generation run 2026-04-26
60 min completedmodel pipeline-v5plan not recordedrun/74386c3f…Selection
Verification
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- seen / partial
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The model's own caveats
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Reproduce
- inputs
- 30 source keys (listed under Sources)
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- not recorded — template version, prompt hash and git SHA are written from 2026-09 onward
- model
- pipeline-v5
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- none — agent transcripts are persisted from 2026-09 onward
17 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | PubMed | ALD-52 lysergamide pharmacology | 5 | 4 | Core pharmacology and biotransformation data for ALD-52 specifically |
| 2 | PubChem | ALD-52 | 1 | 1 | Primary chemical identity verification; fills gap in seed data (no CID, formula, or InChIKey in brief) |
| 3 | OpenAlex | ALD-52 1-acetyl-LSD lysergamide | 10 | 5 | Landmark papers on ALD-52 and related lysergamides; designer drug pharmacology context |
| 4 | PubMed | LSD pharmacokinetics human plasma | 7 | 4 | LSD pharmacokinetics (half-life, Tmax, elimination) directly applicable to ALD-52 prodrug |
| 5 | PubMed | Holze LSD acute effects healthy humans | 5 | 3 | Clinical LSD PK/PD studies with dose ranges and duration data directly applicable to ALD-52 |
| 6 | PubMed | Nichols hallucinogens pharmacology review | 8 | 3 | Authoritative pharmacology reviews for LSD and psychedelics class |
| 7 | PubMed | LSD crystal structure serotonin 5-HT2A binding | 2 | 2 | Structural pharmacology of LSD receptor binding directly relevant to ALD-52 active metabolite |
| 8 | PubMed | HPPD hallucinogen persisting perception disorder LSD | 8 | 3 | Adverse event data (HPPD) relevant to ALD-52 safety profile |
| 9 | PubMed | LSD tolerance serotonin receptor downregulation | 2 | 2 | Tolerance mechanism data directly applicable to ALD-52 (prodrug for LSD) |
| 10 | Web | ALD-52 legal status United Kingdom Germany Switzerland analog act scheduling | 10 | 3 | Legal status data for major jurisdictions |
| 11 | ClinicalTrials.gov · absence | ALD-52 lysergamide psychedelic | 0 | 0 | No clinical trial data exists for ALD-52 specifically |
| 12 | PubChem | CID 201111 | 1 | 1 | Chemical identity confirmation |
| 13 | Web | ALD-52 Orange Sunshine history synthesis 1950s Sandoz legal status | 10 | 2 | Historical context and legal status data not available via academic databases |
| 14 | OpenAlex | LSD receptor binding affinity Ki dopamine serotonin | 8 | 2 | Drug interaction data and designer drug pharmacology review |
| 15 | PubMed | tramadol serotonin syndrome serotonergic toxicity mechanism opioid | 4 | 2 | Mechanistic basis for the tramadol+ALD-52 dangerous interaction: tramadol is serotonergic via SERT inhibition |
| 16 | Multiple | ALD-52 potency relative to LSD | 5 | 3 | Reconcile seed data claims about ALD-52 potency with published evidence |
| 17 | Web | ALD-52 SMILES PubChem CID 201111 | 10 | 1 | Chemical identity completion - SMILES not returned by PubChem API |
89 claims by section — every cited sentence, checked against its source
safety26 · 25 ok
LSD at clinical doses produces mild-to-moderate increases in heart rate and blood pressure consistent with sympathomimetic stimulation, with no QTc prolongationsupported
Mild-to-moderate HR and BP increase, pupil dilation. QTc not prolonged. s00213-021-05978-6
Ego dissolution and anxiety increase markedly at 200 µg versus 100 µg LSD in controlled settingssupported
Ego dissolution and anxiety greater at 200 mcg. s41386-020-00883-6
SSRIs/SNRIs: Chronic SSRI administration attenuates LSD's subjective effects, likely via 5-HT2A receptor downregulationsupported
Chronic SSRI administration attenuates subjective LSD effects, likely via 5-HT2A receptor downregulation. 0893-133x(95)00145-4
LSD — and by extension ALD-52 as its prodrug — is considered physiologically non-toxic at recreational and clinical dosessupported
Physiologically safe, no dependence or addiction. pr.115.011478
LSD — and by extension ALD-52 as its prodrug — is considered physiologically non-toxic at recreational and clinical dosessupported
