Replies to post #157933 on Biotech Values

[NP1986]

Not only in regards to the overall health of the patients with MF vs ET/PV but also it's unclear how much of a driver the Jak allele burden is in these various disease settings.

As I recall, the data from the Jakafi trials suggest that mutant JAK allele burden is not a predictor of efficacy.

[iwfal]

GERN and INCY -

A few or two ago I also dug up the allele burden data for Jakafi vs imetelstat. The comparison does look good for imetelstat, but like you I'm mindful of the caveats.

Found ET (data). For Jakafi. It exists in two locations and they don't completely agree - which I have not figured out. Bottom line is that it looks like imetelstat does a substantially better job of controlling excess platelets than jakafi. Of course this is about a comparison across trials and the imetelstat ET patients did start with somewhat lower platelet count to begin with. Nonetheless... .

Jakafi data in ET:

See link to presentation in this PR.

See results tab in Clinical Trials.

Further commentary:

1) HU appears, both across diseases and across different cell types, to be consistently not-quite-as-good as jakafi. Or, in other words it isn't like, for instance, jakafi is just much better at controlling WBC than HU, but much worse at controlling platelets. FWIW.

2) imetestat data for wbc or hematocrit or spleen size in ET doesn't appear to have been measured. GERN just generally seems to run minimal trials - collecting very little data other than primary endpoint and SAE.

3)AE for the imetelstat ET trial showed a substantial rate of ALT/AST abnormalities - which is not something listed as an AE in any of their solid tumor trials. An oddity I cannot yet explain.