5-MeO-MiPT

# Research Output: 5-MeO-MiPT

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## Chemical Identity

**Verified via PubChem (CID 2763156) and cross-referenced with ChemicalBook/Cayman Chemical:**

| Field | Value | Source |
|---|---|---|
| CAS Number | 96096-55-8 | [Ref 23] |
| PubChem CID | 2763156 | [Ref 23] (api_verified) |
| Molecular Formula | C15H22N2O | [Ref 23] (api_verified) |
| Molecular Weight | 246.35 g/mol | [Ref 23] (api_verified) |
| IUPAC Name | N-[2-(5-methoxy-1H-indol-3-yl)ethyl]-N-methylpropan-2-amine | [Ref 23] (api_verified) |
| InChIKey | HEDOODBJFVUQMS-UHFFFAOYSA-N | [Ref 23] (api_verified) |
| SMILES | COc1ccc2[nH]cc(CCN(C)C(C)C)c2c1 | [Ref 23] |
| Chemical Class | Indole / Substituted tryptamine | — |

**Physical properties** (web-retrieved, not from peer-reviewed literature): Freebase melting point ~72–74°C; hydrochloride salt melting point 162–163°C. Freebase soluble in DMSO, ethanol, and DMF (~30 mg/mL); insoluble in water. HCl salt soluble in water [Ref 23].

**Discrepancies with seed data:** The brief's seed data left SMILES, molecular formula, molecular weight, InChIKey, and PubChem CID blank. All have now been confirmed via PubChem API lookup [Ref 23].

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## Pharmacology

### Receptor Binding and Functional Activity

5-MeO-MiPT is primarily a full agonist at the serotonin 5-HT₂A receptor. Blough et al. (2014 [Ref 16]) measured a 5-HT₂A EC₅₀ of approximately 7.82 ± 1.5 nM with Emax of 101 ± 3% in a functional assay — confirming full agonist activity. Arrestin recruitment at 5-HT₂A was very weak (EC₅₀ >10,000 nM), suggesting G-protein-biased signaling.

At the serotonin transporter (SERT), Blough et al. (2014 [Ref 16]) found SERT IC₅₀ >10,000 nM, effectively inactive as a reuptake inhibitor. This is corroborated by Nagai et al. (2007 [Ref 10]) who found 5-MeO-MiPT inhibited monoamine reuptake only weakly and had minimal effect on monoamine release in rat synaptosomes. Rickli et al. (2016 [Ref 2]) similarly found that, unlike 5-MeO-AMT and certain other tryptamines, 5-MeO-MiPT did not significantly interact with SERT or the norepinephrine transporter (NET).

**FLAG: 5-HT₁A status.** The seed data classifies 5-MeO-MiPT as a 5-HT₁A receptor agonist. Blough et al. (2014 [Ref 16]) found the compound inactive at 5-HT₁A at 10 µM. However, Warren et al. (2024 [Ref 14]) demonstrated that 5-methoxytryptamines as a class engage 5-HT₁A (studied via cryo-EM with 5-MeO-DMT), and the structure-activity relationship data suggest 5-methoxy substitution promotes 5-HT₁A engagement. The 5-HT₁A agonist designation in the seed data may be inferred from structural class rather than direct 5-MeO-MiPT-specific binding data. This requires editorial review.

At the G-protein level, Nonaka et al. (2007 [Ref 9]) showed 5-MeO-MiPT stimulates [³⁵S]GTPγS binding in rat brain membranes. Potency rank among 5-methoxytryptamines: 5-MeO-DMT > 5-MeO-DALT > 5-MeO-AMT ≥ 5-MeO-MIPT > 5-MeO-DIPT > DPT ≥ AMT [Ref 9].

Ray (2010 [Ref 11]) profiled 25 psychedelics at 51 receptors using NIMH-PDSP data, demonstrating psychedelic drugs interact with a broader array of monoamine targets than previously believed. The psychedelic tryptamine class (contextualizing 5-MeO-MiPT's broader receptor profile) engages 5-HT₂A, 5-HT₂B, 5-HT₁A, 5-HT₆, 5-HT₇, and in some cases sigma receptors [Ref 11].

