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Thanks Mojo-- Great Caltech article!
My immunologist friend confirms that there is an ocean of PS on the membrane of an HIV virion compared to the viral spikes (GP120/GP41) that are so few and far between.
Your image of both arms of the MAb anchoring to the abundant PS nodes helps to explain why 11.31 is so much more powerful than other broadly neutralizing antibodies.
Seems like a lot of related research is all being published in April and May and all points in the same direction. Look again at the current story on the JBM anti-PS blog where the Director of IAVI says:
"But here, too, there is progress to report. Scientists have identified new antibodies capable of neutralizing a wide spectrum of HIV types circulating worldwide. These antibodies may now provide the keys to NEW VULNERABLE TARGETS on the surface of HIV, which can be exploited for vaccine design."
Yes, PS is a "vulnerable" target because it is not part of the virus and does not evolve and modify over time.
But now it also seems that part of the "vulnerability" of the PS target is that PS nodes are close enough together on the viral membrane to allow for the "two-arm" anchoring Caltech identifies as the key to a successful antibody.
By targeting the ocean of proximate PS nodes, Bavi and 11.31 would seem to answer HIV's strategy for "circumventing the bivalent effect that is so key to the potency of antibodies." http://www.eurekalert.org/pub_releases/2009-04/ciot-css042209.php
Abstract #3005 posted by CJ is the first time we have learned the breakdown of the patients between Stage III (advanced/recurrent) breast cancer and Stage IV (metastatic).
Stage IV is the the most advanced stage amounting to a death sentence. See the two descriptions of Stage IV from medical websites below.
I find it amazing that PPHM got a 71% Overall Response Rate in a population WHERE 13 OF 15 WERE ON DEATH ROW.
Does anyone have the ability to go back to the old Roche/Genentech abstracts for Avastin Ph II breast cancer and see how many of those patients were Stage IV?
Yes, Bavi has gotten higher ORR rates than Avastin, but did we also achieve that result in a sicker, more desperate patient population?
_________________
Stage IV Treatment Options
In stage IV breast cancer, the cancer has spread elsewhere in the body. Affected areas may include the bones, brain, lungs, or liver. Because multiple areas may be involved, focused treatments like surgery or radiation alone are not sufficient. So far, treatment of stage IV breast cancer does not provide a cure for the disease.
http://www.webmd.com/breast-cancer/treatments-stage?page=4
Stage IV Breast Cancer
Overview
Patients diagnosed with Stage IV or metastatic breast cancers have disease that has spread from the affected breast to one or more distant sites in the body. Historically, metastatic breast cancer has been considered incurable; the goal of treatment has been to provide relief from symptoms and prolong the duration and quality of life.
http://patient.cancerconsultants.com/CancerTreatment_Breast_Cancer.aspx?LinkId=53877
KT-- Thanks. Excellent point.
I believe the transfer agent would give the O/S figure on a fully-issued (fully-diluted) basis, which of course would include these warrants.
DIA-- Thanks for this report.
I view this as good news because Mgmt is in a news embargo regarding GA PFS data until the ASCO abstract goes public. If the GA abstract is indeed released on May 14, the Company will have a full two weeks before the last trading day in May to get the stock over $1.00 for Russell rebalancing purposes.
My understanding is that final Russell adjustments are made in June but you can only be considered part of of the June group if your pps is above $1.00 as of last trading day in May.
My bet is we see PRs updating all three Ph II trials between May 15 -29.
News of a small licensing transaction and online publication of the Duke/Haynes article in Nature Medicine during those last two weeks of May wouldn't hurt either.
From history in prior years, I'm sure PPHM has their eye on the May 29 date and is saving some PR ammunition for that time.
ASCO's official 2009 policy regarding online public release of abstracts is found in the link at bottom of this post.
