ALD-52
ALD-52 is a psychedelic lysergamide structurally related to LSD, first synthesized by Albert Hofmann at Sandoz in 1957.1 It functions as a prodrug that readily converts to LSD in the body, producing virtually indistinguishable effects at comparable potency.21 The compound gained notoriety through false claims that it was distributed as 'Orange Sunshine' during the 1960s counterculture era.1 Like LSD, it is not considered addictive or toxic, though unpredictable adverse psychological reactions remain possible.3
Contents
Dosage & Duration
Dosage
Potency is close to that of LSD, with sources reporting roughly 90 to 100 percent of LSD's potency; toxic dose and long-term effects are unstudied. Combination with MDMA is strongly synergistic and unpredictable, warranting markedly reduced doses of both.
Duration
Subjective Effects
Effects vary widely by individual, dose, and context.
Cognitive
In comparison to other lysergamides such as LSD and 1P-LSD, ALD-52 is less stimulating and is associated with a more relaxed mental state. The most prominent of these cognitive effects generally include:
Visual
Distortions
Geometry
The geometry of ALD-52 is very similar to that of its close relative LSD. The geometry of ALD-52 is suspected (but not confirmed) to lead to level 8A geometry (similar to LSD).
Hallucinatory States
Auditory
Reagent Testing
Loading reagent data
Pharmacology
Pharmacodynamics
ALD-52 functions as a prodrug for LSD, with a large percentage of the administered dose metabolizing into LSD in the body.2 The conversion to LSD has been confirmed with human liver enzymes in vitro and in rodents in vivo.2 Through its metabolite LSD, ALD-52 acts as a partial agonist at multiple serotonin receptor subtypes, including 5-HT1A, 5-HT2A, 5-HT2B, 5-HT2C, and 5-HT6 receptors, with the psychedelic effects believed to primarily stem from activity at the 5-HT2A, 5-HT2C, and 5-HT1A receptors. The parent compound ALD-52 itself shows dramatically reduced affinities for the serotonin 5-HT1A and 5-HT2A receptors compared to LSD, with markedly reduced activational potency and efficacy at the 5-HT2A receptor, while agonistic activity at the 5-HT2B and 5-HT2C receptors was lost entirely.2 ALD-52 is also expected to act as an agonist at dopamine receptors such as D2 through its conversion to LSD.
Pharmacokinetics
ALD-52 acts as a prodrug that is readily converted to LSD following administration.2 The formation of LSD from ALD-52 is primarily mediated by CYP3A4, which catalyzes the deacetylation of ALD-52 into LSD. This conversion can be largely blocked by the strong cytochrome P450 inhibitor ketoconazole. CYP2D6 is also involved in hydroxylation processes.4 In addition to LSD as the primary metabolite, ALD-52 is metabolized into N-deethyl ALD-52 and N6-demethyl ALD-52 (nor-ALD-52).2 Circulating levels of LSD following administration are virtually identical between ALD-52 and the related prodrug 1P-LSD.2
Dangerous
Highest riskThese combinations are considered extremely harmful and should always be avoided. Reactions to these drugs taken in combination are highly unpredictable and have a potential to cause death.
Unsafe
AvoidThere is considerable risk of physical harm when taking these combinations, they should be avoided where possible.
Caution
Use cautionThese combinations are not usually physically harmful, but may produce undesirable effects, such as physical discomfort or overstimulation. Extreme use may cause physical health issues. Synergistic effects may be unpredictable. Care should be taken when choosing to use this combination.
