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Underlying mechanisms involve improved glycemic control, but also increased nitric oxide bioavailability, reduced oxidative stress and, for certain molecules, a direct inhibition of platelet activation and aggregation

Clinical claims are sourced from peer-reviewed literature, regulatory documentation, and manufacturer specifications

Most treatment discontinuations were due to gastrointestinal AE and occurred during the rapid escalation phase this may be mitigated with more gradual dose escalation at phase 3 trials

Other recognized adverse effects include injection site reactions, increased heart rate, pancreatitis, and gallbladder disease