4-HO-MiPT

# Research Output: 4-HO-MiPT (Miprocin)

**PSX ID:** PSX-0069  
**Research Date:** 2026-04-20  
**Substance Readiness Classification:** Emerging / Sparse data (readiness < 0.3)

---

## Chemical Identity

**Confirmed via PubChem (CID 10082683) [Ref 1 — database lookup]:**

| Property | Value |
|---|---|
| IUPAC Name | 3-[2-[methyl(propan-2-yl)amino]ethyl]-1H-indol-4-ol |
| Molecular Formula | C₁₄H₂₀N₂O |
| Molecular Weight | 232.32 g/mol |
| InChIKey | RXKGHZCQFXXWFQ-UHFFFAOYSA-N |
| CAS Number | 77872-43-6 |
| PubChem CID | 10082683 |
| SMILES | CC(C)N(C)CCC1=CNC2=C1C(=CC=C2)O |

**Notes on seed data discrepancies:**
- The brief had empty SMILES, PubChem CID fields — these are now confirmed from PubChem database lookup.
- The brief's IUPAC name matches the PubChem record exactly.
- Molecular formula and weight are confirmed.

**Physical Properties (from Shulgin TiHKAL [Ref 3] and Chadeayne et al. 2020 [Ref 1]):**
- Free base melting point: 123–124°C (per TiHKAL entry #22 [Ref 3, Ref 23])
- The compound rapidly discolors (oxidizes) without inert atmosphere storage and freezing; stability is poor under ambient conditions [Ref 3]
- A stable crystalline fumarate salt form has been characterized: bis(4-hydroxy-N-isopropyl-N-methyltryptammonium) fumarate, with structure confirmed by X-ray crystallography (Chadeayne et al. 2020 [Ref 1])
- In the fumarate crystal, tryptammonium and fumarate ions are held in one-dimensional chains by N–H···O and O–H···O hydrogen bonds, further consolidated by N–H···π interactions [Ref 1]

**FLAG:** No published data on aqueous solubility or log P for 4-HO-MiPT. Free base stability is poor; fumarate salt is preferred for storage. These values are absent from the literature.

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## Pharmacology

### Primary Mechanism of Action

4-HO-MiPT is a serotonergic psychedelic acting primarily as an agonist at the serotonin 5-HT₂A receptor, consistent with all 4-hydroxytryptamine class compounds (Nichols 2018 [Ref 15]; Glatfelter et al. 2022 [Ref 5]; Repke et al. 1985 [Ref 2]).

The 4-hydroxytryptamine scaffold (shared with psilocin/4-HO-DMT) confers nanomolar affinity at 5-HT₂A receptors, which is the principal mediator of hallucinogenic/psychedelic effects (Nichols 2018 [Ref 15]). Glatfelter et al. (2022 [Ref 5]) demonstrated that 4-hydroxy and 4-acetoxy tryptamines display similar receptor target profiles and efficacies at 5-HT₂A, and that only tertiary amines (including N-methyl-N-alkyl variants) produce the head twitch response (HTR), a rodent behavioral proxy for hallucinogenic effects.

The unsymmetrical nitrogen substitution in 4-HO-MiPT (N-methyl + N-isopropyl) is noted by Repke et al. (1985 [Ref 2]) as producing increased potency compared to symmetrical dimethyl homologues (psilocin) in at least some MIPT analogs.

### Receptor Binding — Published Data

**⚠ FLAG (safety-critical):** No published Ki or EC₅₀ binding affinity data exists for 4-HO-MiPT itself at any receptor. The following findings are inferences from structural class data and must be clearly labeled as such in article prose.

**By class/structural analogy (4-hydroxytryptamine tertiary amines):**
- 5-HT₂A receptor: nanomolar affinity (primary psychedelic target); 4-substituted compounds show high selectivity for 5-HT₂A vs. 5-HT₁A and 5-HT₂C (Kozell et al. 2023 [Ref 6])
- 5-HT₁A receptor: agonist activity expected at class level; 4-substituted compounds show less 5-HT₁A binding than 5-substituted compounds (Kozell et al. 2023 [Ref 6]; Blair et al. 2000 [Ref 11])
- 5-HT₂C receptor: low to moderate affinity expected at class level (Kozell et al. 2023 [Ref 6])
- Serotonin transporter (SERT): some non-ring-substituted tryptamines bind SERT, but this is less consistent for 4-substituted compounds (Kozell et al. 2023 [Ref 6])

**Adjacent compound data (Glatfelter et al. 2023 [Ref 4]):** The Glatfelter 2023 study tested N,N-dialkyl variations on 4-HO, 4-AcO, and 4-PrO tryptamines — but used N-methyl-N-propyl (n-propyl, MPT) rather than N-methyl-N-isopropyl (MiPT). 4-HO-MiPT was not directly included in this study. ⚠ Note: isopropyl ≠ n-propyl; these have distinct steric profiles.

