MiPT

# Research Output: MiPT

## Chemical Identity

**Confirmed via PubChem CID 29935323 [Ref 9 (PubChem)]:**

| Property | Value | Source |
|---|---|---|
| Preferred IUPAC name | N-[2-(1H-indol-3-yl)ethyl]-N-methylpropan-2-amine | PubChem CID 29935323 |
| Systematic name | N-methyl-N-isopropyltryptamine | Repke et al. 1985 [Ref 10] |
| CAS number | 96096-52-5 | WikiDoc [Ref 9] / Cayman Chemical |
| PubChem CID | 29935323 | PubChem |
| Molecular formula | C₁₄H₂₀N₂ | PubChem |
| Molecular weight | 216.32 g/mol | PubChem |
| InChIKey | KTQJVAJLJZIKKD-UHFFFAOYSA-N | PubChem |
| SMILES | CC(C)N(C)CCC1=CNC2=CC=CC=C12 | WikiDoc [Ref 9] |
| Melting point (free base) | 82–83 °C | TiHKAL [Ref 8] |

**Discrepancies with seed data:** The brief does not list SMILES, molecular formula, molecular weight, InChIKey, or PubChem CID. All five fields are now confirmed via PubChem API. CAS number (96096-52-5) and SMILES are additionally confirmed by WikiDoc [Ref 9]. The IUPAC name in the seed data ("N-methyl-N-isopropyltryptamine") is a common name, not a formal IUPAC name; the formal IUPAC name is confirmed above.

**Physical properties:** MiPT freebase is a colorless oil that spontaneously crystallizes. Notably, it is described as unusually stable to air oxidation over extended periods compared to many other tryptamine freebases, which typically decompose rapidly in the presence of light and oxygen [Ref 8; Ref 9].

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## Pharmacology

### Primary Receptor Activity

**5-HT₂A receptor — primary psychedelic target:**
Blough et al. (2014 [Ref 5]) measured MiPT at the 5-HT₂A receptor using a calcium mobilization assay in cells expressing the human 5-HT₂A receptor:
- **EC₅₀ = 44.9 ± 1.7 nM**
- **Emax = 74 ± 5%** (partial agonist; full agonist = 5-HT reference)

This classifies MiPT as a moderately potent partial agonist at 5-HT₂A, consistent with its psychedelic activity at oral doses of 10–25 mg. For comparison, the closely related 5-methoxy analog (5-MeO-MiPT) has an EC₅₀ of approximately 7.82 nM — approximately 6-fold more potent, consistent with the methoxy group's known potency-enhancing effect in this series [Ref 5].

**5-HT₂A β-arrestin recruitment:** Inactive. MiPT does not recruit β-arrestin at the 5-HT₂A receptor [Ref 5]. This is consistent with a G protein-biased or functionally selective pharmacological profile, though this has not been characterized further for MiPT specifically.

**⚠ FLAG — 5-HT₁A agonist classification in seed data is not confirmed:**
The seed data categorizes MiPT as a "Serotonin 1A receptor agonist." Blough et al. (2014 [Ref 5]) measured MiPT at 5-HT₁A receptors and found it **inactive at concentrations up to 10 µM**. Kozell et al. (2023 [Ref 16]) tested 21 substituted tryptamines and found that non-ring-substituted tryptamines (the class MiPT belongs to) generally exhibit variable and often low affinity at 5-HT₁A, unlike 5-substituted compounds which consistently show high 5-HT₁A affinity. No published source confirms 5-HT₁A agonism for MiPT. The generation agent should update pharmacological class to reflect only confirmed 5-HT₂A activity.

### Monoamine Transporters

Blough et al. (2014 [Ref 5]) found MiPT to be **inactive as a reuptake inhibitor** at SERT, DAT, and NET (Ki >10,000 nM for all three). However, Cozzi et al. (2009 [Ref 1]) demonstrated that MiPT exhibits **substrate behavior** (not blocker behavior) at the serotonin transporter:
- SERT uptake inhibition KI = **8.88 ± 4.7 µM** (substrate)
- VMAT2 inhibition KI = **20 ± 4.3 µM** (substrate)

High binding-to-uptake ratios at both transporters support the classification of MiPT as a transporter **substrate** rather than an uptake blocker, analogous to amphetamine at the dopamine transporter. This mechanism may allow MiPT to accumulate within neurons and activate intracellular sigma-1 receptors [Ref 1], though no direct sigma-1 binding data for MiPT has been published.

