MXiPr

# Research Output: MXiPr (Methoxisopropamine)

**PSX ID:** PSX-0268  
**Research Date:** 2026-05-09  
**Substance Readiness:** Sparse/Emerging (< 0.3) — primary literature is very limited; most pharmacological context derived from structural analogs

---

## Chemical Identity

### Verified Data (PubChem CID 163192824)

| Field | Value | Source |
|---|---|---|
| Preferred IUPAC name | 2-(isopropylamino)-2-(3-methoxyphenyl)cyclohexan-1-one | PubChem [Ref 17] |
| Alternate IUPAC | 2-(3-methoxyphenyl)-2-(propan-2-ylamino)cyclohexan-1-one | PubChem API |
| Molecular formula | C₁₆H₂₃NO₂ | PubChem [Ref 17] |
| Molecular weight | 261.365 g/mol | PubChem [Ref 17] |
| SMILES | CC(C)NC1(CCCCC1=O)c1cccc(OC)c1 | HandWiki [Ref 17] |
| InChIKey | FTQIVDGNGXPEKP-UHFFFAOYSA-N | PubChem [Ref 17] |
| PubChem CID | 163192824 | Confirmed via API |
| CAS number | Not officially assigned / "unknown" in MedKoo | Multiple sources |

**Note on CAS number:** Some commercial sources list "72242-03-6" for MXiPr, but MedKoo explicitly marks CAS as "unknown." This number could not be cross-verified against a primary registry. The generation agent should flag this for editorial verification.

**Note on molecular weight discrepancy:** The seed brief contains no molecular weight. Some vendor sources erroneously list ~273 g/mol, which corresponds to the HCl salt (261.36 + 36.46 ≈ 297.82... or possibly a different compound). The confirmed free base MW from PubChem is 261.365 g/mol. The Cayman Chemical reference standard is listed as the hydrochloride salt (Item 31545).

### Synonyms Confirmed
- Methoxisopropamine (preferred common name)
- MXiPr (primary abbreviation in literature)
- MXiP (alternative abbreviation)
- Isopropyloxetamine
- Isopropyxetamine
- 3-MeO-2′-Oxo-PCiPr (substitutive nomenclature)

### Structural Relationships
MXiPr is the N-isopropyl homologue of methoxetamine (MXE). Structurally, replacing MXE's N-ethyl group with an N-isopropyl group gives MXiPr. It is directly related to:
- **MXE** (methoxetamine, N-ethyl) — the parent research chemical
- **MXPr** (methoxpropamine, N-propyl) — same series, one carbon longer
- **DMXE** (deoxymethoxetamine) — same N-ethyl chain but lacks the 3-methoxy group
- **Deschloroketamine (DCK)** — lacks the 3-methoxy, has N-methyl
- **Ketamine** — the clinical parent compound (2-chloro, N-methyl instead of N-isopropyl/3-methoxy)

The Frankenfeld et al. 2024 study designates MXiPr as "deschloro-N-isopropyl-ketamine," placing it in the deschloroketamine derivative series (Frankenfeld et al. 2024 [Ref 1]).

---

## Pharmacology

### Primary Target: NMDA Receptor

**Substance-specific data:**  
Irie et al. (2022 [Ref 11]) determined the IC₅₀ of MXiPr at NMDA receptors to be **0.661 µM** using patch-clamp electrophysiology in NMDAR-expressing cartwheel interneurons of mice. An in silico docking study in the same paper confirmed that MXiPr interacts within the NMDAR channel pore. This is the only published, peer-reviewed pharmacological measurement specific to MXiPr.

Comparative IC₅₀ values from the same paper (Irie et al. 2022 [Ref 11]):
- MXE: 0.524 µM
- DMXE: 0.679 µM
- MXiPr: **0.661 µM**
- N-desethyl MXE: 1.649 µM
- O-desmethyl MXE: 0.227 µM

This places MXiPr's NMDA potency between MXE and DMXE, and ~25% less potent than MXE at the receptor level. The authors explicitly identified MXiPr and DMXE as "serious concerns" given their potent NMDAR blockade and online availability since 2020 (Irie et al. 2022 [Ref 11]).

**Mechanism:** NMDA receptor antagonism is uncompetitive and open-channel blocking — the same mechanism as ketamine, PCP, and MXE. Activation of the NMDA receptor by glutamate/glycine is required before the drug can enter and block the ion channel. This is thought to underlie the dissociative, hallucinogenic, and analgesic properties of this compound class (Zanos et al. 2018 [Ref 7]; Wallach & Brandt 2018 [Ref 4]).

