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5.43, exactly half of the current average
Also interesting, given that so many people like to complain about the costs of getting a drug approved in the US:
http://www.thepharmaletter.com/file/113474/new-study-shows-japan-most-expensive-for-investing-in-clinical-trials-followed-by-australia.html
It was either as you say "a hundred million here, . . ." or simply "a million here, . . . ." Notwithstanding what appears below, I think "billion" is plainly wrong. I remember the time and the context, and it wasn't "billion." At the time, "billion" was "real money" in anyone's book and didn't need to appear in multiples to so qualify.
The truth appears to be lost in the mists of time, but googling the variants gives 200,000 hits for "billion," 60,000 hits for "million," 500 hits for "a hundred million," and only 6 hits for "100 million."
I have the faintest memory of it as "million," but I have probably invented more memories than you.
"I used to work for a hedge fund . . . too many thieves on wallstreet stealing money."
So these first posts of yours are your conscience speaking?
Not our boy, boyo.
I must disclaim that I am a physician or play one on TV, nor do I have any biochemical expertise.
The handle is an old private joke.
Big Pharma has paid what by now probably amounts to more than a BBBillion dollars in fines for just that, so don;t laugh too loudly.
"bavi would train the immune system to respond to any PS on the outside of any cell"
Correct me if I'm wrong, but I have always thought that the immune response is directed at offending (non-self) material, not the PS. I recall that in one or more of the viral studies, the immune effect to that virus persisted long after the bavi would have cleared, but nobody was claiming that residual immunity was effective against all envelope viruses, as would seem to be the case if the immune system operated against the exposed PS.
Isn't it more correct to say that bavi prevents the exposed PS on affected (cancerous and virally infected) cells from triggering that part of the immune system that merely clears away dead matter and does not "learn" anything, and allows (or causes?? - maybe someone can help here) the more powerful part of the immune system (the one that actually learns, makes antibodies, kills cells, and causes inflammation) to go after, and manufacture antibodies to, the non-self (i.e. cancerous) portions of the affected cells, or the virus or virus fragments?
In short, doesn't bavi respond to the PS, which allows the immune system to respond to the real problem?
I'm happy to let all concerns about the validity of the Ph2 data be answered by a partnership. After that happens, I really want to see who persists in bad-mouthing the data, and I would love to hear their explanation of how the partner got conned.
Take a break for a few years, come back when the stock finally shudders into life, and what do I find?
Same old ****.
When I think of the energy wasted . . . .
I wonder what our effective float really is. Doesn't seem like it took much news, or much volume, to produce today's result.
You ask Whats happened with our research on viral hemorrhagic diseases?
Didn't you hear? It was all a dream.
5 million shares in new or increased positions, 100,000 in decreased or sold out positions.
That's a ratio of 50:1.
Today the breast cancer indication for Avastin was taken away by the FDA.
Either this is a price-manipulation scam in an American market run by crooks, or there is a yet-to-be-disclosed problem with autoimmunity or some other practical problem.
My bet is on the former, because that's why the board flies are here.
Use of MABs to control viruses targeting, apparently targeting viral proteins themselves rather than envelopes built from host cells.
"Monoclonal antibodies are the largest class of biotherapeutic drugs. When administered to infected organisms to blunt the propagation of pathogenic viruses, they may also induce a long-lasting and protective antiviral immune response similar to that achieved by vaccination.
* * *
Until now, the only mechanism of action of antiviral monoclonal antibodies that was really considered by the medical and scientific communities was the neutralization and direct elimination of viruses in infected organisms [except for those seeming few who know about PPHM].
* * *
The team identified an unexpected mechanism enabling the monoclonal antibodies to induce protective antiviral immunity. This mechanism is based on their ability to recognize not only circulating viral particles but also certain viral proteins expressed at the surface of infected cells. These new findings may help to trigger protective immunity. They should be borne in mind by the biologists who design and develop therapeutic antiviral monoclonal antibodies.
In mice, a short and early course of therapeutic monoclonal antibodies targeting both the viruses and the cells infected by these viruses thus enables permanent recovery from a fatal chronic infection. If this observation can be extrapolated to humans, it will result in a therapeutic benefit not only for patients but also for society, in that it will help to significantly reduce the cost of monoclonal antibody therapies, which remains prohibitive in most cases.
http://www.sciencedaily.com/releases/2010/06/100611124651.htm
"Naked Bavi"
Excellent point, esp. as I had read the PR hastily and thought that the PRIMA was riding on the MAB.
You were 'made' almost as soon as you showed up here.
