Educational use only — not medical advice. This guide summarizes information reported in published research and community practice for educational purposes. It is not medical advice and not a recommendation to use any compound. Any doses, schedules, or combinations shown are examples of what has been reported, not instructions for you. Many peptides described here are research compounds that are not FDA-approved for the uses discussed and may be investigational or restricted. Effects, risks, and legal status vary; individual needs and results vary. Consult a qualified, licensed healthcare professional before making any decision. Do not use this content to diagnose, treat, or dose yourself.
5-Amino-1MQ at a glance
- What it is
- 5-Amino-1MQ (5-amino-1-methylquinolinium) — a small-molecule quinolinium compound and a selective inhibitor of NNMT. Despite being sold alongside this library's peptides, it is not a peptide: it has no amino acid chain.
- Researched for
- Preclinical metabolic, muscle and kidney research as an NNMT inhibitor. Six years of animal work across four organ systems, and still no human clinical trial — ClinicalTrials.gov returns zero registered studies.
- Commonly reported range
- Community sources describe oral doses of roughly 50–150 mg per day — anecdotal, not derived from any human study. Mouse efficacy work used 10 and 32 mg/kg/day subcutaneously.
- Route reported
- Oral capsule or powder is overwhelmingly what is sold and discussed. The published animal work found oral bioavailability of only 3.5% in mice, with a peak blood level below the concentration needed to inhibit the target enzyme — the single most important fact on this page.
- Reported frequency
- Daily, per community and commercial sources. The 2024 mouse efficacy study dosed once daily; the earlier 2018 study dosed three times daily.
- Mechanism
- Selective NNMT (nicotinamide N-methyltransferase) inhibition, proposed to preserve intracellular NAD+ and SAM and reduce fat-cell lipogenesis — demonstrated in cells and mice, never in humans.
- Half-life
- Measured in mice in 2024, not in humans: terminal half-life 6.3 h after intravenous dosing, 12.8–13.3 h subcutaneous, 14.8 h oral. Note that blood levels stayed above the enzyme-inhibiting concentration for only about 2–4 hours after injection, so half-life overstates the duration of target engagement.
- Regulatory status
- Not FDA-approved for any use; no registered clinical trial; not on any FDA bulk-drug-substance compounding list. Research/educational use only.
Reported ranges from research/community — examples, not recommendations.
What it is / mechanism
5-Amino-1MQ is a selective, cell-permeable inhibitor of nicotinamide N-methyltransferase (NNMT), a cytosolic enzyme that methylates nicotinamide — consuming the methyl donor SAM in the process — to form 1-methylnicotinamide, diverting nicotinamide away from the NAD+ salvage pathway. The research rationale is that inhibiting NNMT preserves intracellular NAD+ and SAM, which in adipocyte models suppresses de novo lipogenesis. The 2018 paper that established the compound (PMID 29155147, Biochemical Pharmacology) did the groundwork properly: it tested membrane permeability using parallel artificial membrane and Caco-2 assays, and it tested selectivity against structurally related methyltransferases and against enzymes of the NAD+ salvage pathway, reporting that the methylquinolinium scaffold with a primary amine substitution was both highly permeable and selective — it did not inhibit the related SAM-dependent methyltransferases. Selectivity data of that kind is often missing for compounds in this market, and it is a point in this one's favour. The mechanism is real, published and specific. It has been demonstrated in cell and animal models and never in a human being.
Researched effects
The animal record has grown considerably since this compound entered the research-chemical market, and it now spans four organ systems. In diet-induced-obese mice (PMID 29155147, 2018), subcutaneous 5-Amino-1MQ at 20 mg/kg three times daily for about eleven days produced roughly 5.1% body-weight loss against continued weight gain in controls, about 35% less epididymal white fat, smaller adipocytes, lower plasma cholesterol and improved glucose tolerance, with no change in food intake. A 2019 study (PMID 30753815) reported that NNMT inhibition activates senescent muscle stem cells and improves the regenerative capacity of aged skeletal muscle. A 2024 study in Scientific Reports (PMID 38969654) treated 22-to-24-month-old mice with an NNMT inhibitor, intensive exercise, or both, and found that sedentary treated mice gained about 40% grip strength over sedentary controls while exercise alone gave 20% — and that the two were additive, reaching 60% combined. A 2024 study in Diabetes, Obesity and Metabolism (PMID 39161060) dosed diet-induced-obese mice once daily for 28–30 days at 10 and 32 mg/kg/day subcutaneously, reporting dose-dependent limits on body-weight and fat-mass gain, improved glucose tolerance and insulin sensitivity, attenuated hepatic steatosis, and normalised ALT and AST. Most recently, a 2026 paper in Cell Reports (PMID 41543936) implicated NNMT in tubular senescence and fibrosis in early chronic kidney disease and found selective inhibition protective in senescent kidney cells, organoids and in vivo. This is a substantial and broadening preclinical programme. Every result in it is from a mouse or a dish.
