Protection against diet-induced obesity (rodent) [1]
NNMT knockdown and pharmacological inhibition reduce fat mass and protect against diet-induced obesity in mice, with improved glucose tolerance and insulin sensitivity.
PrecisePep/Peptide Library/5-Amino-1MQ
Metabolic & Adipose Regulation
5-Amino-1MQ
5-amino-1-methylquinolinium · NNMT inhibitor
Not a peptide at all — a small-molecule enzyme inhibitor that blocks NNMT in fat cells, raising intracellular NAD⁺ and, in mice, converting stored fat into burned fat. No human has ever been studied on it.
00 Overview
First, a category correction. 5-Amino-1MQ is a quinolinium small molecule, not a peptide. It is stocked alongside peptides and discussed in the same protocols, but it has a different chemistry, a different route (orally active, because it crosses membranes) and a different regulatory character. A site called PrecisePep should say so on the page rather than let the shelf it sits on define what it is.
The mechanism is genuinely interesting. NNMT — nicotinamide N-methyltransferase — consumes nicotinamide and SAM to produce 1-methylnicotinamide. It is highly expressed in white adipose tissue and is upregulated in obesity. Inhibiting it does two things at once: it preserves nicotinamide for NAD⁺ salvage, raising intracellular NAD⁺, and it lifts a brake on sirtuin signalling. The reported net effect in adipocytes is a shift from a storage phenotype toward energy expenditure.[1][2]
The evidence stops at rodents. NNMT knockdown and inhibition protect against diet-induced obesity in mice, with reduced fat mass and improved insulin sensitivity — a reproducible and well-characterised finding.[1] There is no human trial of 5-Amino-1MQ. Not a small one, not a negative one, none.
Zero human data is not the same as new
The NNMT literature dates to the early 2010s. More than a decade later there is still no registered human trial of this inhibitor. Compounds with strong rodent obesity data and commercial interest usually reach humans; when they do not, the reasons are worth asking about rather than assuming the science is simply ahead of the clinic.
// Mechanism of action
NNMT inhibition. NNMT methylates nicotinamide using S-adenosylmethionine as the methyl donor. In adipose tissue this consumes nicotinamide that would otherwise re-enter the NAD⁺ salvage pathway, and it consumes SAM, the cell's universal methyl donor. Inhibiting the enzyme conserves both.
Raised intracellular NAD⁺. More nicotinamide available for salvage means more NAD⁺, which is the substrate sirtuins require. This is a fundamentally different route to raising NAD⁺ than supplying precursors such as NMN or NR — it reduces consumption rather than increasing supply, and it does so tissue-selectively where NNMT is highly expressed.
SIRT1 activation and adipocyte phenotype. Increased sirtuin activity is associated with a shift in adipocytes toward lipolysis and energy expenditure and away from storage, and with improved mitochondrial function in skeletal muscle.
Methyl-group economics. The SAM-sparing effect is the underexplored half of this mechanism. SAM is the methyl donor for DNA methylation, neurotransmitter synthesis and much else. Chronically altering its consumption in a major tissue is not obviously a small intervention, and nobody has looked at it in a human.
01 Reported benefits
Effects that have been reported. A study-tier entry means a result was published — not that the effect is established, reproducible, or transferable from a rodent to a person.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Increased intracellular NAD⁺ and SIRT1 activity [2]
Demonstrated in adipocyte and muscle models — the mechanistic core, and reproducible.
Improved muscle regeneration in aged mice [3]
NNMT inhibition reported to enhance muscle stem cell function and regenerative capacity in aged animals, extending the interest beyond adipose tissue.
NNMT is upregulated in human obesity [4]
Human adipose tissue expression data supports the target being relevant in people, which is what makes the absence of a human trial notable rather than merely incomplete.
No human interventional study exists
No trial has administered 5-Amino-1MQ to humans at any dose for any duration.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Fat loss in humans without appetite suppression
The community use case, and the reason it appears in stacks alongside incretins — a substrate-utilisation mechanism rather than an intake-reduction one. Entirely untested in humans.
Improved muscle preservation during caloric deficit [3]
Extrapolated from the muscle regeneration work, and the reason it is proposed alongside aggressive fat-loss agents.
Healthspan and longevity effects via sirtuin signalling
The general NAD⁺/sirtuin longevity argument, inheriting every unresolved question that field carries.