### Secondary Targets

**Sigma-1 receptor:** Not directly measured for MXiPr. The seed data lists sigma-1 agonism as a pharmacological class property. MXE and related β-keto-arylcyclohexylamines have been shown to have sigma receptor affinity (Roth et al. 2013 [Ref 3]), but this has not been confirmed for MXiPr in published literature. This is a structural class inference requiring substance-specific measurement.

**Serotonin transporter (SERT):** Roth et al. (2013 [Ref 3]) demonstrated that MXE possesses affinity for SERT. Whether MXiPr shares this property is unknown; no published binding study has evaluated MXiPr at SERT. The N-isopropyl substitution may alter SERT affinity relative to the N-ethyl parent.

**Dopamine/norepinephrine transporters:** No published data for MXiPr.

**FLAG for generation agent:** All secondary receptor data for MXiPr relies on class inference from MXE data. There are no published multi-target binding studies for MXiPr itself.

### Pharmacokinetics

**Metabolism (Frankenfeld et al. 2024 [Ref 1]):**
The most detailed published data on MXiPr's pharmacokinetics is from a metabolic fate study of five deschloroketamine derivatives including MXiPr, conducted in male Wistar rats (in vivo, urine collected over 24h at 2 mg/kg body weight) and pooled human liver microsomes (in vitro). Primary metabolic pathways identified were:
1. **N-dealkylation** — loss of the isopropyl group (principal pathway, analogous to DCK and MXE metabolism)
2. **Hydroxylation** — on the aromatic ring and/or cyclohexane ring
3. **Multiple oxidations** — combinations of the above
4. Phase II: **glucuronidation** and **N-acetylation**

Across all five DCK derivatives studied, 29 phase I and 10 phase II metabolites were detected. Compound-specific metabolites for MXiPr were identified by LC-HRMS/MS, enabling targeted urinary detection; however, GC-MS screening only detected non-specific acetylated N-dealkylation metabolites (Frankenfeld et al. 2024 [Ref 1]).

The analogous metabolism of MXPr (N-propyl congener) includes N-despropyl(nor)MXPr, O-desmethyl MXPr, and dihydroMXPr (Goncalves et al. 2022 [Ref 15]), providing comparative context.

**Half-life:** No human pharmacokinetic studies published. The seed data lists a tolerance half-life of 5 days, which likely refers to functional (receptor-level) tolerance duration rather than plasma elimination half-life. No plasma half-life data from published studies.

**Bioavailability:** No published data. Common administration routes are insufflation and oral (seed data). Oral bioavailability of MXE-class compounds is generally reduced relative to insufflation due to first-pass metabolism.

**CYP enzyme involvement:** Not specifically studied for MXiPr. Arylcyclohexylamines are generally metabolized via CYP2B6 and CYP3A4 (as established for ketamine; Zanos et al. 2018 [Ref 7]). This is a class inference, not confirmed for MXiPr.

**Stereochemistry:**
The chiral center at C2 of the cyclohexanone ring means MXiPr exists as two enantiomers (R and S). Seibert et al. (2025 [Ref 2]) developed enantioseparation methods for 11 ketamine derivatives including MXiPr using CE-UV and HPLC-UV with optical rotation detection. Enantiomers were partially or fully separated; the enantiomer elution order was determined. However, no functional data comparing the pharmacological potency or safety profiles of R- vs. S-MXiPr has been published. For reference, S-ketamine is approximately twice as potent as R-ketamine at NMDA receptors (Zanos et al. 2018 [Ref 7]); whether MXiPr shows comparable enantioselectivity is unknown.

---

## History

### Discovery and First Appearance

MXiPr first appeared on online research chemical markets in **late 2020**, according to multiple sources. The first formal laboratory identification was made by the **National Forensic Laboratory of Slovenia in December 2020** (cited in Tanaka et al. 2022 [Ref 12]; confirmed in HandWiki [Ref 17]). The compound was not previously described in pharmaceutical or academic literature before its emergence as a research chemical.

