Human glucagon-like peptide-1 stimulates insulin release after a meal, but the enzyme DPP-4 degrades it within a couple of minutes, which makes it useless as a drug in its natural form. John Eng, working at a Bronx veterans hospital, screened Gila monster venom on the reasoning that lizard venoms disturb the pancreas, and isolated exendin-4: a peptide about 53 percent identical to GLP-1 that binds the same receptor and is not a DPP-4 substrate, so it persists for hours.
The synthetic form, exenatide, was approved by the FDA in 2005 for type 2 diabetes. It was the first GLP-1 receptor agonist on the market, and the class it opened now includes widely used drugs developed on the same receptor rather than from lizard venom itself.
Two things are commonly overstated. Later GLP-1 agonists are not made from Gila monster venom; they are separately engineered peptides. And the lizard's own bite, while genuinely venomous and very painful, has not been reliably shown to have caused a healthy adult human death in modern records.