MDMAMescalinePsilocybin

Psilocybin therapy of psychiatric disorders is not hampered by hERG potassium channel-mediated cardiotoxicity

Clinical concentrations of psilocin do not cause significant inhibition of the human ether-a-go-go-related gene (hERG) potassium channel. Therefore hERG channel blockade is unlikely to explain reported psilocybin-associated QT prolongation or other cardiotoxic effects.

Authors

  • Hackl, B.
  • Todt, H.
  • Kubista, H.

Published

International Journal of Neuropsychopharmacology
individual Study

Abstract

Psilocybin, a hallucinogen contained in “magic” mushrooms, holds great promise for the treatment of various psychiatric disorders, and early clinical trials are encouraging. Adverse cardiac events after intake of high doses of psilocybin and a trial reporting QT interval prolongation in the electrocardiogram attributed to the drug’s main metabolite, psilocin, gave rise to safety concerns. Here we show that clinical concentrations of psilocin do not cause significant human ether-a-go-go-related gene (hERG) potassium channel inhibition, a major risk factor for adverse cardiac events. We conclude that hERG channel blockage by psilocin is not liable for psilocybin- associated cardiotoxic effects.

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Research Summary of 'Psilocybin therapy of psychiatric disorders is not hampered by hERG potassium channel-mediated cardiotoxicity'

Editorial

βBlossom's Take

This is a useful safety counterweight in the psilocybin literature because it tests one specific cardiac worry rather than leaving all QT concerns at the level of speculation. By showing that clinical psilocin concentrations do not significantly inhibit hERG, it helps narrow the mechanism behind reported ECG effects and keeps later clinical monitoring questions properly focused.

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