Methylnaphthidate

Sources

2 strong · 12 moderate · 3 weak

Studies and references cited across this article, graded by evidence strength.

Values approved

121/121 (100%)

Data points an editor reviewed and accepted for publication.

Value Provenance

Dosing

oraltrace

Field	Published	AI Proposed	Confidence
Threshold	4 mg	4 mg	low
Low	10–15 mg	10–15 mg	low
Common	15–30 mg	15–30 mg	low
Strong	30–50 mg	30–50 mg	low
Heavy	50+ mg	50+ mg	low
Editorial	All oral dose values carried forward from existing DB community consensus. No published dose-finding studies exist for methylnaphthidate. One self-report at 34.8 mg oral described effects as 'mild stimulant' — consistent with common-to-strong range. Dose values are safety-critical and unverified by controlled study.
	ReasoningReasoning All oral dose values carried forward from existing DB community consensus. No published dose-finding studies exist for methylnaphthidate. One self-report at 34.8 mg oral described effects as 'mild stimulant' — consistent with common-to-strong range. Dose values are safety-critical and unverified by controlled study. Evidence basis: community_consensus_large

insufflatedtrace

Field	Published	AI Proposed	Confidence
Threshold	—	—	low
Low	4–8 mg	4–8 mg	low
Common	8–14 mg	8–14 mg	low
Strong	14–28 mg	14–28 mg	low
Heavy	28+ mg	28+ mg	low
Editorial	Insufflated dose values carried forward from existing DB community consensus. No threshold value available in seed data or community reports — omitted rather than fabricated. Insufflated doses approximately half of oral, consistent with expected higher intranasal bioavailability. All values unverified by controlled study.
	ReasoningReasoning Insufflated dose values carried forward from existing DB community consensus. No threshold value available in seed data or community reports — omitted rather than fabricated. Insufflated doses approximately half of oral, consistent with expected higher intranasal bioavailability. All values unverified by controlled study. Evidence basis: community_consensus_large

Duration

oral

Field	Published	AI Proposed	Confidence
Onsettrace	1–10 minutes	1–10 minutes	low
Editorial	Oral onset from existing DB community consensus (1–10 minutes). No published human PK data.
	ReasoningReasoning Oral onset from existing DB community consensus (1–10 minutes). No published human PK data. Evidence basis: community_consensus_large
Peaktrace	1.5–2 hours	1.5–2 hours	low
Editorial	Oral peak from existing DB community consensus (1.5–2 hours). No published human PK data.
	ReasoningReasoning Oral peak from existing DB community consensus (1.5–2 hours). No published human PK data. Evidence basis: community_consensus_large
Offsettrace	1.5–2 hours	1.5–2 hours	low
Editorial	Oral offset from existing DB community consensus (1.5–2 hours). No published human PK data.
	ReasoningReasoning Oral offset from existing DB community consensus (1.5–2 hours). No published human PK data. Evidence basis: community_consensus_large
Totaltrace	2–5 hours	2–5 hours	low
Editorial	Oral total from existing DB community consensus (2–5 hours). One anecdotal report described 5–7 hours at 34.8 mg, suggesting upper bound may be underestimated at higher doses. No published human PK data.
	ReasoningReasoning Oral total from existing DB community consensus (2–5 hours). One anecdotal report described 5–7 hours at 34.8 mg, suggesting upper bound may be underestimated at higher doses. No published human PK data. Evidence basis: community_consensus_large
After effectstrace	1–8 hours	1–8 hours	low
Editorial	Oral aftereffects from existing DB community consensus (1–8 hours). Wide range reflects individual variation and dose-dependence. No published human PK data.
	ReasoningReasoning Oral aftereffects from existing DB community consensus (1–8 hours). Wide range reflects individual variation and dose-dependence. No published human PK data. Evidence basis: community_consensus_large

