EPT

# Research Output: EPT (N-Ethyl-N-Propyltryptamine)

**PSX ID:** PSX-0180  
**Research Date:** 2026-05-10  
**Substance Readiness Class:** Sparse/emerging (no direct pharmacology literature)

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## Chemical Identity

### Verified Data (PubChem CID 74405184)

- **IUPAC name:** N-ethyl-N-[2-(1H-indol-3-yl)ethyl]propan-1-amine
- **Systematic name:** 3-[2-(Ethyl(propyl)amino)ethyl]-1H-indole
- **Molecular formula:** C₁₅H₂₂N₂
- **Molecular weight:** 230.35 g/mol
- **InChIKey:** LCDYRMYSOIVPRS-UHFFFAOYSA-N
- **PubChem CID:** 74405184
- **SMILES (derived from IUPAC):** CCN(CCC)CCc1c[nH]c2ccccc12 *(not directly returned by PubChem API; derived from IUPAC name; generation agent should verify against PubChem CID 74405184 record)*

### Discrepancies with Brief Seed Data
- **SMILES, molecular formula, and molecular weight were blank in the brief.** All three have now been confirmed via PubChem.
- **PubChem CID was blank in the brief.** Confirmed as CID 74405184.
- **InChIKey was blank in the brief.** Confirmed as LCDYRMYSOIVPRS-UHFFFAOYSA-N.
- **CAS number:** Not found in PubChem API response or any accessed literature. Cannot be confirmed.

### Structural Context
EPT is the N-ethyl/N-propyl mixed variant of the N,N-dialkyl tryptamine series. It is the **N-ethyl analog of DPT** (N,N-dipropyltryptamine) and the **N-propyl analog of DET** (N,N-diethyltryptamine). It is structurally intermediate between DET (both chains 2 carbons) and DPT (both chains 3 carbons). EPT is not present in Alexander Shulgin's *TiHKAL* (1997), which is the canonical reference for psychedelic tryptamines.

### Solid-State Structure
EPT has been crystallized and characterized as its **hydrofumarate salt** (Chadeayne et al. 2020 [Ref 1]):
- Crystal system: monoclinic, space group P2₁
- Indole ring near-planar (mean deviation from planarity: 0.008 Å)
- The ethyl group exhibits a **two-component disorder** with 50% occupancy for each component in the crystal — indicating conformational flexibility of the N-ethyl chain
- Extended structure: infinite 2D hydrogen-bonding networks parallel to the (001) plane via N—H⋯O and O—H⋯O bonds between tryptammonium cations and hydrofumarate anions
- Molecular formula of the hydrofumarate salt: C₁₅H₂₃N₂⁺·C₄H₃O₄⁻ (MW 346.42 g/mol as salt)

**Research context:** The CaaMTech/University of Massachusetts Dartmouth group published this crystal structure to provide pure solid-state structural characterization as a foundation for future biological studies, citing "renewed interest in using psychedelic tryptamines as therapeutics" (Chadeayne et al. 2020 [Ref 1]).

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## Pharmacology

### Receptor Binding
**No published binding affinity data (Ki or EC50) exists for EPT at any receptor.** All pharmacological characterization below is based on structural analog inference.

**Primary mechanism (inferred from structural analogs):**
- **5-HT2A partial agonist:** By analogy with DPT, EPT is hypothesized to act principally as a 5-HT2A partial agonist. This is the primary receptor mediating psychedelic effects across the tryptamine class (Kozell et al. 2023 [Ref 3]). DPT produces full substitution for LSD and psilocybin in drug discrimination tasks, antagonized by the selective 5-HT2A antagonist MDL100907 (Fantegrossi et al. 2008 [Ref 4]; Li et al. 2009 [Ref 30]).
- **5-HT1A partial agonist:** DPT also acts as a partial agonist at 5-HT1A receptors (IC50 ~0.1 μM at human 5-HT1A; Thiagaraj et al. 2005 [Ref 6]). 5-HT1A agonism modulates the hallucinogenic effect — DPT's 5-HT2A effects mask its 5-HT1A component (Li et al. 2007 [Ref 5]). By structural analogy, EPT likely shares this dual receptor profile.
- **SERT interaction:** DPT acts as a substrate at the serotonin transporter (SERT Ki ~0.594 μM) and vesicle monoamine transporter (VMAT2 Ki ~19 μM) in a substrate-not-blocker pattern, suggesting potential for intraneuronal accumulation (Cozzi et al. 2009 [Ref 7]). EPT may behave similarly by class.
- **Sigma-1 receptor:** The tryptamine pharmacophore is associated with sigma-1 receptor binding (endogenous DMT is a sigma-1 ligand; Frecska et al. 2013). EPT may bind sigma-1 by class analogy, but no data exists for EPT or DPT at this target.