Kozell et al. (2023 [Ref 16]) additionally noted that among 21 tryptamines studied, **non-ring-substituted tryptamines (the class containing MiPT) most consistently exhibited SERT binding**, consistent with the Cozzi 2009 substrate findings.

### Structural Basis of Oral Activity

Shulgin's hypothesis (TiHKAL [Ref 8]), consistent with the Repke et al. (1985 [Ref 10]) findings, is that MiPT's oral activity arises from the unsymmetrical N-methyl/N-isopropyl substitution pattern: the larger isopropyl group provides steric protection against monoamine oxidase (MAO) metabolic inactivation, allowing the compound to survive first-pass metabolism and reach the CNS, where the smaller methyl group then fulfills a functional role analogous to N,N-dimethyl compounds. This is in contrast to DMT, which is rapidly degraded by intestinal and hepatic MAO-A and requires co-administration with an MAOI for oral activity.

Repke et al. (1985 [Ref 10]) confirmed that MiPT (the "Ar H" unsubstituted compound in their series) showed **substantial increase in potency as well as oral activity** compared to the symmetrical N,N-dimethyl homologue (DMT), supporting this MAO-protection hypothesis.

### Metabolic Pathways and CYP Enzymes

No published pharmacokinetic or metabolic studies specific to MiPT have been identified. Metabolic pathway data must be inferred from close structural analogs.

For **5-MeO-MiPT** (the 5-methoxy analog), Grafinger et al. (2017 [Ref 7]) identified the following in vitro and in vivo metabolic pathways via LC-HRMS/MS:
- Primary routes: **N-demethylation** (removing the methyl group) and **hydroxylation**
- Additional routes: N-oxide formation, combined demethylation + hydroxylation
- In a forensic case: blood concentration 160 ng/mL, urine 3,380 ng/mL
- Recommended biomarkers: 5-methoxy-N-isopropyltryptamine (N-demethylation product), 5-OH-MiPT (hydroxylation product)

For **5-MeO-2-Me-DIPT** and analogs (a structurally related substituted tryptamine), Caspar et al. (2017 [Ref 18]) identified CYP enzyme involvement:
- **CYP1A2, CYP2C19, CYP2D6, CYP3A4** — hydroxylation
- **CYP2C19, CYP2D6** — O-demethylation
- **CYP2C19, CYP2D6, CYP3A4** — N-dealkylation
- Phase II: glucuronidation and sulfation of phase I metabolites

By structural analogy, CYP2D6 and CYP3A4 involvement should be assumed for MiPT until substance-specific data are available. This is relevant for interactions with CYP inhibitors/inducers.

**FLAG:** No published human PK data (Tmax, bioavailability, half-life, protein binding) for MiPT. All metabolic data is by structural analog inference. Flag for editorial review.

### Receptor Panel Context

Ray (2010 [Ref 2]) profiled 25 psychedelic drugs at 51 receptors, transporters, and ion channels (NIMH-PDSP). The study does not appear to specifically include MiPT (the compound list focuses on phenylalkylamines and more common tryptamines), but provides essential context on the multi-receptor nature of psychedelic drug action — psychedelic drugs interact with up to 42 of 49 assayed sites.

