National Geographic : 2013 Feb
78 national geographic • february 2013 drug derived from pit viper venom, reached clinics in Europe in 1968. Today Arvin has been replaced by other viper venom anticoagulants. The Brazilian pit viper’s venom led to the development in the 1970s of a class of drugs called ACE inhibitors, now widely used against hypertension. Researchers began by asking why Brazilian banana plantation workers bitten by these snakes collapsed with crashing blood pres- sure. The researchers then teased out the key pressure-lowering component in the venom. But drug-company managers needed convincing that what comes from snake fangs would save human lives. And you can’t just put venom in a pill and hand it to patients, so the useful com- ponent of the venom had to be modified at the molecular level—resized and tinkered with to survive the harsh effects of the human digestive system. Eventually a synthetic version made it to human trials, and in 1975 the first oral drug for hypertension, captopril, was approved for use. The ACE inhibitor class of drugs pioneered by captopril now treats tens of millions worldwide, with multibillion-dollar sales. The molecular gifts of toxic animals offer hope in the fight against a host of debilitating diseases. Heart patients owe gratitude to the Eastern green mamba, a deadly African tree snake whose venom impairs its victim’s nerves and blood circulation. Researchers at the Mayo Clinic fused a key peptide from the venom with a peptide from cells in the lining of human blood vessels to make cenderitide, the subject of clini- cal trials. It is intended not only to lower blood pressure and reduce fibrosis (the growth of ex- cess connective tissue) in a failing heart but also to shield the kidneys from an overload of salt and water. “ That’s the beauty of this drug,” says Mayo cardiovascular researcher John Burnett.