From the discovery of a mysterious blood-pressure–lowering effect in the venom of a Brazilian pit viper to the development of the first ACE inhibitor, we trace how scientists transformed a deadly toxin into lifesaving medicine. We follow the work that identified bradykinin-potentiating peptides in snake venom and revealed that angiotensin-converting enzyme could be blocked—leading to the creation of captopril and later drugs such as enalapril and lisinopril. Along the way, landmark experiments and clinical trials showed that ACE inhibitors do far more than lower blood pressure, reshaping the treatment of heart failure and chronic kidney disease by targeting maladaptive activation of the renin–angiotensin–aldosterone system.

• (00:00:00) - ACE Inhibitor Story Continues: Shutting off RAAS
• (00:01:00) - Recap: The RAAS Refresher
• (00:02:36) - Venom Mystery : Why Pit Viper Bites Cause Hypotension
• (00:05:02) - Venom and the ACE Connection: John Vane's Lab
• (00:06:20) - Interview With a Pit Viper: Snake’s Take on Pharma
• (00:09:18) - Venom Into Medicine: Turning Raw Venom into a Drug
• (00:10:04) - Captopril: The First ACE Inhibitor
• (00:11:04) - Better ACE Inhibitors: Captopril to Enalapril to Lisinopril
• (00:12:35) - Maladaptive RAAS Activation: Heart Failure Activates Renin
• (00:19:36) - Maladaptive RAAS Activation: Kidney Failure Activates Renin
• (00:24:24) - Episode Conclusion: ACE Inhibitors Transform Cardiorenal Medicine