This part is also typical pumper mode.

{{Possibly most exciting in the mid-to-long term in our view, could be ongoing investigations involving immune checkpoint inhibitors, such as those targeting PD-1/PD-1L or CTLA-4. Peregrine is
currently conducting pre-clinical studies and could begin clinical work yet this calendar year.}}


Everybody and their uncle is talking about how wonderful their drug will be in combination with drugs targeting PD-1. Hell, SNTA just showed some preclinical data of Genetespib with such drugs too, and it was impressive. So what. It is absurd, and likely a touch desperate to be citing pre-clinical data as some major price driver.

The idea of some partnership this year for PPHM seems quite far-fetched, unless it was some horrid deal for them. At least Piper guy didn't spew forth sheer non-sense that Bavi is going to get a breakthrough designation as some pumpers on seeking alpha or the IHUB board keep saying.

I love the old unnamed sources comments. Reuters claimed last week that their unnamed sources said Pfizer wasn't interested in ONXX because it was too expensive. Bloomberg today cited unnamed sources as listing Pfizer as one of the companies interested in ONXX.

Cyncical trader, thanks for the article. If it pans out, I could see how such a drug would be a boon for paralysis patients.

{{SNTA—What did you find idiotic?}}

Perhaps simplistic would have been a better word.

{{Here's the Street's Adam Feurstein with the super cynical take: "If you close your eyes tight, ignore real data, and drink subgroup-flavored Kool-Aid, ganetespib wins."}}

What was idiotic was when Feuerstein said SNTA pulled out the >6 month group out of thin air.

It isn't as SNTA zeroed into 5% of the patients. They identified a patient population early in the Galaxy I trial and have been collecting more data on this group as the trial progressed. Perhaps Feuerstein didn't recognize that the latest ACSCO update had a large batch of newer patients, this significant benefits for Ganetespib are quite clear in patients. What is key is that benefits remain clear, but that there still remain a decent number of censored patients in around the 6-8 months, which more in the Ganetespib + DOC arm than DOC only. How these play out when the data matures is the key.

I like reading his comments, but Adam Feuerstein can sure say some idiotic things.

{{As opined on the CC today our guys expect a large synergistic effect from a combination bavi/PD-1 or PD-1L trial and preclinical work on such is now being done. }}

Robert, that is what a lot of companies are saying after the impressive data from the PD-1 and PD-L1 at ASCO. The key is for such companies to actually provide clinical data to back it up.

{{I suspect CLDX, rightly or wrongly, is being linked to the ONXX buyout scenario. As the bids start to go up for ONXX, CLDX may continue its meteoric rise as well. It may not be rational, but who says the Market is rational? I'm just riding the wave here.}}

Bladerunner, I don't know enough to make an intelligent comment on CLDX, but they now have a market cap of $1.7 billion. I don't think they have any drugs beyond phase II. Is that correct? From a superficial perspective, it looks a bit like EXEL when they surged to around a $1.5 billion market cap last year then were cut in half.

Could some CLDX shareholders give me a brief intro as to why they are so high on the company's prospects?

Thanks.

Vinny

Stopping the formation of plaques in Alzheimers may be counter-productive. Recent data suggests that the soluble oligomers are the toxic form and plaques are a means of detoxification or miminizing that toxicity. That would explain why so many Alzheimer's drugs designed to impede plaque formation have failed.

http://www.fightaging.org/archives/2013/05/alzheimers-drug-candidate-provides-benefits-in-mice-without-clearing-amyloid-plaques.php

{{The SEC said it believes that the defendants are in, or trading through accounts in, the Canary Islands and Beirut. }}

It wasn't me!

{{You say "The PPHM data in 2nd line NSCLC is trivia, insignificant and limited." It is obvious that the FDA does not advance drugs to Phase III trials based on data which is trivia ,insignificant and limited. Your bias is showing.}}

dia76ca, your post is exactly why I made the comment. The FDA allowing a drug to move to a phase III trials only takes a reasonable assessment that doing so won't cause patients harm. By combining any drug with docetaxel, all a drug would have to do for NSCLC is not increase docetaxel toxicity nor reduce its efficacy. That is it. The Bavi phase II NSCLC trial was corrupted, and the attempt by PPHM to somehow salvage something rests on a very small patient group in the 3mg/kg arm, close to half of whom are censored more than a year after the final data was collected. That makes it both trivial and insignificant.

