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Preclinical studies with SAR425899 clearly demonstrated dual receptor agonism in vitro and in preclinical in vivo studies, with a higher potency for the GLP1R than for the glucagon receptor in order to counterbalance the GCGR mediated increase of blood glucose levels through GLP-1 agonism 11,12,13

Those patients were then compared with a control group of similar individuals, also with diabetes or obesity, but who were not treated with a GLP-1

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