From reading the "Embargo Policy" at bottom left of this PDF link, it would seem that the big abstract on Ph II GA data slated for "oral presentation" does not fall into either of the first two categories of abstracts that will be released online at 6:00 pm on Thursday May 14 because our oral presentation is not "publish only." However, the abstract on the U.S. Ph I data will probably be released on May 14 at 6:00 pm.
If being selected for "oral presentation" means that we are "plenary", i.e. presented orally in front of the full audience, then the big abstract we are all waiting for will be released either Sat or Sun morning May 30 or 31.
http://www.asco.org/ASCO/Communications/Communications%20Download/FINALAM09CorporateandInstitutionalPRPolicies.pdf
"Nature Medicine is published monthly. Articles are archived online in text and PDF formats; access is by subscription only.
Its 2007 impact factor was 26.382, making it the highest cited research journal in preclinical medicine.[2] It is also among the highest impact of primary (non-review) scientific journals."
Source: http://en.wikipedia.org/wiki/Nature_Medicine
Of course just because Wikipedia says it doesn't make it true.
"I believe this initial PPHM-Duke Nature-Med. pub. will concern the data presented at AIDS-VACCINE’08 in CapeTown 10-14-08, concentrating on the “most potent” mab from that study, PGN632, aka 11.31."
CJ-- I agree. The data that will be published soon in Nature Medicine from the CHAVI 005 protocol is clearly PPHM's stuff. This is obvious from looking at Tony Moody's page on the Duke website where he is identified as the leader of the CHAVI 005 project (here's the link: http://humanvaccine.duke.edu/modules/moody/index.php?id=1) and then looking at the list of contributors to the Cape Town abstract, which includes Moody, Haynes, Thorpe and Steve King. Here's an image from the top of that abstract. You can see that PPHM also got mentioned by name.
SO WHAT HAPPENED LAST TIME NATURE MED. PUBLISHED OLD PRE-CLINICAL PPHM DATA. Answer: The stock ran from $0.22 to $0.38 when PPHM put out its Nov 24, 2008 PR on Nature's publication of 2-year old Thorpe pre-clinical data.
This time around, it's none other than Barton Haynes, Moody and CHAVI who did the research that Nature will publish on PPHM's antibodies. And this time around 11.31 was compared to a panel of other "broadly neutralizing" antibodies. We already know 11.31 completely outperformed the other antibodies Haynes and Moody reviewed on stage in Cape Town.
Remember, in the science world it's not real until it's published in a major peer-reviewed journal. Nature Medicine is unquestionably the most prestigious, high-impact journal in the world. If you don't believe it, just Google "Nature Medicine." Not to mention that Barton Haynes is the most high-impact scientist in the HIV global community.
Just like Thorpe's old research discussed in the Nov 24 PR went unnoticed until Nature applauded it, so also Moody's oral Cape Town presentation of the 005 protocol results will go relatively unnoticed until Nature highlights this paradigm shift for all to see and believe.
If you need a little primer on why Moody's Cape Town presentation represents such a paradigm shift in viral immunotherapy, you can get a good, plain English overview of the Haynes/Moody/Thorpe/King abstract (i.e. the one that will be presented soon in Nature Medicine on PPHM's antibodies) at this link: http://anti-ps.blogspot.com/2009/01/cape-town-wrap-up-anti-lipid-antibodies.html
IT'S DEFINITELY HAPPENING.
Auditors include, or do not include, the "going concern" sentence in the cover letter that accompanies their audited financial statements. The "going concern" statement (or absence thereof) is based on the facts as they exist on the date the audit is completed and the cover letter is written, not as of the fiscal year end.
The audited financial statements for PPHM's FY ending 4/30/09 have to be filed with the SEC by July 15, 2009. The auditors cover letter will be dated the same day that the financial statements are filed with the SEC. Last year, this cover letter (which included the "going concern" qualification) was dated July 10, 2008. The auditor's letter is included as page F-1 of the PPHM Annual Report.
