Biotech Values

[mcbio]

You may be right. At the MLNM gave no indication that they were working to improve the linker that they got form IMGN they way Genentech has. However, there was talk that one of the big factors for the failure of the PSMA drug was that the target is shed copiously into the circulation. As you can imagine, this can produce a kind of "sink" for the toxin-PSMA Ab construct, reducing the amount that gets to the tissue.

pgs: Curious if you have any comments on PGNX's early results for its PSMA ADC for prostate cancer that I posted on in #msg-67357499 and, most recently, #msg-71663954. Namely, do you find the early results encouraging and do you think they lend credence to the possibility that the prior failures of PSMA Abs may have been due to the specific drugs themselves, not the target? Also, how strongly do you think large drops in circulating tumor cells will correlate to a potential OS benefit? Note in the most recent Phase 1 ASCO GU update poster that while some patients seem to derive no benefit, there were also patients that saw large drops in their CTCs. Specifically, looks like 2/4 patients in the 2.0 mg/kg group and 2/3 patients in the 2.2 mg/kg group saw large and sustained drops in CTCs from baseline. Separately, PSA declines don't necessarily correlate as only 1 of those 4 patients that had a large drop in CTCs also had a large drop in PSA. I do believe that drawing conclusions based on PSA changes tends to be a bit controversial though. So, is the drop in CTCs the more important endpoint to focus on here?