Reference

Last reviewed: 29 Apr 2026
Sources cited: 5

Compound class286.11 g/mol (iodide salt)

Selective NNMT (nicotinamide N-methyltransferase) inhibitor — small-molecule peptidomimetic (not a peptide)

5-amino-1-methylquinolinium — a small-molecule quinolinium derivative. Selectively inhibits NNMT to prevent nicotinamide methylation, conserving NAD+ salvage substrate and SAM methyl-donor pools. Not a peptide; included in the encyclopedia because it overlaps heavily with NAD-axis metabolic stacks.

5-Amino-1MQ

Last verified: 2026-04-29

At a glance


Also known as	5-Amino-1-methylquinolinium, 5A1MQ, 5A1MQ iodide
Class	Selective NNMT (nicotinamide N-methyltransferase) inhibitor — small-molecule peptidomimetic
Typical route	Oral capsule
Half-life	Not formally characterised in human PK studies; preclinical work suggests several hours; community uses once-daily dosing as the practical pattern
Molecular weight	286.11 g/mol (iodide salt)
Sequence / structure	Not a peptide. A small-molecule quinolinium derivative — 1-methylquinolinium with an amino group at the 5-position.
UK status	Not approved as a medicine. Sold as a research chemical.
US status	Not FDA-approved. Not DEA-controlled. Sold as a research chemical labelled “not for human consumption.”

What it is

5-Amino-1MQ is the encyclopedia compound that occupies the NAD-axis-adjacent metabolic space through a different mechanism than NMN, NR, or NAD+ itself. Where those compounds raise NAD+ levels by feeding the salvage pathway, 5-Amino-1MQ prevents NAD+ loss by inhibiting NNMT (nicotinamide N-methyltransferase) — the enzyme that consumes nicotinamide (a NAD+ recycling intermediate) and methyl groups from S-adenosyl-methionine (SAM).

The mechanistic case is genuinely interesting: NNMT is upregulated in obesity, type 2 diabetes, and certain cancers. Its activity drains both nicotinamide (which would otherwise recycle back to NAD+) and methyl groups (which would otherwise serve other methylation reactions). Inhibiting NNMT theoretically frees up nicotinamide to recycle to NAD+ and conserves methyl-donor pools — addressing the metabolic dysfunction at a different point in the pathway than NMN supplementation does.

The biohacker community uses 5-Amino-1MQ for fat loss, body recomposition, and metabolic optimisation — primarily framed as a “fat loss peptide” despite not being a peptide. The pharmacology supports the framing: preclinical work in obese mice shows dose-dependent reductions in body weight, fat mass, and adipocyte size, with improved insulin sensitivity and glucose tolerance.

The clinical reality is that no human trials of 5-Amino-1MQ exist. All human use is extrapolation from rodent work and community experience. This is the central editorial weight on this profile — the mechanism is plausible, the preclinical data is favourable, and the human evidence base is essentially empty.

It is not a peptide and does not activate the GH/IGF-1 axis. It does not produce the cardiovascular, growth-promoting, or hormonal effects of the GH cluster.

Mechanism

5-Amino-1MQ is a selective small-molecule inhibitor of NNMT, the enzyme that catalyses methylation of nicotinamide (NAM) to 1-methylnicotinamide (1-MNA) using S-adenosyl-methionine (SAM) as the methyl donor.1 5

The downstream cascade after NNMT inhibition:

Reduced 1-methylnicotinamide (1-MNA) production — 1-MNA is the metabolic by-product that signals NNMT activity is high
Increased intracellular NAD+ — nicotinamide that would have been methylated and excreted instead recycles back to NAD+ via the salvage pathway
Conserved SAM and methyl-donor pools — methyl groups that would have been consumed in nicotinamide methylation remain available for other methylation reactions
Suppressed lipogenesis in adipocytes — directly demonstrated in vitro
Increased energy expenditure — preclinical data in obese mice
Improved insulin sensitivity and glucose tolerance — preclinical data

The compound is selective for NNMT and does not inhibit related SAM-dependent methyltransferases or enzymes in the NAD+ salvage pathway. This selectivity is mechanistically important — it means the compound’s effects come through the NNMT-specific pathway rather than broadly disrupting methylation biology.