insufflated

Field	Published	AI Proposed	Confidence
Onsettrace	3–6 minutes	3–6 minutes	low
Editorial	Insufflated onset from existing DB community consensus (3–6 minutes). No published human PK data.
	ReasoningReasoning Insufflated onset from existing DB community consensus (3–6 minutes). No published human PK data. Evidence basis: community_consensus_large
Peaktrace	1–2 hours	1–2 hours	low
Editorial	Insufflated peak from existing DB community consensus (1–2 hours). No published human PK data.
	ReasoningReasoning Insufflated peak from existing DB community consensus (1–2 hours). No published human PK data. Evidence basis: community_consensus_large
Offsettrace	1–2 hours	1–2 hours	low
Editorial	Insufflated offset from existing DB community consensus (1–2 hours). No published human PK data.
	ReasoningReasoning Insufflated offset from existing DB community consensus (1–2 hours). No published human PK data. Evidence basis: community_consensus_large
Totaltrace	90–180 minutes	90–180 minutes	low
Editorial	Insufflated total from existing DB community consensus (90–180 minutes). Approximately half of oral duration, consistent with faster absorption and elimination. No published human PK data.
	ReasoningReasoning Insufflated total from existing DB community consensus (90–180 minutes). Approximately half of oral duration, consistent with faster absorption and elimination. No published human PK data. Evidence basis: community_consensus_large
After effectstrace	1–2 hours	1–2 hours	low
Editorial	Insufflated aftereffects from existing DB community consensus (1–2 hours). No published human PK data.
	ReasoningReasoning Insufflated aftereffects from existing DB community consensus (1–2 hours). No published human PK data. Evidence basis: community_consensus_large

Safety

Toxicity Profiletrace

Field	Published	AI Proposed	Confidence
Acute	moderate	moderate	low
Chronic	moderate	moderate	low
Organs Affected	cardiovascular, central nervous system, thermoregulatory	cardiovascular, central nervous system, thermoregulatory	low
Editorial	Acute and chronic toxicity rated moderate per work-notes, inferred entirely from DAT/NET/SERT reuptake inhibitor pharmacological class and methylphenidate structural analogy. Cardiovascular risk (hypertension, tachycardia, arrhythmia, vasoconstriction), CNS excitotoxicity (seizure risk), and thermoregulatory disruption (hyperthermia) are the primary inferred organ systems. Absence of case reports likely reflects low prevalence, not low risk. Evidence discount applied: class-inferred data warrants low confidence.
	ReasoningReasoning Acute and chronic toxicity rated moderate per work-notes, inferred entirely from DAT/NET/SERT reuptake inhibitor pharmacological class and methylphenidate structural analogy. Cardiovascular risk (hypertension, tachycardia, arrhythmia, vasoconstriction), CNS excitotoxicity (seizure risk), and thermoregulatory disruption (hyperthermia) are the primary inferred organ systems. Absence of case reports likely reflects low prevalence, not low risk. Evidence discount applied: class-inferred data warrants low confidence. Evidence basis: structural_analogy

Dependence Profiletrace

Field	Published	AI Proposed	Confidence
Physical	negligible	negligible	medium
Psychological	high	high	medium
Compulsive Redosing	high	high	medium
Dose Escalation	moderate	moderate	medium
Editorial	Psychological dependence rated high based on Lile et al. 2003 NHP reinforcing efficacy data showing HDMP-28 = cocaine = methylphenidate on progressive-ratio schedules. Physical dependence negligible per phenidate class analogy. Compulsive redosing high per NHP reinforcement data. Dose escalation moderate per methylphenidate tolerance patterns. Human dependence data absent — confidence medium rather than high because NHP data is strong but no human confirmation exists.
	ReasoningReasoning Psychological dependence rated high based on Lile et al. 2003 NHP reinforcing efficacy data showing HDMP-28 = cocaine = methylphenidate on progressive-ratio schedules. Physical dependence negligible per phenidate class analogy. Compulsive redosing high per NHP reinforcement data. Dose escalation moderate per methylphenidate tolerance patterns. Human dependence data absent — confidence medium rather than high because NHP data is strong but no human confirmation exists. Evidence basis: animal_study