**Adjacent compound data (Glatfelter et al. 2023 [Ref 4]):** For 4-HO-DiPT (N,N-diisopropyltryptamine — the diisopropylamino variant), binding at 5-HT₂C was notably weaker than other N,N-dialkyl psilocin analogs, suggesting that bulkier N-alkyl substitutions may differentially affect receptor selectivity. 4-HO-MiPT's asymmetric methyl/isopropyl combination occupies a structural space between smaller and larger N-substituents.

**Potency relative to psilocin (human, from TiHKAL [Ref 3]):** Shulgin reports that 20 mg of 4-HO-MiPT was "fully equivalent to 50 mg of psilocin," indicating approximately 2.5× greater oral potency than psilocin in human self-experiments. This is the only published human potency comparison and is uncontrolled.

**⚠ FLAG:** The Psychedelic Science Review [Ref not independently verified] cites a "McKenna et al. 1990" study reportedly showing greater potency than psilocin at 5-HT₁A, 5-HT₂A, and 5-HT₂B, and a "Klein et al. 2020" study showing 25% less potency than psilocin in HTR assays. Neither of these studies could be located in PubMed, OpenAlex, or Crossref. These claims remain unverified and should not be cited in article prose without primary source retrieval.

### Mechanism of Psychedelic Action (Class-Level)

Current evidence identifies 5-HT₂A Gq-protein signaling (not β-arrestin2 recruitment) as the key pathway underlying psychedelic effects; Gq efficacy at 5-HT₂A predicts psychedelic-like activity in rodent HTR assays (Wallach et al. 2023 [Ref 18]). 4-HO-MiPT, as a 4-hydroxytryptamine, is expected to function as a Gq-activating 5-HT₂A partial agonist, consistent with its hallucinogenic profile (Repke et al. 1985 [Ref 2]).

5-HT₁A co-agonism is a class feature of 4-hydroxytryptamines and mediates sedative, hyperthermic, and hypolocomotor effects at higher doses, attenuating the 5-HT₂A-mediated HTR in rodents (Halberstadt et al. 2011 [Ref 10]; Glatfelter et al. 2023 [Ref 4]).

### Pharmacokinetics

**No published pharmacokinetic studies exist for 4-HO-MiPT.** The following is inferred by class analogy.

**Psilocin comparator (Brown et al. 2017 [Ref 19]):** Oral psilocin/psilocybin PK in humans: Tmax for psilocin ~90–120 min; elimination half-life ~2–3 hours. However, psilocin is the N,N-dimethyl analog; the N-methyl-N-isopropyl substitution in 4-HO-MiPT alters steric bulk and lipophilicity, potentially affecting absorption rate and metabolic susceptibility.

**Expected metabolic pathways (by analogy with 4-OH-EPT, Bergh et al. 2024 [Ref 16]):** For the closely related 4-hydroxy-N-ethyl-N-propyltryptamine (4-OH-EPT), major metabolic pathways in human liver microsomes include:
- N-dealkylation (loss of the larger alkyl group)
- Hydroxylation (ring and/or side chain)
- Carbonylation
- Double bond formation

For 4-HO-MiPT, N-deisopropylation (yielding 4-HO-NMT, 4-hydroxy-N-methyltryptamine) and N-demethylation are the most likely primary routes. Phase II glucuronide and/or sulfate conjugation is expected, as observed for psilocin (class analog).

**⚠ FLAG:** CYP enzyme involvement is unknown for 4-HO-MiPT. MAO (monoamine oxidase) involvement, which is significant for some tryptamines, has not been characterized. This gap is safety-relevant for MAOI interaction warnings.

