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Native GLP-1 has an extremely short half-life due to rapid degradation by dipeptidyl peptidase-4 (DPP-4), and GLP-1 receptor agonist analogues are engineered with structural modifications to confer resistance to enzymatic cleavage and extend circulating activity in experimental systems

And so the thinking behind that is perhaps there are other complexes that are unique to the different solid tumors

These structural modifications result in approximately 98% albumin binding in physiological buffers and an extended plasma half-life compared to unmodified GLP-1 analogs in preclinical pharmacokinetic studies