### Discriminative Stimulus Effects

Gatch et al. (2021 [Ref 7]) trained rats to discriminate DOM (2,5-dimethoxy-4-methylamphetamine) from saline and found 5-MeO-MiPT fully substituted for DOM with potency ≤ DOM. This confirms DOM-like hallucinogen discriminative stimulus effects and implies similar abuse liability to classical psychedelics [Ref 7].

### Pharmacokinetics

No published human PK studies (Tmax, bioavailability, elimination half-life) are available for 5-MeO-MiPT in controlled settings.

**Metabolic pathway (human, in vitro/in vivo):** Grafinger et al. (2018 [Ref 3]) characterized 5-MeO-MiPT metabolism in pooled human liver microsomes (pHLM) and forensic samples. Seven phase I metabolites were identified in vitro; 4 in blood and 7 in urine in the forensic case. The five most abundant metabolites were produced via N-demethylation and O-demethylation/hydroxylation. Recommended urinary biomarkers: 5-MeO-NiPT (N-demethylation), 5-OH-MiPT (O-demethylation), 5-MeO-MiPT-N-oxide (N-oxidation), and OH-5-MeO-MiPT (hydroxylation) [Ref 3].

**CYP enzymes:** No direct CYP phenotyping has been published specifically for 5-MeO-MiPT. By structural analogy with closely related 5-methoxy tryptamines (e.g., 5-MeO-2-Me-DIPT; Caspar et al. 2017), CYP1A2, CYP2C19, CYP2D6, and CYP3A4 are implicated in hydroxylation, O-demethylation, and N-dealkylation reactions. **FLAG: This is class-level inference, not substance-specific data.**

**Blood/urine concentrations (forensic case):** Blood 160 ng/mL; urine 3,380 ng/mL in the Grafinger 2018 case [Ref 3]. Polydrug context (cocaine, cocaethylene, methylphenidate also detected); clinical interpretation requires caution.

**Oral vs. smoked potency:** Shulgin's TiHKAL entry (1997 [Ref 19]) noted that 5-MeO-MiPT is "several times more potent when taken orally than when smoked" — the inverse of 5-MeO-DMT. This suggests significant first-pass conversion to an active metabolite or superior oral bioavailability, but the mechanism has not been formally investigated. The oral dose range reported by Shulgin was 4–6 mg; smoked range 12–20 mg [Ref 19].

### Serotonin Reuptake Inhibition Discrepancy

The seed data classifies 5-MeO-MiPT as a "serotonin reuptake inhibitor." This is disputed by Blough et al. (2014 [Ref 16]) (SERT IC₅₀ >10,000 nM) and Nagai et al. (2007 [Ref 10]) (weak reuptake inhibition in rat synaptosomes) and Rickli et al. (2016 [Ref 2]) (no significant SERT interaction). Cayman Chemical product description notes SERT/NET inhibition, likely a vendor-level pharmacological inference that is not consistently supported by primary literature. **FLAG for editorial review: "Serotonin reuptake inhibitor" pharmacological classification may be incorrect based on primary data.**

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## History

5-MeO-MiPT was first synthesized and pharmacologically characterized by David Repke, David Grotjahn, and Alexander Shulgin (Repke et al., 1985 [Ref 15]), published in the *Journal of Medicinal Chemistry* (Volume 28(7), pp. 892–896, DOI: 10.1021/jm00145a007). This paper evaluated eight N-methyl-N-isopropyltryptamines with varying aromatic oxygen substituents for hallucinogenic activity in humans. 5-MeO-MiPT (their compound 4, the 5-methoxy derivative) was noted to show "a substantial increase in potency as well as oral activity when compared to the symmetrical dimethyl homologues." 4-HO-MiPT was described as producing the most classic hallucinogenic profile [Ref 15].

Shulgin subsequently described 5-MeO-MiPT in greater detail in his 1997 book *TiHKAL* (Tryptamines I Have Known and Loved), entry #40 [Ref 19]. TiHKAL includes the compound's synthesis, self-experiment reports (multiple authors), dosage guidance, and qualitative effects. The book entry notes 6-MeO-MIPT and 7-MeO-MIPT showed no significant psychoactivity, making the 5-position critical for activity [Ref 19].