---

## History

### Discovery and First Synthesis

The earliest PubMed-indexed published source for MiPT is:

**Repke DB, Grotjahn DB, Shulgin AT. "Psychotomimetic N-methyl-N-isopropyltryptamines. Effects of variation of aromatic oxygen substituents." J Med Chem. 1985;28(7):892-896. PMID: 4009612 [Ref 10].**

Shulgin was a co-author on this foundational paper, which synthesized and evaluated **eight MiPT analogues** (with varying aromatic oxygen substituents) for hallucinogenic activity in man. Key findings:
- The unsubstituted MiPT ("Ar H," compound 1) and 5-MeO-MiPT ("Ar 5-OCH₃," compound 4) showed **substantial increase in potency and oral activity** compared to their N,N-dimethyl homologues (DMT and 5-MeO-DMT respectively)
- 4-HO-MiPT (compound 2) was described as "the most interesting in overall effect, producing a classic hallucinogenic profile"
- 5-MeO-MiPT (compound 4) produced "a state characterized by heightened conceptual stimulation lacking in visual phenomena"

**Note on "1981" claim:** Multiple secondary web sources claim MiPT was "first synthesized by Repke et al. in 1981." No PubMed-indexed paper from 1981 by Repke et al. on MiPT was found. The earliest verifiable published record is the 1985 JMC paper (PMID 4009612). The 1981 date may refer to unpublished laboratory notes, conference presentations, or may be a secondary source error. **FLAG for editorial review.**

### TiHKAL Synthesis and Characterization

Shulgin AT and Shulgin A. *TiHKAL: Tryptamines I Have Known and Loved* (1997) [Ref 8], entry #47, provides:
- Two synthetic routes from tryptamine
- Dosage: 10–25 mg oral; 20 mg by insufflation also reported
- Duration: **3–4 hours** (oral)
- Physical: colorless oil, spontaneously crystallizes, MP 82–83°C, unusually stable to air oxidation
- Self-experiment reports at various doses

### Appearance as NPS

MiPT was encountered as a **novel designer drug in Europe by approximately 2005**, according to multiple concordant secondary sources. Unlike its analogs 5-MeO-MiPT (first identified in Italy 2014; [Ref 17]) and 5-MeO-DiPT, MiPT has remained relatively rare in the recreational and forensic literature.

Erowid documents MiPT as "very uncommon and has nearly no history of human use" in its vault description, consistent with the sparse published literature.

---

## Subjective Effects

Published subjective effects data derives primarily from: (1) Repke et al. (1985 [Ref 10]) — human self-experiments by Repke, Grotjahn, and Shulgin; and (2) TiHKAL entry #47 (Shulgin [Ref 8]).

### Dose-Dependent Effects (from Repke/Shulgin self-experiments)

**Low dose (5–10 mg oral):**
- "A very good feeling," mild excitement
- Mild stimulant and psychedelic qualities
- No significant perceptual changes reported

**Common dose (10–25 mg oral):**
- "Considerable excitement, central stimulation"
- Brightened colors
- Auditory effects (music enhancement consistent with reported effects)
- "Almost no visuals" compared to related tryptamines — MiPT is notably characterized by **psychedelic/entheogenic effects over sensory/hallucinogenic activity**

**Insufflated (20 mg):**
- Rapid onset reported
- "Orange overlay" visual tinting
- Primarily psychedelic over hallucinogenic effects

### Effect Character

MiPT is distinguished from related tryptamines by its emphasis on cognitive/mental effects over visual perceptual distortion. This aligns with the pharmacological profile: partial 5-HT₂A agonism (Emax 74%) with no β-arrestin recruitment, absent 5-HT₁A activity, and minimal monoamine transporter activity. The 5-MeO congener further develops this cognitive emphasis — Repke et al. (1985 [Ref 10]) found 5-MeO-MiPT produced "heightened conceptual stimulation lacking in visual phenomena" — consistent with the seed data effects taxonomy.

### Duration

**⚠ Duration discrepancy across sources:**
- TiHKAL (Shulgin [Ref 8]): **3–4 hours**
- WikiDoc [Ref 9]: **4–6 hours**
- Seed data (DB): **3–8 hours** (total oral)

The seed data range (3–8 hours) encompasses both published values but extends to 8 hours, which is not documented in either primary source. The TiHKAL value (3–4 hours) from Shulgin's own experiments is the most directly sourced. The wider range in the seed data may reflect inter-individual variation or heavier doses. **FLAG for editorial review: seed data duration upper bound (8 hours) not confirmed by primary sources.**

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## Safety & Toxicity

### Toxic Dose / LD50

**No published LD50 data for MiPT in any species.** The seed data correctly notes "toxic dose is unknown." This is consistent with the extremely sparse clinical/toxicological literature on this compound.