Evidence & regulatory status
- Evidence: strong and expanding preclinical data across obesity, skeletal muscle, ageing and kidney models, from 2018 through 2026. Zero human clinical trials — a ClinicalTrials.gov search returns no registered study of 5-Amino-1MQ, and the two studies the registry returns for NNMT generally are a terminated hydroxychloroquine trial and an endometrial gene-expression study, neither of which tests an NNMT inhibitor.
- The route problem, which is this compound's central issue: 5-Amino-1MQ is sold and taken almost entirely as oral capsules, and the 2024 pharmacokinetic work found oral bioavailability in mice of just 3.5%, with an oral peak concentration of 14.5 ng/mL against a mouse NNMT IC50 of 78 ng/mL. Oral dosing did not reach the concentration that inhibits the target enzyme. Every efficacy result for this compound comes from injection.
- Why oral absorption fails, since it is not a formulation problem that better capsules would fix: the same study reports the compound is highly soluble — over 100 mg/mL in phosphate-buffered saline and over 10 mg/mL in simulated gastric fluid — and barely binds plasma protein (7%). It attributes the low oral bioavailability to limited intestinal absorption plus heavy first-pass metabolism, supported by a half-life under 7 minutes and clearance of 57.9 mL/min/kg in mouse hepatocytes.
- Regulatory: not FDA-approved for any use and not on any FDA bulk-drug-substance compounding list. Mouse results should not be assumed to predict human outcomes at any dose or by any route — and here the species gap is compounded by a route gap.
Dosage — reported ranges (overview)
Community and commercial sources commonly describe oral doses of roughly 50–150 mg per day, typically in capsules. That figure does not come from any human study, and the animal literature does not support the route it is given by. The 2024 efficacy work used 10 and 32 mg/kg/day by subcutaneous injection; the 2018 work used 20 mg/kg three times daily, also subcutaneous. Converting animal doses to human ones is not a straight multiplication and this page does not attempt it, but the direction of the problem is worth naming: with 3.5% oral bioavailability measured in mice, an oral capsule delivers a small fraction of what the same milligram figure would deliver by injection, and the one time oral dosing was measured directly, the resulting blood level sat below the concentration that inhibits NNMT. There is no human trial establishing any effective or safe dose for this compound by any route.
A printable protocol sheet with a reconstitution reference and an injection log comes with All-Access Lifetime.
Reconstitution — bac-water math
Most reported and commercial use of 5-Amino-1MQ is oral rather than reconstituted, unlike most compounds in this library — the concentration math below is provided for research completeness and parity with the rest of the calculator tool, not because injectable use is standard or recommended. It is worth noting that the published animal work is entirely parenteral, so the mismatch between how the compound is studied and how it is sold runs in the opposite direction to the usual one. The math itself: 5-Amino-1MQ ships as a powder and can be reconstituted with bacteriostatic water; concentration in mg per unit = total mg in vial ÷ (mL of bacteriostatic water × 100) on a U-100 insulin syringe, where 100 units = 1 mL. Worked example for a 50 mg vial, with every row staying within a single syringe's 100-unit capacity:
| Bac water added | Concentration | 5 mg (concentration-math example only) | 10 mg (concentration-math example only) |
|---|
| 1 mL | 50 mg/mL | 10 units | 20 units |
| 2 mL | 25 mg/mL | 20 units | 40 units |
| 3 mL | 16.7 mg/mL | 30 units | 60 units |
This is concentration math, not a dose recommendation.
Injection / administration basics
Oral capsule and powder use is what is actually sold and discussed commercially for 5-Amino-1MQ, while the research that established its mechanism and preclinical effects is entirely parenteral — subcutaneous in the efficacy studies, with intravenous and oral arms in the pharmacokinetic work. Those animal protocols are research-animal designs, not human administration guides, and this page's concentration math is reference material only. This is general educational information, not a personal use protocol; a qualified professional should guide any actual use.
