ALD-52

(6aR,9R)-4-acetyl-N,N-diethyl-7-methyl-6,6a,8,9-tetrahydroindolo[4,3-fg]quinoline-9-carboxamide

Overview

ALD-52 belongs to Psychedelics / Ergolines.

Key safety note: ALD-52 is a potent psychedelic active at roughly 100 µg: accurate low dosing (ideally volumetric) is essential.[1]
Effects
Subjective effects vary. What a substance feels like depends on dose, individual physiology, mindset, and setting. The points below describe commonly reported effects, not guaranteed, uniform, or desirable outcomes.
  • Broadly LSD-like, but often reported as slightly less potent and less visual than LSD, with a mellower, less anxiety-provoking headspace
  • A pronounced, stimulating body high with tactile enhancement
  • A long experience (~8–14 h) with a gradual come-up and a long come-down
Dosing & duration
Harm-reduction note: These are commonly cited reference ranges, not a recommendation or a “safe” dose. Potency, purity, body chemistry, tolerance, and drug combinations vary widely. Start low, go slow, wait for full effects before redosing, and never assume an unknown product matches these figures. Missing data is not evidence of safety.

Oral. Active at roughly 0.5–1 µg/kg orally (~35–70 µg for a 70 kg adult). Shulgin's TiHKAL lists ~50–175 µg and community harm-reduction sources a common range around 100–175 µg. As a prodrug that converts to LSD, it is dosed like LSD: start low, and use volumetric dosing of a solution for accuracy.

Dose ranges

Threshold

~30 µg

Light

30–100 µg

Common

100–175 µg

Strong

175–325 µg

Duration

onset

20–40 min

peak

3–5 h

total

8–14 h

Chemical & Physical Properties
FormulaC22H27N3O2
Molar mass365.5 g/mol
StateNot reported
Melting pointNot reported
Boiling pointNot reported
DensityNot reported
Vapor pressureNot reported
pKaNot reported
LogP2.8 (predicted, XLogP3)
SolubilityNot reported
Refractive indexNot reported
Identifiers & Synonyms
CAS3270-02-8
CAS (enantiomer)
PubChem CID201111
InChIKeyFJOWXGYLIWJFCH-OXQOHEQNSA-N
InChIInChI=1S/C22H27N3O2/c1-5-24(6-2)22(27)16-10-18-17-8-7-9-19-21(17)15(13-25(19)14(3)26)11-20(18)23(4)12-16/h7-10,13,16,20H,5-6,11-12H2,1-4H3/t16-,20-/m1/s1
SMILESCCN(CC)C(=O)[C@H]1CN([C@@H]2CC3=CN(C4=CC=CC(=C34)C2=C1)C(=O)C)C

Synonyms

  • 1-Acetyl-LSD
  • 1A-LSD
  • N-Acetyl-LSD
  • Acetyl-LSD
  • 1-Acetyllysergic acid diethylamide
Pharmacodynamics & Biochemistry

A semi-synthetic lysergamide: the N1-acetyl derivative of LSD (1-acetyl-LSD). It behaves as a readily converted prodrug of LSD: hepatic CYP3A4 deacetylates it to LSD, and its psychedelic effects are largely attributed to that conversion (formation of LSD can be blocked in vitro by CYP3A4 inhibitors). In its own right ALD-52 is a much weaker direct agonist than LSD, with markedly reduced affinity and activational potency/efficacy at the serotonin 5-HT2A and 5-HT1A receptors, N1-acylation of the ergoline is known to lower 5-HT2 affinity, so little of its activity is thought to come from the parent molecule itself. In humans it is reported to be roughly 90–100% as potent as LSD, with a very similar onset and duration, consistent with LSD being the main active species.

Biological targets

  • 5-HT2A

Binding & functional measurements

TargetMeasurementSpecies
5-HT1A receptorKi 1,054 ± 367 nMHuman
5-HT2A receptorEC50 38 nM
Emax 25 ± 2%		Human
5-HT2A receptorKi 174 ± 43 nMHuman
5-HT2A receptorEC50 12 nM
Emax 29 ± 1%		Mouse
5-HT2C receptorKi 10 ± 3.5 nMHuman
Pharmacokinetics
BioavailabilityNot reported
TmaxNot reported
Half-lifeNot established in humans (rapidly deacetylated to LSD)
VdNot reported
Protein bindingNot reported
MetabolismA prodrug: hepatic CYP3A4 deacetylates ALD-52 to LSD, which is thought to mediate most of its effects. In vitro, LSD formation is largely blocked by CYP3A4 inhibitors. Human pharmacokinetics, including a formal elimination half-life, have not been established, but the overall duration of action (~8–14 h) is similar to that of LSD
ExcretionNot reported
Toxicology & Safety
Harm-reduction note: Toxicity and risk depend on dose, route, purity, combinations, setting, and individual health factors. Missing harms should never be interpreted as evidence of safety.

Not reported

ALD-52 is a potent psychedelic active at roughly 100 µg: accurate low dosing (ideally volumetric) is essential. Because it is a prodrug that converts to LSD, its effects and risks broadly mirror those of LSD: a long experience (about 8–14 hours), possible anxiety or confusion, transient increases in blood pressure and heart rate, and the potential to precipitate or worsen psychosis in vulnerable people. Dedicated human safety and toxicity data are very limited and largely inferred from LSD. As with all serotonergic drugs, avoid combining it with other serotonergic agents. Limited data must never be read as evidence of safety.[1]

Legal Status
Legal note: Legal status can change over time and may vary by country, region, formulation, analogue status, prescription context, and enforcement practice. Always confirm with current official sources before relying on this section.
Interactions & Contraindications

Drug interactions

Lithium, Tramadol Markedly raise the risk of seizures and psychosis with serotonergic psychedelics, avoid.
Stimulants (amphetamines, cocaine) Add cardiovascular strain, anxiety and paranoia.
Cannabis Can strongly and unpredictably potentiate the effects and increase the chance of a negative reaction.
SSRIs, SNRIs, MAOIs Add to serotonergic load.

Contraindications

Personal or family history of psychosis, schizophrenia or bipolar disorder
Cardiovascular disease, hypertension or arrhythmia significant or uncontrolled disease or hypertension.
Concurrent MAOI, SSRI/SNRI or other serotonergic medication includes concurrent lithium or tramadol (seizure/psychosis risk).
Settings where impairment or dissociation risks injury (driving, water, heights) long (~8-14 h) duration and potency call for a prepared, supported setting.
Usage & Context
  • Research.
  • Recreational.
Sources & Evidence

Further Information