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Summary sheet: ALD-52
Chemical Nomenclature
Common names ALD-52, 1-Acetyl-LSD, 1A-LSD, 1A-LAD, Orange Sunshine
Substitutive name 1-Acetyl-N,N-diethyllysergamide
Systematic name (6aR,9R)-4-Acetyl-N,N-diethyl-7-methyl-4,6,6a,7,8,9-hexahydroindolo-[4,3-fg]-quinoline-9-carboxamide
Class Membership
Psychoactive class Psychedelic
Chemical class Lysergamide
Routes of Administration

WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.

Threshold 30 µg
Light 30 - 100 µg
Common 100 - 175 µg
Strong 175 - 325 µg
Heavy 325 µg +
Total 8 - 14 hours
Onset 20 - 40 minutes
Come up 1 - 2 hours
Peak 3 - 5 hours
Offset 3 - 5 hours
After effects 4 - 24 hours

DISCLAIMER: PW's dosage information is gathered from users and resources for educational purposes only. It is not a recommendation and should be verified with other sources for accuracy.


1-Acetyl-N,N-diethyllysergamide (also known as ALD-52, 1-Acetyl-LSD, 1A-LSD, 1A-LAD, and mistakenly as Orange Sunshine) is a lesser-known psychedelic substance of the lysergamide class that produces LSD-like psychedelic effects when administered. It's structurally related to psychedelic lysergamides like LSD and 1P-LSD and is reported to produce largely indistinguishable effects.

ALD-52 was originally discovered by Albert Hofmann in his study of LSD analogs,[1] but it did not enter mainstream awareness until the 1960s through Western youth counterculture. ALD-52 gained public notoriety when it was supposedly distributed as LSD in the 1960s under the now-famous name "Orange Sunshine." This was later disproven (see section below).

Alexander Shulgin touches briefly on the subject of ALD-52 in the commentary section of LSD-25 in the book TiHKAL ("Tryptamines I have Known and Loved").[2] His writings are based on second-hand accounts which state that doses in the 50-175 µg range result in various effects that are not particularly distinct from LSD. His reports indicate that it produces less visual distortion than with LSD as well as less anxiety and tenseness, while also being somewhat less potent than LSD. Another report found the two substances to be indistinguishable.[2]

As with LSD itself, ALD-52 does not meet the criteria to be considered addictive or toxic by the scientific community.[3][4] Nevertheless, unpredictable adverse reactions such as anxiety, paranoia, delusions and psychosis are always possible, particularly among those who are predisposed to psychiatric disorders.[5] While these negative reactions or "bad trips" can often be attributed to factors like user inexperience or improper preparation of set and setting, they are known to happen spontaneously among even highly experienced users as well. It is highly advised to approach this very potent, long-lasting hallucinogenic substance with the proper amount of preparation, and harm reduction practices if using it.

History and culture

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In 1968 and 1969, a famous batch of LSD known as "Orange Sunshine" was synthesized by Nick Sand and Tim Scully and made widely available in California. This "Orange Sunshine" was long held by the hippie generation to be ALD-52 until 2005, when it was revealed by Nick Sand that "Orange Sunshine" was just a particularly well made batch of LSD dosed at 300 micrograms per unit. This was confirmed by Tim Scully in a 2017 Reddit AMA, where Scully explained that the claim that "Orange Sunshine" was technically not LSD arose from an "ill-advised desperate defense strategy that failed miserably" during his trial for LSD manufacture.[6]


ALD-52, or 1-Acetyl-N,N-diethyllysergamide, is a semisynthethic molecule of the lysergamide chemical class. ALD-52 is a substituted derivative of lysergic acid. ALD-52's structure contains four rings, a bicyclic hexahydroindole fused to a bicyclic quinoline group. This core structure of ALD-52 is an ergoline derivative, and has tryptamine and phenethylamine structures embedded within it. ALD-52 contains a N,N-diethylcarboxamide functional group bound to R8 of the chemical structure. It is additionally substituted at carbon 6 with a methyl group.

ALD-52 is homologous to 1P-LSD, which contains a propionyl group bound to CH3CO- instead of the acetyl group bound to the same location. It is unknown how these differences account for differences in the two compound's activity.