### Role of 5-HT₂A in Tolerance

Rapid tolerance to psychedelic effects is mediated by 5-HT₂A receptor downregulation following agonist exposure (de la Fuente Revenga et al. 2022 [Ref 13]). The mechanism is β-arrestin-2-independent. Cross-tolerance between psychedelics (DOI and LSD demonstrated) occurs via the same receptor-level mechanism. These findings directly support the observed tolerance profile for 4-HO-MiPT (tolerance building almost immediately, cross-tolerance within the psychedelic class).

---

## History

**Synthesis (1981):** 4-HO-MiPT was first synthesized and characterized by David B. Repke, Wilfred J. Ferguson, and Dennis K. Bates in 1981 as part of a series of N-alkyl-substituted psilocin analogs. The paper — "Psilocin analogs II. Synthesis of 3-[2-(dialkylamino)ethyl]-, 3-[2-(N-methyl-N-alkylamino)ethyl]-, and 3-[2-(cycloalkylamino)ethyl]indol-4-ols" — was published in the Journal of Heterocyclic Chemistry (Vol. 18, No. 1, pp. 175–179) [Ref 20]. This was part of a continuing series investigating psilocin SAR; earlier work by Repke and Ferguson (1977, J Heterocyclic Chem) had established the 4-hydroxytryptamine scaffold's synthetic accessibility.

**Human pharmacology (1985):** The psychedelic effects of 4-HO-MiPT and related N-methyl-N-isopropyltryptamine analogs in humans were first formally described by Repke, Grotjahn, and Shulgin (1985) in the Journal of Medicinal Chemistry (Vol. 28, No. 7, pp. 892–896) (PMID 4009612 [Ref 2]). Eight MiPT analogs were synthesized and evaluated for hallucinogenic activity in man. The 4-hydroxy congener was described as the "most interesting in overall effect, producing a classic hallucinogenic profile." The study also noted that, for some analogs (MiPT itself and 5-MeO-MiPT), unsymmetrical nitrogen substitution increased potency compared to the dimethyl homologues.

**TiHKAL documentation (1997):** Alexander Shulgin provided an extended account of 4-HO-MiPT's synthesis, properties, and subjective effects as entry #22 in TiHKAL: The Continuation (Shulgin & Shulgin, 1997 [Ref 3]). This remains the most detailed human pharmacology record available for the compound.

**Crystal structure (2020):** Chadeayne, Pham, Golen, and Manke (2020) published the first detailed crystal structure of 4-HO-MiPT as its fumarate salt in Acta Crystallographica Section E (PMID 32280495 [Ref 1]). This work was part of a research program on crystalline forms of psychedelic tryptamines at the University of Massachusetts Dartmouth.

**Therapeutic patent (2023):** US Patent US11780808B2 was granted for crystalline bis-miprocin fumarate, proposing therapeutic applications in psychiatric and neurological disorders. No clinical trials have been conducted [Ref — patent, web_retrieved].

**Research chemical market emergence:** 4-HO-MiPT has appeared on research chemical markets as "miprocin" primarily as a fumarate salt (20 mg pellet forms are commercially advertised). The compound circulates as a psilocin analog. Exact date of initial market appearance not documented in peer-reviewed literature; the Swedish scheduling in November 2005 suggests market presence by at least that date.

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## Subjective Effects

Published descriptions of 4-HO-MiPT's subjective effects come from two primary sources: the controlled human experiment reported by Repke et al. (1985 [Ref 2]), and Shulgin's detailed self-experiment accounts in TiHKAL (1997 [Ref 3, Ref 23]).

**Repke et al. (1985 [Ref 2]):** Described 4-HO-MiPT as producing a "classic hallucinogenic profile" — qualitatively the most interesting compound in the MIPT series. No specific phenomenology was detailed in the peer-reviewed abstract beyond this characterization.

**TiHKAL entry #22 (Shulgin 1997 [Ref 3, Ref 23]):** Shulgin described:
- Vivid closed-eye imagery (CEVs) with intense color alteration
- Sensory enhancement, particularly music appreciation
- Altered time and distance perception
- Erotic effects (enhanced sexual arousal)
- "Bodiless flight" sensations and drifting in/out of body experiences
- Physical sensations including muscle tremors and jaw clenching (bruxism)
- At higher doses: sedative qualities with motor incoordination
- Visual phenomena including tracers, after-images, and color enhancement (consistent with DB effects taxonomy entries)

**Effect profile consistency:** The documented effects from TiHKAL align closely with the Psychedex effects taxonomy for 4-HO-MiPT (perception, body, thinking, transpersonal categories in the brief). No contradiction between seed data effects and published descriptions was identified.