Concern: NNMT in cancer biology [5]
NNMT overexpression is associated with tumour aggressiveness in several cancers, and NNMT inhibition has been explored as an anti-cancer strategy. That direction is reassuring — but it also means this enzyme sits inside cancer biology, and chronic manipulation in healthy people has not been studied.
Concern: methyl-donor and SAM effects
Sparing SAM in a major tissue alters methyl-group availability. The downstream implications for methylation-dependent processes are unexamined.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
Gradual fat loss over 8–12 weeks without appetite change
The characteristic report, and it is the one most vulnerable to confounding — this compound is almost never run alone.
Improved energy and workout capacity
Reported and consistent with the NAD⁺ mechanism, unmeasured.
Subtle or absent effects
Non-response is reported at least as often as response, which is what would be expected from a compound with no established human dose.
Taken orally, unlike almost everything else in these protocols
Supplied as capsules or as a powder for oral use. The 50 mg vials in peptide catalogues are an odd format for an orally active small molecule.
02 Adverse effects & risks
Adverse effects, contraindications and unknowns. The grey-market tier is where under-reporting is worst: uncontrolled use produces no systematic safety surveillance at all, so absence of a reported harm is not evidence of safety.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
No human safety data of any kind
No toxicology in humans, no pharmacokinetics, no adverse-event surveillance.
Well tolerated in rodent studies [1]
Animal work reports no notable toxicity at effective doses over the study durations used.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Unknown consequences of chronic enzyme inhibition
NNMT is expressed in liver as well as adipose tissue and participates in xenobiotic methylation. Chronic systemic inhibition is not a targeted intervention.
Methyl-group and SAM balance
Altering SAM consumption has theoretical implications for methylation-dependent processes including epigenetic regulation.
Interaction with NAD⁺ precursors
Combining a consumption-reducing mechanism with a supply-increasing one is the obvious stack, and it is also the scenario with the least characterisation.
Oral dosing without pharmacokinetics
Bioavailability, half-life and tissue distribution in humans are unknown, so the relationship between an oral dose and tissue exposure is guesswork.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
Mild nausea or GI upset
Occasionally reported with oral dosing.
Flushing
Occasionally reported, plausibly related to nicotinamide-pathway effects.
Few adverse reports overall
Reflecting short courses and low usage volume as much as any safety property.
03 Dosing ranges
Figures below are documented, not recommended. Study ranges come from published protocols in the stated model; grey-market ranges are what the research community reports using and carry no safety validation of any kind.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Rodent dosing does not convert [1]
Animal studies use milligram-per-kilogram dosing by intraperitoneal or oral route. No validated allometric conversion to a human dose exists, and none of the community figures derive from one.
No human dose has been established
Every figure in circulation originates from vendor suggestion and community practice.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Oral is the route the evidence used
The animal work that motivates all of this dosed orally or intraperitoneally, and 5-Amino-1MQ is a membrane-permeable small molecule with oral activity in those models. Any subcutaneous figure is a departure from the evidence base, not a refinement of it.
The first-pass argument for injecting
The stated grey-market rationale: subcutaneous administration bypasses hepatic first-pass metabolism, so a smaller dose should produce the same or greater systemic exposure. That is standard pharmacological reasoning — and it requires knowing the oral bioavailability to size the reduction, which nobody does, because no human pharmacokinetic study exists for either route.
Injection may work against the tissue target
The counter-argument, and it is rarely raised. NNMT is highly expressed in liver as well as adipose tissue, and an orally absorbed compound reaches the liver first at high concentration. Bypassing that may reduce exposure at a tissue the mechanism depends on, not increase it.
Morning dosing
Convention aligned with the metabolic framing. No pharmacological basis by either route.
Cycled rather than continuous
Given chronic enzyme inhibition with no human characterisation, defined courses limit total exposure.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
50–150 mg daily, oral
The original and still most common community range, taken as capsules in the morning.
5–10 mg daily, subcutaneous
The dominant injectable figure now circulating, roughly a tenth of the oral dose. The reduction is reasoned from first-pass avoidance rather than measured, so the true equivalence could be anywhere.
10–20 mg daily, subcutaneous
A higher injectable tier reported by users who found the lower range subtle. At the top of this range the injected dose approaches a meaningful fraction of the oral one, which suggests the first-pass reasoning is being abandoned in practice.
Vials sized for injection, not capsules
The 50 mg vial format is itself the clearest signal of where the market has moved. At 10 mg subcutaneous daily a 50 mg vial is five days; at 5 mg it is ten.