Recreational use emerged in the 2000s via online research chemical markets. The compound acquired the street name "Moxy." It was first identified in forensic/law-enforcement contexts in Italy in 2014 (Bassi et al., 2024 [Ref 1]) and was seized in Germany and Switzerland by at least 2016 (Grafinger et al., 2018 [Ref 3]). It has appeared in NPS monitoring databases in Japan (Nonaka 2007 [Ref 9]) and has been detected in Chinese drug markets [Ref 20].

A DEA proposed rulemaking in January 2022 sought to place 5-MeO-MiPT in Schedule I of the US Controlled Substances Act. This proposal was withdrawn in July 2022, with the DEA requesting a new scientific and medical evaluation from the Department of Health and Human Services [Ref 21].

No institutional or clinical research program has been associated with this compound historically; its entire documented pharmacological profile derives from self-experiments (Repke/Shulgin 1985, TiHKAL 1997), forensic case reports, and preclinical animal studies.

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## Subjective Effects

No controlled human studies exist. Published subjective effects derive from Shulgin's self-experiment data (TiHKAL, 1997 [Ref 19]) and limited clinical case descriptions.

**Shulgin's TiHKAL reports (oral, 4–6 mg):**
- Onset: rapid, ~10–15 minutes
- Physical stimulation and tingling sensations
- Enhanced conceptual/philosophical thinking
- Altered depth perception with minor wave patterns in peripheral visual field
- At these doses: no frank visual hallucinations reported
- Notably erotic/aphrodisiac effects mentioned across multiple reports
- Duration: 4–6 hours orally

**Smoked route (12–20 mg per TiHKAL):** Less potent weight-for-weight, shorter duration.

The effects taxonomy in the seed data (visual drifting, object transformations, internal hallucinations, music enhancement, time distortion, emotional and empathy enhancement, thought connectivity, pattern recognition, personal insight, depersonalization) is consistent with the broader class profile of 5-HT₂A agonist psychedelics but is **not directly supported by published controlled studies** for 5-MeO-MiPT specifically. These reflect user-report-based observations from platforms such as PsychonautWiki and Erowid, rather than peer-reviewed data.

**Reported adverse subjective effects (user reports/case data):**
- At higher doses: pronounced body load, vasoconstriction, nausea, tachycardia
- Stimulation can be overwhelming; anxiety and paranoia reported at higher doses
- The 2007 Japanese case (Shimizu [Ref 8]) and 2016 forensic case (Grafinger [Ref 3]) both describe agitated, disinhibited behavior

**Duration comparison:** Seed data states total duration 5–8 hours both oral and smoked. TiHKAL reports 4–6 hours orally. These are broadly consistent; the seed data's upper range may reflect higher doses. No contradictions flagged, though the seed data is not sourced from controlled studies.

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## Safety & Toxicity

### LD50 and Acute Toxicity (Animal)
Altunci et al. (2021 [Ref 4]) performed the first published in vivo acute toxicity and histotoxicological study of 5-MeO-MiPT. The full LD50 data and specific dose values were not accessible from the available abstract. The paper is the foundational reference for animal acute toxicity — **FLAG: LD50 value(s) not verified from abstract; generation agent should note this is unverified.**

The zebrafish model data (Zhao et al., 2024a [Ref 5]; Zhao et al., 2024b [Ref 6]) demonstrates behavioral inhibition, anxiety-like behavior, disruption of the liver-brain pathway, metabolic alterations (amino acid, lipid, energy metabolism), and histopathological tissue damage following chronic 5-MeO-MiPT injection over 30 days. Signaling: acts via Gαq/11-PLCβ pathway, inhibiting DAG-Ca²⁺/PKC/ERK while enhancing Ca²⁺/CREB [Ref 5].

### Preclinical Mouse Study with Human Case Context
Bassi et al. (2024 [Ref 1, 24]) derived their mouse study from an Italian human poisoning case. Mouse effects included: initial tachycardia followed by bradycardia and rebound tachycardia; biphasic blood pressure changes (initial fall, then systolic and diastolic elevation); motor impairment at pharmacologically relevant doses [Ref 24].

### Human Case Reports

**Case 1 (Italy, 2014; Bassi 2024 [Ref 24]):** 23-year-old male presenting with tachycardia (107 bpm), hypertension (150/90 mmHg), catatonia, drowsiness, and muteness. Symptoms resolved within 24 hours under supportive care.