Withdrawal Profiletrace

Field	Published	AI Proposed	Confidence
Severity	mild	mild	low
Symptoms	dysphoria, hypersomnia, increased appetite, psychomotor retardation, cognitive slowing	dysphoria, hypersomnia, increased appetite, psychomotor retardation, cognitive slowing	low
Fatal	No	No	low
Medical Supervision	Not required	Not required	low
Editorial	Withdrawal inferred from stimulant class analogy with methylphenidate. No methylnaphthidate-specific withdrawal data exists. Stimulant withdrawal (dysphoria, hypersomnia, increased appetite, psychomotor retardation) is well-characterized for the DAT inhibitor class but not life-threatening.
	ReasoningReasoning Withdrawal inferred from stimulant class analogy with methylphenidate. No methylnaphthidate-specific withdrawal data exists. Stimulant withdrawal (dysphoria, hypersomnia, increased appetite, psychomotor retardation) is well-characterized for the DAT inhibitor class but not life-threatening. Evidence basis: animal_study

Tolerance Profiletrace

Field	Published	AI Proposed	Confidence
Buildup	moderate	moderate	low
Half-life	5 days	5 days	low
Full Reset	10 days	10 days	low
Cross-tolerances	methylphenidate, ethylphenidate, isopropylphenidate, cocaine	methylphenidate, ethylphenidate, isopropylphenidate, cocaine	low
Editorial	Tolerance buildup rated moderate per work-notes, inferred from methylphenidate class analogy. Half-life of ~5 days and full reset of ~10 days estimated from methylphenidate tolerance patterns ('days to weeks for partial tolerance, 1–2 weeks full reset' from work-notes). Cross-tolerances with other DAT inhibitors expected via shared mechanism.
	ReasoningReasoning Tolerance buildup rated moderate per work-notes, inferred from methylphenidate class analogy. Half-life of ~5 days and full reset of ~10 days estimated from methylphenidate tolerance patterns ('days to weeks for partial tolerance, 1–2 weeks full reset' from work-notes). Cross-tolerances with other DAT inhibitors expected via shared mechanism. Evidence basis: structural_analogy

Effects & Profile

Contraindications

Field	Published	AI Proposed	Confidence
other MAOI usetrace	absolute	absolute	low
Editorial	Class-level absolute contraindication for all monoamine reuptake inhibitors. No methylnaphthidate-specific case data exists; inferred from DAT/NET/SERT inhibitor pharmacology and methylphenidate structural analogy.
	ReasoningReasoning Class-level absolute contraindication for all monoamine reuptake inhibitors. No methylnaphthidate-specific case data exists; inferred from DAT/NET/SERT inhibitor pharmacology and methylphenidate structural analogy.
cardiovascular Pre-existing cardiovascular diseasetrace	absolute	absolute	low
Editorial	Class-level absolute contraindication for sympathomimetic stimulants. All cardiovascular risk is inferred from DAT/NET reuptake inhibitor class and methylphenidate analogy; no substance-specific data.
	ReasoningReasoning Class-level absolute contraindication for sympathomimetic stimulants. All cardiovascular risk is inferred from DAT/NET reuptake inhibitor class and methylphenidate analogy; no substance-specific data.
psychiatric History of psychosis or bipolar disordertrace	relative	relative	low
Editorial	Class-inferred relative contraindication from DAT inhibitor pharmacology. No methylnaphthidate-specific psychiatric adverse event data exists.
	ReasoningReasoning Class-inferred relative contraindication from DAT inhibitor pharmacology. No methylnaphthidate-specific psychiatric adverse event data exists.
other Concurrent serotonergic medication (SSRIs, SNRIs, triptans)trace	relative	relative	low
Editorial	Class-inferred from SERT inhibitor pharmacology. The SERT component distinguishes this contraindication from methylphenidate (which has negligible SERT activity). No substance-specific serotonin toxicity cases reported.
	ReasoningReasoning Class-inferred from SERT inhibitor pharmacology. The SERT component distinguishes this contraindication from methylphenidate (which has negligible SERT activity). No substance-specific serotonin toxicity cases reported.
neurological Seizure disorderstrace	relative	relative	low
Editorial	Class-level relative contraindication for stimulant-class compounds. No methylnaphthidate-specific seizure data; inferred from methylphenidate and DAT/NET inhibitor class.
	ReasoningReasoning Class-level relative contraindication for stimulant-class compounds. No methylnaphthidate-specific seizure data; inferred from methylphenidate and DAT/NET inhibitor class.

