Is 5-Amino-1MQ a peptide?

No. It is a small molecule taken as an oral capsule. It appears alongside peptides because it is sold in the same places, not because it has anything chemically in common with them.

Has it been tested in humans?

No published human study exists. Not for weight loss, not for safety, not for pharmacokinetics. Everything known about it comes from cells and mice.

Where does the dose on the bottle come from?

The manufacturer. There is no human study to derive a dose from, and no published scaling from the animal work either.

Weight loss

5-Amino-1MQ

5-Amino-1-methylquinolinium · 5A1MQ

PreclinicalReviewed 16 Aug 2026

5-Amino-1MQ is a small molecule, not a peptide. It appears on this site for the same reason MK-677 does. It is sold in the same places — to the same people — alongside compounds it has nothing chemically in common with. It is taken orally as a capsule and nothing about it is reconstituted or injected.

It inhibits nicotinamide N-methyltransferase, an enzyme that is markedly overexpressed in the fat tissue of obese animals and people. NNMT consumes nicotinamide, a precursor of NAD+, and methylates it into a form the body excretes. Blocking it should therefore do two things at once: raise NAD+ availability, and change how fat cells handle energy. In mice this works well. One study in diet-induced obese mice found reduced fat mass and smaller fat cells with no change in how much the animals ate.

There the evidence stops. No human trial of 5-Amino-1MQ has been published, for weight loss or anything else. There is no human pharmacokinetic data — no established dose — and no safety data. Every dose figure printed on a capsule bottle is a manufacturer's choice, and NNMT is expressed in the liver and other tissues as well as fat, so what long-term inhibition does elsewhere is simply unknown.

How it works

NNMT methylates nicotinamide, removing it from the salvage pathway that regenerates NAD+. Inhibiting the enzyme leaves more nicotinamide available, which in animal studies raises NAD+ in fat tissue.

It also raises cellular levels of S-adenosylmethionine, the methyl donor NNMT consumes. That has downstream effects on methylation throughout the cell, which is a broader consequence than the NAD+ story usually acknowledges.

NNMT is strongly overexpressed in the adipose tissue of obese animals and people. Which is what made it a target. Whether it is a cause of the metabolic problem or a consequence of it is not settled, and that distinction matters for whether inhibiting it should help.

The enzyme is not confined to fat. It is highly expressed in the liver, and elevated in several cancers, where its role is an active research question. Systemic inhibition affects all of these tissues, and nothing establishes what that means over time in a person.

Quick reference

Commonly described dose: 50 mg–150 mg
How often: Once daily, often described in courses of several weeks
Route: Oral
Timing: Commonly described in the morning, with or without food.
Storage once mixed: Not applicable

These describe what sources report, not what you should do. Full detail and provenance in the dosing section below.

Price index

Per-milligram pricing across vendors arrives with the directory. We are recording prices now so the history exists when the page ships.

Vocabulary on this page

Concentration: How much peptide there is in each millilitre of solution, once the vial has been reconstituted.
Reconstitution: Adding liquid to a freeze-dried peptide powder to turn it into a solution that can be drawn into a syringe.
Peptide: A short chain of amino acids: the same building blocks as a protein, in a chain short enough to behave differently.

The whole glossary →

Regulatory status — United States

Not approved anywhere, for any purpose, and never studied in a published human trial. Sold as a capsule, often labelled as a dietary supplement or a research chemical. Neither category requires evidence of effect or safety before sale.

Last reviewed 16 Aug 2026. Regulatory positions in this category change frequently; we date this line so you can see how current it is.

NNMT inhibitors and the NAD+ story: a chain of plausible links

What it is studied for

Each entry states the evidence behind it. We do not rank indications by effectiveness — for most compounds here, that would be a claim nobody can support.

Fat loss

Published review

The reason it is sold.

EvidenceReduced fat mass and adipocyte size in diet-induced obese mice, without a change in food intake. No human study of any kind has been published.

Raising NAD+

Published review

The mechanistic rationale.

EvidenceDemonstrated in mouse adipose tissue. Not measured in humans, and not compared against NAD+ precursors that have been studied in people.

Muscle preservation and regeneration

Community practice

A claim that appears in marketing.

EvidenceBased on animal studies of NNMT inhibition in aged muscle. No human data.

Identity and clearance

Molecule

Class: Small molecule: a quinolinium compound, not a peptide or protein
Molecular weight: 159.2 Da

Included here because of where it is sold, not because it belongs to the same chemical family as anything else on this site.

Dose protocols reported in sources

Displayed for reference only. Every row says where it came from, and a trial protocol and a community convention are not the same kind of information. None of this is fed into the calculator, and none of it is a recommendation.

Dose protocols reported in sources, with the source of each.
Goal	Dose	Frequency	Route	Units, 50 mg vial	Source	Start this protocol
Commonly sold capsule strength	50 mg – 150 mg	Once daily, often described in courses of several weeks	Oral50 to 150 mg daily. These figures come from what manufacturers put in capsules, not from any study. There is no published human pharmacokinetic data to derive a dose from, scaled from mice or otherwise.	from 100 u	Manufacturer	Start this

Start this copies a row into a protocol of your own, which you can then edit. Where a source gave a dose range or an ambiguous frequency, those fields arrive empty — we will not pick a number on your behalf.