MXiPr emerged as part of a wave of methoxetamine analogs designed to circumvent the scheduling of MXE, which was controlled in Japan, the UK, Germany, and many other jurisdictions by the mid-2010s. The structural strategy — replacing the N-ethyl group with N-isopropyl — mirrors a broader pattern in NPS design: minor N-alkyl substitution variations to circumvent generic scheduling definitions while preserving the pharmacological core (Wallach & Brandt 2018 [Ref 4]; Wallach & Brandt 2018 [Ref 16]).

Tanaka et al. (2022 [Ref 12]) reported the identification of MXiPr alongside MXPr and DMXE in **seized illegal products in Japan**, representing the first published forensic identification of MXiPr. Irie et al. (2022 [Ref 11]) from the same research group (National Institute of Health Sciences, Japan) subsequently published the first pharmacological characterization, measuring NMDA IC₅₀.

The compound has since been detected in France by a harm reduction drug-checking service (Marseille, October 2024 [Ref 14]) and was flagged in the context of emerging ketamine analogues patterns by the French Addictovigilance Network (Mezaache et al. 2026 [Ref 13]).

### Regulatory History

- **December 2020:** First identified, National Forensic Laboratory, Slovenia
- **April 2021:** Prohibited in Hungary
- **~2021:** UK Class B designation (Misuse of Drugs Act 1971); Germany NpSG designation
- **~2021–2022:** Identified in Japanese illegal product seizures
- **2022:** Published in peer-reviewed forensic literature (Tanaka et al. 2022 [Ref 12]; Irie et al. 2022 [Ref 11])
- **October 2024:** Detected in drug-checking services, Marseille, France [Ref 14]

---

## Subjective Effects

**No controlled human studies exist for MXiPr.** All effect descriptions come from anonymous self-reports on harm reduction and research chemical community platforms (web_retrieved [Ref 22]).

Published sources (Irie et al. 2022 [Ref 11]; Tanaka et al. 2022 [Ref 12]) confirm the pharmacological basis for dissociative effects via NMDA antagonism but do not describe human subjective phenomenology.

### Dose-Dependent Phenomenology (User Reports Only [Ref 22])

**Low-to-moderate doses (roughly 5–30 mg insufflated):**
- Primarily stimulating rather than sedating
- Sensation of bodily lightness and weightlessness (described as particularly prominent)
- Tingling body sensation localized to hands, feet, and head
- Mild dissociation and mood elevation
- Analgesic effects
- Described as resembling nitrous oxide at threshold/light doses

**Higher doses (roughly 30–60+ mg insufflated):**
- Transition to sedation
- Stronger dissociation — described as "hole"-like (complete ego dissolution/disconnection) at heavy doses
- Internal hallucinations and conceptual thinking
- Warm, dreamy afterglow following the acute phase

**Aftereffects:**
- Body load reported lasting up to 2 days after even small doses in some reports [Ref 22]
- Afterglow described as euphoric and warm — potentially contributing to compulsive redosing

### Duration (Seed Data, Consistent with Community Reports [Ref 22])

Insufflation:
- Onset: 2–5 minutes
- Total: 1.5–4 hours
- Aftereffects: 2–12 hours

Oral:
- Onset: 20–60 minutes
- Total: 2–5 hours
- Aftereffects: 4–48 hours

**FLAG:** All duration data is unconfirmed by controlled studies. The seed data values are derived from community consensus. The aftereffect duration of up to 48 hours oral is a wide range that would benefit from editorial review.

### Effect Profile Assessment

Based on class pharmacology and the NMDA IC₅₀ data, the following effects profile is pharmacologically plausible for MXiPr:

The NMDA antagonism mechanism directly explains: dissociation, amnesia, depersonalization, derealization, analgesia, motor control impairment, and the dose-dependent dissociative depth. Sigma-1 agonism (if confirmed) would contribute to: antidepressant effects, euphoria, and potentially visual distortion. The absence of a ketone reduction site compared to some analogs and the bulky N-isopropyl group may influence SERT affinity and metabolic half-life relative to MXE.

**FLAG for generation agent:** Effects listed in the seed database (42 effect slugs) are all marked as community_consensus_large/medium provenance with null intensity/frequency values. No peer-reviewed source provides human phenomenological data. All effect assignments should be derived from structural class inference from MXE, with appropriate confidence labeling.