Timeline Phases

oral

Field	Published	AI Proposed	Confidence
Onsettrace	300–600 sec(i=0.05)	300–600 sec(i=0.05)	low
Editorial	Oral timeline derived from existing DB community consensus: onset 1–10 min, peak 1.5–2 h, offset 1.5–2 h, total 2–5 h, aftereffects 1–8 h. One anecdotal report suggested 5–7 h at 34.8 mg. No published human PK data. Come_up phase interpolated from onset-to-peak gap. All values class-inferred from methylphenidate analogy and community reports.
	ReasoningReasoning Oral timeline derived from existing DB community consensus: onset 1–10 min, peak 1.5–2 h, offset 1.5–2 h, total 2–5 h, aftereffects 1–8 h. One anecdotal report suggested 5–7 h at 34.8 mg. No published human PK data. Come_up phase interpolated from onset-to-peak gap. All values class-inferred from methylphenidate analogy and community reports. Evidence basis: community_consensus_large
Come uptrace	600–1800 sec(i=0.30)	600–1800 sec(i=0.30)	low
Editorial	Oral timeline derived from existing DB community consensus: onset 1–10 min, peak 1.5–2 h, offset 1.5–2 h, total 2–5 h, aftereffects 1–8 h. One anecdotal report suggested 5–7 h at 34.8 mg. No published human PK data. Come_up phase interpolated from onset-to-peak gap. All values class-inferred from methylphenidate analogy and community reports.
	ReasoningReasoning Oral timeline derived from existing DB community consensus: onset 1–10 min, peak 1.5–2 h, offset 1.5–2 h, total 2–5 h, aftereffects 1–8 h. One anecdotal report suggested 5–7 h at 34.8 mg. No published human PK data. Come_up phase interpolated from onset-to-peak gap. All values class-inferred from methylphenidate analogy and community reports. Evidence basis: community_consensus_large
Peaktrace	5400–7200 sec(i=1.00)	5400–7200 sec(i=1.00)	low
Editorial	Oral timeline derived from existing DB community consensus: onset 1–10 min, peak 1.5–2 h, offset 1.5–2 h, total 2–5 h, aftereffects 1–8 h. One anecdotal report suggested 5–7 h at 34.8 mg. No published human PK data. Come_up phase interpolated from onset-to-peak gap. All values class-inferred from methylphenidate analogy and community reports.
	ReasoningReasoning Oral timeline derived from existing DB community consensus: onset 1–10 min, peak 1.5–2 h, offset 1.5–2 h, total 2–5 h, aftereffects 1–8 h. One anecdotal report suggested 5–7 h at 34.8 mg. No published human PK data. Come_up phase interpolated from onset-to-peak gap. All values class-inferred from methylphenidate analogy and community reports. Evidence basis: community_consensus_large
Resolutiontrace	5400–7200 sec(i=0.40)	5400–7200 sec(i=0.40)	low
Editorial	Oral timeline derived from existing DB community consensus: onset 1–10 min, peak 1.5–2 h, offset 1.5–2 h, total 2–5 h, aftereffects 1–8 h. One anecdotal report suggested 5–7 h at 34.8 mg. No published human PK data. Come_up phase interpolated from onset-to-peak gap. All values class-inferred from methylphenidate analogy and community reports.
	ReasoningReasoning Oral timeline derived from existing DB community consensus: onset 1–10 min, peak 1.5–2 h, offset 1.5–2 h, total 2–5 h, aftereffects 1–8 h. One anecdotal report suggested 5–7 h at 34.8 mg. No published human PK data. Come_up phase interpolated from onset-to-peak gap. All values class-inferred from methylphenidate analogy and community reports. Evidence basis: community_consensus_large
Afterglowtrace	3600–28800 sec(i=0.15)	3600–28800 sec(i=0.15)	low
Editorial	Oral timeline derived from existing DB community consensus: onset 1–10 min, peak 1.5–2 h, offset 1.5–2 h, total 2–5 h, aftereffects 1–8 h. One anecdotal report suggested 5–7 h at 34.8 mg. No published human PK data. Come_up phase interpolated from onset-to-peak gap. All values class-inferred from methylphenidate analogy and community reports.
	ReasoningReasoning Oral timeline derived from existing DB community consensus: onset 1–10 min, peak 1.5–2 h, offset 1.5–2 h, total 2–5 h, aftereffects 1–8 h. One anecdotal report suggested 5–7 h at 34.8 mg. No published human PK data. Come_up phase interpolated from onset-to-peak gap. All values class-inferred from methylphenidate analogy and community reports. Evidence basis: community_consensus_large

