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BlendMetabolicNo human studies cited

5-amino-1MQ with SLU-PP-332

5-amino-1MQ with SLU-PP-332 (oral metabolic blend)

Written by Reviewed Sep 2026

Also known as: Exercise mimetic blend, Oral fat loss stack, M-51

In plain English, from Aaron

This is how I would explain it to a friend. The evidence, with the numbers, is further down the page.

An oral capsule with two lab chemicals in it, usually 50 mg of one and 0.25 mg of the other. It is sold as exercise in a pill. Neither chemical has ever been given to a human being in a published study. Not one.

What people take it for

  • Losing fat without training.
  • Better endurance.
  • Raising cell energy levels.
  • A pill instead of a needle.

What the trials actually showed

Nobody has tested the mix, in people or animals. And neither ingredient has ever been tested in a person by itself. 5-amino-1MQ blocks the enzyme that throws away a cell fuel molecule. In lab dishes it raised that fuel inside fat cells. In mice fed a high fat diet, a strong version of it reversed their obesity. Cells and mice. SLU-PP-332 switches on a set of genes that exercise switches on. In a muscle cell line it raised energy output. In mice it grew more of the endurance type muscle fibre and let them run longer. Mice again. Now the ratio. 50 mg against 0.25 mg is 200 to 1. The exercise mimetic people came for is half of one percent of what they swallow. A common tablet version adds 125 micrograms of BPC-157, which is a quarter of one percent of the tablet, by mouth, with zero absorption data.

What people report

Reports, not trial results

The good

  • Better endurance in training after two or three weeks.
  • Less appetite and slow fat loss, credited to the first ingredient.

The bad

  • Nothing at all. Very common.
  • Flushing and a warm feeling after dosing.
  • Nausea and stomach discomfort.
  • People argue about whether any of it is even absorbed, because nobody has measured it in a person.
  • It comes in a capsule with a dose printed on it, which makes it look like a supplement. It is not one, and it is not legal as one.

Where these come from: Peptide and nootropic forums plus seller product pages. People talking, using unverified material, usually while also training.

My bottom line

Both of these came out of serious labs and both are interesting. They are also at the very start of a road that normally takes ten years. A capsule with a dose on the bottle skips all of it.

An opinion, not a finding. I am a coach, not a doctor.

Overview

An oral capsule combining two research chemicals, commonly 50 mg of 5-amino-1MQ with 0.25 mg of SLU-PP-332, a 200 to 1 ratio by mass. Neither compound has ever been given to a human being in a published study. Both literatures are mice, and a common tablet variant adds 125 micrograms of BPC-157 on top, which is an oral route with no evidence for a peptide FDA found had no adequate human data.

This is the exercise-mimetic capsule, sold on the idea that one molecule raises cellular NAD by blocking its disposal and the other switches on the genetic programme exercise switches on. Both ideas come from real laboratories and real papers. Neither has been tested in a person.

5-amino-1MQ is a nicotinamide N-methyltransferase inhibitor. In the foundational work, methylquinolinium analogues showed high membrane permeability and high selectivity, not inhibiting related methyltransferases or NAD salvage pathway enzymes, and reduced intracellular 1-methylnicotinamide while raising intracellular NAD+ in cultured adipocytes. A potent inhibitor was then assessed in diet-induced obese mice on a high fat diet, where it reversed high fat diet-induced obesity. Cells and mice.

SLU-PP-332 is a synthetic pan agonist at the estrogen-related receptors with highest potency at ERR alpha. It increased mitochondrial function and cellular respiration in a skeletal muscle cell line, and in mice it increased type IIa oxidative muscle fibres and enhanced exercise endurance while inducing an ERR alpha dependent acute aerobic exercise gene programme. Mice again.

The arithmetic is unusually lopsided. At 50 mg of 5-amino-1MQ with 0.25 mg of SLU-PP-332, the first is 200 times the second by mass and 99.5% of the active content. A buyer who read about the exercise mimetic is mostly swallowing the NNMT inhibitor. A common tablet variant uses 50 mg, 0.5 mg and 125 micrograms of BPC-157, which makes the peptide 0.25% of the tablet.

