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Plontke SK, Siedow N, Wegener R, Zenner HP, Salt AN
Those seeking structured, medically guided care: These treatments arent meant to be used on your own
We found that the rapid depletion of SNIP1 induces widespread splicing defects, resembling the effects of CDK11 inhibition with OTS964
However, there is no peak of insulin levels (see above)
What they found (summary): Amylin is a critical partner of insulin in metabolism, the loss of amylin in T2DM is as significant as the loss of insulin The AMY1 receptor in the area postrema is the primary target for the appetite effect Amyloid aggregation is the main problem with native amylin, proline substitutions (the Pramlintide strategy) are essential The half-life of native amylin is only 13 minutes, that is why lipidated analogs like Cagrilintide are necessary Perspective: amylin + GLP-1 combinations are the natural evolution of metabolic pharmacotherapy Why it matters: This is the reference article for amylin pharmacology