insufflated

Field	Published	AI Proposed	Confidence
Onsettrace	300–300 sec(i=0.10)	300–300 sec(i=0.10)	low
Editorial	Insufflated timeline derived from existing DB community consensus: onset 3–6 min, peak 1–2 h, offset 1–2 h, total 90–180 min, aftereffects 1–2 h. Work-notes specify 4 phases for insufflated (onset/peak/offset/afterglow). Compressed temporal course compared to oral. No published human PK data. All values community-reported and class-inferred.
	ReasoningReasoning Insufflated timeline derived from existing DB community consensus: onset 3–6 min, peak 1–2 h, offset 1–2 h, total 90–180 min, aftereffects 1–2 h. Work-notes specify 4 phases for insufflated (onset/peak/offset/afterglow). Compressed temporal course compared to oral. No published human PK data. All values community-reported and class-inferred. Evidence basis: community_consensus_large
Peaktrace	1800–3600 sec(i=1.00)	1800–3600 sec(i=1.00)	low
Editorial	Insufflated timeline derived from existing DB community consensus: onset 3–6 min, peak 1–2 h, offset 1–2 h, total 90–180 min, aftereffects 1–2 h. Work-notes specify 4 phases for insufflated (onset/peak/offset/afterglow). Compressed temporal course compared to oral. No published human PK data. All values community-reported and class-inferred.
	ReasoningReasoning Insufflated timeline derived from existing DB community consensus: onset 3–6 min, peak 1–2 h, offset 1–2 h, total 90–180 min, aftereffects 1–2 h. Work-notes specify 4 phases for insufflated (onset/peak/offset/afterglow). Compressed temporal course compared to oral. No published human PK data. All values community-reported and class-inferred. Evidence basis: community_consensus_large
Resolutiontrace	3600–5400 sec(i=0.40)	3600–5400 sec(i=0.40)	low
Editorial	Insufflated timeline derived from existing DB community consensus: onset 3–6 min, peak 1–2 h, offset 1–2 h, total 90–180 min, aftereffects 1–2 h. Work-notes specify 4 phases for insufflated (onset/peak/offset/afterglow). Compressed temporal course compared to oral. No published human PK data. All values community-reported and class-inferred.
	ReasoningReasoning Insufflated timeline derived from existing DB community consensus: onset 3–6 min, peak 1–2 h, offset 1–2 h, total 90–180 min, aftereffects 1–2 h. Work-notes specify 4 phases for insufflated (onset/peak/offset/afterglow). Compressed temporal course compared to oral. No published human PK data. All values community-reported and class-inferred. Evidence basis: community_consensus_large
Afterglowtrace	3600–5400 sec(i=0.10)	3600–5400 sec(i=0.10)	low
Editorial	Insufflated timeline derived from existing DB community consensus: onset 3–6 min, peak 1–2 h, offset 1–2 h, total 90–180 min, aftereffects 1–2 h. Work-notes specify 4 phases for insufflated (onset/peak/offset/afterglow). Compressed temporal course compared to oral. No published human PK data. All values community-reported and class-inferred.
	ReasoningReasoning Insufflated timeline derived from existing DB community consensus: onset 3–6 min, peak 1–2 h, offset 1–2 h, total 90–180 min, aftereffects 1–2 h. Work-notes specify 4 phases for insufflated (onset/peak/offset/afterglow). Compressed temporal course compared to oral. No published human PK data. All values community-reported and class-inferred. Evidence basis: community_consensus_large

