The Drug That Nausea Kept From Becoming a Psychedelic Mystery
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The Drug That Nausea Kept From Becoming a Psychedelic Mystery
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Nausea ended nearly every human trial before quipazine could show whether it was psychedelic - at 25 mg oral doses subjects had severe gastrointestinal distress, while rodents and monkeys showed clear LSD-like effects. How did a compound that substituted fully for LSD in animals fail so completely in people?
In this episode, we trace quipazine’s discovery in 1966, its pharmacological profile across serotonin receptors, and the contrasting human and animal data that left researchers baffled. Can the same molecule trigger vomiting and mimic psychedelics at once, and what does that tell us about translating animal models to human consciousness?
Person: quipazine
Date: 1966 (first appearance in literature)
Dose (human): 25 mg oral produced nausea and gastrointestinal distress
Receptor affinity: strongest for 5-HT3; also binds 5-HT2A, 5-HT2B, 5-HT2C, 5-HT1B, 5-HT1A
Animal finding: substituted fully for LSD in rodents and monkeys; produced head-twitch response in rodents
- The literature records a single footnoted human report listing a 0.5 mg dose with an effect noted (printed with "sic").
- At 25 mg oral in human subjects quipazine caused nausea, flatulence, cramps, and diarrhea with no LSD-like effects observed.
- Quipazine’s strongest receptor affinity is for 5-HT3, a receptor whose activation provokes nausea and vomiting in humans.
- In 1977 rodents given quipazine showed the head-twitch response, blocked by the 5-HT2A antagonist ketanserin.
- Drug discrimination studies found quipazine substituted fully for LSD, DOM, and in reverse tests LSD, mescaline, and psilocybin substituted fully for quipazine in animals.
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