Looks like we have some panicking shorts appearing. I will assume that you are either a short trying to misinform or some kind of paid agent trying to drive the stock price down. It is a pitiful attempt.
<HSP90 is ubiquitous, a chaperone needed for many house keeping proteins. Maybe oncogene/mutant proteins need more HSP90's help?>
All anti-cancer treatments affect normal cellular proteins. The key is to affect cancer cells more, or mutant oncogenes which drive cell proliferation more than their wild-type counterpart.
Their is indisputable data for a large number of mutant proteins which illustrates are they are far more dependent on HSP90 for their stability and or their folding into an active form. Your question here vividly illustrates that you know little or nothing about HSP90 inhibitors. I was especially amused when you claimed in another post to have significant experience in HSP90s but don't even know this basic fact.
<The best data I found was phase II breast cancer, but n is so small. I am not convinced.>
Look at the ALK+ in lung cancer. Yes the breast cancer data was small, but there was still some interesting indications of efficay. That trial was also for Ganetespib as single agent, and NSCLC is for Ganetespib + Dox so they are hardly comparible.
Actually thinking about what you posted. Yes all the institutions and alike, see no credibility in SNTA. None of the big institutions do any type of homework, they just have a dart board and pick there stocks from that. I do not think so. There has been a lot of Credibility shown from Trials etc over the Months.
I use my own analysis, never listening to an analyst. I believe Mr. Thomas Wei at Jefferies is a parrot only.
I personally worked with Chaperones. So I do have some hand-on experiences many years ago. At the presentation, it looks only the oncogene proteins bind to HSP90. How about other house keeping proteins.
If you look at the experimental data carefully, you will find SNTA only uses 5nM concentration, not higher. You know why? Because of toxicity. Has the management told you or warned you? no!
Then take a look at what 5nM of G (Ganetespib) does? It could only inhibits a few proteins to a much less extension.
Since some oncogenes are over expressed, they may got preferentially inhibited. But I did not find their data at presentation.
Above is my pre-clinical evaluation.
More importantly, the existing clinical data do not support the following three big claims:
I just could find any statistical significant data to support the above claims.
At best, I would say the efficacy is anecdotal. A few cases only. For example, as a single agent in phase II breast cancer presented in ASCO11, only 2 pts of 22 (9%) showed any activity (CR+PR+SD) that last > 6 months, which is a significant reduction of efficacy rate at 9 of 22 at month 5. This raised serious questions:
1) is the efficacy real? Confirmed? (Only confirmed response rate is reliable). 2) durable?
I will go through the data again this weekend.
Anyway, I find SNTA has its characteristic that has not changed since its elesclomol debacle. They like to present lots, lots of scientific reasons/circumstantial evidence to show their scientific excellence, but not clinical excellence.
I have a bad feeling. History more then often repeats if we do not change our behaviors.
Well that's a bit of an unfair characterization of what pick is saying. What would show real credibility for SNTA is if a big Japanese pharma were to step up and say "Your work shows promise,we will partner with you and give you "x" multimillion dollars." Until then,no matter how "interesting" or "exciting" the work is, there is no way of valuing the company.