I did read some people here praising as great news that there may be an interim analysis in the proposed Bavi phase III trial for 2nd line NSCLC. So, when did PPHM officially state this? What did PPHM provide as benchmarks for this interim analysis in the PPHM public announcement? Since you brought up SNTA, I will mention what they did in regards to their FDA approved phase III trial for 2nd line NSCLC using Ganetespib + Docetaxel, which has already begun treating patients. They stated that 2 interim analyses were planned, and gave the expected approximate dates for each, as well as the expected trial completion data. Based on the trial size, SNTA provided the probability for reaching statistical significance at each interim and the final data summary based on a Hazard ratio (HR) of 0.7, 0.6 and 0.5. Obviously this doesn't guarantee success, but you want the company in which you have invested your hard earned money to provide parameters and benchmarks. If PPHM provide nothing of the sort regarding their proposed phase III trial, you have to wonder if they know what they are doing, or how frank and honest they are being with investors. In this regard, I still don't see any reports where PPHM divulged what the MOS was in the control arm of their recently reported data for Bavi in 1st line NSCLC.

I suggest you stop such umbrage when someone doesn't share your rosy views of Bavi. I never said Bavi was crap, or a placebo as others have done. Maybe Bavi will find the right combination drug to work with, but I haven't seen data to support it yet. You have to be cold and hard when investing your money, and bad management is extremely hard to overcome. I know because I underestimated this in the past, and paid dearly for it. I will end with a quote showing some relevant wisdom from "The Godfather" movie. "It's not personal, it's just business."

{{Do your ONXX gains cover your SNTA losses?}}

Don't worry about me. The recent SNTA downturn placed me back at even on SNTA so I don;t have any SNTA losses. By the way, bought back more at $4.60 so I now have more shares than I did before the 2nd interim ASCO data. I have owned ONXX for many years and my average price is a shade over $30 ($30.13 to be exact).


{{You win some...you lose some.}}

Yes.


{{Don't worry about the PPHM data ...the FDA likes it!}}

The PPHM data in 2nd line NSCLC is trivia, insignificant and limited. The FDA is allowing PPHM to move forward because they are using Bavi in a combo with a drug that has efficacy on its own.

ONXX is my largest holding. It was more than 60% of my portfolio before the big jump today, so you know I am smiling. ONXX is a major buyout prospect because they have 3 drugs on the market, with Kyprolis being the major driver. They are also partnered with PFE for another drug called palbociclib, which was granted breakthrough status in breast cancer after increasing PFS from about 7 months to 27 months.

PPHM won't need to have multiple drugs on the market to be bought. They will need a good deal of excellent data from solid, well controlled and large trials. They have noting of the sort to date.

According to the Supreme Court, ONXX should be arrested for prostitution. No I haven't been drinking this afternoon. Well, I have been drinking but not THAT much.

This paragraph was just posted on yahoo finance.

{{NEW YORK (Reuters) - Cancer drugmaker Onyx Pharmaceuticals Inc (ONXX) said on Sunday it rejected a roughly $10 billion takeover offer from larger biotechnology company Amgen Inc (AMGN) as too low but still is considering selling itself.}}


Since the Supreme Court ruled that corporations are people, selling oneself for a price is called prostitution. I rest my case. :)

jbog, Congratulations on your investment successes, and I hope you have more. I was speaking of how you come across, not the value of your contributions. Yes it is important to counter-group think.

Perhaps I was unfair in linking you with Kobers' comments. You do have a good track record, and I will never forget how you were so right about GTCB. There is no doubt that had both Dew and heeded your comments, we would have been far better off. You specifically spoke of the financial crush GTCB was dealing with, and it was on target. I whined about it but didn't act by selling, which was my only real option. Dew finally came to the same conclusion and sold off before rATIII approval. I held on and after rATIII approval, the price surged to where I could have sold off and broke even, maybe even gotten a little profit, but I was too stubborn and too greedy. That is the lesson I won't forget. Thanks for trying to teach me that very early on regarding GTCB. This is when the wisdom of "The Godfather" movies comes into play. It's not personal, it's just business.