Bottom line: As long as the Company closes a new financing transaction before June 30, 2009 (or July 10 at the latest, i.e. just before the July CC), there won't be a "going concern" statement in the auditor's cover letter.
"... after a maximum of six treatment cycles."
Looks like they got 9 of 14 OTRs before all 14 had finished the 6 treatment cycles.
The PR on Feb 11 reported 7 of 14 OTRs after two 4-week cycles. Just under 11 weeks have passed since the Feb 11 PR. That's enough time for two--- but not three--- more treatment cycles (because each cycle is 4 weeks, plus I think there is one week off between cycles-- can anyone confirm this week off between cycles?).
Yes, some of the first patients in Stage 1 may have done "... a maximum of six treatment cycles," but a fair reading of the PR would seem to be that they got 9 of 14 OTRs after "UP TO" 6 treatment cycles.
It would seem that the two additional OTRs reported today were achieved after just 4 treatment cycles.
Question for CJ.
Could you please remind us of where we will be on the Georgia Breast study time line when that data is updated for ASCO?
I appreciate very much Jake's post that our total ORR on all three trials is 28/45 or 62%. But as I understand things, what will really turn heads is the DURABILITY of our ORR compared to Avastin, not that our ORR is 10 or 20 percent points higher than Avastin.
How many months out will our Georgia patients be at ASCO time compared to month 7(?) or 8(?) when PFS started going to hell for Avastin?
Thanks so much.
Thanks CJ. One correction to your post. You say:
"Note: the last StageA parent was DOSED ~10-20-08, ~26 wks from 4-20-09. 6 cycles at 3wks each = 18 weeks. Not sure when the post- 6th-cycle scan occurs, plus add in min. 4 weeks for the confirmation, plus time to evaluate & report… Obviously, all this for the last 3 didn’t occur/report by the 4-20-09 Prelim. Data PR."
Actually, all we know from the Oct 20, 2008 PR is that the last of 21 patients was ENROLLED, not dosed, as of Oct 20. From the time when enrollment completed for the last 3 patients (i.e. when all exclusion and inclusion criteria have been med and patient has signed the enrollment papers) until the time dosing started for those last 3 patients, could easily be another 3-4 weeks. When these extra weeks are added to the 18 weeks required for 6 cycles, and then another 4 weeks are added for the mandatory wait time before the confirmation scan can be done, you're up to 25-26 weeks.
This just adds further support to your point, namely, that the last 3 patients are doing their confirmation scans this month and it will take another 1-2 weeks to analyze and incorporate the data from those final 3 confirmation scans.
But it does look like we could get another update on the 17 evaluable India lung patients during ASCO week when the Georgia breast data is released.
I've never been so eager to see these beautiful spring days fly by.
I'll bet we get another PR on the India lung patients in the run up to ASCO reporting that 11 of 11 OTRs have been confirmed by repeat scans.
Management would love to have a good reason to republish this lung data concurrently with data from the two breast trials so all the ASCO reporters can easily do the addition on total confirmed OTRs in all three trials.
As Joe Shan said in the CC, it's the consistency of the data across all three Bavi trials that is so stunning.
Lurker, You may be right. I took a closer look at the Orange County case file and it says "Request for dismissal without prejudice--Party". I was thinking it was a voluntary dismissal of the Complaint.
As you point out, It appears to be a dismissal of a party,
For anyone who wants to go into the court files, the Case No. is 07CC00544.
"The fact that they are seeking the dismissal "without prejudice" would seem to indicate that they have not settled with that party."
Not true. A voluntary dismissal by a plaintiff "without prejudice" usually means there has been some kind of settlement, but the plaintiff is reserving the right to come back to the court for a court judgment if the defendant violates, or fails to fulfill, the terms of the settlement. A private settlement agreement between the parties does not have the force of a court order, so one side or the other always wants to reserve the right to re-open the case and get a court order if settlement terms are breached.
If the settlement agreement was signed yesterday, I think the Company has something like three business days to get out the PR.