**Case 2 (Germany/Switzerland, 2016; Grafinger 2018 [Ref 3]):** Police-encountered naked man exhibiting agitation and aggressive behavior. Blood 5-MeO-MiPT concentration 160 ng/mL; urine 3,380 ng/mL. Polydrug context (cocaine, cocaethylene, methylphenidate also detected). Seven urinary metabolites identified in this case.

**Case 3 (Japan, 2007; Shimizu 2007 [Ref 8]):** 27-year-old male with substance intoxication after ingesting what he thought was pure methylone; analysis revealed ~60% methylone (120 mg) and ~38% 5-MeO-MIPT (76 mg). Resulted in substance-related mental disorder presentation.

### Organ Toxicity
Zebrafish chronic exposure studies demonstrated liver-brain pathway disruption, with evidence of brain damage and hepatic involvement (Zhao 2024a [Ref 5]; 2024b [Ref 6]). The Gαq/11-PLCβ pathway activation implicates secondary messenger disruption in multiple tissues. No specific human organ toxicity data available.

### Psychological Risks
As a 5-HT₂A agonist, risks consistent with the psychedelic class include anxiety, panic reactions, and the potential for hallucinogen-persisting perception disorder (HPPD), though no published case reports of HPPD specifically attributed to 5-MeO-MiPT were found. The strong stimulation component and cardiovascular effects at higher doses add unique risk factors compared to classical 5-HT₂A agonists.

### Toxicity Assessment Note
The seed data classifies acute and chronic toxicity as "low" with the note "Inferred from pharmacological class — not sourced from literature." This classification is **partially supported** by case data showing resolution of acute intoxication within 24 hours under supportive care [Ref 24], but the zebrafish chronic exposure data [Refs 5, 6] and mouse cardiovascular data [Ref 1] suggest meaningful toxicity potential that warrants caution. The "low toxicity" label should be flagged for editorial review given the limited human data.

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## Harm Reduction

No published harm reduction protocols are specific to 5-MeO-MiPT. The following is derived from published clinical and pharmacological evidence:

**Cardiovascular risk:** Based on the Italian human case [Ref 24] and mouse data [Ref 1], the compound produces tachycardia and hypertension. Individuals with pre-existing cardiovascular conditions (hypertension, arrhythmias, structural heart disease) face elevated risk.

**Drug-drug interactions:** As a serotonergic compound (5-HT₂A agonist with weak serotonin effects), combination with MAOIs presents a theoretical serotonin syndrome risk — a class-level concern for all serotonergic psychedelics (Hassan et al., 2017 [Ref 25]). Tramadol (listed as "dangerous" in seed data) is itself a serotonin reuptake inhibitor and weak opioid agonist; combination with serotonergic psychedelics elevates serotonin syndrome risk.

**Reagent testing:** The compound's electrochemical signature has been characterized using glassy carbon and graphite screen-printed electrodes (LOD 0.015 µmol/L; applicable to forensic seized samples, web-retrieved, [Ref 23 context]). Ehrlich reagent (reacts with indole ring) should be positive. Simon's reagent reaction profile requires verification in specific literature.

**Polydrug avoidance:** Forensic cases consistently show 5-MeO-MiPT ingestion alongside other stimulants (cocaine [Ref 3]) or entactogens (methylone [Ref 8]). Polydrug combinations complicate clinical management.

**Dose control:** The substantial difference in oral vs. smoked potency (oral ~4–6 mg active; smoked ~12–20 mg per TiHKAL [Ref 19]) makes dosing error possible. Users switching routes without adjusting dose face overdose risk.

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## Tolerance & Dependence

**Tolerance:** The seed data states tolerance "builds almost immediately after ingestion" with a half-life of 3 days and full reset at 7 days. This profile is consistent with the mechanistic literature on 5-HT₂A receptor agonist tolerance: de la Fuente Revenga et al. (2022 [Ref 17]) demonstrated rapid 5-HT₂A receptor downregulation in mouse frontal cortex following DOI administration, with progressive tolerance developing over 4 days and single-dose tolerance observable at 24 hours. Cross-tolerance between classical psychedelics (DOI and LSD) was confirmed, mediated through 5-HT₂A activation [Ref 17].

