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c/glp1science·submitted 1 year ago by u/zeynep_villalobos

[Question] how do you actually verify half-life

Questionbranch of 6 comments

how do you actually verify half-life. I am not trying to be the "source?" guy. I would just like a source. Glucose-dependent insulin secretion is why hypoglycaemia risk is low as monotherapy: the effect scales with glycaemia rather than acting unconditionally. Tolerance to the gastric effect develops with continued…

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6 comments, started 1 year ago
u/emil_agyeman412 points·1 year ago

Long half-life in this class comes from structural modification that promotes albumin binding and resists enzymatic degradation. Weekly dosing is a consequence of the molecule, not a convenience decision.

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u/gradient_goblin119 points·1 year ago

a mechanism you can state is not a mechanism you have demonstrated

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u/mod_ambulatoryadmin89 points·1 year ago

albumin binding is most of the half-life story

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u/neha_krastev606 points·1 year ago

the peripheral and central stories are not in competition

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u/hassan_ostergaard423 points·1 year ago

the peripheral and central stories are not in competition

Disagreeing with this specific inference — that is a preclinical result being read as human pharmacology.

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u/enzo_danquah199 points·1 year ago

glucagon agonism sounds paradoxical until you read the energy expenditure work

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The mechanism layer: incretin physiology, receptor distribution, gastric emptying, central appetite signalling, glucagon-receptor contribution, amylin co-agonism, and the pharmacokinetics that make weekly dosing possible. Papers get cited by journal and year or they get a [needs source] reply.

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