Further information: Serotonergic psychedelic

ALD-52 through its metabolite LSD acts as a partial agonist at most serotonin receptor subtypes, including the 5-HT1A, 5-HT2A, 5-HT2B, 5-HT2C and 5-HT6 receptors.[7] It can also be expected to act as an agonist at dopamine receptors such as D2.[8] The psychedelic effects are believed to come from ALD-52's efficacy at the 5-HT2A, 5-HT2C, and 5-HT1A receptor subtypes.[9][10][11][12]

ALD-52, alongside 1P-LSD and 1B-LSD, act as prodrugs for LSD, though it is unclear as to whether it is capable of exerting its own effects as a parent substance.[13] It has been found that ALD-52 metabolizes into two distinct metabolites, N-deethyl ALD-52 and N6-demethyl ALD-52 (nor-ALD-52) in addition to its' primary metabolite LSD. ALD-52 is metabolized by CYP3A4 which does the N6-deallylation. Additionally, CYP2D6 is involved in the hydroxylation process.[13]

Subjective effects

Anecdotal reports from many users suggest that the effects of ALD-52 are virtually identical to LSD. In comparison to other psychedelics such as psilocin, LSA and ayahuasca, ALD-52 is significantly more stimulating and fast-paced regarding the specific style of its physical and cognitive effects, as is the case with other lysergamides.[clarification needed]

Anecdotal reports from the community tend to report ALD-52 as being slightly less potent and visual, with a mellower, less anxiety-provoking headspace that comes at the expense of less depth, giving it the reputation for being a more recreational variant of LSD. It has been speculated that this is due to a slightly extended, less jarring come up period that allows the user to become more acclimated to the changes in head space. As one increases the dose, it is reported to lose this character and converge with the effects of a high-dose LSD experience.

Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), an open research literature based on anecdotal user reports and the personal analyses of PsychonautWiki contributors. As a result, they should be viewed with a healthy degree of skepticism.

It is also worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects. Likewise, adverse effects become increasingly likely with higher doses and may include addiction, severe injury, or death ☠.

Physical effects

Visual effects

Cognitive effects

Multi-sensory effects

Combination effects

  • Alcohol - Alcohol's central depressant effects can counteract some of the anxiety and bodily tension produced by ALD-52. However, alcohol can cause dehydration, nausea and physical fatigue which can negatively impact the tone of the trip. Users are advised to pace themselves and drink a portion of their usual amount.
  • Benzodiazepines - Benzodiazepines are highly effective at reducing the intensity of ALD-52's effects through the general suppression of brain activity.
  • Cannabis - Cannabis strongly intensifies the sensory and cognitive effects of ALD-52. Extreme caution is advised when using this combination as it can significantly increase the chances of a negative psychological reaction like anxiety, confusion and psychosis. Users are advised to start off with only a fraction of their usual cannabis dose and take long breaks between hits to avoid over intake.
  • Dissociatives - ALD-52 enhances the cognitive, visual and general hallucinatory effects of dissociatives. Dissociative-induced holes, spaces, and voids and internal hallucinations become more vivid and intense on ALD-52. These effects correspond with an increased risk of confusion, delusions, and psychosis.
  • MDMA - ALD-52 and MDMA are highly synergistic and mutually enhance each other's physical, cognitive, and visual effects. The synergy between these substances is unpredictable so it is advised to start with markedly lower doses than one would take for each individually. There is some evidence that suggests that co-administration of LSD with MDMA increases the neurotoxicity of the latter,[14][15][16] and this may extend to A and this may extend to ALD-52.

Experience reports

Anecdotal reports which describe the effects of this compound within our experience index include:

Additional experience reports can be found here:

Toxicity and harm potential

The toxicity and long-term health effects of recreational ALD-52 use do not appear to have been studied in any scientific context and the exact toxic dose is unknown. This is because ALD-52 is a research chemical with a very limited history of human use.

Anecdotal evidence from people within the community who have tried ALD-52 suggests that there are no negative health effects attributed to simply trying the drug by itself at low to moderate doses and using it very sparingly (although nothing can be completely guaranteed). Independent research should always be conducted to ensure that a combination of two or more substances is safe before consumption.

