The "(sic)" Dose: How Quipazine Haunted Psychiatry's Psychedelic Moment
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The "(sic)" Dose: How Quipazine Haunted Psychiatry's Psychedelic Moment
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A tiny notation in a scientific paper - “0.5 mg (sic)” - froze researchers because the number was real and inexplicable, and the compound it described was never meant to be a psychedelic. Quipazine activated both the 5‑HT2A receptor linked to hallucinogens and the 5‑HT3 receptor that causes severe nausea, leaving animal studies screaming psychedelic signals while human trials reported only sickness; how could the same molecule tell such different stories?
In this episode, we lay out the sequence of experiments, results, and interpretations that turned quipazine into a scientific paradox, from rodent head‑twitches and LSD substitution to primate vomiting and a discontinued 25 mg human trial; can receptor overlap explain why quipazine’s psychedelic promise never reached people?
Person: James Winter
Date: 1994
Dose in publication: 0.5 mg (sic)
Human trial dose: 25 mg
Animal result: full substitution for LSD in drug discrimination studies
- Rodents given quipazine produced a rapid repetitive head‑twitch response matching LSD and mescaline patterns.
- In drug discrimination experiments rodents trained on LSD could not distinguish quipazine from LSD, indicating full substitution.
- Monkey trials at psychedelic‑range doses produced projectile vomiting described as severe, linked to 5‑HT3 activation.
- Human volunteer trial at 25 mg resulted in nausea with no reported LSD‑like subjective effects and was discontinued.
- James Winter proposed in 1994 that 5‑HT3 receptor activation prevented reaching 5‑HT2A‑mediated effects at tolerable doses.
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