The mechanism complements NAD+ precursor supplementation rather than competing with it. NMN feeds the NAD+ pool; 5-Amino-1MQ prevents nicotinamide loss from the pool. Stacking is mechanistically defensible and is a common community pattern.

Routes of administration

Oral (the standard and only viable route)


Bioavailability	Sufficient for the documented preclinical effects; exact human bioavailability not characterised
Onset	Subjective effects, where present, typically appear over 4–8 weeks
Duration	Once-daily dosing maintains effect at steady state
Typical dose	50–150 mg orally once daily
Equipment	None — capsule, swallow with water
When this route makes sense	Default. The molecule was designed for oral activity.

Morning dosing is the dominant convention. Some users dose with food to improve subjective tolerance; the absorption impact is not formally characterised.

Other routes

Not used. Sublingual, intranasal, and injection routes have no established practice and no preclinical or clinical data.

What the evidence says

Honest summary: 5-Amino-1MQ has clean preclinical evidence in rodents and a plausible mechanism. There are no human clinical trials. All human dosing is extrapolation from rodent work via allometric scaling. The compound is genuinely investigational despite being widely sold.

Preclinical evidence (the entirety of the evidence base)

The Brachs et al. and Neelakantan et al. preclinical studies demonstrate:1 5

Dose-dependent reduction in body weight, white adipose mass, and adipocyte size in diet-induced-obese mice
Improved oral glucose tolerance and insulin sensitivity
Suppressed hyperinsulinaemia
Reduced lipogenesis in adipocytes in vitro
Selectivity for NNMT without inhibition of related methyltransferases or NAD+ salvage enzymes

The mechanism is well-supported preclinically. The translation to human outcomes is the unresolved question.

Human evidence

No human clinical trials of 5-Amino-1MQ have been published. Community use is based on:

Allometric dose scaling from mouse studies (effective mouse doses of ~5 mg/kg translate to ~50–100 mg in adult humans)
Community-reported subjective effects (variable; not systematically studied)
The mechanistic plausibility

This is a narrower evidence base than any of the GH-cluster compounds in this encyclopedia — even the failed-Phase-2 compounds (ipamorelin’s ileus trial, AOD-9604’s obesity trial) at least had controlled human efficacy data. 5-Amino-1MQ has none.

What the evidence does NOT show

No human clinical trials at any stage
No long-term safety data in humans at any duration
No human pharmacokinetic data characterising absorption, half-life, distribution, or metabolism
No comparative data vs metformin, GLP-1 agonists, or any other metabolic intervention
No data on cycling, dose-response, or optimal duration in humans

The compound’s evidence base is the most preclinical-only of any compound in this encyclopedia. Users should treat this as a different category of evidence weight than even AOD-9604 (which at least failed a controlled human trial) or NMN (which has multiple positive human trials).

Typical use patterns

Standard biohacker protocol

50 mg orally once daily for the first 1–2 weeks (assess tolerance)
100 mg orally once daily as the standard maintenance dose
Some users titrate to 150 mg daily for higher dose-response
Cycle 8–12 weeks on, 4–8 weeks off — community precaution given the absence of long-term safety data

Sensitive-start protocol

25–50 mg orally once daily for 2–3 weeks
Hold before considering an increase
Many sensitive users find 50 mg sufficient indefinitely

Stacking

NMN or NR — common pairing; mechanistically complementary (precursor supply + degradation pathway inhibition). The combined effect on NAD+ levels is plausibly larger than either alone, though not directly studied.
GLP-1 agonists — common in the metabolic-optimisation crowd. Both compounds independently reduce body weight and improve insulin sensitivity. Combined effect is plausible but not directly studied; monitor glucose closely.
AOD-9604 — both compounds target fat loss through different mechanisms. Stacking is mechanistically defensible.
Methyl-donor supplements (TMG, B12, folate) — not strictly necessary because NNMT inhibition conserves methyl groups rather than consuming them, but commonly added in NAD-stack formulations.
Caffeine, yohimbine — common in fat-loss stacks. No documented direct interactions.