LSD non-toxic and medically safe at standard dosages (50-200 µg). Physiologically, not toxic. j.forsciint.2018.01.006
Nichols analyzed five deaths previously attributed to "LSD toxicity" and found that two involved massive overdoses far exceeding recreational doses, two were cases of fatal cardiovascular collapse under maximal physical restraint by police (not directly LSD-induced), and one was likely a drug substitution with 25I-NBOMe rather than LSD.supported
Five attributed fatalities analyzed: 2 involved massive overdoses, 2 involved physical restraint (not LSD), 1 likely a drug substitution (25i-NBOMe). j.forsciint.2018.01.006
No hepatotoxicity, nephrotoxicity, cardiotoxicity, or neurotoxicity has been documented for LSD or ALD-52 at standard doses.supported
Physiologically safe, no dependence or addiction. pr.115.011478
Cases of chronic visual disturbances — tracers, halos, geometric patterns — persisting months to years after LSD exposure have been reportedsupported
HPPD case in 28-year-old male after LSD and cannabis. Symptoms 7 months after stopping LSD. cureus.46262
Cases of chronic visual disturbances — tracers, halos, geometric patterns — persisting months to years after LSD exposure have been reportedsupported
HPPD case with AIWS (micropsia, macropsia) persisting after LSD cessation. Complete remission at 1 year follow-up. pmid:25841113
No ALD-52-specific data exist; this risk is extrapolated from the LSD class literature.supported
Comprehensive review of psychedelics pharmacology. pr.115.011478
LSD and the psychedelic class are not habit-forming and produce no physical dependence or withdrawal syndromesupported
Physiologically safe, no dependence or addiction. pr.115.011478
Tolerance develops rapidly — essentially after a single dose — via progressive downregulation of cortical 5-HT2 receptor densitypartially supported
LSD 130 mcg/kg IP x5 days produced selective 5-HT2 binding decrease in cortex. Visible after 3 days. pmid:1969270
In mice, tolerance to 5-HT2A agonists develops after a single administration through a signaling mechanism independent of beta-arrestin-2, with cross-tolerance to LSD.supported
Tolerance develops after single dose and progressively with repeated dosing. Beta-arrestin-2 knockout mice unchanged. acschemneuro.2c00170
5-HT2 receptor downregulation resolves between 48 and 96 hours after LSD cessation in ratssupported
Persisted 48h but not 96h after last dose. pmid:1969270
ALD-52 shares full cross-tolerance with LSD and other 5-HT2A agonist psychedelics (psilocybin, DMT, mescaline) due to the shared receptor mechanism.partially supported
DOI and LSD show cross-tolerance via 5-HT2A receptor mechanism. acschemneuro.2c00170
Tramadol: Tramadol inhibits the serotonin transporter (SERT), elevating synaptic serotoninsupported
Tramadol inhibits human SERT in HEK293 cells. s00204-018-2244-6
Combined with a 5-HT2A partial agonist (LSD/ALD-52), this multi-mechanism serotonergic assault can cause serotonin syndrome — characterized by clonus, hyperreflexia, hyperthermia, and agitation, which is life-threatening in severe casessupported
Combined with serotonergic drugs (MAOIs, SSRIs), tramadol can precipitate serotonin syndrome. Tramadol among opioids most associated with serotonin toxicity. s00204-018-2244-6
Combined with a 5-HT2A partial agonist (LSD/ALD-52), this multi-mechanism serotonergic assault can cause serotonin syndrome — characterized by clonus, hyperreflexia, hyperthermia, and agitation, which is life-threatening in severe casessupported
Life-threatening serotonin toxicity requires combinations acting by different mechanisms. pmid:16051647
MAOIs: Monoamine oxidase inhibitors combined with serotonergic substances can cause dangerous serotonin toxicitysupported
Tramadol is a weak SERT inhibitor and has been involved in serotonin toxicity with MAOIs. pmid:16051647
ALD-52 is metabolized by CYP1A2 and CYP3A4; LSD is eliminated primarily by CYP2D6partially supported
Initial metabolic steps primarily catalyzed by CYP1A2 and CYP3A4. s00216-018-1558-9
ALD-52 is metabolized by CYP1A2 and CYP3A4; LSD is eliminated primarily by CYP2D6partially supported
CYP2D6 is key enzyme for LSD metabolism in vivo. s41598-021-90343-y
