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5-Amino-1MQ

5-Amino-1-methylquinolinium; 5-Amino-1MQ iodide; NNMT inhibitor (lead methylquinolinium analog)

Checked Oct 28, 2026

The short answer

D

No human evidence yet for fat loss and metabolic health in people

Grade D for fat loss: it reduced body weight and fat mass in diet-induced obese mice, and there is no human trial of any kind, so it is not tested in humans.

Approved?
Not approved for any use.
Safety: D, uncharacterized
There is no human safety data, and NNMT is up in several cancers, so long-term effects of blocking it are unknown.
The full answer: what it is for, the dose, the units

What people take it for: People take it for fat loss, metabolic health and energy, usually as an oral capsule. It is a small molecule that blocks the enzyme NNMT, not a peptide.

D

Does it work for fat loss and metabolic health in people? D, no human evidence yet. Result: not tested in humans.

Grade D for fat loss: it reduced body weight and fat mass in diet-induced obese mice, and there is no human trial of any kind, so it is not tested in humans.

No approval for any use.

Safety: D, uncharacterized. There is no human safety data, and NNMT is up in several cancers, so long-term effects of blocking it are unknown.

Do not use if: No human contraindications are formally established because there are no trials.

Could it be placebo? No controlled trial exists for any human use, so a placebo effect cannot be ruled out for the energy and focus effects people report.

The dose people use, and the units to draw

No verified dose statement found. No label, human trial, or named clinician source states a human dose, and the only dose in the published work is a mouse dose.

SourceDoseHow often and howWho it was forLink
Neelakantan et al. 2018, Biochemical Pharmacology (mouse study)20 mg/kgSubcutaneous, three times daily for 11 days (Figure 5 legend)Diet-induced obese mice, not humans; cannot be converted to a human doseFigure 5 legend

No human dose is stated by any label, human trial, Examine, Attia, Huberman Lab or Dr. Abud Bakri source we could find (no Examine page, no episode found, checked 2026-10-28). Dose ranges printed on this site before had no named non-seller source and are removed.

Reported by the named source, never prescribed by us.

How many units do I draw?

Use the calculator: units = (dose in mg divided by vial mg, times water mL) times 100 on a U-100 syringe. The calculator does not tell you what dose to use. Open the dose calculator

Why it might work
  1. Oral absorption and membrane permeability
    5-Amino-1MQ (5-amino-1-methylquinolini
  2. Selective NNMT inhibition in adipose tissue
    Inside the cell
  3. NAD+ and SAM conservation in adipocytes
    By blocking the NNMT reaction
  4. Increased adipocyte energy expenditure and fat mass reduction (mice)
    The downstream consequence

Assumed pathway, not shown in people.

Assumed mechanism: 5-amino-1MQ inhibits nicotinamide N-methyltransferase (NNMT), which normally methylates nicotinamide using SAM as the methyl donor (producing 1-methylnicotinamide). NNMT is markedly upregulated in obese white adipose tissue. By inhibiting it, the compound is thought to spare nicotinamide for NAD+ salvage (raising NAD+) and conserve SAM, increasing adipocyte energy expenditure and fat oxidation (via downstream SIRT1/PGC-1a signaling) while suppressing lipogenesis. This is well supported in mice and cells but unproven in humans.

The trials, claim by claim

The 'No registered human trial' line is a registry-status statement, so it shows a Status tag rather than a letter.

  • People use it for fat loss and metabolic health, stacking it with GLP-1 drugs, GH secretagogues, and peptides. The NNMT target is real and mechanistically compelling.
  • The evidence is almost entirely in mice. One key study (Neelakantan 2018) showed significant fat loss in diet-induced obese mice at 20 mg/kg/day. No controlled human trial has been published or registered anywhere.
  • The catch is the cancer biology. NNMT is upregulated in a long list of tumors, and inhibiting it chronically in a human system, with no human safety data, is a genuine open question nobody can answer yet.
D

NNMT knockdown in adipose tissue protects mice against diet-induced obesity (the founding target-validation finding in mice).

Result: not tested in humans

Kraus et al., Nature 2014 - antisense oligonucleotide knockdown in mice and cell studies. Animal/in-vitro only; establishes the target, not human efficacy.

Kraus 2014, Nature (PMID 24717514) - PubMed
D

The membrane-permeable methylquinolinium NNMT inhibitor (5-amino-1MQ class) reverses high-fat-diet-induced obesity in mice, reducing body weight, adipose mass and adipocyte size.

Result: not tested in humans

Neelakantan et al., Biochemical Pharmacology 2018 - diet-induced obese mouse model, ~20 mg/kg dosing, plus adipocyte cell work. No human subjects.

PubMed: Selective and membrane-permeable NNMT inhibitors reverse high-fat-diet obesity in mice (Neelakantan, Biochem Pharmacol 2018)
D

NNMT inhibition raises intracellular NAD+ and SAM and suppresses lipogenesis in adipocytes.

Result: not tested in humans

In-vitro adipocyte studies; mechanistic, cell-level only.

NNMT NAD+ adipocyte lipogenesis - PubMed search
Status

No registered human clinical trial of 5-amino-1MQ exists for any indication.