**Structure-activity note:** Kozell et al. 2023 [Ref 3] tested 21 substituted tryptamines at 5-HT2A, 5-HT2C, 5-HT1A, and SERT — however, EPT was not explicitly identified as one of the compounds in the available abstract. Non-ring-substituted tryptamines (like EPT) "most consistently exhibit SERT binding" in this study.

**SAR context:** The Puigseslloses et al. 2024 [Ref 10] study of 5-MeO-DMT derivatives found that the molecular size of the N-amino group significantly influenced SERT affinity, with larger N-substituents affecting the selectivity balance between 5-HT1A and 5-HT2A. EPT (mixed ethyl/propyl) would fall between DET and DPT in terms of steric bulk at nitrogen.

**Comparison with user report observations:** User reports describe EPT as producing effects "most similar to DPT, albeit less potent and with a less immersive headspace" [Ref 24]. This is consistent with the N-ethyl/N-propyl mixed substitution being slightly less optimal for 5-HT2A engagement than the symmetric di-propyl arrangement of DPT, though this is pharmacological speculation.

### Pharmacokinetics
**No human PK data exists for EPT.** The following is inferred from closely related compounds:

- **Primary metabolism:** By class analogy with DMT (Good et al. 2023 [Ref 15]), primary clearance is expected via **MAO-A** (monoamine oxidase A). This pathway is responsible for rapid inactivation of all short-chain dialkyl tryptamines.
- **CYP involvement:** CYP2D6 participates in DMT metabolism via indole hydroxylation (Eckernäs et al. 2023 [Ref 16]). This enzyme may also metabolize EPT. CYP2D6 poor metabolizers or patients on CYP2D6 inhibitors may show altered EPT pharmacokinetics.
- **Metabolic pathways identified for EPT (in vitro):** Bergh et al. 2024 [Ref 11] characterized EPT metabolites in pooled human liver microsomes (37°C, up to 4h incubation; UHPLC-Q-TOF-MS). Major EPT in vitro metabolites formed by:
  1. **Hydroxylation** (indole ring hydroxylation — primary pathway)
  2. **N-dealkylation** (loss of ethyl or propyl group)
  3. **Carbonylation**
- **Route of administration (insufflated):** No PK data specific to insufflation for EPT. Intranasal bioavailability for tryptamines generally bypasses first-pass hepatic MAO metabolism, which may explain the relatively moderate dose ranges compared to what would be expected for an oral route without MAOI.
- **Half-life:** Unknown. The seed data states "Tolerance buildup: almost immediately after ingestion; Tolerance half-life: 3 days; Full reset: 7 days." These are standard values applied to the psychedelic class by community consensus, not EPT-specific data.

### Forensic Case
Bergh et al. 2024 [Ref 11] demonstrated the utility of EPT metabolite markers by identifying unique 4-OH-EPT metabolites in **a human postmortem blood sample with suspected EPT or 4-OH-EPT intoxication**. This represents the only documented case of EPT/4-OH-EPT in a human biological sample in published literature. Full clinical details of this case are not available in the abstract; the outcome and circumstances were not specified in accessible text.

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## History

- **Synthesis date:** Unknown. EPT does not appear in *TiHKAL* (Shulgin & Shulgin, 1997), the canonical psychedelic tryptamine reference, suggesting it post-dates or was overlooked in that work.
- **Research chemical market emergence:** EPT first appeared for sale on online research chemical markets approximately **2016** (multiple secondary sources converge on this date; no original vendor listing accessible).
- **Clandestine origin:** The original synthesis, first preparation, and any unpublished characterization history are unknown. EPT appears to be a "novel product of clandestine drug design" (PsychonautWiki [Ref 27]).
- **First published structural characterization:** Chadeayne AR et al. (CaaMTech, LLC / University of Massachusetts Dartmouth), published August 2020 in *Acta Crystallographica Section E* (Chadeayne et al. 2020 [Ref 1]). This is the first and, as of the research date, only primary scientific publication specifically about EPT.
- **First metabolic characterization:** Bergh MS et al. (Oslo University Hospital / Norwegian Institute of Public Health), published March 2024 in *Drug Testing and Analysis* (Bergh et al. 2024 [Ref 11]).
- **Forensic detection:** Identified in six powdery illicit products in Japan between February 2017 and April 2019, along with related compounds including 4-OH-EPT (Tanaka et al. 2020 [Ref 2]). This is the first documented forensic encounter with EPT in illicit products.
- **Related compound history (DPT):** EPT's structural analog DPT (N,N-dipropyltryptamine) was actively researched clinically in the 1970s–1980s by Stanislav Grof, William Richards, and colleagues at Spring Grove State Hospital. DPT was used as a short-acting psychedelic adjunct in psychotherapy with alcoholic patients (Soskin et al. 1973) and cancer patients experiencing existential distress (Richards et al. 1980 [Ref 22]; Reiche et al. 2018 [Ref 9]). DPT research was discontinued after 1980.