As with other psychedelic substances, there are relatively few physical side effects that have been reported associated with acute ALD-52 exposure. Although no formal studies have been conducted, it is likely that as with LSD itself,[17] ALD-52 is able to be considered non-addictive, with an extremely low toxicity relative to dose. It is also likely that as with LSD, there are little to no negative physical, cognitive, psychiatric or other toxic consequences associated with acute ALD-52 exposure.

However, as with LSD and psychedelics in general, it is possible that ALD-52 can act as a potential trigger for those with underlying psychiatric conditions. It is advised to be extremely cautious if it is known that a family member has bipolar disorder or schizoaffective disorder as those with a personal or family history of mental illness are generally advised not to use this substance, particularly outside of a supervised medical setting.

It is strongly recommended that one uses harm reduction practices when using this substance.

Tolerance and addiction potential

Although no formal studies have been conducted, it is not unreasonable to assume that like LSD itself, ALD-52 is not habit-forming and that the desire to use it can actually decrease with use.

Tolerance to the effects of ALD-52 is built almost immediately after ingestion. After that, it takes about 5-7 days for the tolerance to be reduced to half and 14 days to be back at baseline (in the absence of further consumption). ALD-52 presents cross-tolerance with all psychedelics, meaning that after the use of ALD-52 all psychedelics will have a reduced effect.


The LD50 of ALD-52 is unknown. Adverse psychological reactions are common especially at higher doses. Some of these include anxiety, delusions, panic attacks and more rarely seizures. Medical attention is usually only needed if suspected of severe psychotic episodes or “fake acid” (such as 25i-NBOMe or DOB). Administration of benzodiazepines or antipsychotics may help to relieve the negative cognitive effects.

Dangerous interactions

Warning: Many psychoactive substances that are reasonably safe to use on their own can suddenly become dangerous and even life-threatening when combined with certain other substances. The following list provides some known dangerous interactions (although it is not guaranteed to include all of them).

Always conduct independent research (e.g. Google, DuckDuckGo, PubMed) to ensure that a combination of two or more substances is safe to consume. Some of the listed interactions have been sourced from TripSit.

Legal status

ALD-52 is currently a gray area compound within many parts of the world. This means that it is not known to be specifically illegal within most countries, but people may still be charged for its possession under certain circumstances such as under analog laws and with the intent to sell or consume.

  • Austria: ALD-52 is technically not illegal but it may fall in the NPSG (Neue-Psychoaktive-Substanzen-Gesetz Österreich) as an analogue of LSD.[19][20]
  • Denmark: ALD-52 is not listed as an illegal substance in Denmark, and its chemical class 'lysergamide' is not banned under the Analogue Act (Some LSD analogues are, however, prohibited).[21]
  • Germany: ALD-52 is controlled under the NpSG (New Psychoactive Substances Act)[22] as of July 18, 2019.[23] Production and import with the aim to place it on the market, administration to another person and trading is punishable. Possession is illegal but not penalized.[24]
  • Latvia: ALD-52 is illegal in Latvia. Although it isn't officially scheduled, it is controlled as an LSD structural analog due to an amendment made on June 1, 2015.[25]
  • Poland: ALD-52 is a NPS class drug in Poland, making it illegal to possess or distribute.[26]
  • Singapore: ALD-52 is a Class A controlled substance.[27]
  • Switzerland: ALD-52 is a controlled substance specifically named under Verzeichnis E.[28]
  • United Kingdom: As of January 7, 2015, ALD-52 is specifically named in the U.K. Misuse of Drugs Act as a Class A controlled substance..[29]
  • United States: ALD-52 is unscheduled in the United States. It may be considered an analogue of LSD, a Schedule I controlled substance under the Controlled Substances Act. As such, the sale for human consumption or the use for illicit non-medical or scientific research could be prosecuted as crimes under the Federal Analogue Act.[30][31]

