Buy ALD-52 (1A-LSD) Cas 3270-02-8

Buy ALD-52 (1A-LSD) Cas 3270-02-8

ALD-52, also known as 1-acetyl-LSD (1A-LSD) and falsely as “Orange Sunshine“, is a psychedelic drug of the lysergamide family related to lysergic acid diethylamide (LSD).^[1][4] It is taken orally.^[1]

The drug acts as a readily converted prodrug of LSD and hence has very similar properties to those of LSD, including in terms of onset, duration, and subjective psychedelic effects.^{[8][9][4][6][1]} LSD itself acts as a non-selective agonist of serotonin and dopamine receptors, including of the serotonin 5-HT_2A receptor, and this mediates its hallucinogenic effects.^[10] ALD-52 is a 1-acyllysergamide, specifically the 1-acetyl derivative of LSD, and is closely related to other 1-acyllysergamide LSD prodrugs, such as 1P-LSD, 1V-LSD, and 1cP-LSD.^[9][6][11] The drug has about 90 to 100% of the potency of LSD.^[6][4][12]

ALD-52 was first described in the literature by Albert Hofmann and colleagues at Sandoz in 1957.^[4][13][14] It was once claimed that the “Orange Sunshine” LSD distributed by Tim Scully and Nick Sand during the 1967 Summer of Love in the United States was actually ALD-52 rather than LSD, but this turned out to be untrue.^{[15][1][16][17]} ALD-52 was first definitely encountered as a novel designer drug in 2016.^[18][4][19] The drug is a key parent compound and inspiration for the 1-acyllysergamide prodrugs like 1P-LSD that were developed by Lizard Labs and emerged as designer drugs in the mid-2010s.^{[9][8][4][20][21]}

ALD-52 was long thought to be a readily converted prodrug of LSD.^[22][8][1] However, this was not empirically confirmed until formal studies were finally done in the 2010s and 2020s.^{[8][4][5][23]}

ALD-52 was clinically studied and found to produce psychedelic effects similar to those of LSD itself and to closely match the time–course of LSD in terms of onset and duration.^[4][6][7] However, in one study, it was claimed that ALD-52 seemed to modify cognition and body image to a greater extent than LSD.^[6][4][24] Both LSD and ALD-52 were reported to be active at doses of 0.5 to 1 μg/kg orally (35–70 μg for a 70-kg person).^[4] Other sources found that ALD-52 was 91% as potent as LSD (with LSD notably having 88% of the molecular weight of ALD-52) or that the two drugs were equipotent.^{[6][22][4][12]}

In his book TiHKAL (Tryptamines I Have Known and Loved), Alexander Shulgin briefly discusses ALD-52, giving a dose range of 50 to 175 μg orally and no onset or duration mentioned.^[1] In other publications however, he gave a dose range of 100 to 200 μg orally.^[25][26] A few different individual accounts of the effects of ALD-52 were described by Shulgin.^[1] 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.^[1] Another claimed that it was more effective than LSD in increasing blood pressure.^[1] One account could not tell ALD-52 and LSD apart.^[1] Per Shulgin, if ALD-52 is a readily converted prodrug of LSD, then they should be equivalent in all regards (aside from a slight difference potency).^[1]

ALD-52 is a readily converted prodrug of LSD and hence has similar pharmacology to LSD.^{[8][9][4][6][1]} This has been confirmed with human liver enzymes in vitro and in rodents in vivo, but still needs to be confirmed with a clinical study in humans in vivo.^[27][4]

In early studies, ALD-52 was found to have 19 or 20% of the toxicity of LSD in rabbits given intravenously, 12.5 or 13% of the pyretogenic effect of LSD in rabbits, and 2.0 to 2.1 times the antiserotonergic activity of LSD in the isolated rat uterus in vitro.^[22][6][12]

The receptor interactions of ALD-52 have been studied.^[4][28] The drug shows dramatically reduced affinities for the serotonin 5-HT_1A and 5-HT_2A receptors compared to LSD itself.^[4][28] It also showed markedly reduced activational potency and efficacy at the serotonin 5-HT_2A receptor relative to LSD, whereas agonistic activity at the serotonin 5-HT_2B and 5-HT_2C receptors was lost entirely.^[4]

An early study reported that ALD-52 surprisingly did not produce the head-twitch response, a behavioral proxy of psychedelic effects, in mice.^[4][29][30] It was subsequently suggested that this could be due to species differences in the metabolism of ALD-52.^[31] However, later research found that ALD-52 does indeed produce the head-twitch response in mice and that the earlier findings were erroneous.^[4] ALD-52 had about 45% of the molar potency of LSD in inducing the head-twitch response, whereas 1P-LSD had about 38%, 1V-LSD 36%, and 1cP-LSD 31% of the molar potency of LSD in this assay.^[9][4]

The preclinical pharmacokinetics and metabolism of ALD-52 have been studied.^[4] A large percentage of the total dose of both ALD-52 and 1P-LSD is metabolized into LSD in rodents.^[4] Circulating levels of LSD following subcutaneous injection in rodents are virtually identical with administration of ALD-52 and 1P-LSD.^[4] The formation of LSD from ALD-52 could be largely blocked by the strong cytochrome P450 inhibitor ketoconazole in a human liver enzyme system in vitro, with CYP3A4 specifically appearing to be responsible for ALD-52 deacetylation into LSD.^[5]