Half-life & frequency rationale
As of 2024 there is a measured half-life for this compound, and it is worth being precise about what was measured and in what. A pharmacokinetic study in Diabetes, Obesity and Metabolism (PMID 39161060) characterised 5-Amino-1MQ — written 5A1MQ there — in mice by three routes. After intravenous dosing at 5 mg/kg, peak concentration was 2,009 ng/mL with a terminal half-life of 6.3 hours, high plasma clearance of 101 mL/min/kg and a large steady-state volume of distribution of 39 L/kg. After subcutaneous dosing at 25 mg/kg, peak concentration reached 7,010 ng/mL within about 15 minutes, with terminal half-lives of 13.3 hours after a single dose and 12.8 hours after five once-daily doses. After oral dosing at 30 mg/kg, the terminal half-life was 14.8 hours but the peak was only 14.5 ng/mL, giving oral bioavailability of 3.5%. Two cautions belong with those numbers. The first is species: these are mouse figures, no human pharmacokinetic study exists, and human values cannot be assumed to match. The second is more interesting, because it is a case where the half-life is genuinely misleading on its own — blood levels stayed above the compound's mouse NNMT IC50 of 78 ng/mL for only about 2 to 4 hours after injection, so a 13-hour terminal half-life describes how long a decaying tail remains detectable, not how long the enzyme is actually inhibited. The oral route illustrates the point at its sharpest: it has the longest terminal half-life of the three, 14.8 hours, and never reached the inhibitory concentration at all. An earlier version of this page said no half-life or bioavailability data existed and advised treating any specific figure as unsourced. That was correct when written and is now out of date; the data exists, it is animal data, and it is reported above with its source.
Side effects, safety & contraindications
No published human safety data exists, because no human study exists. Community-reported effects — nausea, GI discomfort, headache — come from anecdotal vendor and forum sources rather than controlled observation. The animal studies are reassuring as far as they go: the 2018 work reported no observed adverse effects at its tested dose, and the 2024 study reported normalised liver enzymes rather than raised ones, which is the opposite of a hepatic safety signal. Neither establishes human safety at any dose or by any route, and the compound has never been through the toxicology that would precede a first human trial. Consult a licensed professional; this is not a safety clearance.
Stacking — overview
Commercial sources sometimes describe 5-Amino-1MQ as complementary to GLP-1 receptor agonists such as semaglutide or tirzepatide for metabolic research interest. That is marketing framing rather than evidence — no clinical trial or peer-reviewed study of any such combination exists in humans, and none exists in animals either. The one combination that has actually been tested in a controlled way is not a drug pairing at all: the 2024 ageing-muscle study combined NNMT inhibition with exercise and found the two additive in mice.
5-Amino-1MQ + GLP-1 research
A commercially promoted pairing with GLP-1 agonists based on theoretical complementary mechanisms — no human or animal study of this combination has been published.
NNMT inhibition + exercise (the tested one)
The only combination with controlled data behind it, and it is in mice: NNMT inhibitor plus intensive exercise produced additive grip-strength gains in aged animals (about 40% from the inhibitor alone, 20% from exercise alone, 60% combined).
Stacking across compounds
The overview above covers 5-Amino-1MQ. The cross-compound material — which pairings are redundant rather than additive, where interaction risk is documented versus merely unstudied, and the blend arithmetic worked end to end — lives in the Peptide Stacking Guide, which is free to read in outline and $39 in full (included with All-Access Lifetime).
Included with this guide
The 5-Amino-1MQ Stacking Module
The overview above is the free summary. The 5-Amino-1MQ Stacking Module goes through each combination in depth — the mechanism-level reason it is proposed, what is actually reported in practice, and the cautions specific to that pairing — plus what to avoid and why. Included with 5-Amino-1MQ Standard Access.
- How to think about stacking 5-Amino-1MQ — 4 principles
- 2 combinations covered in detail
- What to avoid, and why — 3 items
- Combination-specific cautions
Combinations covered: Metabolic / longevity stack, Body Recomposition Stack.
For how combinations are grouped by research context, the named blends, and why a pre-mixed blend vial cannot be calculated from its total milligrams, see the peptide stacks guide.
Storage & handling
- Unmixed powder: store cold and dry; long-term storage is typically at −20 °C, and the powder is stable refrigerated in the short term.
- If reconstituted: refrigerate at about 2–8 °C, keep away from light, and do not freeze once mixed. Most commercial product is sold and used as oral capsules or powder rather than reconstituted.
References
Primary sources for this guide: PMID 39161060 (Diabetes, Obesity and Metabolism, 2024) for the mouse pharmacokinetics by intravenous, subcutaneous and oral routes, the 3.5% oral bioavailability, the 78 ng/mL mouse NNMT IC50, the hepatocyte stability data and the 28–30 day efficacy study; PMID 29155147 (Biochemical Pharmacology, 2018) for the original selectivity, permeability and diet-induced-obesity results; PMID 30753815 (Biochemical Pharmacology, 2019) for muscle stem cells and aged skeletal muscle; PMID 38969654 (Scientific Reports, 2024) for the NNMT-inhibition-plus-exercise study in aged mice; PMID 35013352 (Scientific Reports, 2022) for calorie restriction combined with NNMT inhibition; and PMID 41543936 (Cell Reports, 2026) for NNMT in tubular senescence and early chronic kidney disease. Registry status checked against ClinicalTrials.gov. An earlier version of this page stated that no pharmacokinetic data existed for this compound; that was accurate when written and has been superseded by the 2024 study rather than left in place.