See also

External links




  1. Troxler, F., Hofmann, A. (1957). "Substitutionen am Ringsystem der Lysergsäure I. Substitutionen am Indol-Stickstoff. 43. Mitteilung über Mutterkornalkaloide". Helvetica Chimica Acta. 40 (6): 1706–1720. doi:10.1002/hlca.19570400619. ISSN 0018-019X. 
  2. 2.0 2.1 Shulgin, Alexander; Shulgin, Ann (1997). "#26. LSD-25". TiHKAL: The Continuation. United States: Transform Press. ISBN 0-9630096-9-9. OCLC 38503252. 
  3. Lüscher, Christian; Ungless, Mark A. (2006). "The Mechanistic Classification of Addictive Drugs". PLOS Medicine. 3 (11). doi:10.1371/journal.pmed.0030437. ISSN 1549-1277. PMID 17105338. 
  4. Nichols, David E. (2016). Barker, Eric L., ed. "Psychedelics". Pharmacological Reviews. 68 (2): 264–355. doi:10.1124/pr.115.011478. ISSN 0031-6997. 
  5. Strassmann, Rick (1984). "Adverse reactions to psychedelic drugs. A review of the literature". Journal of Nervous and Mental Disease. 172 (10): 577–595. doi:10.1097/00005053-198410000-00001. ISSN 0022-3018. OCLC 1754691. PMID 6384428. 
  6. "Earth"; "Jon Hanna"; "Spoon" (March 14, 2016). "Ask Erowid : ID 3189 : Was Orange Sunshine actually ALD-52?". Erowid. Retrieved January 1, 2020. 
  7. Aghajanian, G. K., Bing, O. H. L. (September 1964). "Persistence of lysergic acid diethylamide in the plasma of human subjects". Clinical Pharmacology & Therapeutics. 5 (5): 611–614. doi:10.1002/cpt196455611. ISSN 0009-9236. 
  8. Marona-Lewicka, D., Thisted, R. A., Nichols, D. E. (July 2005). "Distinct temporal phases in the behavioral pharmacology of LSD: dopamine D2 receptor-mediated effects in the rat and implications for psychosis". Psychopharmacology. 180 (3): 427–435. doi:10.1007/s00213-005-2183-9. ISSN 0033-3158. 
  9. Titeler, M., Lyon, R. A., Glennon, R. A. (February 1988). "Radioligand binding evidence implicates the brain 5-HT2 receptor as a site of action for LSD and phenylisopropylamine hallucinogens". Psychopharmacology. 94 (2). doi:10.1007/BF00176847. ISSN 0033-3158. 
  10. Burris, K. D., Breeding, M., Sanders-Bush, E. (September 1991). "(+)Lysergic acid diethylamide, but not its nonhallucinogenic congeners, is a potent serotonin 5HT1C receptor agonist". The Journal of Pharmacology and Experimental Therapeutics. 258 (3): 891–896. ISSN 0022-3565. 
  11. Krebs-Thomson, Ph.D., K. (May 1998). "Effects of Hallucinogens on Locomotor and Investigatory Activity and Patterns: Influence of 5-HT2A and 5-HT2C Receptors". Neuropsychopharmacology. 18 (5): 339–351. doi:10.1016/S0893-133X(97)00164-4. ISSN 0893-133X. 
  12. Moreno, J. L., Holloway, T., Albizu, L., Sealfon, S. C., González-Maeso, J. (April 2011). "Metabotropic glutamate mGlu2 receptor is necessary for the pharmacological and behavioral effects induced by hallucinogenic 5-HT2A receptor agonists". Neuroscience Letters. 493 (3): 76–79. doi:10.1016/j.neulet.2011.01.046. ISSN 0304-3940. 
  13. 13.0 13.1 Wagmann, L., Richter, L. H. J., Kehl, T., Wack, F., Bergstrand, M. P., Brandt, S. D., Stratford, A., Maurer, H. H., Meyer, M. R. (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. doi:10.1007/s00216-018-1558-9. ISSN 1618-2642. 