---

## Safety & Toxicity

### Substance-Specific Data

**Lethal dose (LD₅₀):** Not established. The seed data notes "toxic dosage is unknown."

**Human overdose cases:** No published case reports involving MXiPr identified in this research.

**Published adverse event data:** None substance-specific.

### Class-Based Inference (FLAG: analog inference)

Fatal cases have been reported for several structurally related arylcyclohexylamine compounds:

- **N-ethyldeschloroketamine (2-Oxo-PCE):** Fatal case reported (Theofel et al. 2019 [Ref 6]). Femoral blood concentration 375 µg/L. Co-administered with venlafaxine.
- **2-Fluorodeschloroketamine (2-FDCK):** Two fatal cases (Riess et al. 2024 [Ref 5]). Blood concentrations 758 and 5,885 µg/L.
- **2F-DCK and 3-MeO-PCE combination:** Fatal intoxication reported (Gicquel et al. 2021 [Ref 9]).

The lethality in analog cases appears associated with high doses, polydrug use (particularly with CNS depressants or serotonergic agents), and underlying health factors. Whether MXiPr shares similar toxicity thresholds cannot be determined from published data.

### Specific Risk Signals

**Seizure risk:** User reports describe seizures occurring at very high doses [Ref 22]. No case reports in published literature confirm this for MXiPr specifically, though NMDA antagonists as a class can affect seizure threshold (Luethi & Liechti 2020 [Ref 20]).

**Uroepithelial toxicity:** Class-based concern. Studies on MXE and ketamine in chronic administration have found evidence of bladder inflammation and fibrosis. Whether MXiPr carries this risk is unknown; no human data or animal histology studies for MXiPr have been published.

**Cardiovascular effects:** Class inference. NMDA antagonists including ketamine produce dose-dependent sympathomimetic cardiovascular effects (tachycardia, hypertension) via central sympathetic stimulation (Zanos et al. 2018 [Ref 7]).

**Prolonged body load:** Anecdotal reports describe a body load lasting up to 2 days after small doses [Ref 22], which is longer than typically described for MXE or ketamine. This may reflect the bulkier N-isopropyl group slowing hepatic N-dealkylation, resulting in a longer functional half-life. This is speculative — no pharmacokinetic data confirm it.

**Psychological risks:** Consistent with the NMDA antagonist class: anxiety, paranoia, cognitive impairment during use; potential for psychological dependence with heavy use. The antidepressant-like properties observed for ketamine and MXE may also be present, which could attract self-medication use (Zanos et al. 2018 [Ref 7]).

---

## Harm Reduction

No published harm reduction guidelines specific to MXiPr exist. The following is derived from class evidence and is appropriate only as a starting framework:

**Testing:** MXiPr does not appear in standard drug testing kits designed for common substances. Reagent color reactions for arylcyclohexylamines (e.g., Mecke, Mandelin, Simon's reagent) may give class-level positive responses but cannot confirm MXiPr identity. FTIR or LC-MS is required for definitive identification. Drug-checking services in France (Marseille, October 2024 [Ref 14]) have successfully identified MXiPr, suggesting appropriate laboratory methods exist.

**Dosing caution:** MXiPr appears more potent than the dose ranges for some related compounds might suggest, given reports of prolonged body load at small doses. Starting with low doses (≤5 mg insufflated) and waiting fully for effects before redosing is critical.

**Combination risks:** CNS depressants (opioids, benzodiazepines, GHB, alcohol) additive with sedation/respiratory depression — potentially fatal. The fatal case involving N-ethyldeschloroketamine + venlafaxine (Theofel et al. 2019 [Ref 6]) highlights the risk of combining arylcyclohexylamines with serotonergic agents.

**Drug checking:** MXiPr has been found in pill form in France (October 2024), indicating it may be substituted for or mixed with other substances in tablet preparations.

---

## Tolerance & Dependence

### Tolerance

No published studies characterize MXiPr-specific tolerance. The seed data states buildup "develops with prolonged and repeated use" with a half-life of 5 days and full reset at 1.5 weeks. These values are derived from community consensus with reference to related compounds (MXE, ketamine class).

The mechanism of tolerance for NMDA antagonists involves receptor upregulation and compensatory glutamatergic changes. Cross-tolerance within the dissociative class (NMDA antagonists) is expected (Luethi & Liechti 2020 [Ref 20]).

**FLAG:** Tolerance half-life (5 days) and reset time (1.5 weeks) in the seed data are community-derived values consistent with MXE class behavior. These are not confirmed for MXiPr in published literature. These values should be treated as structural analog inferences.

### Dependence

**Physical dependence:** No published data for MXiPr. Class-based (ketamine/MXE): moderate physical dependence possible with heavy use.

