did the career thing long enough.
Register for free to join our community of investors and share your ideas. You will also get access to streaming quotes, interactive charts, trades, portfolio, live options flow and more tools.
Register for free to join our community of investors and share your ideas. You will also get access to streaming quotes, interactive charts, trades, portfolio, live options flow and more tools.
md/silverback says IR implied there would be no loan...we shall see.
is the randomness of the free market keeping us at 1.66 day after day?
i think not.
forumuser... institutions never pay close to retail...
i'm hoping there's bidding going on as posted by silverback...
this stock has leaked inside info like a sieve for years...you'd think there would be some positive action if we were 'close'...
indeed, dia...cheynew deserves an answer. do you have inside info, or are you imagining that 'in talks' means they're close?
that would mean they've been close for 7 or 8 years so far...
i don't know how much is new hiring and how much may be replacing folks who have left. i hope it's the former, but nobody here has been able to verify it so far.
can somebody do that?
pw... sabotage or something akin to it has played a role, i certainly agree, but nobody seems to be putting much stock in the salvaged trial and the science. pphm's credibility is below 'poor'.
as i've said too often...a deal has to happen very soon, or we'll be diluted into oblivion. the Street certainly subscribes to that according to the pps...
dia.. of course you disagree.
why is it that you and a few others never question why we can't get out of our own way regarding failed attempt after failed attempt on the part of management to increase and sustain the market value of this company?
a big pharma now faces backlash if they pay up for anti-PS when PD-1 is all the rage. Our leverage may have actually weakened, again, due to the PD-1 hype.
if front line nsclc comes in mediocre, it'll get very ugly around here, as in 'look out below', imo.
a deal should have been completed LONG ago... years have been wasted in developing trials for the additional indications...
what are they doing?????????????????????????????????????
All the talk about immune therapy for cancer is great. Too bad the reporters and big money think Pd 1 is VHS and we are BetaMax (if they even know we exist)
Bought more last week on a pullback in advance of ASCO. That buy is now underwater.
12 years. It is amazing that with all of Thorpe's great work these clowns cannot make it worth anything.
the early bid/ask suggests another big dump today. for cryin' out loud...it gets so old, doesn't it?
Dr...there is no way partnering meetings would be advanced at asco. any outfit seriously interested would have been having plenty of meetings with pphm already, and no company would be waiting to conveniently meet at asco in order to save on air fare and hotels.
a deal is either done and waiting on legalese, or they're bullshitting us all.
these discussions don't go on for years for a 2-bit microcap. if there's no deal during the summer, in time to support p3 roll-out from the very start, run for the hills before the 50% dilution starts.
we were supposed to be focused on asco...for what? news that apparently is going to take us lower than before asco?
make a deal already. jeez.
dew...so the 11.7 for the pphm 3mg NSCLC was just the placebo effect when almost no other control, let alone treatment arm, has ever produced that? you're saying pphm and their crappy CRO were lying, and the fda didn't care?
Dew... you are sharp enough to know that the pancreatic patients were mostly at the end of the line when they started, with little hope...and with badly compromised immune systems, which don't portend high hopes, particularly for a drug intended to work with the immune system to fight the cancer... you are also sharp enough to know that, since it wasn't a late-stage trial, analysis of subsets, where there were signs of potentially effective treatment compared to soc, it could be worth pursuing given the now-apparent fact that the drug seems to have some efficacy across several afflictions. by focusing on pancreatic, while nsclc and breast both had interesting results, and picking out the weakest of the 3 trials they addressed, your criticism comes across as disingenuous. you and this board both expect more than than from participants here. jeez..one AF is enough...please stay on the higher ground.
nsclc, which is the primary target for now, seems to warrant continuing attention, and i suspect you know it. you do want effective treatments to be developed, don't you? shouldn't all of the new treatments which demonstrate potential effectiveness continue to be pursued till they're shown not to, particularly when it's been such a difficult and underfunded slog with a drug with a new moa that isn't automatically popular since it's so different?
while your bias continues, it looks like it ain't over yet for little ol' pphm.
but they sure could use some money, eh???!!!
Dew...if it gets half-way to Roth's target, I'll be thrilled!!!!!