Related peptide guides
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Guide FAQ
Quick answers about guide scope, access, and educational use context.
What is 5-Amino-1MQ's half-life?
In mice, measured in 2024: 6.3 hours after intravenous dosing, 13.3 hours after a single subcutaneous dose (12.8 hours with repeated daily dosing), and 14.8 hours after oral dosing. There is still no human pharmacokinetic study, so no human half-life exists. One caveat matters more than the numbers: blood concentrations stayed above the level that actually inhibits NNMT for only about 2–4 hours after injection. The terminal half-life measures how long a residual tail stays detectable, not how long the target is engaged, and for this compound the two are very different.
Does 5-Amino-1MQ work when taken orally?
The one study that measured it directly says it barely enters circulation. In mice, oral bioavailability was 3.5%, and the oral peak blood concentration was 14.5 ng/mL against a mouse NNMT IC50 of 78 ng/mL — meaning the oral route never reached the concentration that inhibits the target enzyme. Every efficacy result reported for this compound, in every study, comes from injection. Since it is sold and consumed almost entirely as oral capsules, this is the most consequential thing on the page. It is also not a solubility problem that a better capsule would solve: the compound dissolves readily in both buffer and simulated gastric fluid, and the authors attribute the low bioavailability to poor intestinal absorption plus rapid first-pass metabolism in the liver, where its half-life in hepatocytes was under 7 minutes.
Is 5-Amino-1MQ a peptide?
No. Despite being sold in this peptide guide library, 5-Amino-1MQ is a small-molecule quinolinium compound with no amino acid chain — chemically distinct from every other guide in this library. That has a practical consequence for verification: the analytical methods used to confirm a peptide's identity, such as peptide mapping, do not apply, and a certificate of analysis for this compound should be read as a small-molecule report.
Has 5-Amino-1MQ been tested in humans?
No. There is no published human clinical trial and no registered one — a ClinicalTrials.gov search returns zero studies of this compound. All efficacy data comes from mice, now spanning obesity, aged skeletal muscle, the microbiome and early chronic kidney disease between 2018 and 2026. The preclinical case has strengthened considerably over those years; the human case has not started.
Is the commonly cited 100 mg oral dose based on human research?
No. Community-reported oral doses of roughly 50–150 mg/day are not derived from any published study. The animal research used subcutaneous injection — 20 mg/kg three times daily in 2018, and 10 or 32 mg/kg once daily in 2024 — a different route, species and dosing basis. Given the 3.5% oral bioavailability measured in mice, the route difference is not a technicality: it is the difference between the amount studied and a small fraction of it.
Does 5-Amino-1MQ have drug interactions?
No interaction studies of any kind have been published, so there is no interaction profile to report — not a clean one and not a concerning one. What can be said is mechanistic: the compound inhibits NNMT, an enzyme in nicotinamide and NAD+ metabolism, so any theoretical interaction would most plausibly involve that pathway. The 2024 pharmacokinetic work adds one relevant observation — the compound undergoes heavy first-pass hepatic metabolism in mice — which is the kind of property that tends to matter for interactions, though no study has examined which enzymes are involved or what else they handle. That is reasoning from mechanism, not evidence, and it is not a basis for assuming either safety or risk alongside anything else. Anyone weighing this compound against existing medication should be doing so with a licensed professional.
Is there a 5-Amino-1MQ certificate of analysis or test report?
A certificate of analysis describes one specific batch — identity, purity by HPLC and mass confirmation — and is supplied by whoever produced the material, not by this guide. Because 5-Amino-1MQ is a small molecule rather than a peptide, it should be read as a small-molecule report: the mass is straightforward to check against the compound's formula, and there is no peptide-mapping section to look for. Our explainer on reading a peptide certificate of analysis covers which fields on a report are checkable and which are not.
Is 5-Amino-1MQ FDA-approved or on an FDA compounding list?
No. It is not FDA-approved for any use and is not on any FDA bulk-drug-substance compounding list. It has no registered clinical trial, which means it has not entered the human development pathway at all.
Why do vendor pages quote confident human half-life and bioavailability numbers?
Because numbers now exist and the species label tends to fall off them. Since 2024 there are real pharmacokinetic figures for this compound — 6.3, 12.8–13.3 and 14.8 hours by three routes, and 3.5% oral bioavailability — and every one of them was measured in mice. A figure quoted without its species is not necessarily invented, but it is being presented as something it is not. The test to apply is simple: ask which study a number came from and what was dosed. For this compound the honest answer is always a mouse, and the bioavailability figure is the one least likely to be quoted at all.
Compliance and trust notes
- Educational content only; no personalized health or outcome claims.
- No personalized use recommendation outputs.
- Use this material for general learning and research-context literacy.