Reconstituted with bacteriostatic water like a peptide
Community practice treats it as a peptide for handling purposes. It is a small molecule with different solubility behaviour, and suppliers do not consistently state a recommended diluent.
8–12 weeks on, then a break
Standard community course length by either route.
| Approach | Dose | Route | Duration |
|---|---|---|---|
| Oral entry | 50 mg | Oral, morning | 8–12 weeks |
| Oral standard | 100 mg | Oral, morning | 8–12 weeks |
| Oral higher-end | 150 mg | Oral, morning | 8–12 weeks |
| Injectable entry | 5 mg | Subcutaneous, morning | 8–12 weeks |
| Injectable standard | 10 mg | Subcutaneous, morning | 8–12 weeks |
| Injectable higher-end | 20 mg | Subcutaneous, morning | 8–12 weeks |
Two routes, one missing number
Oral doses cluster around 50–150 mg. Injectable doses cluster around 5–20 mg. The tenfold gap is derived entirely from the assumption that subcutaneous administration avoids first-pass metabolism — a reasonable assumption with no number attached to it, because the oral bioavailability of 5-Amino-1MQ in humans has never been measured.
If oral bioavailability is high, the injectable doses are a tenth of what people think they are taking. If it is very low, they may be considerably more. Nobody can tell you which, and the confidence with which both ranges circulate is not supported by anything.
04 Synergy & interactions
Combination effects. Almost no peptide combination has been studied as a combination in humans; stack logic is overwhelmingly mechanistic inference and community practice. Each linked compound has its own page.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
No combination studies exist
No study has combined 5-Amino-1MQ with anything.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
5-Amino-1MQ + NAD⁺ precursors
Reduce NAD⁺ consumption while increasing supply. The most mechanistically coherent pairing available for this compound, and completely unstudied.
With incretin agonists
Appetite suppression plus a substrate-utilisation mechanism — the rationale for its place in the 15-Compound Matrix metabolic pillar.
With MOTS-c
Both raise NAD⁺-dependent signalling by different routes. Also both push in the AMPK/sirtuin direction, which sits awkwardly alongside anabolic goals in the same stack.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
Part of the 15-Compound Matrix metabolic pillar
Grouped with retatrutide and cagrilintide in the metabolic and adipose regulation matrix.
Stacked with NAD⁺ and NMN
Common in longevity-oriented protocols.
05 Protocols
Whole schedules — dosing, titration, cycle length, and off-time — as documented in trials, as proposed from mechanism, and as circulated in the research community. Reproduced for study and comparison only.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
No human protocol exists
No registered trial, no clinical protocol.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Defined courses, oral, with metabolic markers measured
Fasting glucose, HbA1c and lipids before and after would at least generate an interpretable individual result, which is more than most self-experiments produce.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
15-Compound Matrix — Q1 metabolic reset
Introduced in the opening quarter alongside retatrutide and cagrilintide, with continuous NAD⁺ support.
Not part of the Gold Standard Protocol
The thirteen-compound protocol does not include it.
05b Condition-specific interest
Every claim for 5-Amino-1MQ traces to the same body of mouse work, and the compound is sold in a format that does not match the route that work used. Both facts are worth stating before the individual claims.
No approval, no trial
There is no human data on 5-Amino-1MQ for any indication, by any route. Not a small trial, not an open-label series — none. The evidence is NNMT inhibition in cell and rodent models. It is also not a peptide; it is a small molecule.
Theorized — mouse, and the mechanism is interesting
Obesity and metabolic health
Pathophysiology
Nicotinamide N-methyltransferase is upregulated in adipose tissue in obesity, where it consumes nicotinamide and methyl groups and is proposed to slow adipocyte energy expenditure.
Mechanistic rationale
Inhibiting NNMT reduced fat mass and improved metabolic parameters in diet-induced obese mice without changing food intake, which is a genuinely interesting result and a different mechanism from anything else in this library. Mouse adipose tissue metabolism differs substantially from human, and this specific field has no human translation yet.
Community reports
Sold primarily for fat loss. Reports are confounded by everything else people change at the same time.
Components carrying the argument: NNMT inhibition — adipocyte energy expenditure
Theorized — mouse
Muscle and sarcopenia
Pathophysiology
NNMT expression rises in ageing and diseased muscle, and NAD+ availability constrains muscle stem cell function.