### Case Reports of Adverse Events

**No published case reports of adverse events or intoxication specifically for MiPT have been identified.** This is consistent with its rarity of use.

**5-MeO-MiPT (close analog) case data available:**
- Grafinger et al. (2017 [Ref 7]): A man found naked, agitated, and aggressively behaving on a public street. Blood: 160 ng/mL 5-MeO-MiPT; urine: 3,380 ng/mL. Polydrug case (also: cocaine, cocaethylene, methylphenidate).
- Bassi et al. (2024 [Ref 17]): Preclinical mouse study of 5-MeO-MiPT derived from a human poisoning case identified in Italy 2014. Motor, sensorimotor, physiological, and cardiorespiratory parameters measured. First published preclinical pharmacotoxicological assessment of this analog.

**Analog inference for MiPT risk profile:** Tryptamine class risks include:
- Cardiovascular stimulation (tachycardia, hypertension) at higher doses — common to 5-HT₂A agonists
- Psychological distress (anxiety, panic, confusion) — documented for all classical psychedelics
- Potential for serotonin syndrome in combination with serotonergic drugs (see Interactions)

### Dependence Liability

No published data on MiPT's dependence liability. Seed data states "not habit-forming." This is consistent with the general tryptamine class: classical 5-HT₂A psychedelics are not associated with physical dependence. Rapid tolerance development (see Tolerance section) reduces reinforcing properties.

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## Harm Reduction

### Drug Interactions

**MAOI interactions (HIGH RISK):** Tryptamines, including DMT and related compounds, are substrates for MAO-A. Combining MiPT with a monoamine oxidase inhibitor (MAOI — including pharmaceutical MAOIs like phenelzine, tranylcypromine, or reversible MAOIs like moclobemide, and the β-carbolines found in ayahuasca) would be expected to markedly potentiate and prolong MiPT's effects and increase serotonin syndrome risk. No published data on this combination exists specifically for MiPT. Malcolm & Thomas (2022 [Ref 11]) review serotonin toxicity risks for serotonergic psychedelics including interactions with SSRIs and MAOIs.

**SSRI interactions:** Combining MiPT with selective serotonin reuptake inhibitors (SSRIs) carries a theoretical serotonin syndrome risk, though the absence of significant SERT inhibition by MiPT [Ref 5] somewhat reduces (but does not eliminate) this risk. SSRIs may also attenuate psychedelic effects via 5-HT₂A downregulation.

**Lithium:** Lithium is a contraindication for use with serotonergic psychedelics. Multiple case reports associate lithium + psychedelic combinations with seizures and severe neurological reactions (class-level caution; no MiPT-specific data).

**Stimulants:** Combining with stimulants (amphetamines, cocaine) may increase cardiovascular load (tachycardia, hypertension). The 5-MeO-MiPT forensic case (Grafinger 2017 [Ref 7]) involved polydrug use with cocaine and methylphenidate.

**Cannabis:** Anecdotally reported to intensify psychedelic effects unpredictably; no MiPT-specific data.

### Testing Recommendations

No MiPT-specific reagent testing data was found in the published literature. By class analogy, Ehrlich reagent (indole-reactive: turns purple/violet for tryptamines) is recommended as a first-line field test to confirm indole ring presence. Folin reagent is also used. LC-MS/MS is confirmed as the gold standard for forensic identification [Ref 19].

### General Harm Reduction

- Start with the lowest effective dose and allow ≥2 hours before redosing
- Do not combine with MAOIs, SSRIs, lithium, or other serotonergic agents
- Set and setting preparation appropriate for psychedelic use duration (3–6 hours)
- Do not operate vehicles or machinery during or for several hours after use
- Have a sober companion present, especially for new users

---

## Tolerance & Dependence

### Tolerance Mechanism

Classical psychedelics, including 5-HT₂A partial agonists, develop tolerance via **receptor downregulation**: repeated activation of 5-HT₂A receptors leads to decreased receptor density in the frontal cortex (de la Fuente Revenga et al. 2022 [Ref 13]).