Dose Tier Summaries

thresholdtrace

low

Barely perceptible stimulation emerges at approximately 4 mg oral. A subtle increase in alertness and wakefulness may be noticed, but effects can be indistinguishable from placebo for many individuals. No significant mood alteration or focus enhancement is expected. Physical effects are minimal — slight elevation in heart rate may occur but is typically imperceptible. Appetite may be marginally reduced. No meaningful functional impairment or sleep disruption is expected at this level. This dose serves primarily as a sensitivity test. Individual response varies; some users may notice nothing at all.

Editorial

Threshold of 4 mg oral from existing DB community consensus. No published dose-finding studies exist for methylnaphthidate; all values are community-reported. Expanded from work-notes threshold outline.

Reasoning

Evidence basis: community_consensus_large

lighttrace

low

Mild stimulation with recognizable phenidate-class character. Focus enhancement and thought acceleration become noticeable, accompanied by modest appetite suppression and increased wakefulness. Mood may shift slightly positive, though distinct euphoria is unlikely at this level. Oral doses range 10–15 mg; insufflated 4–8 mg. Physical effects include mild cardiovascular activation — slightly elevated heart rate and subtle vasoconstriction. Dry mouth and mild dehydration sensation may appear. Insufflated administration produces faster onset (3–6 minutes vs. up to 10 minutes oral) with a compressed duration. Sleep may be mildly disrupted if taken in the evening. Functional impairment is minimal; most users remain fully operational.

Editorial

Light dose ranges from existing DB (oral 10–15 mg, insufflated 4–8 mg). Effects inferred from phenidate class and methylphenidate analogy. No controlled human data. Work-notes outline expanded with substance-specific texture.

Reasoning

Evidence basis: community_consensus_large

commontrace

low

Clear stimulant effects dominate — sustained focus enhancement, motivation enhancement, and thought acceleration are pronounced. Appetite suppression becomes significant. The SERT component may contribute mild mood elevation with possible entactogen-adjacent warmth not typical of purely catecholaminergic phenidates. Time alteration — typically perceived acceleration — may be noticed. Oral doses range 15–30 mg; insufflated 8–14 mg. Cardiovascular effects become noticeable: elevated heart rate, mild abnormal heartbeat awareness, and vasoconstriction. Bruxism, dry mouth, and dehydration sensation emerge. Pupil dilation is likely. Excessive sweating may occur with physical activity. Insomnia is expected if dosed within 6–8 hours of intended sleep. The offset phase brings cognitive fatigue, mild irritability, and reduced motivation as dopaminergic rebound begins.

Editorial

Common dose ranges from existing DB (oral 15–30 mg, insufflated 8–14 mg). Effects profile assembled from work-notes effects list at common dose intensity values. SERT-mediated mood qualities noted per research output DAT/SERT ratio ~4.8.