Why a user would choose 5-Amino-1MQ over NMN

Different mechanism — pathway preservation rather than precursor supply; potentially complementary
Theoretical methyl-group conservation — relevant for users with methylation issues
Fat-loss-focused framing — community use is more weight-loss-oriented than NMN

Why a user would choose NMN over 5-Amino-1MQ

Human evidence base — NMN has multiple controlled human trials; 5-Amino-1MQ has none
Regulatory legitimacy — NMN is a lawful supplement in the US (post-September 2025); 5-Amino-1MQ remains research-chem-only
Long-term safety data (modestly) for NMN; essentially none for 5-Amino-1MQ

For sensitive systems

5-Amino-1MQ is genuinely uncharacterised in sensitive-systems populations because the human evidence base is preclinical. The mechanism (selective NNMT inhibition) is not directly relevant to mast-cell, autoimmune, or autonomic biology in ways that would predict consistent flare patterns.

Start dose for sensitive users. 25–50 mg orally once daily for 2–4 weeks. Hold before considering an increase.

Ramp. If 50 mg is well tolerated, 100 mg is the standard community target. The dose-response data in humans is essentially absent.

Expected adjustment profile (extrapolated from community reports):

Mild GI symptoms — uncommon but reported, typically in the first few days
Mild energy changes — variable; some users report subtle improvements over 2–4 weeks
Headache — uncommon
Subjective fat-loss effects — slow if present, accumulate over 8–12 weeks

What’s not normal and warrants stopping: persistent GI symptoms, unusual fatigue, headache that doesn’t resolve. The absence of human safety data means any unexpected symptom warrants stopping and reassessing rather than waiting it out.

For MCAS / histamine-sensitive users. No specific histamine activity documented. The mechanism is not directly mast-cell-relevant. Most users in this population tolerate the compound; outliers exist.

For POTS users. No documented cardiovascular effects. Generally well-tolerated. Monitor as usual.

For UARS / chronic fatigue / ME/CFS. A subset of users in this population reports modest energy improvements over 4–8 weeks of dosing. The mechanism (NAD+ pathway support, mitochondrial metabolism) is plausible. Worth a 4–8 week trial; expect modest signals if any.

For active or recent cancer history. Worth specific caution. NNMT is upregulated in many cancers, and NNMT inhibitors are being investigated as cancer therapeutics (i.e. the inhibition pattern that would kill cancer cells is the same pattern users want for fat loss). The implications for cancer survivors are uncharacterised — does inhibiting NNMT in healthy cells help or hinder if there are residual cancer cells? No data. Get oncology input before using 5-Amino-1MQ in any cancer survivorship context.

For diabetes (type 1 or type 2). Generally promising preclinically; no human data. Monitor glucose markers as standard.

Interactions worth considering:

NMN, NR, NAD+ IV — mechanistically complementary; common stack.
GLP-1 agonists — combined effects on glucose handling not characterised.
Methylation cofactors (TMG, B12, folate) — supportive; mechanism actually conserves methyl groups, so theoretical synergy is smaller than for NMN.
No documented direct drug interactions but the compound is uncharacterised in human PK studies.

Reasonable expectations

Onset. Subjective effects, where present, typically appear over 4–8 weeks. Body composition changes accumulate over 8–12 weeks if at all.

Response rate. Community-reported response varies widely. Some users report measurable fat loss over an 8–12 week cycle; others report no measurable change. Without controlled trial data, the population-level response rate is genuinely unknown.

What the evidence actually supports.

