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And so, another working week will soon draw to a close. Not a moment too soon, yes? This is, you may recall, our treasured signal to daydream about weekend plans. Our agenda is especially modest. We hope to tend to the Pharmalot campus, take our short person for a dollop of ice cream, and promenade with the official mascot. And what about you? This is a fine time to enjoy the great outdoors, so perhaps a jaunt to the beach or a hike up a mountain is in order. You could engage in a little spring cleaning. Or simply catch up on your reading. Well, whatever you do, have a grand time, and be safe. Enjoy, and see you soon. …

A pharmaceutical turnaround artist has teamed up with a former Martin Shkreli acolyte in an effort to depose him, recruiting a few industry lifers with a new plan for the former Turing Pharmaceuticals, STAT reports. If they succeed, step one would be undoing the 4,000% price increase on the drug that transformed Shkreli from an anonymous entrepreneur into the reviled “pharma bro.” “I want to right the wrongs,” Jason Aryeh, a health care investor, told STAT. “I want to throw the bad guys out. There isn’t a bigger, badder guy than Martin Shkreli.”

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  • Current human clinical trials indicate that aducanumab does not reliably lead to meaningful clinical benefit in symptomatic or asymptomatic Alzheimer’s. The current aducanumab data are uncompelling. Some critics of “the amyloid hypothesis” have seized this moment of ambiguity about aducanumab as evidence that the amyloid hypothesis must be wrong. There are 28 disease-causing mutations in the amyloid precursor gene APP alone: all cause Alzheimer’s, and all do so apparently because each mutation accelerates accumulation of a neurotoxic amyloid “oligomer”. Trialists can reliably purge the brain of all detectable amyloid but — so far — not in a way as to cause reliably a meaningful clinical benefit. Though disappointing, wholesale rejection of the amyloid hypothesis is unjustified. The advantage of aducanumab (and lecanemab and donanemab) is that they purge all detectable amyloid while “moving the needle” on clinical trajectory (albeit to a degree unlikely to be noticeable to patients or families). However, laboratory evidence indicates that while some amyloid oligomers are toxic, there are also oligomers that can be inert or even beneficial. We are hamstrung by our current inability to distinguish amyloid oligomer subtypes in the living brain. The challenge is to identify the “right” at-risk population for subject selection and marry them to the “right” dosing and timing scheme so as to deplete harmful amyloid oligomer subtype(s) at the disease stages when these subtypes are important. Biogen is obliged to establish a protocol leading reliably to a meaningful clinical benefit.

  • It is indeed late in the day to observe this development, but I have asked on “these pages” more than …. Thrice, did the prices for the the PharmaBro drug ever get lowered?
    Now that I have this not unexpected answer (NO), I should ask about those 2 Valiant drugs that went up some …. 700 pct? I should indeed, but will I?

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