**Potency note:** Shulgin stated that 20 mg of 4-HO-MiPT was "fully equivalent to 50 mg of psilocin" — suggesting approximately 2.5× greater oral potency than psilocin [Ref 3]. This is a single uncontrolled human report.

**Duration profile:** 
- TiHKAL reports: onset 10–20 minutes, plateau reached at approximately 40–60 minutes, total duration 4–6 hours, with residual effects potentially extending beyond this.
- Brief/PsychonautWiki reports: onset 15–45 minutes, come-up 20–60 minutes, peak 1.5–2.5 hours, total 4–6 hours, aftereffects 2–12 hours.
- **Minor discrepancy:** TiHKAL onset (10–20 min) is somewhat faster than the brief's range (15–45 min). Both ranges are plausible given interindividual variability; the brief's broader range is conservative. No flag required — the brief range encompasses TiHKAL's report.

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## Safety & Toxicity

### LD₅₀ / Lethal Dose
No LD₅₀ data exists for 4-HO-MiPT in any species. No lethal human doses have been published. The brief correctly states "toxic dose is unknown" [confirmed].

### Human Adverse Events
No published case reports of 4-HO-MiPT overdose, severe toxicity, or fatality were identified in PubMed, OpenAlex, or the comprehensive NPS adverse events review (Mohr et al. 2022 [Ref 17], which covers 2017–2020). The NPS toxicology reviews (Tittarelli et al. 2015 [Ref 8]; Malaca et al. 2020 [Ref 9]) do not specifically reference 4-HO-MiPT adverse events.

**⚠ FLAG:** The absence of published adverse event reports should not be interpreted as confirmed safety. It reflects sparse literature coverage of an emerging compound rather than documented safety data.

### Psychological Risks
By class analogy with 4-hydroxytryptamines and tryptamine psychedelics:
- Acute psychological distress (anxiety, panic, dysphoric ideation) is possible, particularly at higher doses, in unfamiliar settings, or in individuals with psychiatric history
- Drug-induced psychosis is theoretically possible (documented for related compound 4-HO-MET in an adolescent — ResearchGate case report identified but not verified through structured APIs)
- Hallucinogen-persisting perception disorder (HPPD) risk exists by class inference; no 4-HO-MiPT-specific cases documented

### Physical Risks
Documented physical adverse effects from TiHKAL [Ref 3]:
- Muscle tremors
- Jaw clenching / bruxism
- Motor incoordination at higher doses
- Nausea (documented in the effects taxonomy; consistent with oral tryptamine class)

### Cardiac/Serotonergic Toxicity
Serotonin syndrome risk is real if combined with serotonergic agents. The tramadol–tryptamine interaction is mechanistically supported: tramadol inhibits SERT and has weak serotonergic agonist activity, creating additive/synergistic serotonin toxicity risk when combined with 5-HT₂A agonists or SERT-releasing agents (Baldo 2018 [Ref 12]).

**⚠ FLAG (safety-critical):** The brief lists tramadol as "dangerous" — this is supported by mechanistic literature (Baldo 2018 [Ref 12]) but no 4-HO-MiPT + tramadol case reports were found. The warning is class-level, not substance-specific. It should be retained.

### Seizure Risk
The brief lists "Seizure threshold reduction" as an effect. No published data on seizure risk for 4-HO-MiPT specifically. Class-level risk of lowered seizure threshold exists for serotonergic tryptamines at high doses. ⚠ FLAG: This effect taxonomy entry cannot be verified against published primary literature for 4-HO-MiPT.

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## Harm Reduction

No published harm reduction guidelines specifically for 4-HO-MiPT exist. The following reflects class-level evidence and published psychedelic harm reduction frameworks:

**Storage and stability:** The free base form rapidly oxidizes and discolors; storage under inert atmosphere (nitrogen or argon) with freezing is required (TiHKAL [Ref 3]). The fumarate salt is more stable (Chadeayne et al. 2020 [Ref 1]).

**Dose sensitivity:** Given Shulgin's 2.5× greater potency relative to psilocin [Ref 3], and the absence of standardized pharmaceutical formulations, accurate weighing with a precision scale is essential. Common recreational doses (15–25 mg) are considerably less than doses of other psychedelics by mass.

