Biotech Values

[biomaven0]

[ALK] is a space (like CML) where preclinical results are highly predictive of clinical results.

In both cases (ALK and CML) we have a cancer driven by a single runaway pathway. If a drug hits that pathway, then it will work, at least for a limited period until there are mutations. So if you have a potent and selective kinase inhibitor it will likely be successful, assuming of course no weird tox issues arise. (By contrast, the situation with Aria's mTOR drug is much more complex - there you poke the pathway in one place and it bulges in two other places and turns inside out somewhere else - the only way you are really going to know if something works in practice is to try it. It's not the mTOR pathway itself that is the root cause of the cancers being treated - it is over-activated because of some other dysfunction, and so inhibiting mTOR doesn't get at the primary driver of the cancer).

The Ariad poster in fact predicted possible ways the pathway might mutate under the Pfizer drug. It was striking that the two mutations that emerged in practice and were disclosed in the NEJM article were among those listed as possible by Ariad. The Ariad drug by contrast seems much more resistant to mutations.

Of course I am making something of a leap here given that all we have seen so far is one clinical publication on the Pfizer drug and one preclinical poster from Ariad. That's why I don't have my entire portfolio in ARIA. :)

Peter