NNMT inhibition mechanism — preclinically supported
Adipose lipolysis and reduced lipogenesis — preclinically supported
Improved insulin sensitivity and glucose tolerance — preclinically supported in rodent models

What the evidence does not support.

Any specific human outcome — no human clinical trials exist
Lifespan or longevity claims — speculative
Cancer prevention or treatment claims — NNMT inhibitors are being investigated as cancer therapeutics, but 5-Amino-1MQ is not a cancer treatment

What not to expect.

Predictable fat-loss outcomes. The compound has no controlled human trial data.
Effect comparable to GLP-1 agonists. Different mechanism, much smaller evidence base.
A clean safety record. The absence of human safety data is not the same as a clean safety record.

Cost

5-Amino-1MQ is not available through licensed pharmacy channels in any major Western market.

Research-chemical UK market:

30 capsules at 50 mg: ~£25–60
30 capsules at 100 mg: ~£40–90
Bulk powder: ~£40–100 for 5 g

Monthly cost at 100 mg/day: approximately £25–60/month, mid-range for research-chem compounds.

Sensitive-start economics. A user starting at 50 mg/day uses half the standard dose. Capsule formulations are convenient at standard doses; powder is more cost-efficient but requires accurate weighing.

Quality variance

The research-chem 5-Amino-1MQ market has typical variance issues. Lab-tested vendors with mass-spec or HPLC certificates are the meaningful quality marker. The compound is small-molecule and chemically stable, so degradation issues are smaller than for peptides — but underdosing and substituted ingredients remain documented concerns.

Reconstitution

5-Amino-1MQ is a small molecule, not a peptide. It does not require reconstitution.

Capsule form: swallow with water. Morning is the dominant convention.

Bulk powder form: weigh on accurate scale. Do not eyeball doses of 5-Amino-1MQ powder. The therapeutic range (50–150 mg) is narrow enough that significant weighing errors materially change the dose-response profile. Bulk powder is the cheapest per-dose route but has the highest dosing-error risk; capsules are safer for most users.

Storage

Capsules: room temperature, dry, away from heat and light. Manufacturer expiry dates apply.
Bulk powder: sealed, dry, room temperature with desiccant. The compound is reasonably stable but hygroscopic over long-term humidity exposure.

What gets miscalculated

Treating 5-Amino-1MQ as a peptide. It’s a small molecule. No reconstitution, no BAC water, no cold chain.
Eyeballing bulk-powder doses. Without an accurate scale, dose precision is impossible.
Stacking with redundant NAD+ pathway compounds expecting amplification. NMN and 5-Amino-1MQ are mechanistically complementary, but the human-trial data on either is thin enough that the combined claim is even thinner.
Skipping cycling. Community 8–12 weeks on / 4–8 weeks off is a precaution against the absence of long-term safety data, not a measured optimisation.

Areas of concern ⚠

The evidence gap (the largest of any compound in this encyclopedia)

No published human clinical trials. The compound is sold widely and used in community protocols entirely on the basis of preclinical rodent work and allometric dose scaling. This is a fundamentally different evidence position than even the failed-Phase-2 compounds in this encyclopedia.

For a sceptical reader: 5-Amino-1MQ is a small-molecule NNMT inhibitor with a plausible mechanism, clean rodent data, no human PK data, and no controlled human efficacy or safety data. Continued community use is reasonable mechanistically but is not supported by the kind of evidence that GLP-1 agonists, semaglutide, or even tesamorelin have.

Cancer / NNMT-inhibition concern (genuinely unsettled)

NNMT is upregulated in many cancers (renal, colon, lung, glioma, pancreatic, breast, others), and NNMT inhibitors are actively being investigated as anti-cancer therapeutics. The implications for healthy users are unsettled in two directions:

Theoretical concern: NNMT inhibition affects methylation biology broadly, and methylation patterns are central to cancer development. Long-term NNMT inhibition in healthy cells could have effects on epigenetic regulation that aren’t yet characterised.
Theoretical benefit: NNMT inhibition is anti-proliferative in cancer cell models. Some users frame this as a potential cancer-prevention benefit. The evidence does not support this claim in healthy users.