Reasoning

Evidence basis: community_consensus_large

strongtrace

low

Pronounced stimulation with significant euphoria and marked cognitive drive. Focus enhancement may paradoxically shift toward cognitive impairment at the upper end of this range as overstimulation disrupts organized thought. Compulsive redosing urge intensifies — non-human primate data shows reinforcing efficacy equal to cocaine. Restlessness and anxiety become more likely. Oral doses range 30–50 mg; insufflated 14–28 mg. Cardiovascular effects are prominent: tachycardia, hypertension, and noticeable vasoconstriction. Bruxism intensifies. Appetite suppression is near-complete. Excessive sweating, trembling, and temperature dysregulation may occur. Pupil dilation is marked. Insomnia is virtually certain for 6+ hours post-dose. The post-acute phase brings depression, irritability, cognitive fatigue, and motivation suppression as monoamine stores are depleted.

Editorial

Strong dose ranges from existing DB (oral 30–50 mg, insufflated 14–28 mg). Compulsive redosing risk supported by Lile et al. 2003 NHP reinforcing efficacy data (HDMP-28 = cocaine = methylphenidate). Effects escalation pattern inferred from stimulant class.

Reasoning

Evidence basis: community_consensus_large

heavytrace

low

Intense, potentially overwhelming stimulation with high risk of adverse effects. Anxiety and paranoia may dominate the experience. Psychotic symptoms — paranoid ideation, peripheral misidentification — become possible with sustained dosing at this level. Cognitive impairment replaces enhancement. Compulsive redosing urge is severe. Oral doses exceed 50 mg; insufflated exceeds 28 mg. Cardiovascular strain is significant: pronounced tachycardia, hypertension, vasoconstriction, and risk of arrhythmia. Hyperthermia risk increases, especially with physical exertion. Bruxism may cause jaw pain. Sleep is impossible for an extended period — wakefulness persists well beyond the subjective stimulant effects. The post-acute rebound is severe: depression, anhedonia, physical fatigue, and cognitive slowing may persist for 12–24+ hours. This dose range carries meaningful acute medical risk with no established safety margin.

Editorial

Heavy dose ranges from existing DB (oral 50+ mg, insufflated 28+ mg). Adverse effect escalation inferred from DAT/NET/SERT reuptake inhibitor class. No LD50 data in any species; no human adverse event case reports. All safety characterization is class-inferred.

Reasoning

Evidence basis: community_consensus_large

History

current version

published Oct 2, 2026system—

versions

2 total · since previous: +0 / −0 citations

publication ledger

publish Oct 2, 2026 · by agent-psx

backfill Jun 4, 2026

Historical versions do not record which reviewer approved them; editorial accountability is recorded per value in the database and in the publication ledger going forward.

