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The cagrilintide dosing protocols are still being established, but the mechanism of action, targeting amylin receptors for appetite regulation, offers a novel pathway distinct from GLP-1 agonism

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demonstrated that administration of AC3174, an exenatide analog, to a high-trans-fat, high-fructose, high-cholesterol diet (HTFD)-induced NASH mouse model led to a reduction in body weight and fat mass as well as in liver and serum lipid levels and to improvement in hepatic steatosis and inflammation [8]

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I would greatly value your perspective on: The evidence regarding GLP-1 use and safety in people with MS Whether the metabolic benefits alone justify considering them in someone with my profile