That BPC-157 addition deserves its own sentence. FDA staff who reviewed BPC-157 in July 2026 counted five human studies totalling fewer than 110 subjects, none by subcutaneous injection and none longer than two weeks, and found mislabelled products in the market. An oral tablet at 125 micrograms is a third route at a dose far below anything anyone injects, with no absorption data at all.

Mechanism of action

5-amino-1MQ inhibits nicotinamide N-methyltransferase, the enzyme that methylates nicotinamide for disposal, which in cultured adipocytes raises intracellular NAD+ and lowers 1-methylnicotinamide. SLU-PP-332 agonises estrogen-related receptors alpha, beta and gamma with highest potency at ERR alpha, inducing an acute aerobic exercise transcriptional programme in mouse skeletal muscle. Both mechanisms are established in cells and rodents and neither has been demonstrated in a person.

Human evidence

There is none, for either compound, by any route. That is the single most important fact about this product.

  • The blend: no published study in any species.
  • 5-amino-1MQ: no human study. Cultured adipocytes and diet-induced obese mice.
  • SLU-PP-332: no human study. A muscle cell line and mice.
  • The BPC-157 tablet variant: FDA counted five human BPC-157 studies totalling fewer than 110 subjects, none by injection under the skin, none longer than two weeks, and found mislabelled products in the market. None of those studies was an oral tablet.
  • No pharmacokinetic data exists for either primary compound in a person, so nothing is known about absorption, distribution or clearance at these doses.

What this does not tell you: Mouse obesity models respond to many interventions that do nothing in people, and the gap between a rodent exercise-mimetic transcriptional programme and a human training adaptation is the entire unanswered question in this field.

What it has been measured to do

Measured in animals or cells, not yet in people

Real results that answer a different question from a trial. Where a human trial is missing on a compound nobody can patent, the reason is usually that no sponsor would ever recover the cost of running one. The record on this one is set out below.

What people using it report

Uncontrolled and self-selected, so it cannot show that anything works. It is still the best guide on this page to what people actually do with 5-amino-1MQ with SLU-PP-332, what they expect, and what goes wrong. The full account, including the negative reports, is below.

32 of the 36 indexed goals have no study of any kind behind 5-amino-1MQ with SLU-PP-332

No trial, no animal work, no cell work on this page reports a result for these. That is an absence of evidence rather than evidence of absence, but it does mean anything you have been told about 5-amino-1MQ with SLU-PP-332 and one of these did not come from a study cited here.

Reading the research record

Both of these molecules came out of serious academic pharmacology and both are interesting. The problem is the distance between where the science is and where the product is. A compound with a promising mouse result and no human pharmacokinetics is at the start of a development process that normally takes a decade, and it is being sold in a capsule with a dose printed on the bottle.

The 200 to 1 ratio is the second thing. Someone buying this for the exercise mimetic is getting a quarter of a milligram of it alongside fifty milligrams of something else. If the ERR agonist is what interests you, this vial gives you a trace of it.

The oral presentation is the third. Capsules and tablets with printed milligram doses are the format of medicines and supplements, not of research chemicals, and the format carries an implication of human testing that has not happened for either ingredient.

The evidence, charted

Fig. 1a · evidence scale

0people have taken this in any study cited here

0 participants · 0 human studies

What this page cites instead is 2 animal studies and 2 reviews. None of it involved giving the compound to a person.

Counted from the citation list on this page. A figure is drawn here only when a human study is cited; an empty one is the finding, not a gap in the page.

Fig. 1b · evidence mix

None of the 4 citations here are human work.

04 citations
  • Animal · given to animals250%
  • Review · summarises other work250%

Counted from the citation list on this page, typed as this page types it. It understates any literature larger than the sources we cite, and a review counts once however many studies it covers.

Fig. 2 · evidence over time

Evidence spans 3 distinct years, 2018 to 2026, counted from the citation list on this page.

Fig. 3 · legal status at a glance

Not approved in any of the four jurisdictions shown. A jurisdiction's classification is a regulatory fact, not a verdict on the science; see Legal status below for the full text and any notes.

Fig. 5 · molecular identity

Modality
Blend
Molecular weight
Not on file
Half-life
Stated in words, not a number

see the exact wording below

Sequence length
None on file

Half-life as stated on file: Not defined for the blend, and not published for either component in people.