I appreciate your unique perspective. "Low of the day." It takes an original mind to detect and label that phenomenon.
Now, 6-7 years later, their financial resources are probably less than they were then?
Please explain, making sure you include the contributions from DTRA and Avid.
This sort of inconsequential PR has recently seemed to coincide with moderate share-price increases. We'll see what happens today.
Not suggesting that the PRs are issued to cover trades known to be in the offing.
Well, if you put your thoughts in red they don't seem as banal.
Those who own zero might have to try harder.
Sometimes I start from the most recent post and work backwards. When I read your post I assumed that Moby'investor's' two contradictory statements were from different posts and that you had done a little digging to assemble them.
Then I get to his most recent querulous and faux-skeptical post and I see that he has contradicted himself in the space of half an inch.
Beautiful.
Please explain. TYVM
For a down day, I liked today's action. Opened off .19, fell to 3.2 or lower twice, but closed off .16, .03 higher than the open.
I am not a technician, but IMO if that isn't that some kind of technical signal, it ought to be.
"We'll see who gets to have the last laugh and when."
Kinda depends on your time frame. What's yours?
Harvard = UMASS??? huh?
I had you pegged here:
http://investorshub.advfn.com/boards/read_msg.aspx?message_id=39581876
WH, whenever JessMeeeeeeee gets challenged he produces a word-processor dump of often irrelevant and usually unedited stuff, as if "quantity had a quality all its own."
"In 1977, Dr. Levinson holds a Ph.D. in Biochemistry from Princeton University and a Bachelor of Science degree in Molecular Biology from the University of Washington."
Edit, edit, edit.
Something is giving way in your facade.
If you think NADA is the future, don't let that old doorknob . . . .
'Distinguishing between talk and reality' is what allows many of us to ignore the drivel pushed here.
Read this 3-YO presentation and if you're still worried, come back next week
INTRODUCTION:
A promising target for tumor vasculature is phosphatidylserine (PS), an anionic phospholipid that resides exclusively on the inner leaflet of the plasma membrane under normal conditions. We have previously shown that PS becomes exposed on the surface of viable endothelial cells (EC) in solid tumors. To target PS on tumor vasculature, a murine monoclonal antibody (3G4) was developed. 3G4 specifically localizes to the vasculature of solid tumors. Treatment of mice with 3G4 inhibits growth of murine and human tumors. Therefore, 3G4 is a promising new therapeutic agent for treatment of solid tumor malignancies. We demonstrate here that the interaction between 3G4 and PS is dependent on antibody binding to the plasma protein beta2- glycoprotein I (B2GPI). B2GPI is a 50 kDa glycoprotein composed of 5 domains, including the positively charged domain V that binds anionic phospholipids. However, the interaction with anionic phospholipids is rather weak under physiological conditions. We show that 3G4 binds B2GPI and enhances the binding of B2GPI to EC induced to expose PS. The data suggest that 3G4 targets tumor vessels by increasing the binding affinity of B2GPI to PS exposed on tumor EC.
PURPOSE OF STUDY:
• To identify the plasma protein required for binding of the novel tumor vascular targeting antibody 3G4 to anionic phospholipids, in particular phosphatidylserine (PS).
• To determine the mechanism by which 3G4 and plasma protein beta2-glycoprotein I (B2GPI) bind cells with exposed PS.
RESULTS – Figure1: “3G4 binds serum protein B2GPI“
A) “3G4 grown in serum-free media does not bind PS in the absence of serum” - Two preparations of the 3G4 antibody were used: 3G4 purified from i) serum-containing media (SCM), and ii) serum-free media (SFM). Microtiter plates were coated with PS and blocked in PBS + 10% FBS or 1% ovalbumin (OVA), which lacks B2GPI. Serial dilutions of 3G4 were performed in PBS + 10% FBS or 1% OVA.
B) “ch3G4 binds strongly to hB2GPI coated plates” - Microtiter plates were coated with B2GPI purified from human serum and blocked in PBS + 1% OVA. Serial dilutions of a human IgG1 chimeric version of 3G4 (ch3G4), control human IgG1 (Erbitux), a commerical mouse anti-human B2GPI (α-B2GPI), and a control mouse antibody (C44) were performed in 1% OVA.
C) Purified human B2GPI (hB2GPI) and 10% human serum were run on a 4-15% gradient Tris-HCl PAGE gel. Protein was transferred to a membrane and immunoblotted with α-B2GPI, 3G4, or C44.
D) “3G4 binds domain II of hB2GPI” - Microtiter plates were coated with recombinant peptides containing serial N-terminal domain truncations of human B2GPI. Serial dilutions of 3G4 were performed as described above.