I tend to buy and hold or add. I did adopt some of your strategy with SNTA. The idea of considering a core position, and designating a part of it as trading shares. I bought low, and twice sold some at a close to double my initial price buy, then bought back more later when the price dropped significantly. I was back to my original total shares with cash in the bank. It is a nice strategy. I then reverted to a bad habit of not selling more when SNTA rose over $11 but decide to wait for the Galaxy 1 update.

As far as Kobers, he was lumping me in with others touting MNTA as a bargain at $20. I don't appreciate when someone attacks me for what someone else says. That is why I threw his own words back at him when he mocked people for owning MNTA at $11, and proceeded to give a lecture along with io_io. Kobers was certainly correct when he derided people calling MNTA a bargain at $20. I am willing let it go now.

Dew, thanks for the link. Lots of rumors in the past about ONXX being bought out, but this was the first that mentioned a specific buyer. Obviously it is not a rumor any more. Like you I did notice that ONXX mentioned other suitors expressed interest.

I will state the obvious. Bayer is almost certainly an interested third party. I will guess that PFE might also be interested based on Palbociclib.

Thanks,

Vinny

P.S. Thanks for the other heads up. For some reason I keep having the same brain fart and saying Roche is the ONXX partner for Palbociclib, when PFE is.

{{I love it when people have the option to choose what timeframe they use when evaluating how great or bad a stock is. Of course they also forget to evaluate what the markets do in general.}}

I am glad you love something jbog as based on your posting history you always seem so negative. Both ONXX and IMGN have far exceeded the market since I have owned them. I own far more of ONXX than I do of MNTA. I own more than twice as many shares of IMGN than MNTA. Kobers was mocking people for owning MNTA when it was $11. Since then it has far exceeded the Dow. Yes, timing is everything.

Thanks for proving you are classless. You can't accept the reality that your incessant attacks against MNTA longs doesn't hold up. You attacked people for owning MNTA when it was $11. It is now $15, for a 36% gain they would have lost if they listened to your "wisdom". In case you can't do math, that gain is a bigger percentage than the loss someone would have take from going from $20 to $15.



{{With shrewd picks like MNTA and GTCB, you appear to be well on your way towards a most comfortable retirement. Good for you. }}

I see you resort to incomplete information to launch personal attacks. Once again that shows you are classless, as well as clueless. I own(ed) other stocks besides those two. I bought into IMGN at $5 just after the FDA declined to approve their T-DM1 armed monoclonal Ab a few years ago. I doubled up at around $8. It is now around $16. Right now my largest holding is ONXX, and I have owned that from the time I owned GTCB. I added over the years since then, and my average price is under $30. ONXX is close to $90 now and rumors of a buyout at $120 by AMGN are being bandied about now. I also owned MEDI and did well when they were bought out. My gains for the latter 3 far exceed my GTCB loss. Unlike you, I have moved on from GTCB, whereas you still are very bitter.

After your unceasing attacks against MNTA and Dew, I asked you many times to tell us what you do own rather than just launch attacks. Like the coward you are, you never posted what you do own or like. In contrast, I have been quite open and up front. I also just increased my shares of SNTA by 20% at $4.60.

{{The 8% royalty on Pfizer's PD-991 is significant and overlooked - that's going to be a very big drug (at least $2 billion in my view). }}

Peter, palbociclib completely slipped my mind. It may well be a block buster for Roche. Do you think that the 8% share to ONXX would be enough to spark some interest for Roche to take over ONXX?

jmkpbers,

At least have the decency to be honest and accurate. What others said or didn't say is irrelevant to what I said and to what you said.

Here are the facts. You were mocking those who held MNTA when it was $11 or $12 but now it is over $15. At least have the decency to acknowledge you were wrong as it is obvious to everybody else.

As far as myself, I am now even on my MNTA investment, and will keep holding.

