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If you are intrigued by SGMO's technology, perhaps this company developing stem cell gene therapy for HIV with core technology from Dr. David Baltimore's lab, is also of interest:
http://www.calimmune.com/home.php and #msg-82723285 and reply.
You're right, this is very confusing as Can-Fite's stake in OPLI is valued higher than market value of CANFY and it was almost two and half times a year ago before Denali (DCMG) changed to OphthaliX (OPLI).
Can-Fite
Market cap is about $26M (97M NIS) see http://www.tase.co.il/TASEEng/General/Company/companyMainData.htm?companyID=001272&subDataType=0&shareID=01094473
Can-Fite (TASE:CFBI; OTC:CANFY)
CF101 Psoriasis Phase II/III quantitative interim results, see slide 12 in the presentation:
http://www.canfite.co.il/upload/2012-12-30_Can-Fite_Overview-English_isa.pdf
Not stat-sig vs placebo at 12 weeks with data from 103 patients, but with additional 188 patients I think it will be.
One odd observation: placebo switchers improved as soon as being put on the 2 mg drug (too quickly) after week 12.
The PR:
http://www.canfite.co.il/upload/2012-12-30%20Psoriasis%20additional%20analysis%20-%20English.pdf
Not following OGXI closely (still following TEVA), but am not optimistic on antisense drugs in general.
Here are several more collaborations Teva dumped (one more that is not mentioned in the slide is MediWound http://www.medical-device.co.il/index.php?option=com_content&view=article&id=7557:teva-cancels-mediwound-collaboration&catid=22:israel-pr-archived-news&Itemid=90 )
I don't understand why they didn't test patients tumors for MUC1 expression level and enrich the trial with those having high expression, that should better respond to stimuvax, as many could have had low MUC1 expression:
http://jcp.bmj.com/content/51/9/667.full.pdf
Calimmune's stem cell gene therapy approach for HIV
It is a very different and exciting approach since it tries to render the immune system resistant to HIV rather than directly disrupt the virus itself and has potential for virus eradication.
Questions/Challenges
First, gene transfer with hematopoietic stem cells is challenging plus there's the risk of mutagenesis occurring in host cells by the vector virus.
It is not clear what level of engrafted genetically modified cells will be in the bone marrow without prior complete myeloablation and what percentage of these cells in peripheral blood would be required for clinical benefit in HIV patients. [Also not clear that the apparent cure of the Berlin patient resulted solely from HIV resistant cells transplant. Chemo, immunosuppressive and other drugs could have had an additive effect especially on HIV reservoirs.]
Even if the level of genetic marking of peripheral blood cells is of clinical benefit, will it remain so long-term? Expression of the therapeutic transcript in the peripheral blood might decline over time allowing viral rebound.
You're right, Aromasin is indicated for use after Tamoxifen treatments. Novartis/Femara and Astra/Arimidex are indicated for 1st line treatment of postmenopausal women with ER+ BC. So they could have used either from this aspect. I can think of why Femara over Arimidex too.
Re: Phase-2 data for PFE’s PD-991
PFE's PD-0332991
PFE's PD-0332991+letrozole vs. letrozole in 1st line ER+/HER2- advanced breast cancer phase II results :
http://www.bloomberg.com/article/2012-12-05/aQxRMpe1_OE4.html
GILD - new NS5A P1 trial
MRK's lead BACE inhibitor - MK-8931
Evolution in the HCV treatment paradigm
If indeed there is different potency in different genotypes as seen in POSITRON trial, ideally we'll have different regimens for them (also for subgroups like naïve, experienced etc), but my guess is there would still be one regimen to start with and a more potent one will follow. One observation that backs this approach is this line from GILD's PR posted by Roy in #msg-81844469:
You are right of course that it is known for some time now that IL28B status is an irrelevant factor when you treat HCV with a potent DAA combo and perhaps (not sure about that) GILD were still genotyping the IL28 locus, but even if so, it would be a response predictor for INF containing treatment (predicts viral clearance) not INF intolerance. So my feeling is that these patients are a bit more intolerant to treatments in general and naïve comply better.
I'm not sure they are as convenient to treat as treatment-naïve.
These patients are not equal to treatment-naïve
I think GIVN is just saying the FDA has not required a PMA for its PillCam COLON 2.
PBTH
PBTH
Two additional caveats:
Phillip Frost holds ~ 20% of the shares.
Phase II is really only a pilot study since (in addition to what you've mentioned) it was also short treatment (one month), patients weren't hGH-naïve, and primary endpoint was IGF-1 levels, these are not the conditions for the future phase III trial.
Yes, it's even very reasonable Servier knew that the 21 patients are responding well also because response was shown in the Turkish trial very quickly (in 4–21 days).
If you meant this ongoing 21 patients trial http://www.controlled-trials.com/ISRCTN15180871 I don't know if results were presented yet and it's also an open-label trial.
Thanks for the correction on Anakinra being an IL-1 antagonist not an antibody, still that doesn't change my point about the two trials design and size.
I amuse I'm stating the obvious here but that pilot XOMA's trial was an open, uncontrolled, in 7 patients only, in Turkey (http://ard.bmj.com/content/71/4/563.abstract).
For the sake of comparison, this is AMGN's Kineret (a different anti IL-1 antibody, which is behind XOMA in Behçet’s disease) pilot trial - randomized, controlled, in 25 patients in US:
http://clinicaltrials.gov/ct2/show/NCT01441076?term=Beh%C3%A7et%E2%80%99s+uveitis&rank=9
Although data from that pilot study are good, I somehow get the feeling of rushing into phase III.
BTW, CSL had a safety problem with the 1st gen plasma derived drug in phase II and started all over with CSL-112.
Not following CSL in particular, just the when they happen to cross another field of interest.
RVX