**Contraindications (class-level):**
- Tramadol: dangerous interaction; serotonin syndrome risk (Baldo 2018 [Ref 12])
- MAOIs: risk of potentiation/serotonin syndrome (class-level; no 4-HO-MiPT-specific data)
- SSRIs/SNRIs: potential serotonin syndrome risk; may also blunt psychedelic effects
- Cardiovascular disease, seizure disorders, personal/family history of psychosis: contraindicated by class
- Lithium: known risk of seizures and adverse cardiac events with classical psychedelics (class-level)

**Testing:** Marquis reagent produces color reactions with 4-hydroxytryptamines (psilocin: black/purple; expected for 4-HO-MiPT by class). No published colorimetric test data specific to 4-HO-MiPT was identified.

**⚠ FLAG:** Cannabis interaction is listed as "unknown" in the brief. Published literature does not address this combination for 4-HO-MiPT specifically, but synergistic intensification of psychedelic effects with cannabis is documented for other serotonergic psychedelics.

---

## Tolerance & Dependence

### Tolerance
**Mechanism:** Rapid 5-HT₂A receptor downregulation following psychedelic exposure (de la Fuente Revenga et al. 2022 [Ref 13]). The mechanism is β-arrestin-2-independent and involves agonist-induced internalization of the receptor. Tolerance to HTR in mice develops within 24 hours of a single exposure.

**Brief data (consistent with literature):**
- Buildup: almost immediately after ingestion ✓ (supported by de la Fuente Revenga et al. 2022 [Ref 13])
- Half-life (tolerance): 3 days ✓ (standard for 5-HT₂A receptor recovery; no 4-HO-MiPT-specific data)
- Full reset: 7 days ✓ (standard for psychedelic class; no 4-HO-MiPT-specific data)
- Cross-tolerance: with other psychedelics ✓ (demonstrated for DOI/LSD cross-tolerance; de la Fuente Revenga et al. 2022 [Ref 13])

**⚠ FLAG:** The 3-day half-life and 7-day full reset figures are community consensus values for the psychedelic class generally, not empirically derived for 4-HO-MiPT specifically. They should be flagged as class-inferred in the article.

### Dependence
The brief states "not habit-forming" — consistent with the class profile of serotonergic psychedelics, which are generally considered to have low abuse potential due to rapid tolerance development and absence of reinforcing dopaminergic reward mechanisms. No published dependence liability assessment exists for 4-HO-MiPT.

---

## Interactions

### Tramadol — DANGEROUS
Tramadol inhibits SERT (serotonin reuptake) and has weak serotonergic activity. Combined with 4-HO-MiPT (5-HT₂A agonist), serotonin syndrome risk is significant (Baldo 2018 [Ref 12]; Mason & Blackburn 1997 [Ref — PMID 9034418]). This is the most critical drug interaction. **Confirmed as a dangerous interaction at class level.**

### Cannabis — UNKNOWN
No published interaction data. Community reports suggest unpredictable synergistic potentiation. The brief lists this as "unknown" — accurate. No change recommended.

### Other Serotonergic Agents (class-level inferences, no 4-HO-MiPT-specific data):
- **MAOIs:** Contraindicated. MAO inhibition blocks the primary metabolic pathway for tryptamines, potentially causing severe serotonin toxicity.
- **SSRIs/SNRIs:** Serotonin syndrome risk; SSRIs may also pharmacodynamically antagonize psychedelic effects via 5-HT₂A receptor downregulation.
- **Lithium:** Risk of seizures and cardiac arrhythmias documented for psychedelics as a class.
- **Stimulants (amphetamines, cocaine):** Increased cardiovascular and psychological risk; no substance-specific data.

**⚠ FLAG:** All interactions except tramadol are class-level inferences. No 4-HO-MiPT-specific pharmacokinetic interaction data exists in the published literature.

---

## Legal Status

| Jurisdiction | Status | Notes |
|---|---|---|
| United States | Unscheduled | Federal Analogue Act (FAA) may apply if sold for human consumption; no known prosecutions as of 2015 (Erowid [Ref 22]) |
| United Kingdom | De facto illegal | Covered by Psychoactive Substances Act 2016 (blanket ban on supply/production of psychoactive substances not on exemption list) |
| Sweden | Scheduled | Classified as hälsofarliga varor (health-hazardous substance) since November 1, 2005 (Erowid [Ref 22]) |
| Germany | Controlled | Covered under Neue-psychoaktive-Stoffe-Gesetz (NpSG) since July 18, 2019 |
| Russia | Schedule I | Controlled as an analog of 4-hydroxytryptamine |
| Netherlands | Research only | Not for human consumption; unscheduled but regulated |
| Canada | Not specifically scheduled | As of 2025; analogue provisions may apply |
| Australia | Unconfirmed | Specific scheduling not confirmed; analogue drug provisions under Criminal Code may apply |
| EU broadly | Unharmonized | No EU-wide scheduling; national laws vary |

