-lab.com/news/cytodyn-reports-significant-fibrosis-reversal-in-smc-lab-studies/

2025.02.28

CytoDyn Reports Significant Fibrosis Reversal in SMC Lab Studies
In a great collaboration with CytoDyn Inc., we are pleased to share promising preclinical results demonstrating the efficacy of leronlimab (a CCR5 antagonist) in liver disease models. Using our STAM (MASH-HCC) and CCl4-induced liver fibrosis models, leronlimab monotherapy successfully reversed liver fibrosis—an area with significant unmet medical need.



These findings suggest that leronlimab’s anti-fibrotic potential may extend beyond liver disease, with possible implications for other fibrotic conditions, such as those affecting the lungs and heart.
We look forward to its continued development and success.



For more details, please see the press release:

CytoDyn Announces Findings of Statistically Significant Fibrosis Reversal Across Studies with SMC Laboratories

Yeah they've been pretty guarded with LA LL details to date. We know the multiple new formulations are key to future plans. I look forward to getting an update along those lines.

I would expect something about the CRC trial before then.

Let's hear it.

There are a ton of members reading along.