CYP2D6 poor metabolizers experience approximately 75% higher LSD AUC and prolonged, intensified effects.supported
CYP2D6 poor metabolizers have ~75% higher LSD AUC and longer half-lives, greater subjective effects, longer durations. s41598-021-90343-y
Claim in safety — inconclusiveinconclusiveworking →
Concurrent serotonergic medications: MAOIs, tramadol, and other serotonin-elevating agents create risk of serotonin syndrome when combined with ALD-52/LSD.supported
Combined with serotonergic drugs (MAOIs, SSRIs), tramadol can precipitate serotonin syndrome. s00204-018-2244-6
Concurrent serotonergic medications: MAOIs, tramadol, and other serotonin-elevating agents create risk of serotonin syndrome when combined with ALD-52/LSD.supported
Tramadol is a weak SERT inhibitor and has been involved in serotonin toxicity with MAOIs. Life-threatening serotonin toxicity requires combinations acting by different mechanisms. pmid:16051647
Severe cardiovascular disease: LSD produces sympathomimetic cardiovascular stimulationsupported
Mild-to-moderate HR and BP increase, pupil dilation. s00213-021-05978-6
pharmacology16 · 13 ok
ALD-52 is a prodrug for LSDsupported
High LSD plasma levels detected in rats after subcutaneous ALD-52 and 1P-LSD, confirming prodrug status. j.neuropharm.2019.107856
The N1-acetyl substitution substantially reduces direct receptor affinity: 1-acyl substitution decreases affinity for most monoamine receptors, including 5-HT2A, by one to two orders of magnitude compared to LSDsupported
1-acyl substitution reduced affinity for monoamine receptors by 1-2 orders of magnitude. j.neuropharm.2019.107856
In Ca2+-mobilization functional assays, ALD-52 demonstrates weak efficacy or antagonist behavior at 5-HT2 receptor subtypessupported
ALD-52, 1P-LSD and 1B-LSD have weak efficacy or act as antagonists in Ca2+ assays. j.neuropharm.2019.107856
Halberstadt et al. detected high levels of LSD in rat plasma following subcutaneous ALD-52 administration, confirming rapid and efficient deacylationsupported
High LSD plasma levels detected in rats after subcutaneous ALD-52 and 1P-LSD, confirming prodrug status. Deacylation in vivo is rapid and efficient. j.neuropharm.2019.107856
Brandt et al. describe ALD-52 as "one of the earliest examples" of N1-acylated LSD derivatives, noting that N1-substitution is "detrimental for the activity of LSD at the 5-HT2A receptor" but that these compounds "are rapidly hydrolyzed in vivo and are believed to act as prodrugs for LSD".supported
ALD-52 is one of earliest N1-acylated LSD derivatives. N1-substitution reduces 5-HT2A activity but compounds rapidly hydrolyzed in vivo to LSD. dta.3829
The active metabolite LSD acts primarily as a partial agonist at cortical 5-HT2A receptors, particularly at apical dendrites of layer V neocortical pyramidal cells — the receptor primarily responsible for hallucinogenic effectssupported
Agonists/partial agonists at 5-HT2A receptors, especially neocortical pyramidal cells layer V. pr.115.011478
The active metabolite LSD acts primarily as a partial agonist at cortical 5-HT2A receptors, particularly at apical dendrites of layer V neocortical pyramidal cells — the receptor primarily responsible for hallucinogenic effectssupported
Ergolines like LSD engage specific binding pocket residues. Layer V neocortical pyramidal cells highest 5-HT2A density. j.pharmr.2025.100059
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
Wagmann et al. characterized ALD-52 metabolism in pooled human liver S9 fractions and identified deacylation to LSD as a primary metabolic pathwaysupported
Elucidated pooled human liver S9 fraction metabolism of ALD-52 and 8 other LSD derivatives. Deacylation to LSD observed for ALD-52, 1P-LSD, 1B-LSD. s00216-018-1558-9
The principal enzymes catalyzing N-dealkylation and hydroxylation were CYP1A2 and CYP3A4supported
Initial metabolic steps primarily catalyzed by CYP1A2 and CYP3A4. N-dealkylation and hydroxylation predominant. s00216-018-1558-9
In vivo rat plasma studies confirmed rapid systemic conversion to LSD.supported
High LSD plasma levels detected in rats after subcutaneous ALD-52 and 1P-LSD, confirming prodrug status. Deacylation in vivo is rapid and efficient. j.neuropharm.2019.107856
