Chemistry:LAE-32

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Lysergic acid ethylamide (LAE-32 or LAE), also known as N-ethyllysergamide, is a psychedelic drug of the lysergamide family related to lysergic acid diethylamide (LSD).[1][2][3] It is the analogue of LSD in which one of the ethyl groups on the amide moiety has been removed.[1][2]

The drug is reported to have some LSD-like effects but is weaker and shorter-lasting, with an active dose reported to be between 0.5 and 1.6 mg by different routes of administration including subcutaneous or intramuscular injection and oral administration.[1][2][4] Side effects like apathy and sedation have been reported.[1]

Analogues of LAE-32 include LSD, MLA-74 (1-methyl-LAE), ALA-10 (1-acetyl-LAE; 1A-LAE), lysergic acid methylamide (LAM), lysergic acid propylamide (LAP), LME-54 (lysergic acid methylethylamide), and LEP-57 (lysergic acid ethylpropylamide; EPLA), among others.[1][2]

LAE-32 was first described in the scientific literature by Albert Hofmann and colleagues by 1955.[5] It was studied by the CIA as part of Project MKULTRA. Documents published by the CIA under the Freedom of Information Act suggest it causes "a schizophrenia-like condition" but it allows people with schizophrenia to remain indifferent to their disorder. The drug has also been studied in psychedelic-assisted psychotherapy.[4] It is not a controlled substance in Canada as of 2025.[6]

See also

  • Substituted lysergamide

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 Shulgin, Alexander; Shulgin, Ann (September 1997). TiHKAL: The Continuation. Berkeley, California: Transform Press. ISBN 0-9630096-9-9. OCLC 38503252. http://www.erowid.org/library/books_online/tihkal/tihkal.shtml.  "LAE-32, N-ethyllysergamide. Different people have observed and reported different effects, with different routes of administration. Subcutaneous administrations of from 500 to 750 micrograms have been said to produce a state of apathy and sedation. Clinical studies with dosages of 500 micrograms i.m. were felt to be less effective than the control use of 100 micrograms of LSD. And yet, oral doses of twice this amount, 1.6 milligrams, have been said to produce a short-lived LSD-like effect with none of these negatives."
  2. ↑ 2.0 2.1 2.2 2.3 "Structure-activity relationships of the classic hallucinogens and their analogs". NIDA Research Monograph 146: 74–91. 1994. PMID 8742795. https://archives.nida.nih.gov/sites/default/files/monograph146.pdf#page=79. 
  3. ↑ "D-Lysergic Acid Diethylamide (LSD): A Review of its Present Status". Clinical Pharmacology and Therapeutics 6 (2): 183–255. 1965. doi:10.1002/cpt196562183. PMID 14288188. https://bibliography.maps.org/resources/download/2117. 
  4. ↑ 4.0 4.1 "Psychedelic treatment of functional neurological disorder: a systematic review". Therapeutic Advances in Psychopharmacology 10. 2020. doi:10.1177/2045125320912125. PMID 32435447. "Giberti and Gregoretti 1959. In an Italian study (not included in Table 2), Franco Giberti and Luciano Gregoretti compared 12 patients with ‘conversion disorder’ in 2–8 weekly sessions of psycholytic therapy with 100 µg LSD and 1–2 weekly sessions with 500 µg of LAE-32 (another LSD analogue that is weaker and shorter-lasting) with 14 patients with obsessive compulsive disorder (OCD). During the dosing sessions, the patients with ‘conversion disorder’ showed amplification of sensory and motor impairment; however, in some cases showed ‘miraculous’ improvement.49 Unfortunately, the authors did not provide outcome data for the patients, rendering this follow up unsuitable for further analysis.". 
  5. ↑ "Amide der stereoisomeren Lysergsäuren und Dihydro-lysergsäuren. 38. Mitteilung über Mutterkornalkaloide". Helvetica Chimica Acta 38 (2): 421–433. 1955. doi:10.1002/hlca.19550380207. ISSN 0018-019X. Bibcode: 1955HChAc..38..421S. https://onlinelibrary.wiley.com/doi/10.1002/hlca.19550380207. Retrieved 5 June 2025. 
  6. ↑ "Controlled Drugs and Substances Act". https://laws-lois.justice.gc.ca/eng/acts/c-38.8/FullText.html. 



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