Peter,

If the AMGN offer is real, I also expect it to just be the opening offer. Bayer sat on their stupid butts for so long, and now there is a very high probability they will enter the game. If ONXX is to be bought, the offer has to be closer to $150 than to $120 to satisfy me. I was astonished that Bayer didn't buy ONXX after Bayer agreed to cede 20% of the Stivarga revenues to ONXX. Don't get me wrong, as a long time ONXX shareholder I am very happy it didn't happen, but anyone could see ONXX was a great takeover target even two years ago.

ONXX is by far the largest position in my portfolio, especially after SNTA cratered. I was reluctant to sell much ONXX even after the Kyprolis approval precisely because I expected a buyout. An ONXX buyout at a large premium would sure as hell take the sting out of the SNTA drop.

Vinny

Peter,

{{The non-rapid group might not progress as quickly, but they've had advanced disease for longer. So those effects counterbalance each other, and no easy way to predict who will survive longer. Think of it this way - assume you have two patients with advanced NSCLC, one was diagnosed six months ago and one was diagnosed yesterday. Which do you predict will survive longer?

You focus on MOS for some reason - the key is the HR, not the MOS, particularly if events might be non-proportionate.

Weakness in the stock seems overdone to me here. The key objection is that this is a subset analysis, but absolute numbers are still pretty decent and effect size looks respectable too.}}


I have been going over the SNTA Galaxy trial data and have become more optimistic. Someone emailed me a figure where they overlaid the arms for both the overall adeno group and the >6 month progressor group. The control arms were essentially identical. The only difference was a very minor divergence that generated the ~1 month MOS difference in MOS, but this divergence was lost quickly. This vividly illustrates your point (as well as others on this board), and my error, of focusing too much on MOS rather than the HR. The overlay of the Ganetespib arm was very interesting as well. I sold off 40% of my SNTA at $4.90, admittedly in a bit of panic and disappointment, but yesterday I bought back half of that at $4.60

Thanks for your thoughts.

geocappy,


{{Couldn't agree more. It is very clear. Would you also agree that they did not say they were done with 1st line lung cancer but they were no longer supporting the "combination" of Bavi + CP. if my memory is right, they have always known that Bavi + Doce was their best combination. Actually, I believe Bavi + irradiation might even be better.}}

Glad to see you are accepting PPHM's word that the combination of Bavi + carboplatin + paclitaxel is a dead end. Companies have real problems admitting failure, and PPHM is more so than most companies I have followed. They appear to be trying to spin this latest failure into a positive. It is a very bad sign that they refuse to provide the MOS for the control arm, but it it not out of character for PPHM.


I acknowledge that I don't know about Bavi + radiation, but why in the world are you so hopeful about Bavi + Docetaxel? You do know they are both taxanes designed to stabilize microtubules, and despite initial hopes, there isn't thought to be much difference clinically between the two. As far as the vaunted 2nd line Bavi NSCLC trial, it was quite small, the 3mg/kg arm had a high percentage of censored patients, and it was corrupted. That doesn't exactly spell powerful reasons to get excited in my book.

Hey jmkobers, MNTA is now up about $2 since your 2nd to last post.

thealias2002

{{In my eyes this trial is not over. I'm sorry,....but it's not. I refuse to accept the data provided as 'final'. }}

It really doesn't matter what you think, what you accept or what you refuse to accept. Below is what PPHM management said. I think you should read the second to last sentence say 10 times until it gets through to you. PPHM makes it quite clear that this avenue is over and will not pursue this avenue. Why do you think PPHM didn't mention the MOS for the control arm? Sometimes what is not show speaks much louder than what is shown.


{{To further focus the strategic direction for potential upcoming trials, Peregrine just completed an analysis of overall survival (OS) data from its Phase II clinical trial comparing bavituximab plus carboplatin and paclitaxel versus carboplatin and paclitaxel alone in front-line patients with Stage IIIb and Stage IV NSCLC. This analysis, with less than 60% of survival events, indicated that while the bavituximab containing treatment arm currently demonstrates a median overall survival of over 14 months, there was not a meaningful enough difference in survival between the two arms of the trial that would support the advancement of this combination. Full results from the trial will be presented at a future scientific meeting or through publication.