For users with active malignancy or recent cancer treatment: get oncology input. The NNMT-cancer relationship is real and the implications for 5-Amino-1MQ supplementation are not characterised.

Long-term safety entirely uncharacterised

There are no controlled long-term safety studies in humans at any duration. The compound was developed as a research tool for studying NNMT biology, not as a clinical drug candidate; the safety database is preclinical only.

Quality and sourcing

Standard research-chem caveats. Capsules from vendors without lab-test certificates are the highest-variance form; powder from lab-tested vendors with certificates is lower-variance but requires weighing accuracy.

Populations where 5-Amino-1MQ is contraindicated or high-risk

Active or recent cancer history (relative contraindication; oncology input needed)
Pregnancy and breastfeeding — no safety data
Under 18 — not studied; no use case justifies the safety unknowns
Severe renal or hepatic impairment — limited data; caution
Active eating disorder — fat-loss compounds generally inappropriate

Measurement and dosing pitfalls

Eyeballing bulk-powder doses — therapeutic range is 50–150 mg; weighing accuracy matters
Skipping cycling and assuming long-term use is safe — no long-term human data
Treating preclinical efficacy as human efficacy — rodent translation is not reliable; allometric scaling is a starting point, not a guarantee

What the community gets wrong

“Like NMN but works on the other side of the pathway.” Mechanistically true, but the human-evidence comparison is wildly asymmetric — NMN has multiple controlled human trials, 5-Amino-1MQ has none.
“Targeted body recomposition.” The mechanism affects whole-body metabolism; “body recomposition” framing oversells the targeting precision.
“Safe because it’s not a peptide.” Not-being-a-peptide doesn’t speak to safety. The absence of human safety data is the relevant fact.
“NNMT inhibitors are being investigated for cancer, so this prevents cancer.” NNMT inhibition is being tested as cancer therapy; that doesn’t translate to cancer prevention in healthy users.

FDA / regulatory status

Jurisdiction	Status	Last verified
US (FDA)	Not approved. Not DEA-controlled. Sold as a research chemical labelled “not for human consumption.” Not eligible for dietary supplement marketing.	2026-04-29
UK (MHRA)	Not approved as a medicine. Sold as a research chemical.	2026-04-29
EU (EMA)	Not approved.	2026-04-29
WADA (sport)	Not specifically prohibited as of the 2026 list, though athletes should consult their governing body — the metabolic mechanism could trigger broader anti-doping considerations.	2026-04-29

Narrative. 5-Amino-1MQ is the encyclopedia compound with the lightest regulatory footprint — not banned, not approved, not on the radar of major regulators. This is partly because the compound has no clinical-trial program that would have triggered regulatory attention. The legal grey area is similar to ipamorelin / CJC-1295 / Melanotan II at the supply level, but without the active regulatory engagement those compounds have.

What to track in Peptrax

Without published human trials, anyone running 5-Amino-1MQ is conducting their own n=1 experiment. The compound’s preclinical efficacy in rodents was dose-dependent; whether that translates to humans is the open question every user is implicitly answering. Precise dose tracking and product-quality logging are how the user participates in that answer rather than handing it to noise.

For most users, the highest-signal log is weekly weight, weekly waist measurement, body-fat tracking, and daily subjective energy/sleep ratings across an 8–12 week cycle. Without controlled trial data, the user is essentially their own n=1 trial — so precise tracking matters more than for compounds with clear evidence bases.

For sensitive-systems users, the priority log is the first 2–4 weeks: any unexpected symptoms, GI changes, energy fluctuations. The absence of human safety data means any unusual signal warrants stopping and reassessing rather than pushing through.

Across all users, logging the brand and batch matters because the research-chem market has documented quality variance. If you see clear effects on one product and nothing on another, that’s product-source signal, not compound failure. The app’s job is to hold that timeline.

For personal tracking and informational purposes only — not medical advice.