ClinicalTrials.gov search returns no Phase 1-3 study of 5-amino-1MQ itself; vendor claims of 'emerging Phase 1' trials are unsubstantiated.

ClinicalTrials.gov search: 5-amino-1MQ (0 results, checked 2026-10-12)
D

NNMT is broadly relevant to obesity and type 2 diabetes biology, supporting it as a metabolic-syndrome target.

Result: not tested in humans

Review of NNMT roles in obesity/T2D; the review itself states clinical trials targeting NNMT have not been reported. Preclinical synthesis.

PubMed: Roles of NNMT in obesity and type 2 diabetes (Liu, Biomed Res Int 2021)
Risks and the label warnings

Adverse events

Reported real-world adverse effects are mild and anecdotal: transient nausea, mild GI/stomach discomfort, occasional headache or jitteriness, mostly early and self-limiting. There is no human safety dataset, no adverse-event registry, and no long-term human data of any kind, so the true frequency and severity of side effects are unknown.

Contraindications

No human contraindications are formally established because there are no trials. Reasonable caution: pregnancy/breastfeeding, active or prior malignancy (given NNMT's cancer associations), significant liver disease, and concurrent methyl-donor or NAD-pathway drugs. Not a substitute for evaluated obesity therapies. Gray-market product purity, identity, and dose accuracy are unverified.

Theoretical concerns

NNMT is upregulated in multiple cancers and participates in liver and CNS one-carbon/SAM metabolism. Chronic systemic NNMT inhibition could theoretically disturb methylation balance (SAM/SAH ratio), nicotinamide/NAD+ handling, and pathways implicated in tumor biology; none of this has been studied in humans. These are mechanism-based concerns, not documented harms.

What nobody knows yet

Essentially everything human: oral bioavailability and PK in people, effective and safe dose, therapeutic window, drug interactions, long-term oncologic and metabolic safety, and whether the striking mouse fat-loss effect translates to humans at all. Tolerance is anecdotally reported after ~4-6 weeks but unverified.

What else could explain the result

Almost always run alongside other interventions that independently drive fat loss: caloric restriction, GLP-1/GIP agonists (tirzepatide/semaglutide), other peptides (e.g., tesamorelin, MOTS-c, AOD-9604), stimulants, training programs, and NAD+ boosters (NMN/NR). Any body-composition change is extremely hard to attribute to 5-amino-1MQ specifically.

Is the vial what it says?

Foundational target biology verified against primary literature: Kraus et al., Nature 2014 (PMID 24717514) and Neelakantan et al., Biochemical Pharmacology 2018 (mouse + cell). NNMT/obesity review PMC8337113 explicitly states clinical trials targeting NNMT have not been reported. ClinicalTrials.gov shows no registered trial of 5-amino-1MQ. Vendor/clinic claims of imminent or 'registered' human trials could not be corroborated and are treated as marketing. Reconstitution/storage and dosing figures are vendor/community sources, flagged as anecdotal.

Half-life and storage

Half-life: No human pharmacokinetic data exist. Rodent/vendor-cited plasma half-life is roughly 4-7 hours (commonly stated ~3.8-6.9 h). Treat as preclinical/unverified for humans.

Once mixed: Sold lyophilized; vendor handling guidance is to store powder frozen (around -20 C), bring to room temperature before opening, reconstitute gently with bacteriostatic water down the vial wall (swirl, do not shake to avoid foaming), then refrigerate the solution at 2-8 C protected from light and use within about 2-4 weeks; do not refreeze. As a small molecule it is generally less fragile than true peptides, but product quality from gray-market sources is unverified.

What I noticed, and what people report

What people report

Volume of reports: mixed. Reports exist but contradict each other.

Low-to-moderate. There is steady marketing chatter and clinic/vendor content, but genuine independent user-experience volume (forums, long-term self-reports) is thin compared with mainstream peptides like BPC-157 or GLP-1 drugs.

Moderately consistent on the mild, early effects (a slight uptick in energy/focus and modest early scale movement); much less consistent on meaningful fat loss, with many reports describing subtle or hard-to-distinguish results and anecdotal tolerance after a few weeks.

Low. The bulk of positive content originates from vendors, medspas, and affiliate sites with a financial interest; independent, disinterested reports are sparse, and almost all users co-administer other fat-loss interventions, undermining attribution.

  • Many users report a mild, stimulant-like lift in energy, focus, and motivation in the first couple of weeks, which is also the effect most prone to placebo. (Anecdote, not proof.)
  • Fat-loss reports are generally modest and slow, and most users describe results as subtle or hard to separate from their concurrent diet, training, or GLP-1/peptide use. (Anecdote.)
  • A recurring theme is apparent tolerance: perceived effects fade over time. (Anecdote, no mechanism confirmed in humans.)
  • Tolerability is usually described as good, with mild early nausea or stomach upset that tends to settle. (Anecdote; no human safety dataset.)

Reports are anecdote, not proof.

Can you tell if it is working?