Safety

Reported effects

EverythingCommunity practice
Unknown — no human safety data exists
This is not a formality. There is no published human study of this compound at any dose, so no adverse event has ever been systematically recorded.
Headache and nauseaCommunity practice
Anecdotally reported
Consequences of inhibiting NNMT outside fat tissuePublished review
Unknown
NNMT is highly expressed in the liver and is elevated in several cancers, where its function is an open question. An oral inhibitor reaches all of it, and no study has looked at what that does over time.
Effects on methylation broadlyPublished review
Mechanistically expected, unmeasured
Blocking NNMT raises S-adenosylmethionine, the cell's main methyl donor. Methylation regulates gene expression throughout the body, and this consequence is rarely mentioned alongside the NAD+ story.

When to stop

Any allergic response: rash, hives, facial swelling or difficulty breathing. Seek urgent care.
Yellowing of the skin or eyes, dark urine, or pain in the upper right abdomen. NNMT is highly expressed in the liver, and nothing establishes what inhibiting it there does.
Persistent nausea, headache or fatigue.
Any new lump or unexplained persistent symptom.

Interactions and situations that need care

Active or previous cancerAvoid
NNMT is elevated in several cancers and its role there is unresolved. It is studied both as a target and as a marker. Inhibiting an enzyme whose function in malignancy nobody understands, with no human data at all, is not a risk anyone can size.
Liver diseaseAvoid
NNMT is expressed most highly in the liver. An oral inhibitor with no human pharmacokinetic or safety data — in someone with existing liver impairment — combines an unknown with a known vulnerability.
Pregnancy and breastfeedingAvoid
No safety data of any kind, and effects on methylation are precisely the sort of thing that matters most during development.
Expecting the mouse result to transferUse caution
Fat loss in diet-induced obese mice is a real finding and a very common one. A great many compounds produce it. Almost none of them go on to work in people. The gap between the two is where most obesity drug candidates have died.

What to expect

HonestlyThere is no human efficacy data for this compound, so there is no evidence-based timeline to give. Any site publishing a week-by-week schedule of expected effects has invented it.

There is no human data. No trial, no pharmacokinetics, no safety study. Nothing published at all.
The mouse result is genuine: less fat mass, smaller fat cells, no change in food intake. Mouse obesity studies are also where most failed drug candidates looked promising.
It is a small molecule taken orally. Nothing here involves reconstitution, syringes or the calculator on this site.
Dose figures come from what manufacturers put in capsules, not from any study in any species scaled to humans.
If raising NAD+ is the goal, precursors like NMN and NR have at least been through human trials. The results were modest, which is itself informative.

Storage and handling

Freeze-dried powder: Capsules or powder at room temperature, dry and out of direct light.
After mixing: Not applicable. This is taken orally, not reconstituted.

Printable one-pager How to reconstitute a vial, step by step

With other peptides

NAD+caution
Both target the same pathway from opposite ends. One supplies NAD+ precursor; the other blocks the enzyme that depletes it. Combining them is not obviously additive, has never been studied in any species, and doubles down on a mechanism with no human outcome data behind it.

Check this against a whole stack

In use

Stacks with 5-Amino-1MQ in them

Documented combinations, with full schedules.

A GLP-1 with 5-Amino-1MQ

Checking your vial

Research chemicals carry no manufacturing standard, so what the vial looks like is often the only quality signal available before you use it. More on assessing quality and COAs.

You cannot assess a capsule by looking at it
Unlike a lyophilised peptide, where a collapsed cake reveals heat damage, a capsule of powder gives no visual information about identity, purity or dose. Third-party testing is the only check available.

Questions

Is 5-Amino-1MQ a peptide?: No. It is a small molecule taken as an oral capsule. It appears alongside peptides because it is sold in the same places, not because it has anything chemically in common with them.
Has it been tested in humans?: No published human study exists. Not for weight loss, not for safety, not for pharmacokinetics. Everything known about it comes from cells and mice.
Where does the dose on the bottle come from?: The manufacturer. There is no human study to derive a dose from, and no published scaling from the animal work either.

References

NNMT inhibition reduces adiposity in diet-induced obese mice, and the wider role of the enzyme
Metabolic and enzymology literature, 2018 · Animal studies with supporting in vitro work
Diet-induced obese mice · Small-molecule NNMT inhibitor, administered daily · Weeks
Reduced fat mass and adipocyte size without a change in food intake, with raised NAD+ in adipose tissue. Also documents high NNMT expression in liver and its elevation in several cancers, where its role remains unresolved.
Commonly sold capsule strengths and reported use
Bioalmanac editorial summary of public sources and product labels, 2026 · Not a study
Records the 50 to 150 mg daily capsule strengths sold and the effects users describe. Carries no evidential weight about safety or effect.

5-Amino-1MQ compared with

5-Amino-1MQ vs MOTS-c

Two metabolic compounds approached from opposite ends: an oral small molecule that inhibits an enzyme, and a mitochondrial peptide. Almost no human data between them.

Related compounds

NAD+

A coenzyme present in every cell, given by injection or infusion in the hope of raising cellular levels. Not a peptide, and poorly absorbed by the routes people use.

Semaglutide

A long-acting GLP-1 receptor agonist approved for type 2 diabetes and for weight management, dosed once weekly.

Tirzepatide

A once-weekly dual agonist that activates both the GIP and GLP-1 receptors, approved for type 2 diabetes and for weight management.

Retatrutide

An investigational once-weekly triple agonist acting on the GLP-1, GIP and glucagon receptors. Not approved anywhere.

Keep this page honest

If something here is wrong, out of date, or missing a source, tell us and we will fix it and say that we did.

Suggest a correction

This page is educational. It describes what published research reports, not what you should do. Peptides discussed here are largely not approved for human use, and nothing on Bioalmanac is medical advice. No clinician reviews these pages.

Page last updated 16 Aug 2026