RESULTS – Figure2: “3G4 enhances binding of B2GPI to cells with exposed PS“
A) “ch3G4 enhances binding of hB2GPI to LPC-treated ABAE cells” - Adult bovine aortic endothelial (ABAE) cells were treated with 200uM lysophosphatidylcholine (LPC) to induce PS exposure. Cells were incubated with 2ug/ml purified hB2GPI prior to or concurrent with ch3G4 (2ug/ml) incubation. ch3G4 binding appears green, nuclei appear blue, and actin filaments appear red.
B) “Nicked hB2GPI does not mediate binding of ch3G4 to LPC-treated ABAE cells” - ABAE cells were treated with LPC as described above. Cells were incubated with hB2GPI or “nicked” hB2GPI in the presence of ch3G4. The lipid binding region of nicked hB2GPI is cleaved, preventing interaction with anionic phospholipids such as PS. The pixel area of ch3G4 binding was quantified and normalized to nuclear area. The binding of nicked hB2GPI to non-induced cells was arbitrarily set to one.
RESULTS – Figure3: “3G4 binding to cells with exposed PS requires a multivalent interaction with B2GPI”
A) “Excess ch3G4 inhibits binding of ch3G4/hB2GPI complexes to LPC-treated ABAE cells” - ABAE cells were treated with 200uM LPC to induce PS exposure. Cells were incubated with 40nM hB2GPI and a titer of ch3G4, fixed, and stained with fluorescent reagents. Images were taken and the pixel area of ch3G4 binding was quantified and normalized to nuclear area. The binding of ch3G4 at 319pM was arbitrarily set to one.
B) “Excess 3G4 Fab inhibits binding of ch3G4/hB2GPI complexes to LPC-treated ABAE cells” - ABAE cells were treated with LPC as described above. Cells were incubated with 40nM hB2GPI, 20nM ch3G4, and a titer of 3G4 Fab. Cells were fixed, stained, and analyzed for ch3G4 binding as described above. The binding of ch3G4 without 3G4 Fab competitor was arbitrarily set to 100.
C) “3G4 Fab does not bind LPC-treated ABAE cells” - ABAE cells were treated with LPC as described above. Cells were incubated with 20nM 3G4, 3G4 F(ab’)2, or 3G4 Fab in 10% FBS; fixed, and stained with fluorescent reagents. 3G4 binding appears green, actin filaments appear red, and nuclei appear blue. D) “Quantification of 3G4 binding area” - The pixel area of 3G4 binding shown in part C was quantified and normalized to nuclear area. The binding of 3G4 to non-LPC treated cells was arbitrarily set to one.
SUMMARY AND CONCLUSIONS:
• 3G4 purified from serum-free supernatants does not bind anionic phospholipids such as PS.
• 3G4 binds serum protein B2GPI, which is known to bind anionic phospholipids.
• 3G4 binds domain II of B2GPI, which is not the domain recognized by many pathogenic anti-B2GPI antibodies found in patients with Anti-phospholipid Syndrome (APS); therefore, 3G4 is safe.
• B2GPI does not bind strongly to the surface of PS-positive cells unless 3G4 is present.
• A non-lipid binding form of B2GPI does not bind PS-positive cells, even in the presence of 3G4.
• Excess 3G4 inhibits binding of 3G4/B2GPI complexes to PS-positive cells, suggesting a divalent interaction between 3G4 and B2GPI is required for binding to PS.
• 3G4 Fab monomer inhibits binding of 3G4/B2GPI complexes to PS-positive cells, but cannot bind PS-positive cells itself.
• Together, the data suggest that formation of a multivalent 3G4/B2GPI complex is required for binding to PS-positive cells in vitro. A similar situation likely exists in vivo.
http://www.curevents.com/vb/archive/index.php/t-29815.html
Search for "Troy Luster"
I'm sure someone has a better version . . . .
Also, is it possible that the newer MABs that do not need to complex w/B2GP1 in order to mask exposed PS, etc., do not present this theoretical problem?
Ask the people here who seem to know the hedge fund dirtbags. It was up .05 a minute ago. It'll probably be up nicely today if the action of November 3, when the article was publ'd online, is any indicator.
And if not, no big deal-- this info is a solid validation of our decision to own the stock, and we'll get our reward (and they'll get theirs, character being fate) soon enuf . . . .
My favorite line:
"Surviving rats were immune to rechallenge with F98 tumor cells. "
I don't think the general public is aware yet of the immune system re-engineering that goes on with our MABs. Today's release re-emphasizes that unique aspect.