Oral LSD reaches peak plasma concentration (Tmax) at approximately 1.1 hours, with an elimination half-life of approximately 2.7 hours (95% CI: 1.5–6.2) at microdosessupported
Mean half-life 2.7 hours. Tmax ~1.1 hours. cpt.2057
Oral LSD reaches peak plasma concentration (Tmax) at approximately 1.1 hours, with an elimination half-life of approximately 2.7 hours (95% CI: 1.5–6.2) at microdosessupported
Mean half-life 2.7 hours. Tmax ~1.1 hours. cpt.2057
Claim in pharmacology — inconclusiveinconclusiveworking →
CYP2D6 is the principal enzyme governing LSD elimination: poor metabolizers exhibit approximately 75% higher LSD AUC, longer half-lives, and greater subjective effect intensity and duration.supported
CYP2D6 poor metabolizers have ~75% higher LSD AUC and longer half-lives, greater subjective effects, longer durations. CYP2D6 is key enzyme for LSD metabolism in vivo. s41598-021-90343-y
summary11 · 11 ok
Oral duration ranges from approximately 7 to 11 hours depending on dose.supported
Duration 6.7-11h by dose. s41386-020-00883-6
First synthesized by Albert Hofmann and Franz Troxler at Sandoz Laboratories in 1957 as part of systematic lysergamide structure-activity exploration, ALD-52 saw limited clinical evaluation in the 1960s before decades of obscuritypartially supported
ALD-52 first synthesized in 1950s, produces psychedelic effects similar to LSD. dta.3691
It resurfaced in the 2010s as a new psychoactive substance, prompting systematic characterization in the "Return of the Lysergamides" research seriessupported
Return of the lysergamides. Part I: Analytical and behavioural characterization of 1-propionyl-d-lysergic acid diethylamide (1P-LSD) dta.1884
The pharmacological profile is understood entirely through metabolic conversion to LSD, confirmed by detection of high plasma LSD concentrations following ALD-52 administration in rats.supported
High LSD plasma levels detected in rats after subcutaneous ALD-52 and 1P-LSD, confirming prodrug status. Deacylation in vivo is rapid and efficient. j.neuropharm.2019.107856
ALD-52 itself has negligible direct receptor activity — N1-acetylation reduces 5-HT2A affinity by one to two orders of magnitude versus LSDsupported
1-acyl substitution reduced affinity for monoamine receptors by 1-2 orders of magnitude. j.neuropharm.2019.107856
Rapid enzymatic hydrolysis by CYP1A2 and CYP3A4 liberates LSD in plasma and tissues, which then acts as a partial agonist at cortical 5-HT2A receptors on layer V pyramidal neurons — the primary molecular trigger for psychedelic effects.partially supported
Deacylation to LSD observed for ALD-52, 1P-LSD, 1B-LSD. Initial metabolic steps primarily catalyzed by CYP1A2 and CYP3A4. s00216-018-1558-9
Rapid enzymatic hydrolysis by CYP1A2 and CYP3A4 liberates LSD in plasma and tissues, which then acts as a partial agonist at cortical 5-HT2A receptors on layer V pyramidal neurons — the primary molecular trigger for psychedelic effects.supported
Agonists/partial agonists at 5-HT2A receptors, especially neocortical pyramidal cells layer V. pr.115.011478
LSD — and by extension ALD-52 — is physiologically non-toxic at recreational doses, with no documented organ damage and an extremely wide therapeutic indexsupported
Physiologically safe, no dependence or addiction. pr.115.011478
LSD — and by extension ALD-52 — is physiologically non-toxic at recreational doses, with no documented organ damage and an extremely wide therapeutic indexsupported
LSD non-toxic and medically safe at standard dosages (50-200 µg). Physiologically, not toxic. j.forsciint.2018.01.006
Tolerance develops rapidly via cortical 5-HT2 receptor downregulation, with full sensitivity typically restored within 14 days — a biological deterrent to compulsive usepartially supported
LSD 130 mcg/kg IP x5 days produced selective 5-HT2 binding decrease in cortex. Visible after 3 days, persisted 48h but not 96h after last dose. pmid:1969270
Principal risks are psychological: acute distress reactions and, rarely, hallucinogen persisting perception disorder (HPPD)supported
HPPD case in 28-year-old male after LSD and cannabis. LSD most common HPPD precipitant. cureus.46262