  14. Armstrong, B. D.; Paik, E.; Chhith, S.; Lelievre, V.; Waschek, J. A.; Howard, S. G. (2004). "Potentiation of (DL)‐3,4‐methylenedioxymethamphetamine (MDMA)‐induced toxicity by the serotonin 2A receptior partial agonist d‐lysergic acid diethylamide (LSD), and the protection of same by the serotonin 2A/2C receptor antagonist MDL 11,939". Neuroscience Research Communications. 35 (2): 83–95. doi:10.1002/nrc.20023. ISSN 1520-6769. 
  15. Gudelsky, Gary A.; Yamamoto, Bryan; Nash, J. Frank (1994). "Potentiation of 3,4-methylenedioxymethamphetamine-induced dopamine release and serotonin neurotoxicity by 5-HT2 receptor agonists". European Journal of Pharmacology. 264 (3): 325–330. doi:10.1016/0014-2999(94)90669-6. ISSN 0014-2999. 
  16. Capela, J. P.; Fernandes, E.; Remião, F.; Bastos, M. L.; Meisel, A.; Carvalho, F. (2007). "Ecstasy induces apoptosis via 5-HT2A-receptor stimulation in cortical neurons". Neurotoxicology. 28 (4): 868–875. doi:10.1016/j.neuro.2007.04.005. ISSN 0161-813X. PMID 17572501. 
  17. Passie, T.; Halpern, J. H.; Stichtenoth, D. O.; Emrich, H. M.; Hintzen, A. "The Pharmacology of Lysergic Acid Diethylamide: A Review" (PDF). CNS Neuroscience & Therapeutics. 14: 295–314. doi:10.1111/j.1755-5949.2008.00059.x. ISSN 1755-5930. Archived from the original (PDF) on May 1, 2013. Retrieved January 1, 2020. 
  18. Talaie, H.; Panahandeh, R.; Fayaznouri, M. R.; Asadi, Z.; Abdollahi, M. (2009). "Dose-independent occurrence of seizure with tramadol". Journal of Medical Toxicology. 5 (2): 63–67. doi:10.1007/BF03161089. ISSN 1556-9039. 
  21. "Samlet liste over euforiserende stoffer opført på bilag 1 til bekendtgørelsen om euforiserende stoffer nr. 557 af 31. maj 2011 og stoffer reguleret herefter via ændringsbekendtgørelser" (in Danish). Lægemiddelstyrelsen [Danish Medicines Agency]. June 13, 2018. Retrieved January 1, 2020. 
  22. "Anlage NpSG" (in German). Bundesministerium der Justiz und für Verbraucherschutz [Federal Ministry of Justice and Consumer Protection]. Retrieved December 10, 2019. 
  23. "Verordnung zur Änderung der Anlage des Neue-psychoaktive-Stoffe-Gesetzes und von Anlagen des Betäubungsmittelgesetzes" (PDF). Bundesgesetzblatt Jahrgang 2019 Teil I Nr. 27 (in German). Bundesanzeiger Verlag. July 17, 2019. pp. 1083–1094. Retrieved January 1, 2020. 
  24. "§ 4 NpSG" (in German). Bundesministerium der Justiz und für Verbraucherschutz [Federal Ministry of Justice and Consumer Protection]. Retrieved December 10, 2019. 
  25. "Noteikumi par Latvijā kontrolējamajām narkotiskajām vielām, psihotropajām vielām un prekursoriem" (in Latvian). VSIA Latvijas Vēstnesis. November 10, 2005. Retrieved January 1, 2020. 
  26. "Rozporządzenie Ministra zdrowia z dnia 21 sierpnia 2019 r. zmieniające rozporządzenie w sprawie wykazu substancji psychotropowych, środków odurzających oraz nowych substancji psychoaktywnych" (PDF) (in Polish). 
  27. "Misuse of Drugs Act: (CHAPTER 185)". March 31, 2008. Retrieved October 22, 2020. 
  28. "Verordnung des EDI über die Verzeichnisse der Betäubungsmittel, psychotropen Stoffe, Vorläuferstoffe und Hilfschemikalien" (in German). Bundeskanzlei [Federal Chancellery of Switzerland]. Retrieved January 1, 2020. 
  29. Advisory Council on the Misuse of Drugs (June 10, 2014). "Update of the generic definition for tryptamines" (PDF). Government Digital Service. p. 12. Retrieved January 1, 2020. 
  30. U.S.C. Title 21 - FOOD AND DRUGS 
  31. PUBLIC LAW 91-513 (PDF), 1970