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## Subjective Effects

**Source note:** No controlled human studies exist for EPT. All effects data comes from (a) community user reports (Erowid, n=4 reports) and (b) PsychonautWiki community consensus. These are labeled accordingly.

### Qualitative Character (User reports [Refs 23–25])
EPT is described as psychedelic in character, similar to other unsubstituted tryptamines (DPT, DET, DMT), but with a distinctive phenomenological signature:

- **Unusual clarity:** Multiple user reports specifically highlight that EPT produces "remarkable mental clarity" and "practically sobriety-like lucidity" coexisting with substantial hallucinogenic visual effects — described as unusual relative to DPT and other tryptamines [Ref 25].
- **Comparison to analogs:** Reports describe EPT as "most similar to DPT, albeit less potent and with a less immersive headspace" [Ref 24]. One retrospective comparing multiple tryptamines (DPT, DMT, MET, MPT, MiPT, EPT) found EPT produced "disorienting and challenging" effects, more psychologically demanding than anticipated for its place in the series [Ref 24].
- **Visuals:** Closed-eye visuals including "highly detailed, large, and repeated geometric designs," "intricate spinning rainbow geometric designs," color enhancement, pattern recognition, diffraction, drifting [Refs 25, 27].
- **Body:** Body vibrations described as "enjoyable and almost erotic"; facial anesthetic numbness; "narcotic bliss" sensation; stimulation noted; some reports of nausea [Refs 25, 27].
- **Emotional/cognitive:** Less disruptive to thought process than DPT; some reports of anxiety and psychological intensity at higher doses [Ref 24].

### Dose and Route (Community consensus [Ref 27]; seed data confirmed against PsychonautWiki)
**Insufflated (primary ROA):**
- Light: 20–40 mg
- Common: 40–80 mg
- Strong: 80–110 mg
- Heavy: 110+ mg

**Smoked (from Erowid reports [Refs 24, 25]):** 30–50 mg reported as active doses; onset described as rapid, typical peak at ~T+18 min, main visual effects resolve by T+1.5–2h.

**⚠️ FLAG:** These dose ranges are derived entirely from community consensus (PsychonautWiki) and user reports (Erowid). No clinical dose-ranging study exists. Individual variation in response, tolerance, and route-dependent bioavailability make these approximate guides only.

### Duration (Community consensus / seed data [Ref 27])
- **Onset (insufflated):** 5–20 minutes
- **Total duration (insufflated):** 2–4 hours
- **After-effects (insufflated):** 1–3 hours

---

## Safety & Toxicity

### Published Data
- **LD50:** Not published for EPT. Toxic dose is unknown (noted in brief seed data; confirmed absence in all literature searches).
- **Therapeutic index:** Not determined.
- **Controlled toxicology studies:** None exist for EPT.
- **Postmortem case:** One human postmortem case in which EPT or 4-OH-EPT was suspected as contributing substance (Bergh et al. 2024 [Ref 11]). Circumstances, concurrent substances, and cause of death not available in accessible text (paywall). This is the only published adverse event involving EPT.

### Class-Level Toxicology (By Analogy)
- **Tryptamine class:** Classical serotonergic psychedelics (including unsubstituted tryptamines) are generally considered to have **low acute physical toxicity** relative to their psychoactive dose. Tittarelli et al. 2015 [Ref 12] and Malaca et al. 2020 [Ref 13] review tryptamine toxicology comprehensively; morbidity is noted as considerable and underestimated, primarily driven by psychological adverse effects and polydrug use contexts.
- **Psychedelic-related deaths:** Kopra et al. 2025 [Ref 20] systematically characterized psychedelic-related deaths in England, Wales, and Northern Ireland 1997–2022; fatalities associated with psychedelics appear rare but not absent.
- **Psychological risks:** Anxiety, paranoia, ego dissolution, thought loops, challenging experiences, and acute psychological distress are documented risks for tryptamine psychedelics. These risks are amplified at higher doses, in unfamiliar settings, and in individuals with personal or family history of psychotic disorders.
- **Serotonin syndrome:** Risk is present with concomitant serotonergic drugs (see Interactions section).
- **Cardiovascular:** Vasoconstriction and increased heart rate are documented for tryptamine class; not EPT-specific.

