The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
the most urgency I ever had was waiting for pcsk9 I better stick him on the market when I read that first paper in the New England Journal of Medicine about 12 years ago on the discovery of this type of you know these these individuals who had missense mutations in that enzyme that lowered their LDL significantly
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Bookmarking — the dossier-vs-overview split is the right call. Most of the time I want overview; sometimes I want receipts.
Would love a "what would change this verdict" RSS feed. Sign me up if it exists.
But PCSK9 is...it looks like it's shaping up to be a terrific example of something that basically all humans can be thought of as having the same disease, and therefore it's a large market could be low cost. Aging is another or a variety of age-related diseases that might have a common core where we are programmed to die at a certain age. The mice diet at two years old, bowhead whales at 200, humans somewhere in between. And so that's probably negotiable. Now, PCSK9 is not solving aging in general. It's a very specific thing that may be common to most humans. It was de-risked because there were a few humans that were walking around that were basically double null for both copies of their PCSK9 from mom and dad. That kind of showed us that it was going to be safe and effective, although there's still quite a bit of long-term studies that have to be shown to make sure it doesn't cause early onset neurodegeneration in the particular way that we're implementing it, which is not germline, which is how it...the people that previously had PCSK9 nulls for germline via natural mutations.