My mistake, it's somewhat debated, but it looks like Ott's study pretty clearly establishes its activity...
From Wikipedia:
Effects in Humans
Fabing & Hawkins (1955)
In 1955, Fabing and Hawkins administered bufotenin intravenously at doses of up to 16 mg to prison inmates at Ohio State Penitentiary. [26] A troubling toxic blood circulation effect causing a purpling of the face was seen in these tests.
A subject given 1 mg reported “a tight feeling in the chest” and prickling “as if he had been jabbed by needles.” This was accompanied by a “fleeting sensation of pain in both thighs and a mild nausea.” [26]
Another subject given 2 mg reported “tightness in his throat”. He had tightness in the stomach, tingling in pretibial areas, and developed a purplish hue in the face indicating blood circulation problems. He vomited after 3 minutes. [26]
Another subject given 4 mg complained of “chest oppression” and that “a load is pressing down from above and my body feels heavy.” The subject also reported “numbness of the entire body” and “a pleasant Martini feeling-my body is taking charge of my mind”. The subject reported he saw red spots passing before his eyes and red-purple spots on the floor, and the floor seemed very close to his face. Within 2 minutes these visual effects were gone, and replaced by a yellow haze, as if he were looking through a lens filter. [26]
Fabing and Hawkins commented that bufotenin’s hallucinogenic effects were "reminiscent of LSD and mescaline but develop and disappear more quickly, indicating rapid central action and rapid degradation of the drug".
Isbell (1956)
In 1956, Dr. Harris S. Isbell at the Public Health Service Hospital in Lexington, Kentucky experimented with bufotenine as a snuff. He reported “no subjective or objective effects were observed after spraying with as much as 40 mg bufotenine”; however subjects who received 10-12 mg injected intramuscularly reported “elements of visual hallucinations consisting of a play of colors, lights, and patterns”.[4]
Turner & Merlis (1959)
Turner and Merlis (1959) [27] experimented with intravenous administration of bufotenine (as the water soluble creatinine sulfate salt) to schizophrenics at a New York state hospital. They reported that when one subject received 10 mg during a 50-second interval, “the peripheral nervous system effects were extreme: at 17 seconds, flushing of the face, at 22 seconds, maximal inhalation, followed by maximal hyperventilation for about 2 minutes, during which the patient was unresponsive to stimuli; her face was plum-colored. Finally, Turner and Merlis reported that:
“on one occasion, which essentially terminated our study, a patient who received 40 mg intramuscularly, suddenly developed an extremely rapid heart rate; no pulse could be obtained; no blood pressure measured. There seemed to have been an onset of auricular fibrillation…extreme cyanosis developed. Massage over the heart was vigorously executed and the pulse returned to normal…shortly thereafter the patient, still cyanotic, sat up saying: ‘Take that away. I don’t like them’.”
After pushing doses to the morally admissible limit without producing hallucinations, Turner and Merlis conservatively concluded: “We must reject bufotenine…as capable of producing the acute phase of Cohoba intoxication”.[4]
McLeod and Sitaram (1985)
A 1985 study by McLeod and Sitaram in humans reported that bufotenine administered intranasally at a dose of 1-16 mg had no effect, other than intense local irritation. When given intravenously at low doses (2-4 mg), bufotenine oxalate caused anxiety but no other effects; however, a dose of 8 mg resulted in profound emotional and perceptual changes, involving extreme anxiety, a sense of imminent death, and visual disturbance associated with color reversal and distortion, and intense flushing of the cheeks and forehead. [28]
Ott (2001)
In 2001, ethnobotanist Jonathan Ott published the results of a study using free base bufotenine via insufflation (5-100 mg), sublingually (50 mg), intrarectally (30 mg), orally (100 mg) and via vaporization (2-8 mg).[29] All tests were self-administered and several volunteers took part in vaporization tests and one colleague well experienced with Anadenanthera took part in insufflation tests confirming the validity of the results of the self-administered tests done by Ott. Ott reported “visionary effects" of intranasal bufotenine and that the "visionary threshold dose" by this route was 40 mg, with smaller doses eliciting perceptibly psychoactive effects. He reported that "intranasal bufotenine is throughout quite physically relaxing; in no case was there facial rubescence, nor any discomfort nor disesteeming side effects".
At 100 mg, effects began within 5 minutes, peaked at 35-40 minutes, and lasted up to 90 minutes. Higher doses produced effects that were described as hallucinogenic, such as "swirling, colored patterns typical of tryptamines, tending toward the arabesque". Free base bufotenin taken sublingually was found to be identical to intranasal use. The potency, duration, and hallucinogenic action was the same. Ott found vaporized free base bufotenin active from 2-8 mg with 8 mg producing "ring-like, swirling, colored patterns with eyes closed".
Ott noted that free base bufotenin taken intranasally and sublingually produced effects similar to those of Yopo without the toxic peripheral symptoms, such as facial flushing, observed in other studies in which the the drug was administered intravenously.
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