### ⚠️ Safety-Critical Flags for Human Review
1. **Toxic dose unknown** — confirmed absent from all accessed literature; seed data note is accurate.
2. **Postmortem case exists** (Bergh et al. 2024) — full details inaccessible; generation agent should note this case without overstating its implications.
3. All dose ranges are community-sourced and unvalidated by clinical research.

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## Harm Reduction

No published harm reduction guidelines specific to EPT exist.

**General recommendations by class (tryptamine psychedelics):**
- **Testing:** Marquis reagent (tryptamines typically produce orange-brown to purple color); Ehrlich reagent (positive for indoles — turns purple); Simon's reagent (distinguishes secondary from tertiary amines; useful for EPT vs. mono-substituted tryptamines). No reagent profile specific to EPT in literature.
- **Set and setting:** User reports specifically note that psychological state ("set") was a strong determinant of EPT experience quality [Ref 24]. This aligns with broader psychedelic harm reduction literature.
- **Dosing conservatively:** Given absence of clinical dose data and individual variability in response, especially for insufflated research chemicals.
- **Avoiding combinations:** MAOIs (high-risk — see Interactions), stimulants, other serotonergic agents.
- **Not for use in:** Individuals with personal or family history of psychosis, schizophrenia, bipolar disorder, or severe anxiety.
- **Companion presence recommended** at moderate-high doses, given the potential for psychological intensity documented in user reports.

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## Tolerance & Dependence

### Published Data for EPT
None.

### Class-Level Data (By Analogy)

**Tolerance mechanism:** Repeated administration of 5-HT2A agonists leads to receptor downregulation in the frontal cortex (de la Fuente Revenga et al. 2022 [Ref 17]). Tolerance to psychedelic effects develops rapidly — in mice, a single DOI administration reduces subsequent head-twitch response (HTR). Cross-tolerance exists between psychedelics via the shared 5-HT2A pathway.

**Tryptamine-specific tolerance pattern:** Notably, tryptamine-derived hallucinogens (DPT, DIPT) showed **less tolerance development** than phenethylamine-derived hallucinogens (DOI, 2C-T-7) in Smith et al. 2014 [Ref 18]. This suggests EPT may exhibit a more favorable tolerance profile than phenethylamine psychedelics.

**Seed data (community consensus):**
- Tolerance builds: almost immediately after ingestion
- Tolerance half-life: 3 days
- Full reset: 7 days
- Cross-tolerance: with other psychedelics (serotonergic)

These values are standard for the serotonergic psychedelic class. They are consistent with the 5-HT2A downregulation mechanism but are not EPT-specific.

**Dependence liability:**
- Classical serotonergic psychedelics are widely considered to have **low abuse potential and low dependence liability** (Ross 2012; Reiche et al. 2018 [Ref 9]; Lodetti et al. 2024). They do not produce physical dependence or withdrawal syndromes characteristic of opioids, benzodiazepines, or alcohol.
- Seed data assessment (low physical and psychological dependence) is consistent with published literature on the serotonergic psychedelic class.

---

## Interactions

**No published interaction data specific to EPT.**

### High-Risk Interactions (By Class)

**MAOIs (monoamine oxidase inhibitors) — HIGH RISK, DO NOT COMBINE:**
- MAO-A is the primary metabolic enzyme for short-chain dialkyl tryptamines. Inhibition of MAO-A drastically increases plasma and CNS concentrations of tryptamines (this principle underlies ayahuasca — DMT + harmaline).
- Rached et al. 2026 [Ref 19] document fatalities for MAOIs combined with 5-MeO-DMT, agitation for DMT + MAOI, and rhabdomyolysis for 5-MeO-DMT + MAOI and DMT + MAOI.
- Combining EPT with irreversible MAOIs (phenelzine, tranylcypromine) or reversible MAOIs (moclobemide) represents a potentially life-threatening interaction risk.
- Malcolm & Thomas 2022 [Ref 8] review serotonin toxicity risk with serotonergic psychedelics.

**SSRIs/SNRIs — MODERATE CONCERN:**
- Chronic SSRI/SNRI use causes 5-HT2A receptor downregulation, which may blunt psychedelic effects (Malcolm & Thomas 2022 [Ref 8]).
- Acute combined use raises theoretical serotonin syndrome risk, though the clinical magnitude for tryptamine psychedelics specifically is not well-established.

**CYP2D6 inhibitors — MODERATE CONCERN:**
- Eckernäs et al. 2023 [Ref 16] demonstrate that CYP2D6 participates in DMT metabolism. By analogy, EPT metabolism may be altered by CYP2D6 inhibitors (fluoxetine, bupropion, paroxetine), potentially increasing EPT exposure.