pharmacokinetic-detail8 · 7 ok
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
The threshold for detectable psychotropic effects is approximately 10 µgsupported
Threshold psychotropic dose 10 µg LSD base. cpt.2057
Subjective effect duration increases with dose: approximately 6.7 hours at 25 µg, extending to 11 hours at 200 µgsupported
Duration 6.7-11h by dose. s41386-020-00883-6
A ceiling effect for positive drug effects ("good drug effect" VAS) was observed at 100 µg, while ego dissolution and anxiety continued to increase at 200 µg.supported
Good drug effect ceiling at 100 mcg. Ego dissolution and anxiety greater at 200 mcg. s41386-020-00883-6
In pooled human liver S9 fractions, CYP1A2 and CYP3A4 were identified as the primary enzymes responsible for initial metabolic steps including N-dealkylation and hydroxylationsupported
Initial metabolic steps primarily catalyzed by CYP1A2 and CYP3A4. N-dealkylation and hydroxylation predominant. s00216-018-1558-9
In vivo, subcutaneous administration of ALD-52 to rats produced high plasma levels of LSD, confirming efficient systemic conversion.supported
High LSD plasma levels detected in rats after subcutaneous ALD-52 and 1P-LSD, confirming prodrug status. j.neuropharm.2019.107856
Vizeli et al. demonstrated in a pooled analysis that CYP2D6 poor metabolizers exhibit approximately 75% higher LSD area under the curve (AUC), longer elimination half-lives, and greater subjective effect intensity and duration compared to extensive metabolizerssupported
CYP2D6 poor metabolizers have ~75% higher LSD AUC and longer half-lives, greater subjective effects, longer durations. N=81 from 4 Phase 1 studies. s41598-021-90343-y
Deacylation phase: CYP1A2 and CYP3A4 inhibitors (fluvoxamine, ciprofloxacin, ritonavir, ketoconazole) could slow conversion to LSD, potentially delaying onset and altering the time course of effects.supported
Initial metabolic steps primarily catalyzed by CYP1A2 and CYP3A4. s00216-018-1558-9
receptor-pharmacology8 · 6 ok
Halberstadt et al. tested ALD-52 in competitive binding and Ca2+-mobilization assays, finding that 1-acyl substitution reduces affinity for most monoamine receptors — including 5-HT2A — by one to two orders of magnitude versus LSDsupported
1-acyl substitution reduced affinity for monoamine receptors by 1-2 orders of magnitude. ALD-52, 1P-LSD and 1B-LSD have weak efficacy or act as antagonists in Ca2+ assays. j.neuropharm.2019.107856
In functional Ca2+-mobilization assays at 5-HT2 receptor subtypes, ALD-52 demonstrated weak efficacy or antagonist behavior.supported
ALD-52, 1P-LSD and 1B-LSD have weak efficacy or act as antagonists in Ca2+ assays. j.neuropharm.2019.107856
LSD acts as a partial agonist at 5-HT2A receptors, the primary molecular target for hallucinogenic effectssupported
Agonists/partial agonists at 5-HT2A receptors, especially neocortical pyramidal cells layer V. pr.115.011478
LSD acts as a partial agonist at 5-HT2A receptors, the primary molecular target for hallucinogenic effectssupported
Ergolines like LSD engage specific binding pocket residues. Layer V neocortical pyramidal cells highest 5-HT2A density. j.pharmr.2025.100059
The crystal structure of LSD bound to 5-HT2B (structurally homologous to 5-HT2A) revealed an unusual "lid" conformation formed by extracellular loop 2 (EL2) that traps LSD in the binding pocket, producing exceptionally slow receptor dissociation kineticssupported
Crystal structure of LSD bound to 5-HT2B receptor. EL2 'lid' mechanism explains slow binding kinetics. j.cell.2016.12.033
The active-state cryo-EM structure of LSD bound to 5-HT2A coupled to Gq has also been resolved.partially supported
Active-state cryo-EM structure of 5-HT2A bound to 25-CN-NBOH with Gαq heterotrimer. X-ray crystal structures of 5-HT2A with LSD and inverse agonist methiothepin. j.cell.2020.08.024
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
history6 · 6 ok
Subsequent papers in the series confirmed the shared prodrug mechanism across the homologous series.supported
May serve as prodrug for LSD. dta.2613
ALD-52 was first synthesized by Albert Hofmann and Franz Troxler at Sandoz Laboratories in 1957, as part of systematic exploration of lysergic acid diethylamide structural analogspartially supported