Mechanistic rationale
NNMT inhibition improved muscle stem cell function and regeneration in aged mice. The mechanism connects to the NAD+ story — NNMT consumes nicotinamide, so inhibiting it preserves the precursor pool. That makes it conceptually adjacent to the NAD+ field with the same translation gap.
Community reports
Used alongside training, which is doing the work.
Components carrying the argument: NNMT → nicotinamide preservation
Actionable
The route mismatch
Pathophysiology
Not a condition.
Mechanistic rationale
The animal work used oral administration. The grey market sells 50 mg vials for subcutaneous injection. Community subcutaneous doses are set at roughly a fifth to a tenth of oral doses on first-pass reasoning — an inference, not a measurement, and there is no pharmacokinetic data for the injected route in any species. The calculator carries a note on this for exactly that reason.
Community reports
Injection is increasingly the default despite the evidence being oral.
Components carrying the argument: —
| Question | Position |
|---|---|
| Human data? | None, by any route |
| Is it a peptide? | No — a small molecule |
| Evidence route | Oral, in mice |
| Market route | Subcutaneous injection |
| Dose basis | Inference from oral, not measurement |
| Adjacent field | NAD+ — same precursor pool, same translation gap |
What actually has evidence for these conditions
For fat loss: an energy deficit that can be maintained, resistance training to protect lean mass, adequate protein, and sleep. The incretin class has the largest pharmacological effect with outcome data behind it. For muscle in ageing: progressive resistance training with 1.2–1.6 g/kg/day of protein has the best evidence of any intervention and improves function, not only mass.
06 Handling, reconstitution & storage
Physical-chemistry reference for laboratory handling of the lyophilised material. Reproduced so that stability and concentration mathematics can be studied — see the calculator for the arithmetic and the reconstitution guide for sterile technique.
Reconstitution
Supplied both as oral capsules and, increasingly, as 50 mg lyophilised vials for subcutaneous use. Reconstituted with bacteriostatic water in community practice, though as a small molecule rather than a peptide its solubility behaviour differs and few suppliers state a recommended diluent. Incomplete dissolution is reported more often than with peptides — inspect for undissolved material before drawing.
Storage
Powder or capsules: dry, cool, protected from light. As a small molecule it is considerably more stable than any peptide on this site. Reconstituted: refrigerated at 2–8 °C.
Common vial sizes
Commonly 50 mg vials for injection; also oral capsules at 50–150 mg.
Stability notes
Small-molecule stability — not subject to the aggregation and denaturation concerns that govern peptide handling. The practical issues here are dissolution and dose accuracy rather than degradation.
07 Legal & regulatory status
Regulatory status changes and differs by country. This is a summary for orientation, not legal advice — check your own jurisdiction.
Not approved anywhere, and not a peptide. 5-Amino-1MQ is an unapproved research chemical with no human clinical data. It is sometimes marketed alongside dietary supplements, which it is not — it has no supplement status, no drug approval and no established human dose.
Regulatory and trial claims re-checked against primary sources on 16 August 2026. Checked: no human data and no regulatory status by any route. Approvals, trial readouts and compounding decisions move faster than anything else on this page — a date here means someone looked, not that nothing has changed since.
Anti-doping
Athletes subject to WADA, USADA, UKAD, NCAA or military testing should assume any peptide is prohibited unless they have verified otherwise against the current WADA Prohibited List. Several classes here (growth-hormone secretagogues, TB-4 analogues, metabolic modulators) are explicitly named. Check the current list — it is republished annually.
§ Sources & further reading
Links resolve to PubMed records, trial registries, publisher pages or primary documents. Where a body of work rather than a single paper is cited, the link opens a PubMed query so the full result set — including newer papers than this page — can be reviewed. Verify every claim against the primary source before relying on it.
- Kraus D, et al. Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity. Nature. 2014;508(7495):258–262.Pre-clinical / animal study
- PubMed: NNMT inhibition, NAD⁺ and sirtuin signalling in adipose tissue (live query)Database or literature search
- PubMed: NNMT inhibition and muscle stem cell / regenerative function in ageing (live query)Database or literature search
- PubMed: NNMT expression in human adipose tissue and obesity (live query)Database or literature search
- PubMed: NNMT in cancer biology and as an oncology target (live query)Database or literature search
Reminder
For educational and research reference only. Nothing on this site is medical advice, a recommendation, or an instruction to administer any substance to a human being. Every figure on this page is a record of what has been reported, not a recommendation. Full disclaimer.