MNTA is up about $1 since you last posted.

I am reconsidering my earlier pessimism regarding SNTA's data at ASCO.

{{Not obvious to me at all. The non-rapid group might not progress as quickly, but they've had advanced disease for longer. So those counterbalance each other, and no easy way to predict who will survive longer.

You focus on MOS for some reason - the key is the HR, not the MOS, particularly if events might be non-proportionate.

Weakness seems overdone to me here. }}


Peter, thanks for your comments. I see what you are saying, and hope that you are correct. Yes I am likely making a newbie error by focusing on the MOS and I know that many on this board have pointed out how un-reliable the MOS can be. However, the issue for me was that I gambled by increasing my shares before the data came in, and the small amount of ONXX I sold didn't cover the entire cost. The SNTA I sold today removed all my margin and left a positive balance, so I can sit and wait if I like.

{{AF, I see, continues to harp on P values in Phase II trials, a non-factor as many here have recognized.

I have no position in SNTA. I continue to be concerned about misleading comments to investors.}}


North4000 it isn't the p value that is troubling. The HR got worse in both Galaxy 1 ITT population, and in the population that is being treated in Galaxy 2, non-rapid progressors. That in itself isn't a disaster, but I did get the cancer to look at the Kaplan-Meier curves as the SNTA web site has updated data for the presentation later today. That is where the were the real story is. A big read flag is that the in the non-rapid progressor group, the MOS is worse that the overall ITT group. The former should have a better prognosis. The HR appears non-proportional with early patients benefiting but after patients doing worse. That alone isn't a disaster. However, when you look closely at the Kaplan-Meier curves, you can see there appears to be a lot more censored patients around the time MOS time point for the control arms, and where the Ganetespib + Doc arm shows good separation.

When I take all this together, it doesn't mean the Galaxy 2 will fail, just that I expect the Galaxy 1 data to show less of a survival benefit for the Ganetespib arm when it is matures. This means the Galaxy 2 trial will take longer and have a lower chance of meeting its primary achieving its primary end point. I think it also means the chances for partnership have dropped, so SNTA will have to raise finds on its own, which will cut into the share price. Feuerstein mentioned the anti-PD-1 data as well. I believe data in NSCLC was primarily in squamous cell lung cancer, which isn't in the the Galaxy trials, but I am sure the anti-PD-1 could enter the NSCLC area more broadly.

I sold off almost 40% of my shares at just over $5 this morning, and will likely cut more. Thanks to everyone on this board for helping me to better evaluate cancer trial data.

Mcbio, looks like you made the correct move by getting out of SNTA with a profit. I had the chance to do the same but took the risk and lost. I sold off half my shares this morning.

entdoc, I think you may be confused.

{{Bavi- was developed as a double-armed MAB vehicle to carry cytotoxins to a specific docking site on vascular endothelial cells, the inner lining cells of blood vessels which nourish cancers and allow them to grow. Bavituximab was originally an anti-angiogenesis MAB in the same category as Avastin, but with a different, exclusive docking site on membrane surface -PS. The idea was to target tumor vasculature. }}

Unless specifically engineered, all IgG monoclonal Abs have two arms which comprise the variable portion of the antibody.



{{Something happened during development: Bavituximab without a payload was immunogenic, stimulating the body's immune system. What happened to loaded Bavi? Rumor has it that when one arm of Bavi is loaded with a small molecule, the other "available" arm cannot bind so readily or solidly to target. }}

Drug conjugates for MAbs can be linked to various portions of the Ab. In fact, multiple conjugates can be added to a single MAb to make it an extremely potent delivery vehicle. If PPHM tried to arm Bavi on one of the variable arms, saw it lose specificity or avidity then stopped rather than try and move the conjugate to other parts of the Ab, like the Fc portion, then they are imbeciles.



{{Again, this is my "understanding" only, but it is said that fully humanized Bavi, now "in production" does not have that issue for reasons more technical than the intent of this post. }}

That sounds like an excuse provided someone who doesn't know what they are talking about. So, why hasn't PPHM announced that the fully humanized Bavi will be made and used as an anti-body drug conjugate?

