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 but resists DPP-4, 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 built on the same receptor rather than from venom.
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 bite, while genuinely venomous and very painful, very rarely kills: a Colorado man died in 2024 after a prolonged bite, which a coroner attributed to envenomation with pre-existing heart and liver disease contributing - the first such death in the United States in almost a century.