full version history suggest a correction contact@psychedex.org

Sources

2 strong · 12 moderate · 3 weak

[1]
weak
NCATS Inxight Drugs - Methylnaphthidate
NIH NCATS · 2024
linkno claims checked
[2]
weak
Methylnaphthidate (HDMP-28) - HandWiki Chemistry
HandWiki contributors · 2023
linkno claims checked
[3]
moderate
Synthesis and pharmacology of site specific cocaine abuse treatment agents: a new synthetic methodology for methylphenidate analogs based on the Blaise reaction
Deutsch HM, Ye X, Shi Q, Liu Z, Schweri MM · 2001 · European Journal of Medicinal Chemistry
pubmed 11461755no claims checked
[4]
weak
Novel Psychoactive Substances Blog - HDMP-28/Methylnaphthidate
Anonymous blogger (novelpsychs.wordpress.com) · 2015
linkno claims checked
[5]
moderate
The reinforcing efficacy of psychostimulants in rhesus monkeys: the role of pharmacokinetics and pharmacodynamics
Lile JA, Wang Z, Woolverton WL, France JE, Gregg TC, Davies HM, Nader MA · 2003 · Journal of Pharmacology and Experimental Therapeutics
pubmed 12954808no claims checked
[6]
moderate
Comprehensive metabolic investigation of dopamine reuptake inhibitor HDMP-28 in equine liver microsomes and Cunninghamella elegans for doping control
Muhammed Ajeebsanu M, Subhahar MB, Karakka Kal AK, Philip M, Perwad Z, Karatt TK, Graiban FM, Joseph M, Jose SV · 2024 · Drug Testing and Analysis
doi.org/10.1002/dta.3642 pubmed 38225724no claims checked
[7]
moderate
Reports of Adverse Events Associated with Use of Novel Psychoactive Substances, 2017–2020: A Review
Mohr ALA, Logan BK, Fogarty MF, Krotulski AJ, Papsun DM, et al. · 2022 · Journal of Analytical Toxicology
doi.org/10.1093/jat/bkac023 pubmed 35445267no claims checked
[8]
moderate
Synthesis of methylphenidate analogues and their binding affinities at dopamine and serotonin transport sites
Davies HM, Hopper DW, Hansen T, Liu Q, Childers SR · 2004 · Bioorganic & Medicinal Chemistry Letters
pubmed 15026075no claims checked
[9]
moderate
Do 2-(Benzoyl)piperidines Represent a Novel Class of hDAT Reuptake Inhibitors?
Jones CB, Eltit JM, Dukat M · 2023 · ACS chemical neuroscience
doi.org/10.1021/acschemneuro.2c00666 pubmed 36745029no claims checked
[10]
moderate
Pharmacological profile of methylphenidate-based designer drugs
Luethi D, Kaeser PJ, Brandt SD, Krähenbuhl S, Hoener MC, Liechti ME · 2018 · Neuropharmacology
doi.org/10.1016/j.neuropharm.2017.08.020 pubmed 28823611no claims checked
[11]
moderate
Differential influences of ethanol on early exposure to racemic methylphenidate compared with dexmethylphenidate in humans
Patrick KS, Straughn AB, Reeves OT, Bernstein H, Bell GH, Anderson ER, Malcolm RJ · 2013 · Drug Metabolism and Disposition
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[12]
moderate
Ethylphenidate as a selective dopaminergic agonist and methylphenidate-ethanol transesterification biomarker.
Patrick KS, Corbin TR, Murphy CE · 2014 · Journal of Pharmaceutical Sciences
doi.org/10.1002/jps.24202 pubmed 25303048no claims checked
[13]
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Ethanol Interactions With Dexmethylphenidate and dl-Methylphenidate Spheroidal Oral Drug Absorption Systems in Healthy Volunteers.
Zhu HJ, Patrick KS, Straughn AB, et al. · 2017 · Journal of Clinical Psychopharmacology
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Monoamine Transporter and Receptor Interaction Profiles in Vitro Predict Reported Human Doses of Novel Psychoactive Stimulants and Psychedelics
Luethi D, Liechti ME · 2018 · International Journal of Neuropsychopharmacology
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Claim Verification

No claim verification has run for this version.

Coverage & Gaps

effect links

86 links · 86 approved · 0 audited0/86 with evidence basis

interactions

4 approved pairs0/4 graded

Methylnaphthidate

Value Provenance

Dosing

oraltrace →

insufflatedtrace →

Duration

oral

insufflated

Safety

Toxicity Profiletrace →

Dependence Profiletrace →

Withdrawal Profiletrace →

Tolerance Profiletrace →

Effects & Profile

Contraindications

Timeline Phases

oral

insufflated

Dose Tier Summaries

History

Sources

Claim Verification

Coverage & Gaps

oraltrace

insufflatedtrace

Toxicity Profiletrace

Dependence Profiletrace

Withdrawal Profiletrace

Tolerance Profiletrace