Take aways from ASH2015

[Fishermangents]

by sdrawkcabeman (repost from Yahoo MB, 6 Dec 2015 1:12 PM)

Points to drive home from the presentation

The emphasis and growing chorus is that there’s a serious unmet need for MF/MDS/AML pts, and that’s the big push coalescing behind Imet. In the Q&A Dr. Baerlocher, Dr. Burington, Dr. Scarlett all stressed it, and the pervading atmosphere here is a palpable excitement for a completely new drug w/a completely new MOA, which, above all else, has a rapid and significantly efficacious effect on the actual diseases.

All studies unequivocally validate Imet’s use as a treatment for myeloid malignancies, and the pivotal P2/3 Imerge exemplifies the investigators’, FDA’s, EMA’s, and the scientific community’s confidence for a drug that achieves unprecedented efficacy in the heme diseases; more to the point, the unprecedented efficacy is in contrast to the utterly inadequate SOC. And this was emphasized repeatedly, Imet simply outperforms SOC. Dr. Burington highlighted how the very modest p.endpoints have been sufficient for NDA and, in that regard, the purpose of both Imbark/Imerge is to demonstrate very plainly that Imet achieves what SOC does, and does it even when pts are R/R to SOC, leaving them totally w/out options. That couldn’t be a stronger argument for registration; now, in that context, add Imet’s CRs/PRs.

Other:

Everyone on that panel acknowledges all toxicities are predictably and completely manageable w/simple dose modulation. And I heard thunder when Dr. Burington relayed Dr. T’s comment RE Imet’s specificity; to paraphrase, considering Imet’s remarkable efficacy, Dr. T expected MORE myelosuppresion but instead saw LESS due to Imet’s clonal specificity, music to regulators’ ears.

Also, MDS RARS/T was selected for splicesome, yet showed no shift in allelic burden; this means Imerge, w/no such qualification, may actually produce CRs/PRs in pts w/out splicesome or w/U2AF1.

[imet]

yahoo!!!!