(better mos than snta)
so...now that the volume is finished, do we drift back down to 1.40 again and wait for another catalyst? we're obviously not going anywhere now...
man, do the institutions hate pphm...
the stock price is no surprise.
the company is essentially broke, and has $150,000,000 in trials still to run.
we need the partnership before too long or we're looking at a massive dilution cycle again. what institutions will buy significant shares before big dilution is off the table?
look at our institutional ownership now and you have your answer.
1.74. well, whoop-dee-do.
af's bash today wasn't much of a bash...
his comments on avastin performance similarity with bleeding reduction is...significant. for someone who has taken such a nasty stance for so long...it's very different.
so we're supposed to focus on asco and partners.
what partners?
IST's, maybe?
vinman... i appreciate your posts...honestly.
here's a recap of the back and forth... people who assume bavituximab is a placebo should read this...there are new discoveries all the time... (thank you, CJ):
jgaddy
Saturday, May 25, 2013 8:14:34 AM
Re: honestabe13 post# 124158
Post # of 124189
Sulaco’s reply to Bval’s Vinmantoo re: Bavi vs. PD-L MOA: post #124163 to Honestabe13 (removed by iH-Admin) reposted with personal ref’s removed… More interesting Bavi science reading evidenced by this exchange between Vinmantoo (strong SNTA advocate http://www.syntapharma.com/pipeline.php Ganatesepib) and contributor Sulaco. (Sulacos’ reply’s prefixed by =>)
Posted by: sulaco 5/24/2013 10:10pm #124163 - reply to honestabe13’s #124158
Vinmantoo - nice try - stating mere opinion as fact…
Re: ”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.”
=> Sorry. Just saying that doesn't count, where's the proof? Who says? Hypoxia can be induced by MANY different biophysical conditions at ANY time. Stating it occurs "later" in tumor development is clearly an opinion, not fact. To boot, hypoxia is clearly not the only mechanism by which flippase everts PS. Many different variations of protein binding do it as well. You would know this if you read the NYAS conference thoroughly.
Re: ”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.”
=> How long did you "look" at it? 5 minutes? It takes HOURS to go through.
Re: ”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.”
=> Again. No proof whatsover is offered by Vinmantoo. Opinion stated as fact. <snip>
Re: ”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, downstream 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.”
=> There are enough self-contradictory sentences here to dismiss <snip>. Rest assured that Bavi does NOT activate "you suppressor T-cells." NO proof, no hypothetical model, and no studies of any kind support this claim.
Re: ”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.”
=> <snip> …you're offering [a slogan] with NO PROOF WHATSOEVER.
Re: ”It's clear that everted PS occurs early on in the cancer timeline.” - Not sure why you think this.”
=> When Bavi induces either complete or partial responses in breast cancer studies, it's reasonable to assume it has outpaced the cancer (kinda hard to do when you're "late") and gained the upper hand.
Re: ”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%!!” - THERE IS NO RELIABLE DATA FOR YOU TO CONCLUDE ANYTHING ABOUT MOS. THE TRIAL WAS SMALL AND CORRUPTED.”
=> Bavi, which the vast majority of investors (including you) invariably fail to realize, applies to MUCH more than lung cancer. It has shown efficacy across MULTIPLE tumors.
Re: ”Additionally: 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.”
=> It's a theoretical model to explain the principle of T-cell ACTIVATION, not suppression. You offer NO models or theoretical proof whatsover for your <snip> claims. Where do you think the modeling occurred to test whether blocking PS eversion stimulated CD4 null to progress to Th1 T-Cell attack? Animal models, Vinmantoo, animal models!
Re: ”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.” - DOWNSTREAM 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.”
=> <snip> on a message board by throwing around bio-immunological jargon is clearly your M.O. Nice try. Come back later, and bring more than mere opinion, please.
Re: ”I can see you read and watch videos. Good for you as that is a great start. However, reading & understanding the complexities and inherent uncertainties are quite a different matter. If you keep reading and then start asking some questions it might help you.”
=> <snip>Time to . . . hit the books. And next time you write, please share the theoretical underpinnings, models, and clinical results (that Bavi all has) to make your downstream inhibition jingle remotely applicable to the argument.
more feedback from biotech values..
i've noticed there hasn't been much pushback from science folks here...
is anybody prepared to challenge the points below??
vinmantoo Member Profile vinmantoo
Friday, May 24, 2013 7:51:30 PM
Re: honestabe13 post# 161616
Post # of 161640
{{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.
vin..thank you for giving this some time. please, however, don't claim that i stated anything about my beliefs about bavituximab. I didn't state any beliefs. i just asked for comments about the science, which are in short order around here vs. bias against pphm, which is not in short order. i just would prefer to separate the two so i can decide how i want to deal with it all....
another response about science of bavituximab
goodJohnhunting Member Level
Friday, May 24, 2013 12:36:42 PM
Re: honestabe13 post# 123973
Post # of 124073
Honestabe,
Although I respect Vinmantoo's opinion, he is way off on his explanation of how Bavituximab works.
