I don’t have a negative bias toward VX-509 or JAK3 inhibitors in general; rather, I’m saying we don’t know enough yet to infer (as you did in #msg-75545834) that JAK3 specificity is an advantage.
We had this discussion when VX509 ph2a data first came out. Compare to two other JAKs in RA space from PFE, LLY at same stage, AE profile was worse. Obviously this could be due to dosing range was really wide in VX509 ph2a trial. So far, couldn't see any advantage over other JAKs from clinical data, unlike Galapagos' JAK1 whose question is whether ph1 data would hold up in larger and longer trial. So the future of VX509 is really up in the air until we see more data from close to chosen dose.
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