No amino acid sequence is on file for 5-amino-1MQ with SLU-PP-332, which is expected: a blend is not built from residues.

Fig. 6 · what is in the vial

99.5%of a 50.25 mg 5-amino-1MQ with SLU-PP-332 vial is 5-amino-1MQ

0 mg50.25 mg total label mass

Label mass from a standard vial, not a dose, and not an assay. The ratio is fixed by the seller, so a draw that hits the amount you want of one component sets the amount of every other component with it. No study has tested this combination in any species.

Key studies & citations

  • Animal2018

    Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice

    Methylquinolinium NNMT inhibitors showed high membrane permeability and high selectivity, not inhibiting related methyltransferases or NAD salvage pathway enzymes. In cultured adipocytes they reduced intracellular 1-methylnicotinamide and increased intracellular NAD+. A potent inhibitor reversed high fat diet-induced obesity in diet-induced obese mice. Cells and mice, with no human exposure.

    Biochemical Pharmacology
  • Animal2023

    Synthetic ERRα/β/γ Agonist Induces an ERRα-Dependent Acute Aerobic Exercise Response and Enhances Exercise Capacity

    SLU-PP-332 is a synthetic pan agonist at all three estrogen-related receptors with highest potency at ERR alpha. It increased mitochondrial function and cellular respiration in a skeletal muscle cell line, and in mice increased type IIa oxidative skeletal muscle fibres, enhanced exercise endurance and induced an ERR alpha dependent acute aerobic exercise gene programme. Mice, with no human data.

    ACS Chemical Biology
  • Review2026

    FDA briefing document on BPC-157 for the July 2026 PCAC meeting

    FDA staff counted five published human studies of BPC-157 totalling fewer than 110 subjects, two of them meeting abstracts only, none dosing longer than two weeks, and none giving the peptide by subcutaneous injection. Staff found no adequate human data and mislabelled products in the market.

    FDA
  • Review2026

    NAD⁺ supplementation for anti-aging and wellness: A PRISMA-guided systematic review of preclinical and clinical evidence

    A systematic review of NAD supplementation evidence across preclinical and clinical work. Relevant here because the NNMT inhibitor's claimed benefit runs through raising cellular NAD, and this review is the current summary of how far raising NAD has translated into measured human outcomes.

    Ageing Research Reviews

What users report

Self-reported experiences, not evidence. Nothing below was measured under controlled conditions, and reports like these cannot separate a real effect from placebo, from the training or diet change that accompanied it, or from what the product actually contained. They are here because knowing what people describe, including what goes wrong, is worth reading alongside the studies.

  • Improved endurance during training after two to three weeks, the main claimed effect.
  • Reduced appetite and slow fat loss, credited to the NNMT inhibitor.
  • Nothing at all, which is very common.
  • Flushing and a warm sensation shortly after dosing, reported on the ERR agonist.
  • Nausea and stomach discomfort.
  • Disagreement about whether any of it is absorbed, since no pharmacokinetic data exists for either compound in a person.

Sources: Forums including r/peptides and r/nootropics, and vendor product pages. Entirely uncontrolled self-report from people taking unverified material, usually while also training.

Frequently asked questions

Has either compound been tested in people?

No. Neither has a published human study of any kind, including pharmacokinetics. Both literatures are cells and mice.

What is the ratio?

Commonly 50 mg of 5-amino-1MQ to 0.25 mg of SLU-PP-332, which is 200 to 1 by mass. The NNMT inhibitor is 99.5% of the active content.

What about the version with BPC-157?

A common tablet adds 125 micrograms of BPC-157, which is 0.25% of the tablet. That is an oral route at a dose well below anything people inject, for a peptide FDA reviewed in 2026 and found had no adequate human data, with no absorption data at all.

Does SLU-PP-332 work like exercise?

In mice it increased oxidative muscle fibres, enhanced endurance and induced an acute aerobic exercise gene programme. In people nobody has looked.

Is it a supplement?

No. Neither compound is a lawful dietary ingredient in the United States. They are research chemicals presented in a dosage form that looks like a supplement.

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