New post today on the Anti-PS Blog has link to UTSW article on Thorpe's work with Bavi.
http://anti-ps.blogspot.com/
Our MAb 11.31 Seems to Be a Focus of Global HIV Vaccine Enterprise
The 2009 priorities of the HIV Enterprise Scientific Plan include this statement:
“4. Create “smarter adjuvants” that are most appropriate for inducing localization of T-cells to gut mucosa. Establish broad-based access to these reagents by researchers.” See http://anti-ps.blogspot.com/2009/03/minutes-from-jan-21-2009-science.html
It’s starting to be clear that these “smarter adjuvants” include in particular PPHM’s MAb 11.31. This was pointed out to me today by a scientist stockholder with whom I discussed last week’s news about Dr. Thorpe’s AACR abstract No.2407. In that abstract Thorpe explains the MOA of MAb 11.31. This abstract will be presented at AACR on April 20th.
I’m not a scientist, but here goes a crude explanation of why our MAb 11.31 is probably one these “smarter adjuvants” that the HIV Enterprise is now focusing on.
The main point of Dr. Thorpe’s AACR abstract No. 2407 is summarized this way:
“We found that 11.31 significantly increased the expression of maturation markers CD40, CD80, CD86 and MHC II on the surface of dendritic cells. 11.31 also significantly increased production of IL-2, IL-6, TNFα, GM-CSF and MIP-1β by immature dendritic cells. Taken together, our results indicate that 11.31 promotes maturation of dendritic cells. 11.31 has the potential to enhance cancer immunotherapy.” This abstract summary is found at: http://anti-ps.blogspot.com/2009/03/anti-phosphatidylserine-antibody_14.html
In a nutshell, here is how Dentritic Cells (or DCs) work. They gobble up foreign critters like tumor cells and viruses and cause little bits of these foreign proteins to be “presented” on the outer surface of the DC, which then attacts T Cells (like CD8) to arrive and destroy tumor cells and viruses that show these same protein fragments. This process, whereby DCs train and educate T Cells to identify the bad guys that need to be attacked, is called “adaptive immunity.” But it can only happen when DCs have become “mature” or “activated.” Young DCs that are not “activated” are not able to “present” foreign antigens on their cell surface and stimulate an army of T-Cell attackers. So any adjuvant like 11.31 that can stimulate the maturation/activation of T Cells is a very important tool in any immunotherapy arsenal.
The significance of AACR abstract No. 2407 is that Dr. Thorpe lays out in great detail the precise MOA by which 11.31 causes Dentritic Cells to become “mature” and “activated” and thereby generate a T-Cell response. At the International AIDS Conference in Capetown, it was announced that the Company’s MAb 11.31 is the most powerful of all the MAb “adjuvants” that trigger a T-Cell response in this way. In particular, the hope is that by using 11.31 as a vaginal microbicide a huge army of T-Cells will be localized at the HIV port of entry.
With this understanding, it’s time to read again what the Global HIV Enterprise has declared to be one of its highest priorities:
“4. Create “smarter adjuvants” that are most appropriate for inducing localization of T-cells to gut mucosa. Establish broad-based access to these reagents by researchers.”
Here’s my translation of the above new AIDS research priority: “Use 11.31 and other ‘smart adjuvants’ to mature and activate Dentritic Cells and thereby stimulate a T-Cell attack against HIV in the vaginal port of entry. Establish broad-based access to 11.31 and PPHM’s other anti-PS MAbs by researchers around the world by encouraging them to order these MAbs from Avid.”
COULD THIS BE THE SOURCE OF ALL THE NEW AVID REVENUES WE ARE HEARING ABOUT???
"This will give us the necessary internal resources to expand the ongoing Bavi Ph.2 studies and TO PREPARE FOR LATER-STAGE CLINICAL TRIALS."
