doi: 10.1111/j.1365-2249.2009.04007.x 520 MackayFSchneiderP
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
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Interestingly, DiR to the brain delivered by COXP micelles was further increased when co-administered with GSH [52] - an encouraging synergistic effect by GSH for GSH transporter mediated brain targeting
it is a synthetic, stabilized fragment created for research purposes
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