{{Yeah, recent comments from MNTA management have left me with low hopes SCOTUS will take up the case at this time. }}

pollyvonwog, you might be correct. Alternatively, maybe MNTA management finally learned it is better to set low expectations so that you can easily beat them with some good news or results.

iwfal,

biotech-researcher was posing his question to me, and he or she appears very sensitive. biotech wrote,


{{vinmantoo, I have been actively following SNTA over the last 12 months and like everything until this news came out in early May:

What: Shares of Synta Pharmaceuticals (NASDAQ: SNTA ) , a clinical-stage biopharmaceutical company focused on researching and developing cancer and chronic inflammatory therapies, fell as much as 17% following an analyst downgrade after Synta disclosed the departure of its president of research & development.

This stunned me as the President of R&D was only there for a few months. What do you see in the company that still makes you so bullish to discount this not so good event? }}



Biotech was wrong about the time-frame for the employment of the former R&D chief, and only mentioned the one analyst who down-graded SNTA without mentioning another who said it was a buying opportunity. This left me with the impression that biotech-researcher thought it was a big negative for SNTA. I gave the following response.


{{He left a $2.6 million/year position at Hospira, was at SNTA for 6 weeks, and they returned to Hospira.
What do you see that is so sinister or has such evil foreboding about this? I see a guy who went from a top position at a large corporation in the town where his family resides, to a small company half-way across the country at a major pay cut. When given the chance to return to his previous company, he grabbed the money and didn't let the door hit him on his backside as he ran back. I wouldn't be surprised if he got a nice bonus to return as well that likely exceeded his $400K salary at SNTA}}

mcbio,

Thanks for the good wishes. When the story about the new R&D head left happened, the MNTA price dropped so I bought 3x. The last time was at $6.83 and the net effect was to increase my shares of SNTA by about 33%. I will also consider selling some SNTA before June 3rd if there is sufficient run-up.

mcbio,

I don't think there is anything wrong with that question, or with you selling SNTA. I also had some discomfort about how the Galaxy trial has changed. My view is that I am willing to wait until after ASCO and the interim update of Galaxy before selling a large percentage chunk of my SNTA. I will sell at least half of my shares, and unless there is a major setback based on the interim data, I will have booked a very nice profit.

He left a $2.6 million/year position at Hospira, was at SNTA for 6 weeks, and they returned to Hospira.
What do you see that is so sinister or has such evil foreboding about this? I see a guy who went from a top position at a large corporation in the town where his family resides, to a small company half-way across the country at a major pay cut. When given the chance to return to his previous company, he grabbed the money and didn't let the door hit him on his backside as he ran back. I wouldn't be surprised if he got a nice bonus to return as well that likely exceeded his $400K salary at SNTA.

Honestabe,

I wasn't directing my comments at you, just to your post as it contained the opinions of someone else who was responding to me. Look I don't know all the answers regarding Bavi or any other anti-cancer therapy. I am making a lot of guesses like many others. I am just trying to improve my chances of being right, and more importantly, of making money by investing in things I know at least a little bit about. I once was invested in AMD, the computer chip maker and read yahoo boards and quickly realized that I had no idea on how to interpret which people with differing opinions were right, so I sold off. I can't guarantee that PPHM is bad investment, just as I can't guarantee that SNTA, a company which I made a big investment recently will be successful. I am just trying to figure things out as best I can and take advantage of the input of the large number very smart and experienced people on this board.

Oops, foprgot one thing.

{{K, so now Bavi fires up CD4 null cells to differentiate into the Th1 arm. This means, your Natural Killers, }}

Natural Killer (NK) cells don't need macrophages to be activated. They are part of the innate immune system. When I was running my laboratory at a cancer center, one of my colleagues was an expert in NK cells, so I do remember a little bit about it, enough to state that they don't need macrophages.

{{Saying that Bavi arrives "late on the scene" with anti-angiogenesis activity (due to late eversion of PS) is patently incorrect. }}

My comment is correct. PS eversion it the tumor vasculature happens under hypoxic conditions, and hypoxic conditions tend to occur later in tumor development.