**Cross-tolerance:** Expected with all classical 5-HT₂A agonist psychedelics (LSD, psilocybin, mescaline, DMT, other tryptamines). The seed data "psychedelic cross-tolerance" designation is consistent with the mechanistic literature [Ref 17].

**Dependence:** The seed data labels 5-MeO-MiPT as "not habit-forming." No published studies on addiction liability specific to 5-MeO-MiPT exist. The zebrafish chronic exposure study (Zhao 2024a [Ref 5]) noted the findings offer "novel insights into the toxicological effects and addiction mechanisms" but did not characterize dependence directly. As a full 5-HT₂A agonist with rapid tolerance, the pattern is consistent with low dependence liability — the rapid tolerance serves as an inherent brake on compulsive use. **FLAG: No controlled human or animal dependence studies exist; the "not habit-forming" label is class-level inference.**

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## Interactions

**Listed in seed data:**

| Drug | Severity (Seed) | Evidence |
|---|---|---|
| Cannabis | Unknown | No published interaction data found |
| PCP | Lethal | **FLAG: No published evidence found to support "lethal" classification. No case reports or preclinical studies of this combination were identified. This interaction severity is unverified and safety-critical.** |
| Cocaine | Dangerous | Partial support: Grafinger 2018 [Ref 3] documents a case involving simultaneous cocaine/5-MeO-MiPT use with severe agitated behavior. However, the study cannot establish causation due to polydrug context. |
| MDMA | Unknown | No published data. Theoretical: both are serotonergic; class-level serotonin syndrome concern. Rickli et al. (2016 [Ref 2]) notes MDMA-like transporter profiles exist for some tryptamines but 5-MeO-MiPT does not significantly interact with SERT. |
| Mescaline | Unknown | No published data. Theoretical pharmacodynamic interaction via 5-HT₂A agonism. |
| Tramadol | Dangerous | No published data specific to this combination. Tramadol's serotonin reuptake inhibition combined with 5-HT₂A agonism raises class-level serotonin syndrome risk (Hassan 2017 [Ref 25]). |

**Class-level serotonin interaction risks:** All MAOIs, other serotonergic compounds, and lithium carry theoretical interaction risks via serotonin syndrome pathways for 5-HT₂A agonist psychedelics.

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## Legal Status

**United States:** Not explicitly scheduled in the federal Controlled Substances Act. The DEA classified 5-MeO-MiPT as an analogue of 5-MeO-DIPT in a March 2005 *Microgram* bulletin, making it potentially prosecutable under the Federal Analogue Act if intended for human consumption. A formal Notice of Proposed Rulemaking to place 5-MeO-MiPT in Schedule I was published January 14, 2022; this was subsequently withdrawn July 27, 2022 [Ref 21], with the DEA requesting a new HHS scientific/medical evaluation. As of April 2026, federal scheduling remains pending.

**US State Level:**
- Florida: Schedule I substance [Ref 20]
- Louisiana: Schedule I (as of June 2013) [Ref 20]
- Minnesota: Banned [Ref 20]

**United Kingdom:** Not listed by name under the Misuse of Drugs Act 1971. However, the UK Psychoactive Substances Act 2016 makes it an offence to produce, supply, or offer to supply any psychoactive substance used for psychoactive effects. It may also fall under the MDA 1971 generic tryptamine definition (ACMD 2014 report) [Ref 20].

**Germany:** Likely controlled under the Neue-Psychoaktive-Stoffe-Gesetz (NpSG, 2016), which generically controls novel psychoactive substances [web-retrieved, not api_verified].

**Austria:** Controlled under Austria's NpSG [web-retrieved].

**China:** Controlled as a Category I psychotropic substance [Ref 20].

**Finland:** Banned December 2014 under new psychoactive substance regulations [Ref 20].

**Japan:** Controlled as a "Designated Substance" under pharmaceutical law; first identified in Japanese NPS context (Nonaka 2007 [Ref 9]) [Ref 20].

