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Interesting that the closer to the conference call the more hysteria there is.
Impossible to set a target right now.
After it tops out and runs into the massive resistance it and begins to stall
Stay tuned for the next target after this Bounce(before the next trounce) ends in a day or two. Recall I said it would bounce. .... after which, KAPLUNK!!
With those dead cat bounces going ever higher, pretty soon that dead cat will reach the moon.
Here, the evidence here is very narrowly tailored to viremia in critical covid-19 cases in which there is immunological exhaustion of CD8+. I'd be dang skeptical about generalizing to viruses in throat or nose tissue and to cases where there is no reason to suspect CD8+ exhaustion.
Additional pathways induced by CCR5, include the PI-30 K pathway and
thereby PDK1 and the serine/threonine kinase protein kinase B (AKT), which in turn induces cell survival, glycolysis, cell proliferation, growth and proliferation of progenitor and stem cells, immune cell differentiation, and the release of eIF4E to promote cap-dependent translation
None of those drugs has ever been tested in combination with leronlimab. If you look at that list they threw every monoclonal antibody and immunomodulator at it, which is complete nonsense.
I pulled one out of the mix at random (Codrituzumab) just to see. Codrituzumab is an Anti-glypican-3 monoclonal antibody. Inhibiting glypican-3 increases caspase-3 which results in tumor cell death. Leronlimab blocking CCR5 also increases caspase-3 leading to tumor cell death. No negative drug interaction and most likely no added benefit.
Tomorrow Is A Good Day To Buy
An example of biotech penny stocks on IHUB
No offense taken. You aren't going to know what my knowledge level is and a year ago I knew very little. It's always best to question because there's a lot of BS flying around.
The reason I am interested in this particular question is because my working hypothesis is that, for the most part, the immune system knows what it is doing.
Also, they do not demonstrate that the inflammation in a cold (sore throat, runny nose) is the result of immune system overreaction; they hypothesize that it is overreaction because they were impressed by how many chemicals were involved: why would there be so many chemicals involved in such a non-serious infection?
They list a bunch of chemicals that they noted were upregulated in rhinovirus infection. RANTES (CCL5) and IL-6 were not mentioned. Dr. Patterson's paper did not show much change in other indicators (besides CCR5 occupancy and viremia), so it's not obvious that leronlimab would help with the inflammation.
Conrad says "Those shares ain't going to move themselves."
Total shares authorized: 1,490,000,00 as of date: 3.31.20
Authorized Shares 5,000,000,000 06/01/2020
I was once pretty sick and went to a Dr and ask for some antibiotics. He asked when my symptoms start and I told him it happened few days back. After hearing what I said, he refused to give me the prescription for the antibiotics. He said it is only effective within the 1st 48 hours
You don't think I know what I'm talking about, no problem. You need outside confirmation, here you go.
Forty-eight hours after inoculation, the expression of 6,530 genes in infected volunteers were significantly either up-regulated or down-regulated compared to the same genes in the control group. In other words, rhinovirus infection triggered a massive immune response in the nasal mucosa. Because rhinovirus is not as destructive as other more serious viral infections, this response appears to be disproportionate to the threat.
The researchers classified the active genes according to function, and found many involved in a process known as chemotaxis, which recruits various immune cells to the site of infection. These particular genes have been correlated with symptoms such as inflammation, congestion and runny nose. Other groups of active genes have also been classified; among them are genes which make antiviral compounds thought to help thwart infections.
"This study shows that after rhinovirus infection, cold symptoms develop because parts of our immune system are in overdrive," said Lynn Jump, Principal Researcher at P&G and study author. "The findings are important because they provide us a blueprint for developing the ideal cold treatment: one that maintains the body's natural antiviral response while normalizing the inflammatory response."
The under cover footage seems to be of stock footage and clips. What's undercover about that? 51 cards short of a deck.
Rashid Ali Buttar is an American osteopathic physician, conspiracy theorist, and anti-vaccine proponent from Charlotte, North Carolina. He is known for his controversial use of chelation therapy for numerous conditions, including autism and cancer.
I saw on Dr. Dalton's twitter he won the IFAH Top 100 Healthcare Leaders Award. He seems in good company.
Vasayo Accoladed The “Top 50 Companies in Health Care” Award at IFAH, Vegas 2019
https://floridajustice.com/vasayo-new-magic-pill-mlm/
Is there a similar problem with rampant IL-6 levels and CD8+ cell exhaustion in common cold? I'm dubious. I'm also dubious that using a powerful immunosuppressant in a normal, mild infection is wise. Normal, acute inflammation is a natural immune system response in fighting off viral infections.
The side effects of the common cold are caused by inflammation. Leronlimab boosts the immune system by downregulating inflammatory M1 macrophages and preferentially upgrading M2 macrophages (CD8+ T-cells) and natural killer T-cells. The exact same MOA as for COVID-19.
However it's not a really cost effective way to treat a cold.
It's 3:20 Pm Eastern Standard Time.
The exhaustive list of indications for Leronlimab has not yet been defined.
Paying $7 B for a non-revenue company is not cheap. You can keep on talking astronomical numbers but market reality is what will drive the final price.
I’m certain there is a silent majority of major shareholders that would entertain $10.
IL-6 inhibitors that do a half-assed job, lower immune response to make fighting the virus harder and have bad side effects are hardly amazing.
Any reasonable offer
These won't be.
Leronlimab - Disease List (updated)
The loosening of restrictions means it will still be around though at a lesser level.
Doctors will perform interventions in the placebo group if necessary which is why leronlimab will be approved on secondary endpoints. Of course the best intervention is leronlimab and I'm sure the results of those who have had intervention will be written up in a supplement to the FDA submission.
Gilead has no SEC financial filings listed before 1996 Even though it's IPO was 1992. So what were they hiding?
I would expect IV to ramp up the same bioavailability within 24 hours that it takes 3 days for via subcutaneous injection.
I'm surprised it's that high. He must have averaged up some. I started buying a bit earlier so I averaged down to .40.
Being large molecule leronlimab has almost no bioavailability if taken orally. That why it's either administered IV or subcutaneous.
Sounds like Gilead circa 1989.
I have a bottle of snake oil to sell you.
As far as Taiwan goes they have a basket trial for cancer starting there.
Not much of a dump if it's going up.
You trust analysts? You must be new to investing. They obviously haven't considered a product that actually works coming along and taking away that market share. But it's sure nice to know how much the drug that's going to do it is worth.
How stupid are those geniuses on Wall Street
So where is CYDY's proof of applying for a uplist?
Only a JAK inhibitor, guess what drug does that and oh so much more. Here's a hint, it's not owned by Gilead. Once again Gilead will suffer.
Roche's Actemra
CYDY is on the OTCQB market which has higher standards than the pink sheet market. Audited annual financials and we follow the SEC Reporting Standard.