{{May I refer you to Dr. Thorpe's outstanding New York Academy of Sciences May 1, 2012 presentation? }}

Thanks. I looked at it. I can see you take your talking points from it almost verbatum.



{{Quote:Bavituximab repolarizes macrophages to their M1 state, which allows them to kill cells that express PS, including the tumor vascular endothelium. It also leads to differentiation of the MDSCs and prompts DCs to mature and to present tumor antigens to T cells. What does this mean? Well, macrophages float around the bloodstream in a depolarized state in the presence of cancer. Bavi repolarizes them, and thereby "re-magnetizes" them. This has NOTHING to do with whatever stage the cancer is in, and the efficacy of the Mab would not be present if "late eversion" of PS occurred as you say. }}

But since the PS eversion happens in tumor vasculature under stress conditions, it is only then Bavi could counteract the phase state change when tumors are large enough to generate hypoxic conditions in the tumor vasculature.

As far as changing the macrophage state, that may begin the process of activating helper-T cells to challenge the tumor, so I can see why PPHM longs are so high on Bavi. However, down stream inhibition trumps upstream activation. What you fail to appreciate is that you suppressor T-cells are designed to shut down the immune response, so even if there is a lot of upstream stimulation, suppressor T-cells will shut down the helper T-cells to ameliorate the anti-tumor response. That is why PD-L inhibitors show so much promise, you unlock the downstream suppression to allow more robust and durable anti-tumor responses. I repeat, downstream inhibition trumps upstream activation.


{It's clear that everted PS occurs early on in the cancer timeline. }

Not sure why you think this.



{{This is why Bavi is showing MOS numbers your friend can only dream of. (60% percent change in second-line NSCLC MOS that was really 100%!!) }}

The is no reliable data for you to conclude anything about MOS. The trial was small and corrupted.



{Additionally:
Quote:Bavituximab can also prompt the development of tumor-specific immunity. In experiments with rats with treatment-resistant glioma tumors, 15% of the animals treated both with radiation and with antibody therapies did not die from those tumors. When the researchers reintroduced glioma tumor cells into these surviving rats, the rats were immune to the cancer. The team determined that spleen cells from these animals could kill gliomas, which indicated the antibody treatment had induced T cell immunity. }}

Please don't cite pre-clinical rat studies as proof of anything.



{{OK, so now Bavi fires up CD4 null cells to differentiate into the Th1 arm. This means, your Natural Killers, interferon-gammas, and other T-cell "Cluster of Designation" (CD) players are fired up to attack the cancer. Again, NOTHING to do with cancer staging and is counterintuitive to your "late PS eversion" hypothesis.}}


Down stream inhibition trumps upstream activation. What you fail to appreciate is that you suppressor T-cells are designed to shut down the immune response, so even if there is a lot of upstream stimulation, they will shut down the response the helper T-cells to ameliorate the anti-tumor response. That is why PD-L inhibitors show so much promise, you unlock the downstream suppression to allow more robust and durable anti-tumor responses. I repeat, downstream inhibition trumps upstream activation.


{{I could go on and on, but you get the point. So few people read, really. }}

I can see you read and watch videos. Good for you as that is a great start. However, reading and understanding the complexities and inherent uncertainties are quite a different matter. If you keep reading and then start ask some questions it might help you.

{{Loe says this asset is often overshadowed by OncoGenex’s own OGX-011, a treatment designed to block the production of clusterin, a cell-survival protein that is over-produced in several malignancies and in response to many cancer treatments.}}

So how does OGX-011 block the production of clusterin?

Abe, jq1234 and others are correct that the guy writing the seeking Alpha article can say what he wants, but empirical evidence from clincial trials says he is completely wrong.

From what I have read about Bavi, it won't have its effect on tumor vasculature until late in tumorigenesis when the tumor becomes large and hypoxic, which can induce PS eversion i the vasculature. This late activity also means Bavi won't affect new metastatic lesions until they become large tumors, which doesn't seem to be a good way fight cancer or to increase OS. That late action also puts Bavi at a disadvantage to angiogenesis inhibitor drugs like Avastin, which inhibit new blood vessel formation and thus can limit tumor growth at early stages, even at new mets.