Snapshot · The Peter Attia Drive
Captopril, designed using a venom peptide from Brazilian pit viper as its structural lead, was approved by the FDA in 1981 as the first oral ACE inhibitor in clinical use.
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At 25:00 · chapter starts 21:00
The story begins in Brazil in the 1940s, where pharmacologist Maurício Rocha e Silva was testing the hypothesis that pit viper venom caused circulatory shock by releasing histamine from blood plasma. The hypothesis was wrong. The venom released something else entirely: a potent vasodilating peptide he named bradykinin. A decade and a half later, Rocha e Silva's graduate student Sérgio Ferreira noticed that bradykinin in plasma was more active than synthetic bradykinin, and traced the discrepancy to a second family of venom peptides — Bradykinin Potentiating Factors (BPFs) — that protected bradykinin from degradation. [1] — Peter Attia "ACE inhibitor chain: 70 years of fieldwork: The entire ACE inhibitor drug class, from bradykinin's discovery in the 1940s to captopril's FD…" 26:30 Ferreira carried powdered BPF to London, to a lab studying pulmonary circulation, where postdoc Kevin Ng had discovered that angiotensin I converts to angiotensin II in the lungs. A key convergence: the same enzyme that destroyed bradykinin was also making angiotensin II — a dual-function regulator sitting at the center of the blood pressure system. Squibb's chemists used the smallest active BPF peptide as a structural lead and designed captopril, the first oral ACE inhibitor, approved by the FDA in 1981. [2] — Peter Attia "Captopril FDA approved 1981 — first oral ACE inhibitor: Captopril, designed using a venom peptide from Brazilian pit viper as its structura…" 25:00 From captopril came enalapril, lisinopril, ramipril, and ultimately the angiotensin receptor blockers. The renin-angiotensin-aldosterone system is now one of the most drugged pathways in medicine. The causal chain from a Brazilian snake farm to tens of millions of lives saved spans 70 years and five countries — and nobody in it set out to treat hypertension.
Maurício Rocha e Silva wasn't looking for bradykinin — he was testing a wrong hypothesis about histamine and circulatory shock. The accidental discovery of bradykinin, then of BPF, then of ACE's dual role in blood pressure, handed medicinal chemists a structural lead for captopril that no one had designed from first principles.
The entire ACE inhibitor drug class, from bradykinin's discovery in the 1940s to captopril's FDA approval in 1981, emerged from roughly 70 years of sequential curiosity-driven research without anyone initially intending to treat hypertension.
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