Dipropyltryptamine

In his book TiHKAL (Tryptamines I Have Known and Loved), Alexander Shulgin lists DPT's dose range as 100 to 250mg orally and its duration as 2 to 4hours. The effects of DPT have been reported to include visuals, being intensely visual at high doses, changes in time perception, feeling like one is in a different place like on a mountain in clouds or in a big castle, enhanced recall of memories and experiences, enhanced emotional expressiveness and self-exploration, entity encounters, and religious feelings. Other reports have stated effects of DPT including visual and auditory hallucinations, increased color intensity, flashes of light and sparkles, apparitions of faces, increased music appreciation, ego dissolution, stimulation, euphoria, relaxation, paranoia, psychosis, anxiety, nausea, dizziness, muscle tremors, and increased heart rate, among others. Its duration is described as much shorter than those of certain other psychedelics like LSD, which can be advantageous in a clinical setting. ==Side effects==

Although tryptamines such as psilocybin and dimethyltryptamine (DMT) have relatively well‑characterized safety, synthetic analogues like DPT lack thorough toxicological evaluation and are mainly associated with anecdotal reports of intoxication and a few cases of fatal outcomes when used recreationally. The pharmacological similarity of DPT to DMT suggests a generally low intrinsic toxicity at controlled doses but a pronounced risk of acute adverse reactions, including agitation, tachycardia, hyperthermia, and serotonergic crisis, particularly in combination with monoamine oxidase inhibitors or other serotonergic substances. The main safety concerns are acute psychophysiological and behavioral disturbances rather than long‑term organ toxicity. Overall, DPT is a potent, short‑acting serotonergic hallucinogen with limited safety data and a toxicity profile comparable to related tryptamines such as DMT and 5-MeO-DMT. == Interactions ==

Pharmacodynamics } formation. Refs: DPT produces the head-twitch response, a behavioral proxy of psychedelic-like effects, in rodents. Unusually among most psychedelics, DiPT did not show evidence of behavioral tolerance in rodents. ==Chemistry==

powder. DPT, also known as N,N-dipropyltryptamine, is a substituted tryptamine related to dimethyltryptamine (DMT). Synthesis The chemical synthesis of DPT has been described. ==History==

DPT was first described in the scientific literature by Speeter and Anthony in 1954. Use of DPT as a designer drug has been documented by law enforcement officials since as early as 1968. It was described as a treatment for alcoholism by Stanislav Grof and colleagues in 1973. The drug was also studied for treatment of anxiety associated with terminal cancer in the late 1970s. ==Society and culture==

Religious use DPT is used as a religious sacrament by the Temple of the True Inner Light, a New York City offshoot of the Native American Church. Legal status Canada DPT is not a controlled substance in Canada as of 2025. Sweden DPT is illegal in Sweden as of 26 January 2016. United Kingdom DPT is a Class A drug in the United Kingdom, making it illegal to possess or distribute. United States DPT is not scheduled at the federal level in the United States, but it could be considered an analog of 5-MeO-DiPT, DMT, or DET, in which case purchase, sale, or possession could be prosecuted under the Federal Analogue Act. Florida "DPT (N,N-Dipropyltryptamine)" is a Schedule I controlled substance in the state of Florida making it illegal to buy, sell, or possess in Florida. Maine DPT is a Schedule I controlled substance in the state of Maine making it illegal to buy, sell, or possess in Maine. ==Research==

Fragile X syndrome DPT has been found to completely prevent audiogenic seizures in mouse models of fragile X syndrome (FXS) at a 10mg/kg dose, with its mechanism of action appearing to be independent of serotonin and sigma σ1 receptor activation. While DPT is an agonist at several serotonin receptors in vitro, its anticonvulsant effects were not blocked by selective serotonin 5-HT2A, 5-HT1A, or 5-HT1B receptor antagonists nor by a selective sigma σ1 receptor antagonist in vivo. The drug's beneficial effects may be mediated by non-serotonergic pathways, possibly involving direct auditory processing modulation. At higher doses, DPT switched from anticonvulsant to proconvulsant action, indicating complex interactions. == See also ==