Partly trackable

Track its one marketed outcome, fat mass / body recomposition, on DEXA plus waist and weight; there is no blood marker, zero human trials, and no way to separate the drug from your diet, so this is confounded n=1 outcome tracking, not verification the compound works.

Bloodwork

No blood proxy

Nothing on a routine panel confirms this one. Anyone who says otherwise is guessing.

5-amino-1MQ inhibits NNMT inside adipocytes; its direct pharmacodynamic readouts (intracellular NAD+, SAM, and 1-methylnicotinamide) live inside cells and are not captured by any routine serum panel, and its claimed systemic metabolic effects are unproven in humans.

Read this before you spend on labs

Routine bloodwork cannot confirm 5-amino-1MQ is working. Its mechanism is NNMT inhibition inside fat cells, read out by intracellular NAD+, SAM, and 1-methylnicotinamide, none of which are orderable LabCorp/Quest tests (serum NAD+ is a research assay, not a routine panel). The only systemic blood signal ever reported was lower plasma total cholesterol in high-fat-fed mice; there is no human PK study, no dose-finding trial, and no placebo-controlled data showing it moves lipids, glucose, HbA1c, or fasting insulin in people. Even if a metabolic marker shifted on a fat-loss protocol, it would be confounded by diet, caloric deficit, and weight change rather than proving the drug's action. Track body composition, weight, and waist instead, those are outcomes, not a blood proxy for the mechanism.

Other ways to track it

DEXA scanDirect readout

DEXA scan, total and regional fat mass, visceral adipose tissue (VAT), and lean/appendicular mass

A working result shows fat mass (and VAT) declining with lean mass held or preserved during a calorie deficit, beyond your pre-compound trajectory. The magnitude in humans is genuinely unknown, no human trial has ever quantified it. Because fat loss is exactly what the deficit alone produces, DEXA can confirm the outcome is happening but cannot attribute it to the drug. If fat mass tracks flat against a controlled deficit, it is not working for you.

NNMT is overexpressed in obese adipose tissue; the mouse-validated effect is reduced white-adipose mass and body weight with no change in food intake, so adipose/VAT is exactly where any real human effect should show up.

Baseline before starting; retest at ~12 weeks. DEXA precision needs a real interval, so do not rescan monthly.How to do it right
Body compositionIndirect / noisy

Waist circumference (navel, fasted) plus morning scale weight, trended weekly

The cheap home proxy for the DEXA signal. A working result shows waist and weight drifting down faster than your baseline trend with diet and training held constant. Waist is a fair abdominal-fat proxy but cannot separate fat from lean or water, and cannot separate drug from deficit, treat a stalled waist against a genuine deficit as not working.

Body weight and abdominal (white) fat are the precise endpoints that moved in mice, and both are measurable at home with no lab.

Collect 1-2 weeks of baseline data before starting; weekly waist, daily weight averaged weekly; read the trend at 8-12 weeks.

Bottom line

5-amino-1MQ has zero human trials, every human fat-loss claim is a mouse-to-man assumption, and the site grades the evidence a D. There is no blood marker for it. Its one marketed outcome (fat loss / body recomposition) is directly measurable on DEXA, with waist and weight as the home proxy, so you can run an honest n=1: lock diet and training, establish your pre-compound trajectory, then watch whether fat mass bends below that line. But none of this proves the drug caused anything, fat loss is exactly what the deficit produces on its own, so at best you are confirming the outcome you are paying for is or is not happening, not that the compound is responsible. If fat mass, waist, and weight all track flat against a real deficit, it is not working for you, regardless of the NAD+ mechanism story.

Logging baseline vs retest is the whole game. The Truth Tracker is our free log for bloodwork, DEXA, genetics, and wearable data, bring your own numbers.

How to track it
History

First documented human use: No controlled human trial has been completed or published. There is no human Phase 1 dose-finding study, no human pharmacokinetic publication, and no registered ClinicalTrials.gov trial of 5-amino-1MQ itself as of October 2026. Documented human exposure is limited to off-label use via gray-market research-chemical vendors and some wellness/medspa clinics, beginning roughly 2021-2023; none of it is controlled or peer-reviewed.

  1. 2014Kraus et al. (Nature) show NNMT knockdown protects mice from diet-induced obesity, validating NNMT as a metabolic target.
  2. 2018Neelakantan et al. (Biochemical Pharmacology) report membrane-permeable methylquinolinium NNMT inhibitors (5-amino-1MQ lead) that reverse diet-induced obesity in mice.
  3. 2021Review literature (e.g., PMC8337113) frames NNMT inhibition for obesity/T2D while noting no clinical trials have been reported.
  4. 2021-20235-Amino-1MQ appears in the gray market as a research chemical and at some wellness/medspa clinics, marketed for fat loss and energy; all human use is off-label and uncontrolled.
  5. 2026Still no published human trial or human PK data. In January 2026 FDA told a 503B outsourcing facility that drugs compounded with 5-Amino-1MQ are not eligible for 503B exemptions because it is not on the bulks list. No FDA-approved use.
All sources

Not medical advice. Grades reflect the evidence as of the date above and will change as data arrives. Reports from users are anecdote, not proof. Talk to a licensed clinician before you act on anything here.