**Psychological dependence:** The warm afterglow and euphoria described in user reports [Ref 22], combined with the antidepressant-like properties of the NMDA antagonist class, suggest psychological dependence potential. The seed data rates psychological dependence as moderate. This is consistent with MXE class experience.

**Withdrawal:** Not characterized for MXiPr. Ketamine/MXE withdrawal involves anxiety, dysphoria, craving, and insomnia.

---

## Interactions

**No published drug interaction data for MXiPr.**

All interaction data is class-based inference (FLAG: structural analog inference only).

### CNS Depressants
Additive CNS depression with benzodiazepines, opioids, alcohol, GHB, and barbiturates. The fatal case of N-ethyldeschloroketamine (Theofel et al. 2019 [Ref 6]) involved co-presence of multiple opioids (morphine, oxycodone, metamizole) and other compounds, illustrating the danger of polydrug use in this class.

### Serotonergic Agents
MXE has demonstrated SERT affinity (Roth et al. 2013 [Ref 3]). If MXiPr shares this property (unconfirmed), combinations with MAOIs, SSRIs, or other serotonergic agents could increase serotonin syndrome risk. The Theofel 2019 fatal case involved venlafaxine (SNRI) [Ref 6], making this interaction category clinically relevant to flag.

### Stimulants
Combination with stimulants may mask sedation, increasing risk of dissociative overdose. Cardiovascular strain from the additive sympathomimetic effects of NMDA antagonists and stimulants is a concern.

### Other Dissociatives
Cross-tolerance with other NMDA antagonists; combined use would increase dissociative intensity unpredictably.

---

## Legal Status

| Jurisdiction | Status | Details | Source |
|---|---|---|---|
| Slovenia | First detection | National Forensic Lab, December 2020 | [Ref 17] |
| Hungary | Prohibited | Production, sale, possession banned; April 2021 | [Ref 17] |
| United Kingdom | Class B | Misuse of Drugs Act 1971 | [Ref 17] |
| Germany | NpSG | Neue-psychoaktive-Stoffe-Gesetz (industrial/scientific use only) | [Ref 17] |
| Canada | Schedule I | Controlled Drugs and Substances Act | [Ref 17] |
| United States | Not federally scheduled | Federal Analogue Act may apply if intended for human consumption; California listed as Schedule I | Web searches |
| Japan | Controlled | Identified in illegal product seizures; regulated under NPS law | [Ref 12] |
| Australia | Unclear | Not confirmed by search; likely covered by analogue provisions of State/Territory drug acts | Not confirmed |

**FLAG:** The US federal status is ambiguous. The Federal Analogue Act (21 U.S.C. § 813) covers substances substantially similar to Schedule I or II controlled substances. Ketamine is Schedule III, which technically places it outside the Analogue Act trigger for analogs. However, MXiPr's structure is also similar to PCP (Schedule II) and structural relationships to Schedule I compounds may vary by prosecutorial interpretation. This requires legal specialist review. The California Schedule I designation may reflect state-level analogue scheduling, not a specific listing of MXiPr.

**FLAG:** The Australian status is unconfirmed by this research. Australia's Poisons Standard (SUSMP) does not appear to have explicitly listed MXiPr based on searches, but State and Territory drug laws may cover it under analogue provisions. The TGA would need to be consulted for confirmation.

---

## Clinical Trials

No clinical trials involving MXiPr are registered on ClinicalTrials.gov. No studies involving MXiPr in therapeutic contexts were identified in any database. This is expected given MXiPr's status as an emerging recreational research chemical with no pharmaceutical development history.

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## Community Feedback Analysis

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

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## Gaps & Flags

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

1. **FLAG [SAFETY-CRITICAL]:** All dose range values (threshold, light, common, strong, heavy) in the seed data are community-derived. No published controlled study has established human dosing parameters for MXiPr. These values are consistent with anecdotal reports and structural analog inference from MXE/DCK derivatives, but have not been verified.

2. **FLAG [SAFETY-CRITICAL]:** The "Heavy: 60+ mg" threshold and the seizure risk at high doses are based solely on user reports [Ref 22]. No published LD50 or toxic dose threshold exists.

3. **FLAG [SAFETY-CRITICAL]:** Duration values — especially the "aftereffects: 4–48 hours (oral)" range — are very wide and unconfirmed. This should be flagged in the article.

