Two oral presentations at ASH

[jpheis]

http://ir.geron.com/news-releases/news- ... t-upcoming

[biopearl123]

Here' s the link for the high risk R/R study: https://ash.confex.com/ash/2018/webprog ... 15163.html

Its worth reading the other abstracts to see how they (don't) compare. Imetelstat has a large number of patients analyzed perhaps the largest. Additional studies confirm JAK failures and dismal prognosis. No OS yet. As genetic mutations get broken down pay special attention to TN (triple negative mutation) patients who had not yet reached MOS. I will wait for Sdraw to analyze both abstracts as he will do a better job than I can. I do encourage people to read all of the relevant abstracts and draw your own conclusions. I don't see too much competition right now. The MDS study also looks quite interesting. I am sure there will be lots of discussion up to and after ASH.

[biopearl123]

Here's the low risk link: https://ash.confex.com/ash/2018/webprog ... 14877.html

[karagozoglu12345]

Bioperl, Sdraw, and others, who have more insight than I in this field, please address my questions and concerns below:

If the data is compelling for MF, as Scarlett put it, why not set clinically meaningful parameters (based on FDA approved cancer drugs, hitherto, that had met MOS endpoint) and inform investors about the decision to take it to Phase 3 in more specific terms such as “at a certain preset threshold date if MOS has not been reached, we will proceed with Phase III in MF indication”? When the only analyst in the CC asked a question about this, Scarlett again chose to avoid any explanation in forthcoming terms and kept going around the circles.

Could the below conjecture be the reason:

Even if Imetelstat extends life at a clinically meaningful length, given the dismal statistics on remission rates while on Imet, perhaps there is a dilemma of longer life vs. quality of life as R/R patients are very sick. Could other meds simultaneously help with the symptoms while Imet extends patients’ lives by modifying the root cause of the disease? Given the patient cohort is R/R, when Jakafi no longer helps is there even a possibility of any other drug to address the symptoms? Also, in the absence of knowledge regarding MOA , it is counter intuitive to me to expect a positive MOS if remission curve is negative ( I am most likely missing a key detail I hope). If there is uncertainty at this juncture, I can see the challenges in deciding on Phase III even if MOS data will turn out positive.

[The-Zete]

karagozoglu12345
Please expand on these 'dismal results' relative to remissions .

[karagozoglu12345]

In the previous CC after negative CD, Scarlett said MF trial showed 1 PR and no CR. Please correct me if my memory is defying.

[biopearl123]

Your memory is correct. This finding is in stark contrast to Dr. Teferri's study which involved patients with much less advanced disease. bp

[karagozoglu12345]

Thank you for confirming my suspicion that Tefferi/Mayo pilot trial involved early stage patients. If Imet provides "disease modifying" spectacular results for the early stage patients, then Janssen trial design focusing on R/R patients was not a good idea by any stretch. The Imet trial for MF should have focused on early stage patients with the end point being progression free survival (PFR). It is quite plausible that these patients would be relatively symptom free (or reduced levels) and live longer lives than the case of Jakafi-R/R point-Imet sequence. In any disease if available drugs heal the root cause of the disease symptoms decrease and eventually disappear. Provided the aforementioned design is successful, Jakafi market could be largely cannibalized by Imet as well. Jakafi would be used only if symptoms while on Imet warrant it. If there is any shred of validity in these considerations, Janssen's design did a huge favor to the competitor. I don't know if Geron had any say in the study design for Imet at Janssen.