**⚠ FLAG:** Australia and Canada legal status is not confirmed against primary legal sources. The Australian TGA Poisons Standard specific entry for 4-HO-MiPT could not be located through database or web searches. Editorial review recommended.

---

## Clinical Trials

**No clinical trials** for 4-HO-MiPT have been registered on ClinicalTrials.gov (confirmed by search). No human clinical trial data exists beyond the uncontrolled human self-experiment data from Repke et al. (1985 [Ref 2]) and Shulgin's TiHKAL accounts (1997 [Ref 3]).

The US Patent US11780808B2 proposes therapeutic applications for miprocin in psychiatric and neurological disorders, but no investigational new drug (IND) application or clinical trial registration has been identified.

---

## Community Feedback Analysis

**No community feedback was submitted in Part A2 of the brief.** Standard research directives from Part B were followed. No community-derived corrections require investigation or flagging.

---

## Gaps & Flags

### ⚠ Safety-Critical Flags

1. **No LD₅₀ or toxic dose data** for 4-HO-MiPT in any species. The brief correctly notes "toxic dose is unknown." This field cannot be populated from the literature.

2. **Tramadol interaction:** Listed as "dangerous" in the brief. Mechanistically supported at class level (Baldo 2018 [Ref 12]) but no 4-HO-MiPT + tramadol case reports exist. Retain the warning; label as class-inferred.

3. **Seizure threshold reduction:** Listed in effects taxonomy. Cannot be verified against published 4-HO-MiPT literature. This is a class-level inference.

4. **SMILES and PubChem CID absent from seed data** — both now confirmed: CID 10082683; SMILES: CC(C)N(C)CCC1=CNC2=C1C(=CC=C2)O. These should be added to the DB.

### Data Gaps

5. **No published Ki/EC₅₀ binding affinity data** for 4-HO-MiPT at any receptor. All pharmacology is class-inferred from structural analogs.

6. **No published human pharmacokinetic studies.** Tmax, bioavailability, half-life, and metabolic CYP enzyme involvement are unknown. Metabolism is inferred from related compound 4-OH-EPT (Bergh et al. 2024 [Ref 16]).

7. **No published adverse event case reports** specifically for 4-HO-MiPT. Psychological risks are inferred from class.

8. **Unverified claims from Psychedelic Science Review:** "McKenna et al. 1990" and "Klein et al. 2020" binding/HTR studies for 4-HO-MiPT could not be located in PubMed or OpenAlex. Do not cite without primary source verification.

9. **Australia legal status** unconfirmed. Canada confirmed as unscheduled as of 2025 per web sources (unverifiable).

10. **Repke 1981 synthesis paper** (J Heterocyclic Chem 18(1):175–179): confirmed via web sources and Semantic Scholar. No DOI or PMID found. Cited as Ref 20 (unverifiable). Predates most databases.

11. **No colorimetric test data** (Marquis, Mecke, Ehrlich reagent reactions) published for 4-HO-MiPT specifically. Ehrlich reagent produces a characteristic purple/blue reaction with indoles generally; specific color characterization unavailable.

12. **MAO metabolism role:** Tryptamine class compounds are typically MAO-A substrates, but MAO involvement in 4-HO-MiPT metabolism is uncharacterized. This has implications for MAOI interaction warnings.

13. **Onset discrepancy (minor):** TiHKAL onset: 10–20 min; brief: 15–45 min. The brief's range is broader but consistent with TiHKAL; no correction required. Range may reflect variability across individuals and doses.

14. **Potency claim (2.5× psilocin):** Derived from a single uncontrolled Shulgin self-experiment. The Psychedelic Science Review cites a contradicting "Klein et al. 2020" finding of reduced potency in rodent HTR assays — but this paper could not be verified. Human subjective potency and rodent HTR potency measure different endpoints and are not directly comparable. The 2.5× figure should be attributed clearly to Shulgin [Ref 3] and framed as a single-source human report.