Actually, his explanation, and what Bavituximab has demonstrated, are completely polar opposites.
Quote: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
The fact remains that PS expression is evident early in many hypoxic conditions. Both, as a result of pathogenic events, and also induced as a result of chemotherapeutic regimen. In that case please tell me how Bavituximab is biased in it's affinity to bind, either late, or early during tumorigenesis. It's not, and therapautic results have clearly been demonstrated in both animal and human models. The same could be said for metastatic extravasation.
thanks, sulaco...i've thrown it back to biotech values for comment...let's see if discussion continues or if it's ignored.
vinmantoo..see bavituximab argument response below..comments?
sulaco Member Profile sulaco
Friday, May 24, 2013 11:59:03 AM
Re: honestabe13 post# 123973
Post # of 124053
Abe, Bavi is NOT Avastin
Saying that Bavi arrives "late on the scene" with anti-angiogenesis activity (due to late eversion of PS) is patently incorrect.
May I refer you to Dr. Thorpe's outstanding New York Academy of Sciences May 1, 2012 presentation?
insert-text-here
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.
It's clear that everted PS occurs early on in the cancer timeline.
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%!!)
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.
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.
I could go on and on, but you get the point. So few people read, really.
Best,
Joe
from biotech values board...after i asked for comments on the new article relative to the science, without bias:
"vinmantoo Member Profile vinmantoo
Friday, May 24, 2013 12:54:59 AM
Re: honestabe13 post# 161587
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. "
ok pphm-science guys...what say you?
vin... thank you for your responsible response. i'll send it over to the pphm board and ask for comments about your argument from science folks there.
jg where did i say it was a superior agent????????????????????
i asked for scientific evaluation, not pompous BS. I DO NOT HAVE A HIDDEN AGENDA!
for crying out loud...what kind of board is this!!!!!???????
more bias with no scientific support.
how are we supposed to get to the science????
Adam Feuerstein ?@adamfeuerstein 53m
Tonight, Seeking Alpha published a bullish article on $PPHM, claiming bavituximab is better than PD-1s. The carnival of stupid runs on.
jg... you did not address the science.
the 'drug' does not claim to act on cancer significantly by itself. it purports to negate to some extent the cancer cells' ability to disguise its presence, allowing chemo agents to become more effective while clearing a path for the immune system to see the unwelcome scourge at the same time once the anti-ps effect sets in. perhaps you should withhold you comments until you familiarize yourself with the MOA, which is still not completely understood.
you did not stick to the science.
scientifically unqualified bloggers need not respond to my question.
Crutch, Dew, Iwfal, vin, Ex, etc...
please comment on this article. I'll appreciate your thoughts. also feel free to critique author qualifications vs anti-pphm columnists, which there have obviously been a bundle of. Please keep the bias to a minimum so the discussions remain on the science.
http://seekingalpha.com/article/1458401-peregrine-pharmaceuticals-the-little-biotech-with-the-golden-goose-of-immunotherapy?source=email_rt_article_title
why be upset at shorters? people moan about 'values' in this country, but the same people keep voting for legislators who have decided that such shenanigans are not immoral, but, in fact, add value.
seems like an icky way to be materially successful to me, but, whatever... i need a shower.
crooked crooked crooked markets. pps sat on my bid price for a good chunk of the last hour and didn't fill
by the way..
pphm's comments that they don't really need to partner to do p3 is hogwash. can you imagine the dilution slaughter?
so we play chicken. wait for the deal, or wait for the dagger.
down .04 on 50,000 shares. blatant orchestration
i guess my point is that the company is valued essentially where it was before the p3 trial was given the green light. is that because the market agrees with dew and af, or because dark forces are managing to keep it down so it can remain a trading toy till somebody opens the wallet? with a number of trials reporting that the stuff seems to help, i guess i'm just irritated that traders dictate the share price, not investors...
market sure loved our news.