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So CagriSema applies two independent signals that both converge on decelerating the stomach: cagrilintide via amylin/AMY receptors in the area postrema and its vagal output, and semaglutide via GLP-1 receptors on vagal afferents and in the brainstem
The compounds anti-inflammatory cytokine modulation and its support for local blood supply via angiogenesis are the most plausible mechanisms for these joint-level effects
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The rate of discontinuation due to adverse events varied from 5% to 19%, predominantly due to gastrointestinal side effects [17]