Charlie, Thanks for re-posting this SK remark. Light bulb went off. Could SK be saying that they want to scale back on Cotara expenses so as to have more money to dedicate to a "LATER-STAGE" Bavi Ph 2-3 trial???
I guess "later-stage" could mean either a bigger Ph II or a Ph II-III.
See new post today on JBM's Anti-PS Blog: http://anti-ps.blogspot.com/
Minutes from the Jan 21, 2009 Science Committee Meeting of the Global HIV Vaccine Enterprise.
SCIENTIFIC PRIORITIES FOR THE ENTERPRISE SCIENTIFIC STRATEGIC PLAN:
CURRENT AND FUTURE
• The chair noted that if the purpose of a vaccine is to stop disease early, efficacy is dependent upon pre-existing, broadly neutralizing antibodies.
• Some hope exists for eliciting broadly neutralizing antibodies. There are some broadly neutralizing antibodies produced by infected patients. However, these antibodies have unusual features and are not elicited frequently. Immunogen design will need to be oriented towards obtaining a similar response.
Below are each group’s s key scientific priorities:
4. Create “smarter adjuvants” that are most appropriate for inducing localization of T-cells to gut mucosa. Establish broad-based access to these reagents by researchers.
6. Increase understanding of (a) the mechanisms through which broadly neutralizing antibodies act on HIV and (b) antibody function beyond neutralization (e.g., complement activation, antibody-dependent cellular cytotoxicity and other Fc functions).
"The ideal scenario is they have enough positive data now and with that are able to find a partner to add a cash infusion and help design and manage the next stage of larger, controlled trials. If that happens prior to any dilution, I believe we'll quickly move beyond $1."
Well said. If they can close either a large gov't/Avid stockpiling deal or a small licensing deal to turn the cash corn this summer without more dilution and more debt, we will surely sail above $1.00.
Flglf4-- I would disagree:
You say: "And the quality of the data will be defined by not only the measurable efficacy and ttp results, but also by the trial size and how it was designed/conducted. I'm really hoping for incredible measurable results, because the other two factors are not working in our favor imo."
Our Phase II trial size is really 150 patients across 3 trials (45+46+49). As Joe Shan said in the recent 3.12 CC: "When looking at the Ph 2 data available to date, what is most encouraging is the consistency of the results across all 3 studies, which are being conducted at over 15 clinical sites."
When you get consistently good data on 150 patients FROM 15 DIFFERENT SITES, the credibility of your data is not in question.
Regarding trial design, the Company went to great trouble to imitate Avastin's Ph II trial design to enable an apples to apples comparison. That's one of the best things we've got going for us.
Regarding trial results, you have to keep in mind that our data may be the first ever in the history of cancer research where the ORs actually increase over time rather than diminish over time due to our apparent ability to trigger an immune response to the tumor. As SK said in responding to Ren in the recent 3.12 CC: "We will have a number of updates coming up as we move into the 2nd parts of the 2 Bavi plus CP [India] studies. As you said, THE RESPONSE RATES ARE CONSTANTLY CHANGING AS WE CONTINUE PATIENT TREATMENT AND FOLLOWUP in the studies. I think we will be ABLE TO GIVE SOME NICE, UPDATED NUMBERS OVER THE COMING WEEKS."
SK is telling us that the "response rates are constantly changing" in the right direction, otherwise the updated numbers wouldn't be "NICE." And remember what Shan said, they are seeing this immune response effect "consistently across all 3 studies."
Actually, I think the upfront payment for an Asian license would be in the range of $20-$60M, but if I said that, people would be distracted, Realist would have a target, and my point would be missed, namely, the sequence is:
1. More Data over March, April May
2. Partnering deal over summer
3. And sale of shares at market price only as a safety backup position to increase negotiating leverage.
"if i was bp i would want the whole thing now."
Exactly. That is precisely why the Company needs a backup plan to raise $7.5M in the open market so they have the credibility and negotiating power to tell BP: "It's either $20 million up front plus royalty on all sales to own the Bavi cancer market in [Asia?] or we don't do the deal. World wide rights are not on the table at this time."
