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It is even possible that the insulin-stimulating, glucagon-suppressing effects of the peptide or a more active synthetic analogue may be useful in the treatment of non-insulin-dependent diabetes, in which both impaired insulin release in response to glucose and persistent hyperglucagonemia are thought to be key pathophysiological abnormalities' (Kreymann, Ghattei, Williams, Bloom)

These developments collectively reshape the ePA landscape for GLP-1 drugs

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