The seed data states tolerance builds "almost immediately after ingestion" — this is consistent with published data on 5-HT₂A receptor agonists, where tolerance is typically evident after a single dose [Ref 13].

### Cross-Tolerance

Classical psychedelics (including LSD, DMT, psilocybin, and tryptamine analogs) share cross-tolerance mediated through the 5-HT₂A receptor. Halberstadt & Geyer (2011 [Ref 12]) confirm that phenylalkylamine and indoleamine hallucinogens induce cross-tolerance. The seed data's cross-tolerance classification as "psychedelic" is confirmed by the published literature.

### Tryptamines vs. Phenethylamines

Smith et al. (2014 [Ref 14]) demonstrated in a mouse head-twitch response model that **tryptamine-derived hallucinogens (DPT, DIPT) showed less tolerance development** than phenethylamine-derived hallucinogens (DOI, 2C-T-7), suggesting that MiPT's tolerance pattern may be less severe than expected from phenethylamine data, though the mechanism remains unclear.

### Tolerance Reset and Half-Life

The seed data states:
- Tolerance buildup: almost immediately after ingestion
- Half-life: 3 days
- Full reset: 7 days

These values are consistent with general psychedelic class data but are not verified by any MiPT-specific published source. **FLAG: tolerance half-life (3 days) and full reset (7 days) are unverified user-report-based estimates; no published pharmacokinetic data for MiPT tolerance kinetics exists.**

---

## Interactions

(See also Harm Reduction for clinical context)

| Interactant | Mechanism | Risk Level |
|---|---|---|
| MAOIs (irreversible) | MAO inhibition → massive MiPT potentiation + serotonin syndrome | Very High |
| MAOIs (reversible, e.g. moclobemide) | Similar but shorter-acting | High |
| SSRIs | Serotonin syndrome risk; may attenuate effects | Moderate |
| Lithium | Seizure risk (class-level contraindication) | High |
| Stimulants (cocaine, amphetamines) | Cardiovascular load (tachycardia, hypertension) | Moderate |
| Cannabis | Intensification of psychological effects | Variable |

No published drug-drug interaction studies specific to MiPT were found. All interaction classifications are based on class-level pharmacological inference [Ref 11; Ref 5; Ref 1].

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## Legal Status

### United States
MiPT is **not explicitly scheduled** under the Controlled Substances Act. However:
- It is structurally related to diethyltryptamine (DET), which is Schedule I
- The Federal Analog Act (21 U.S.C. § 813) could be applied if MiPT is intended for human consumption, given its structural and pharmacological similarity to Schedule I tryptamines
- In January 2022, the DEA proposed placing five related tryptamines (4-OH-DiPT, 5-MeO-AMT, **5-MeO-MiPT**, 5-MeO-DET, DiPT) in Schedule I, but this was subsequently withdrawn (July 2022) following public comment challenges. MiPT (the unsubstituted compound) was **not among the five named** in the DEA proposal.

### United Kingdom
MiPT is a **Class A controlled drug** under the Misuse of Drugs Act 1971, captured by the **generic tryptamine definition** that came into force January 7, 2015 (Circular 001/2015). The generic definition covers tryptamine ethers and ring-substituted analogs, and MiPT is explicitly named in secondary sources covering the generic clause.

### Canada
MiPT is **not explicitly listed** in Schedule III (hallucinogens) of the Controlled Drugs and Substances Act. As of 2025, it remains legally uncontrolled at the federal level in Canada, though this may be subject to change.

### Australia
Australia-specific scheduling data for MiPT could not be confirmed from publicly available sources. The Therapeutic Goods Administration (TGA) Poisons Standard contains a Schedule 9 (prohibited substance) list for psychedelic compounds, but whether MiPT is captured by a generic definition or is explicitly listed could not be verified. **FLAG: Australian scheduling status requires editorial verification.**

### China
As of September–October 2015, China lists **5-MeO-MiPT** as a controlled substance. No specific data was found for unsubstituted MiPT under Chinese regulations.