Seems the plan is:
1. Use April and May to release new cancer data at AACR and ASCO, and hopefully some Duke/Haynes publications as well.
2. Once another round of strong new data is on the table, close a regional Bavi license in June with upfront royalty in the range of $7.5M to $30M. My guess is it will be an Asian license with Mary Boyd's contacts in Japan or China.
3. If BP plays hard ball and refuses to offer fair terms in the license negotiations, have backup option to sell $7.5M worth of shares at market price without warrants. The combination of $7.5M plus the second $5M from loan plus Avid revenues is enough to operate for another full year and keep BP honest.
"When you look at how the articles yesterday reveal that Bavi may reduce VEGF and Avastin mops it up...you can see how they might work together."
Thanks DIA76 for this statement. I think you hit the nail on the head much more than I did yesterday. The big point is not that Bavi is more efficient or "better" than Avastin. The big point is that they can work together and compliment each other.
Nicely said. Thanks
Why would DNA allow Bavi to slip into the hands of a different BP that runs a head-to-head competition between the two drugs. It would make more sense for DNA to pay top dollar, acquire rights to Bavi, and thereby both deepen and guarantee its dominant market position.
My apologies for getting excited this morning. Caption should have read:
KEY GENENTECH SCIENTIST AND CREATOR OF AVASTIN ACKNOWLEDGES THAT PS IS A VIABLE UPSTREAM TARGET FOR REGULATING DOWNSTREAM VEGF.
Sorry if my shorthand was offensive. In saying an Anti-PS target is "better" than an Anti-VEGF target, I was assuming that everyone knows that upstream targets are always more efficient for regulating a downstream event than targeting the downtream event itself. Assuming safety is not an issue, this increase in efficiency does indeed mean that targeting PS is "better" than targeting VEGF directly.
That's the whole point of the article that Napoleone Ferrara (creator of Avastin) edited. You might want to read it. Here's the link: http://anti-ps.blogspot.com/
IMO
What get's me excited
is that this JBM post and the article discussed at the top of the blog by Friemark and McDonald (now both affiliated with PPHM) explains why MoJo's chart shows Avastin results dropping off over time.
What else would you expect if exposed PS and the other upstream events (i.e. mirovesicles that deliver EGFR that stimulates VEGF) are still causing more VEGF to be secreted.
Here's the link
to the Genentech story comparing anti-PS with anti-VEGF.
http://anti-ps.blogspot.com/2009/02/genentech-looking-at-blocking-ps-as.html
GENENTECH ADMITS ANTI-PS IS BETTER THAN ANTI-VEGF
Must-read post just hit the JBM Blog.
Clear implication of article, which is edited by the creator of Avastin, is that:
"Exposed PS thus appears to be an upstream target which can inhibit excess VEGF secretion from ocurring in the first place. Avastin attaches to VEGF in an attempt to slow blood vessel growth, but the VEGF is still being secreted in the area, Avastin simply keeps cleaning it up." Better approach is to block the PS which causes VEGF to be secreted.
PFS = TTP
Are not PFS and TTP just two different terms for the same measurement?
Thanks MoJo, You nailed it.
The RECIST guidelines in your pdf are worth downloading for future reference. Thank you.
As CJ said, the whole point here is to be sure we are comparing apples to apples when the Bavi GA data comes out. I am delighted to see that the 43-week mark is indeed the correct comparison if the GA PR comes out in mid-March
Thanks CJ. Very helpful discussion.
If anyone out there can confirm that PFS data is measured from the start of dosing (and not from the last week of the dosing protocol), that would be most helpful. It would confirm that the GA PFS data we get in mid-March (hopefully) should indeed be compared with how Avastin did at the 43 week mark.
If 43 weeks is the correct measuring mark on Mojo's chart, that means all we need is for 7 of the 14 patients to still be Progression Free and Bavi will have doubled Avastin's efficacy, not to mention its much better safety profile.