4. **FLAG [SAFETY-CRITICAL]:** No human overdose case reports specific to MXiPr have been published. The toxicity risks stated in the article must be explicitly attributed to class inference, not MXiPr-specific data.

### Contradictions Between Seed Data and Published Sources

5. **FLAG:** The seed data does not list a SMILES, molecular formula, molecular weight, InChIKey, or PubChem CID. These are now confirmed: SMILES = CC(C)NC1(CCCCC1=O)c1cccc(OC)c1; Formula = C₁₆H₂₃NO₂; MW = 261.365; InChIKey = FTQIVDGNGXPEKP-UHFFFAOYSA-N; CID = 163192824.

6. **FLAG:** The seed data lists "Sigma-1 receptor agonist" as a pharmacological class. This is a plausible class inference but has not been confirmed by published binding studies for MXiPr specifically. The generation agent should note this is class-inferred, not substance-confirmed.

7. **FLAG:** CAS number is uncertain. Some commercial sources list 72242-03-6; MedKoo lists CAS as "unknown." This discrepancy should be verified against a primary registry before publication.

### Areas Relying on Structural Analogy Rather Than Substance-Specific Data

8. **FLAG [ANALOG INFERENCE]:** Sigma-1 receptor agonism — inferred from MXE (Roth et al. 2013 [Ref 3]).
9. **FLAG [ANALOG INFERENCE]:** Serotonin transporter activity — unknown for MXiPr; inferred from MXE.
10. **FLAG [ANALOG INFERENCE]:** CYP enzyme involvement (CYP2B6, CYP3A4) — inferred from ketamine metabolism.
11. **FLAG [ANALOG INFERENCE]:** Uroepithelial/bladder toxicity — class concern from MXE studies; not documented for MXiPr.
12. **FLAG [ANALOG INFERENCE]:** Tolerance half-life (5 days) and reset (1.5 weeks) — community consensus from MXE class; not measured for MXiPr.
13. **FLAG [ANALOG INFERENCE]:** Cross-tolerance with other dissociatives — class inference; not specifically tested.
14. **FLAG [ANALOG INFERENCE]:** All drug interaction data — no published MXiPr-specific interaction studies exist.

### Unresolved Research Gaps

15. **SMILES verification:** The SMILES CC(C)NC1(CCCCC1=O)c1cccc(OC)c1 was retrieved via HandWiki (web_retrieved), which cites PubChem. This should be confirmed against the PubChem compound page directly.

16. **Enantiomer pharmacology:** Seibert et al. 2025 developed enantioseparation methods for MXiPr but published no comparative potency or safety data for R- vs. S-MXiPr. The pharmacologically active stereoisomer is unknown.

17. **US legal status:** Requires legal specialist review. The Federal Analogue Act applicability is ambiguous given ketamine's Schedule III status.

18. **Australia legal status:** Could not be confirmed. Requires consultation with TGA or state drug control authorities.

19. **Mezaache et al. 2026 [Ref 13]:** This paper (published 2026) covers emerging ketamine analogues in France and may contain specific MXiPr data (detected cases, health outcomes). The abstract was insufficient to confirm whether MXiPr is specifically discussed. Full-text review is recommended before generation.

20. **Seibert et al. 2025 [Ref 2]:** The full enantioseparation paper may contain detailed analytical characterization data (NMR, MS) useful for the chemistry section. Full-text access was not available during this research.

21. **Tanaka et al. 2022 [Ref 12]:** Published in Japanese (Yakugaku Zasshi). Full analytical characterization data (NMR, MS spectra, structural confirmation) may be in the paper body but was not accessible from the English abstract. A Japanese-language review or translation of the analytical section would benefit the chemistry section.

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## Source Quality Summary

| Source Type | Count | Notes |
|---|---|---|
| Primary research (peer-reviewed) | 6 | Refs 1, 2, 11, 12, 13, 15 |
| Review articles | 6 | Refs 4, 7, 8, 16, 19, 20 |
| Case reports | 3 | Refs 5, 6, 9 |
| Web-retrieved (institutional) | 2 | Refs 17, 18 |
| Web-retrieved (harm reduction/community) | 3 | Refs 14, 21, 22 |

**Only Refs 11 and 12 (Irie 2022 and Tanaka 2022) provide substance-specific primary data on MXiPr.** All other data is either class/analog-based or community-report-based. The generation agent should apply conservative confidence framing throughout the article, particularly in pharmacology, dosing, and safety sections.