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Clinical trials have shown that canagliflozin reduces major adverse cardiovascular events (MACE) [15], while empagliflozin decreases cardiovascular mortality by 38% and heart failure hospitalizations by 32% in patients with T2DM at high cardiovascular risk [16]

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[1] These effects typically diminish over time as patients develop tolerance, usually within the first few weeks of therapy

Tryptophan 33 in GLP-1R is required for PF-06882961 signaling Prior to the selection of animal models for in vivo pharmacology studies, we characterized the potential for species differences in GLP-1R activation with our small-molecule agonists