If 11 of 14 patients are still in PFS at 43 weeks, Bavi will have trippled Avastin's eficacy (e.g. 78% vs. 24%
14 patients is a very small patient population, but a DOUBLING or a TRIPPLING of efficacy results is a very large increase.
Remember, 5 more patient cohorts (second part of GA, two parts for India lung and two parts for India breast) will be rolling in with the same PFS data over the next three months. No wonder Mary Boyd will be in a position to license Bavi this summer.
CJ -- Thanks and one more question please.
Do you know whether Avastin PFS data is counted from the first day of dosing in the formal protocol (i.e. start of week 1) or from the last day (i.e. end of week 8) ?
When I count the months lapsed between July 2nd and March 2nd, I get 8 months. I assume you get 10 months because you are counting from the start of the 8-week dosing period.
If Avastin's PFS data is in fact measured from the start of dosing, than I agree any data that PPMH releases in mid March should be compared to Avastin as of the 10 month mark.
CJ- Please help me with this
It seems 11 of 14 patients GA breast patients had finished the eight weeks of dosing by the PR on June 2, 2008 and 14 of 14 had finished by the PR on July 2.
Thus by March 2, 2009 (i.e. shortly before the next CC), there will be 8 months of survival and TTP data on all 14 patients and 9 months of this data on 11 of them.
Could you please post Mojo's chart again. When does Avastin survival and TTP data start to fall off? My recollection is that it's about month 6 or 7.
Given they are always looking for something good to say just before the CC, it sure seems that the GA data is ripe for a comparison with Avastin in mid March, i.e. just before the CC and just before SK's March 18 presentation at Cowen and Company.
Thanks.
Jessme-- You are showing the same ignorance about how M&A works that you have showed about how the markets work.
An NDA (Non Disclosure Agreement) is signed as the first step in starting every dialogue about non-public information. Signing an NDA does not mean you pull up your skirts all the way. I've done lots of M&A work and I know the smart sellers only pull up their skirts ankle high. They leave the rest to the imagination.
Other theories, like the one Geocappy posted in 33227, are just as possible as mine. All I am trying to point out is that over-the-top Bidding Wars don't happen by accident. They happen because of careful tactics and design.
Hiding your Gold
In this emerging world of disappearing BP patents and hostile biotech takeovers, it’s very smart to keep your gold hidden until you have so much clinical proof that the size and value of your hoard of gold cannot be questioned.
I think that is why PPHM is only flashing a small taste of its copper and silver clinical data. It would be against the best interests of shareholders to flash survival and TTP data on 14 patients in India or Georgia when the risk is so high that a hostile raider could come in and argue convincingly that $1.20 per share is a very fair price.
IMO, it makes mores sense to hide the really important survival and TTP data (i.e. the real gold in comparing Bavi to Avastin) from the BPs until you have so much of it on so many patients in so many different trials that your claim to have replaced Avastin as the new standard of care IS IRREFUTABLE. By waiting until ASCO in late May to reveal how much gold we really have, the Company assures a BP bidding war where all the BPs have to admit the true value of our pipeline at the same time and everyone is forced to offer full price for the real market value of our pipeline.
As much as I would like to see the Company start waving its PR flag today, I have to admit that saving our best data to ASCO and releasing it all at once is the correct way to generate a BIDDING WAR. Releasing a little bit of gold dust about 14 patients here and 14 patients there is good way to invite hostile bidders who want to steal us off the table for 1/3 of what we are worth.
_________________________
Separately, can someone please confirm that the “two cycles” mentioned in today’s PR means 8 weeks. If this is correct, then we are looking today at clinical data where Avastin achieved 30.5% ORR in 18 weeks (six cycles), Bavi achieved 41% ORR in 12 weeks (four cycles) on the same tumor type, and Bavi achieved a 50% ORR in 8 weeks (two cycles) on a different tumor type.
