I think this may be promising (and I am usually very skeptical of topicals and chemicals these days because most of them produce inconsistent results).
While Janus Kinases have a number of different roles, it may be that they’re involved in hair growth signaling (perhaps downstream of the prostaglandins?)
Dr. Christiano’s statement that some drugs and signaling agents which activate the growth phase of dormant follicles (I think you can include Minoxidil and PGE2 in this category), by experience, usually work in an uneven and sometimes patchy or unpredictable way, as opposed to this JAK inhibitor which is producing even, very substantial hair growth by switching the growth phase from telogen to anagen.
Remember that the very final step in most kinds of hair loss (different types of alopecias including MPB) entails signaling the follicle to have much shorter growth phase, and remain in dormant phase for longer and longer periods. So ultimately when you have MPB, the affected follicles have insignificant growth phases and very long resting phases. That results in shedding, shorter and shorter, finer and finer hairs until the follicle no longer produces a hair.
DHT sensitivity seems to trigger a pathway which involves things like PGG2 Synthase, excess PGD2 production (and possibly suppressed PGE2), and a few other things, all of which ultimately suppress the activiity of stem cells, reducing the numbers of progenitor and DP cells, which mimics a dormant follicle.
Now it looks like Janus Kinase (JAK) is involved. What is very interesting here as Dr. Christiano says, is the evenness and extent of the regrowth, which to me, suggests that JAK is located very far downstream in this complicated mess. Maybe it’s the final biochemical step, or one of the last, before stem cell suppression?