Tolerance
Psychedelics (all serotonergic psychedelics will have reduced effects following ALD-52 use)
Harm Potential
Addiction & Dependence
Psychosis Risk
Unpredictable adverse reactions including anxiety, paranoia, delusions, and psychosis are possible, particularly among those predisposed to psychiatric disorders.36 These reactions can occur spontaneously even among experienced users. ALD-52 may act as a potential trigger for those with underlying psychiatric conditions, and use is discouraged for individuals with a personal or family history of bipolar disorder or schizoaffective disorder.3
Seizure Risk
Although no cases of ALD-52-induced seizures have been documented, it is believed to have a similar seizure risk as LSD. LSD is thought to lower the seizure threshold, though seizures are very rarely reported and believed to only be a risk to those predisposed to them, particularly when combined with physically taxing conditions such as dehydration, undernourishment, overheating, or general fatigue.78
History & Culture
Discovery and Early Research
ALD-52 was first synthesized and described in the scientific literature by Albert Hofmann and Franz Troxler at Sandoz in 1957 as part of Hofmann's broader study of LSD analogs. The properties and effects of ALD-52 were studied and reported in the late 1950s and early 1960s, though it remains
Trip Reports
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Legality
By Country
References
Source Pages
Citations
- (January 2025). Analytical and behavioral characterization of 1-dodecanoyl-LSD (1DD-LSD). Drug Testing and Analysis, 17(1), 101–109. https://doi.org/10.1002/dta.369112345
- (August 2020). Pharmacological and biotransformation studies of 1-acyl-substituted derivatives of d-lysergic acid diethylamide (LSD). Neuropharmacology, 172. https://doi.org/10.1016/j.neuropharm.2019.10785612345678
- Schlag AK, Aday J, Salam I, Neill JC, & Nutt DJ. (2022). Adverse effects of psychedelics: From anecdotes and misinformation to systematic science. 36(3), 258-272. https://doi.org/10.1177/026988112110691001234
- (July 2019). In vitro metabolic fate of nine LSD-based new psychoactive substances and their analytical detectability in different urinary screening procedures. Analytical and Bioanalytical Chemistry, 411(19), 4751–4763. https://doi.org/10.1007/s00216-018-1558-91
- (2016). Psychedelics. https://doi.org/10.1124/pr.115.0114781
- Sabé M, Sulstarova A, Glangetas A, De Pieri M, Mallet L, Curtis L, Richard-Lepouriel H, Penzenstadler L, Seragnoli F, Thorens G, Zullino D, Preller K, Böge K, Leucht S, Correll CU, Solmi M, Kaiser S, & Kirschner M. (2024). Reconsidering evidence for psychedelic-induced psychosis: an overview of reviews, a systematic review, and meta-analysis of human studies. 30(3), 1223-1255. https://doi.org/10.1038/s41380-024-02800-51
- Freidel N, Kreuder L, Rabinovitch BS, Chen FY, Huang RST, & Lewis EC. (2024). Psychedelics, epilepsy, and seizures: a review. 14. https://doi.org/10.3389/fphar.2023.13268151
- Soto-Angona Ó, Fortea A, Fortea L, Martínez-Ramírez M, Santamarina E, Gil López FJ, Knudsen GM, & Ona G. (2024). Do classic psychedelics increase the risk of seizures? A scoping review. 85, 35-42. https://doi.org/10.1016/j.euroneuro.2024.05.0021
- (n.d.). One account found that there was less visual distortion than with LSD, that there was seemingly less anxiety than with LSD, and that it was somewhat less potent than LSD.<r. https://doi.org/10.1002/dta.261312
- Shulgin AT, & Shulgin A. (1997). TiHKAL: Tryptamines I Have Known and Loved. Transform Press.1
- Normand B. (21 January 2017). Cosmo Feilding Mellen: Interview with a Sunshine Maker. Psymposia. https://www.psymposia.com/magazine/cosmo-feilding-mellen-interview-with-a-sunshine-maker/1
- (31 October 2017). Acid Trip: Denver's Secret LSD Labs Fueled the Psychedelic Revolution. Denver Westword. https://www.westword.com/news/denvers-underground-lsd-labs-fueled-the-psychedelic-revolution-9644844/1
- (2019-07-18). Verordnung zur Änderung der Anlage des Neue-psychoaktive-Stoffe-Gesetzes und von Anlagen des Betäubungsmittelgesetzes. https://www.bundesgesundheitsministerium.de/service/gesetze-und-verordnungen/detail/verordnung-zur-aenderung-der-anlage-des-neue-psychoaktive-stoffe-gesetzes-und-von-anlagen-des-btmg.html1
- (2014-12-10). The Misuse of Drugs Act 1971 (Amendment) (No. 2) Order 2014. https://www.legislation.gov.uk/uksi/2014/3271/made1
- (n.d.). Drug Scheduling — DEA Diversion Control Division Controlled Substance Schedules. https://www.deadiversion.usdoj.gov/schedules/schedules.html1
Further Reading
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