---

## Clinical Trials

**No clinical trials** involving MiPT were found on ClinicalTrials.gov. A search returned zero results for "MiPT" or "N-methyl-N-isopropyltryptamine."

MiPT is not under clinical investigation as of the research date (April 2026). It is not in clinical development for any psychiatric or medical indication.

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## Community Feedback Analysis

**No community feedback submitted.** (Part A2 of the brief was empty.)

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## Gaps & Flags

### Critical Flags (Safety-Relevant)

1. **⚠ PHARMACOLOGICAL CLASS ERROR — 5-HT₁A agonist classification:**
   Seed data classifies MiPT as a "Serotonin 1A receptor agonist." Blough et al. (2014 [Ref 5]) found MiPT **inactive at 5-HT₁A at concentrations ≥10 µM.** Kozell et al. (2023 [Ref 16]) confirms non-ring-substituted tryptamines (MiPT's class) show variable and generally low 5-HT₁A activity, contrasted with 5-substituted compounds which show high 5-HT₁A affinity. No published source supports 5-HT₁A agonism for MiPT. **Recommend removing "Serotonin 1A receptor agonist" from pharmacological class.**

2. **⚠ DURATION UPPER BOUND UNVERIFIED:**
   Seed data states total duration 3–8 hours (oral). Primary source (TiHKAL [Ref 8]) reports 3–4 hours; WikiDoc [Ref 9] reports 4–6 hours. The 8-hour upper bound has no primary source support. The generation agent should propose a revised range with the flag noted.

3. **⚠ TOXIC DOSE UNKNOWN:**
   No LD50 or toxic dose data exists for MiPT in any species. This is a safety-critical gap.

### Data Gaps

4. **No human pharmacokinetic studies:** No published Tmax, Cmax, bioavailability, plasma half-life, protein binding, or volume of distribution data for MiPT.

5. **Tolerance kinetics unverified:** Seed data values for tolerance half-life (3 days) and full reset (7 days) are not confirmed by published sources. These are user-report-based estimates consistent with general psychedelic class data.

6. **No MiPT-specific case reports:** No adverse event, intoxication, or overdose case reports for MiPT specifically. Risk assessment relies on analog (5-MeO-MiPT) and class-level data.

7. **Australia scheduling unconfirmed:** Cannot verify whether MiPT is explicitly captured under Australian Poisons Standard Schedule 9.

8. **Synthesis date discrepancy (1981 vs. 1985):** Secondary sources claim MiPT was "first synthesized by Repke et al. in 1981." The earliest PubMed-indexed publication is Repke et al. (1985, PMID 4009612). No 1981 paper was found. The 1985 date should be treated as the verified first publication date.

9. **CYP enzymes for MiPT not published:** Metabolic pathway data inferred from 5-MeO-MiPT (Grafinger 2017 [Ref 7]) and 5-MeO-2-Me-DIPT (Caspar 2017 [Ref 18]). CYP2D6, CYP3A4 involvement assumed but not directly measured for MiPT.

10. **SMILES not returned by PubChem API:** The SMILES CC(C)N(C)CCC1=CNC2=CC=CC=C12 is sourced from WikiDoc [Ref 9] (cross-referenced with InChIKey from PubChem), not from the PubChem API response. This should be verified via PubChem web interface or ChEMBL.

11. **Sigma-1 receptor binding:** Cozzi et al. (2009 [Ref 1]) proposed that high SERT-to-uptake ratios allow tryptamines including MiPT to accumulate intraneuronally to levels sufficient for sigma-1 receptor activation. No direct sigma-1 binding data (Ki) for MiPT has been published.

### Areas Relying on Structural Analogy

- Metabolic pathway (CYP enzymes): inferred from 5-MeO-MiPT and 5-MeO-2-Me-DIPT analogs
- Cardiovascular effects: inferred from 5-MeO-MiPT forensic case and tryptamine class data
- Drug interaction severity ratings: inferred from class-level serotonergic mechanism, no MiPT-specific interaction studies
- Sigma-1 receptor contribution to effects: hypothesized from Cozzi 2009 [Ref 1] DMT/tryptamine data