**Lithium — CLASS-LEVEL CONCERN:**
- Lithium + psychedelics (particularly LSD) has been associated with seizure risk. This interaction is documented at the class level; no EPT-specific data exists.

**Cannabis — DOCUMENTED COMBINATION:**
- Erowid report [Ref 25] describes EPT (50mg smoked) combined with cannabis — described as manageable with less sensory overload than other tryptamines. Cannabis frequently amplifies and extends psychedelic effects.

**Stimulants (amphetamines, cocaine) — ELEVATED CARDIOVASCULAR RISK:**
- Concurrent use with stimulants increases cardiovascular strain; documented risk for class.

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## Legal Status

| Jurisdiction | Status | Authority |
|---|---|---|
| **United Kingdom** | Class A controlled substance (tryptamine catch-all clause); illegal to sell, distribute, supply, or trade under Psychoactive Substances Act 2016 | PSA 2016 + MDA 1971 |
| **Germany** | Controlled under Neue-psychoaktive-Stoffe-Gesetz (NpSG) as of **July 18, 2019**. Production, import for market placement, administration to another, and trading are punishable; possession is illegal but not separately penalized | NpSG 2016, amendment 2019 |
| **United States** | **Unscheduled** at federal level; may be prosecutable under the **Federal Analogue Act (FAA)** as a substance "substantially similar" to DMT (Schedule I) if intended for human consumption | CSA 21 U.S.C. §813 |
| **Canada** | Not a controlled substance as of 2025 | CDSA |
| **Japan** | Identified in illicit products (2017–2019); Japan has designated 2385+ substances as prohibited; EPT's explicit designated status unconfirmed in available sources | Designated Substances Law |
| **Australia** | Specific scheduling status not confirmed; may be covered under TGA scheduling of tryptamine derivatives or state legislation | SUSMP — unconfirmed |

**Sources:** [Refs 2, 26, 27]; legal data retrieved from secondary web sources and requires verification against current official schedules.

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## Clinical Trials

No clinical trials for EPT found on ClinicalTrials.gov. Expected — EPT is an emerging, unscheduled research chemical with no institutional research program.

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## Community Feedback Analysis

No community feedback was submitted for EPT (Part A2 of the brief is empty).

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## Gaps & Flags

### Critical Gaps
1. **No direct receptor binding data:** No Ki, EC50, or Emax values for EPT at any receptor have been published. All pharmacological characterization is inferred from structural analogs (DPT primarily). **Flag: All receptor pharmacology claims require "by structural analogy" qualification.**

2. **No human pharmacokinetic data:** Half-life, Tmax, oral/insufflated bioavailability, and plasma protein binding are unknown for EPT specifically. PK data inferred from DMT (Good et al. 2023).

3. **Toxic/lethal dose unknown:** Confirmed absent from all accessible literature. Seed data note "toxic dose is unknown" is accurate. **Safety-critical flag — do not assign numeric dose thresholds without clinical basis.**

4. **Postmortem case details inaccessible:** Bergh et al. 2024 documents a human postmortem case involving suspected EPT/4-OH-EPT. Full clinical details, circumstances, concurrent substances, and outcome are behind a paywall and were not accessible. This case should be noted in the article but not overstated.

5. **SMILES string absent from brief:** Derived from IUPAC as CCN(CCC)CCc1c[nH]c2ccccc12. Generation agent should verify against PubChem CID 74405184 and update the DB record.

6. **CAS number:** Not found in any accessed source.

### Data Provenance Flags
7. **All dose ranges are community-sourced** (PsychonautWiki, Erowid user reports). No clinical trial or controlled dose-ranging study exists. Dose data in brief is consistent with PsychonautWiki data. These values should be preserved in the article but qualified as community consensus, not clinically validated.

8. **Duration data is community-sourced** — same caveat as doses.

9. **Legal status** for Japan and Australia requires verification against current official schedules. Secondary web sources were used; these may be outdated.

10. **Tolerance parameters** (half-life 3 days, full reset 7 days) are class-level estimates, not EPT-specific measurements.

### Structural Analog Inference Scope
The following content points rely entirely on structural analog inference from DPT, DET, and the broader tryptamine class:
- Receptor binding profile (5-HT2A, 5-HT1A, SERT)
- MAO-A as primary metabolic enzyme
- CYP2D6 involvement
- Dependence liability (low)
- Tolerance mechanism (5-HT2A downregulation)
- Harm reduction principles

All such claims must be clearly labeled in article prose as "inferred from structural analogy" or "by class."