**Canada, Australia:** No specific legislation found for 5-MeO-MiPT in available sources. May be covered under analogues provisions or general NPS frameworks, but this is unverified. **FLAG for generation agent: Legal status in Canada and Australia not confirmed from available sources.**

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## Clinical Trials

No registered clinical trials for 5-MeO-MiPT were found on ClinicalTrials.gov (search conducted April 2026). One web source mentioned Mindstate Design Labs had sought permission to test 5-MeO-MiPT as a potential treatment for depression, anxiety, and PTSD as of 2024, but no registered trial was found to verify this claim. **FLAG: This claim requires verification.**

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## Community Feedback Analysis

No community feedback was submitted in Part A2 of the brief.

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## Gaps & Flags

### Safety-Critical Values Not Verified Against Published Sources

1. **PCP interaction classified as "lethal"** — No published case report, animal study, or mechanism exists in the reviewed literature to support this specific classification. This is safety-critical. The generation agent must not present this as verified without a source.

2. **LD50 value not available** — Altunci et al. (2021 [Ref 4]) is the published acute toxicity study, but the abstract does not report specific LD50 values and full text was not accessible. The generation agent should not cite a specific LD50.

3. **"Low" acute/chronic toxicity** — The seed data notes this is inferred from pharmacological class. The zebrafish chronic exposure studies (Zhao 2024a,b [Refs 5, 6]) and mouse cardiovascular study (Bassi 2024 [Refs 1, 24]) suggest meaningful toxicity; this classification should be presented with caveats.

4. **Tramadol "dangerous"** — Classified in seed data but no specific interaction study found. Class-level mechanism (serotonin syndrome via SERT inhibition + 5-HT₂A agonism) provides biological plausibility [Ref 25].

### Contradictions Between Seed Data and Published Sources

5. **5-HT₁A agonist classification** — Blough et al. (2014 [Ref 16]) found 5-MeO-MiPT inactive at 5-HT₁A up to 10 µM. The Warren et al. (2024 [Ref 14]) Nature paper on 5-methoxytryptamines characterizes 5-HT₁A engagement at the class level but uses 5-MeO-DMT as the primary ligand. The 5-HT₁A agonist label in the seed data is plausible but not directly verified for 5-MeO-MiPT.

6. **Serotonin reuptake inhibitor classification** — Blough 2014 [Ref 16] (SERT IC₅₀ >10,000 nM), Nagai 2007 [Ref 10], and Rickli 2016 [Ref 2] all suggest minimal SERT interaction. This classification appears inaccurate for 5-MeO-MiPT based on available primary data. **This is a structural data discrepancy that should be addressed in the pharmacological class field.**

7. **TiHKAL onset 10–15 min vs. seed data 20–40 min (oral)** — Shulgin's entry reports onset within 10–15 minutes [Ref 19]; seed data states 20–40 minutes. These may reflect different dosing levels or individual variability. The discrepancy is worth flagging for editorial review. The seed data values (20–40 min) are more consistent with typical oral tryptamine pharmacokinetics.

### Areas Relying on Structural Analogy or Class Inference

8. **CYP enzyme involvement** — CYP1A2, CYP2C19, CYP2D6, CYP3A4 inferred from structural analogues (Caspar et al. 2017 for 5-methoxy-2-methyl-DIPT). No CYP phenotyping published specifically for 5-MeO-MiPT.

9. **Dependence/habit-forming characterization** — Based on class-level inference; no controlled dependence studies for 5-MeO-MiPT.

10. **MDMA and cannabis interaction severities** — Classified as "unknown" but serotonergic interaction mechanisms exist for both; these deserve more detailed interaction notes in the article.

### Data Absent from Literature

11. **No controlled human pharmacokinetic studies** — No published Tmax, half-life, volume of distribution, or bioavailability data for 5-MeO-MiPT.
12. **No human dose-response studies** — All human data derives from self-experiments (Shulgin, TiHKAL) and forensic/clinical case reports.
13. **No long-term safety data in humans** — Chronic effects not studied in humans.
14. **No published HPPD cases** specifically attributed to 5-MeO-MiPT.
15. **Legal status in Canada and Australia** — Not confirmed from available sources.
16. **Stereochemistry** — 5-MeO-MiPT has no chiral center in the tryptamine ethylamine chain; the isopropyl group on nitrogen does not create chirality. No stereoisomer issues identified; confirmed by SMILES structure [Ref 23].