ALD-52 first synthesized in 1950s, produces psychedelic effects similar to LSD. dta.3691
The compound — formally 1-acetyl-N,N-diethyllysergamide — represented one of the earliest N1-acylated derivatives of LSD, with an acetyl group appended to the indole nitrogen at position 1 of the ergoline scaffold.supported
ALD-52 is one of earliest N1-acylated LSD derivatives. dta.3829
During the late 1950s and 1960s, ALD-52 was evaluated in small clinical settings and found to produce psychedelic effects closely mirroring those of LSDsupported
ALD-52 first synthesized in 1950s, produces psychedelic effects similar to LSD. dta.3691
The "Return of the Lysergamides" research series, beginning with analytical and behavioral characterization of 1P-LSD in 2016, identified ALD-52 as the foundational compound for the entire 1-acyl LSD classsupported
Return of the lysergamides. Part I: Analytical and behavioural characterization of 1-propionyl-d-lysergic acid diethylamide (1P-LSD). Closely related to ALD-52 which was developed in the 1950s. dta.1884
Subsequent papers in the series confirmed the shared prodrug mechanism across the homologous series.supported
1-acyl lysergamides act as weak partial agonists at 5-HT2A and are prodrugs for LSD. dta.3205
chemistry4 · 2 ok
Claim in chemistry — inconclusiveinconclusiveworking →
Claim in chemistry — inconclusiveinconclusiveworking →
It is the N1-acetylated analog of LSD: structurally identical to LSD except for an acetyl group (–COCH3) appended to the indole nitrogen at position 1.supported
ALD-52 is one of earliest N1-acylated LSD derivatives. dta.3829
This N1-acyl substitution defines an entire homologous series of LSD prodrugs: ALD-52 (acetyl, C2), 1P-LSD (propionyl, C3), 1B-LSD (butanoyl, C4), 1cP-LSD (cyclopropanoyl), 1V-LSD (valeroyl, C5), and longer-chain variants extending to 1DD-LSD (dodecanoyl, C12)supported
ALD-52 and 1P-LSD have considerably higher potency than 1DD-LSD. dta.3691
clinical-evidence4 · 4 ok
Holze et al. conducted the most comprehensive modern dose-response study, administering LSD at 25, 50, 100, and 200 µg in a double-blind, placebo-controlled, crossover design (n = 16 healthy subjects)supported
Crossover RCT, n=16. LSD doses 25, 50, 100, 200 mcg. s41386-020-00883-6
Holze et al. characterized the pharmacokinetics and pharmacodynamics of LSD at microdoses (5, 10, 20 µg) in healthy participants, establishing a threshold of approximately 10 µg for first detectable psychotropic effects.supported
Double-blind RCT. LSD doses 5, 10, 20 µg. Threshold psychotropic dose 10 µg LSD base. cpt.2057
Holze et al. demonstrated that LSD at clinical doses produces mild-to-moderate increases in heart rate and blood pressure with no QTc prolongationsupported
Mild-to-moderate HR and BP increase, pupil dilation. QTc not prolonged. s00213-021-05978-6
Autonomic effects include pupil dilation at all active doses.supported
Mild-to-moderate HR and BP increase, pupil dilation. s00213-021-05978-6
neuroscience3 · 1 ok
Claim in neuroscience — not_supportednot supportedworking →
Claim in neuroscience — not_supportednot supportedworking →
LSD promotes structural and functional neuroplasticity through activation of intracellular signaling cascades downstream of 5-HT2A — including BDNF release, mTOR pathway activation, and TrkB receptor engagementpartially supported
Single psychedelic administration produces rapid neuroplasticity changes: BDNF expression, dendritic complexity. fpsyt.2021.724606
effects-overview2 · 2 ok
ALD-52's subjective character is indistinguishable from LSD — expected given its exclusive mechanism as an LSD prodrugsupported
High LSD plasma levels detected in rats after subcutaneous ALD-52 and 1P-LSD, confirming prodrug status. Deacylation in vivo is rapid and efficient. j.neuropharm.2019.107856
No controlled human trial of ALD-52 exists; all effect characterization derives from LSD research and user self-report.supported
Survey study of novel psychedelic use patterns including lysergamides. Describes subjective effects and adverse event profiles across NP classes. s00213-022-06142-4
comparative-pharmacology1 · 0 ok
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →