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And the catalog presents oral and injectable GLP-1s side by side without explaining the meaningful clinical difference between them

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[4] A more potent, binding-protein-resistant analog such as IGF-1 LR3 would, by mechanism, be expected to retain this hypoglycemic potential, and because it evades the buffering system that normally tempers free IGF-1 activity, the metabolic effect could in principle be less predictable

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