I like the direction of this data !
It seems Bavi got a better response rate with only 2/3 of the dosing Avastin used.
If you go to the top right column on page 2 of the Avastin Ph II pdf (the one that you can link to from JBM's blog today at http://anti-ps.blogspot.com/), you will see that Avastin lung patients in that Ph II study ...
"...RECEIVED UP TO SIX CYCLES OF CARBOPLATIN/PACLITAXEDL."
Each chemo cycle of C-P is three weeks. So PPHM's Bavi data announced today (i.e. 41% response rate) comes from the end of 12 weeks and the Avastin data (i.e. 31.5% response rate) comes from the end of 18 weeks of treatment.
I wonder when we will get to see our 18 week data, Maybe PPHM's minimalist approach to this PR was due to ASCO considerations.
Mojo, I couldn't agree more with your post highlighting the safety differences. Given that Bavi's safety profile is so much better than Avastin, it is all the more striking that Bavi's efficacy surpasses Avastin in just 2/3 of the time and with only 2/3 of the dosing.
Why are you so afraid of Jazz' blog ?
Jessme-- this is the second or third time I've seen you shutter at the mention of Jazz's blog. It's such a great source of factual and relevant information, I would think we should all want everyone to become more familiar with those posts.
Are you showing your agenda again ?
My present to myself has a different wrapper.
I chose to believe that the Jan 6, 2009 deadline for the submission of abstracts to be presented at ASCO's May meeting is the controlling factor in the timing of PRs on the two India Bavia trials.
I believe the ASCO submission has to disclose all prior PRs regarding the subject matter of the abstract, and after the abstract is submitted on Jan 6, no further PRs are allowed or there is a risk the abstract will be rejected.
Thus, due to ASCO policies, I think Jan 6 may be the deadline for the Company to put out "Top Line" interim Bavi India data.
When SK said yesterday he hopes to be at ASCO "on a number of different fronts," I would like to believe this means presentation of data on the full 46 patients in the Georgia docetaxol trial plus the initial 21 patients in the India lung trial plus the initial 15 patients in the India breast trial. That would mean presenting data on a total of 82 cancer patients all treated with the same Bavi drug in a substantially identical 8-week protocol.
That sounds to me like the type of Ph II data that could get ASCO's attention.
I'll bet they are crunching Georgia and India numbers furiously between now and Jan 6. Might as well have the benefit of all the data crunching before you chose the adjectives you use when you put out Top Line data on Monday Jan. 5. It's just a guess but it makes some sense.
"I may have the erroneous impression that Haynes prefers an antibody other than Bavi, if Table 4 of the patent is correct."
I think that is a correct impression, at least for anti-viral therapy where the amount of exposed PS is so overwhelming that the availability of B2GP1 becomes a serious limiting factor on Bavi's efficacy. The same is not the case in the cancer tumor environment.
I think they developed PBN632 and other similar fragments that don't need the B2GP1 co-factor so that they can pump in a huge dose of the Mab and it will ALL get sucked up by exposed PS on the HIV and related microparticles. If they used classic Bavituximab in an HIV setting, only a small portion of the Mabs would attach to PS because the body only produces a small amount of the B2GP1 co-factor at any one time.
I think this is also why in cancer applications they have to spread the dosing out over 8 weeks so the body can generate more B2GP1 serum each week-- so that Bavi can go to work again.
Turns out "antibody" is a defined term in the patent.
Charlie points out in post 30883 that "All the claims have the limitation that there's an antibody involved and that it's the antibody that is targeting PS."
But in patent text posted in 30889 it says:
"The term "antibody" is thus used to refer to any antibody-like molecule that has an antigen binding region, and this term includes antibody fragments such as Fab', Fab, F(ab').sub.2, single domain antibodies (DABs), Fv, scFv (single chain Fv), linear antibodies, diabodies, camelized antibodies and the like."