5-Amino-1MQ (5-amino-1-methylquinolinium) is a small molecule compound, not a peptide, with a molecular weight of approximately 159 Da. It was developed at the University of Texas at Austin through structure-activity relationship studies aimed at finding selective, membrane-permeable inhibitors of nicotinamide N-methyltransferase (NNMT), an enzyme that had been identified as dramatically overexpressed in obese adipose tissue.
NNMT catalyzes the methylation of nicotinamide (a form of vitamin B3) using S-adenosylmethionine (SAM) as the methyl donor, producing 1-methylnicotinamide (1-MNA) and S-adenosylhomocysteine (SAH). When NNMT is overactive (as in obesity), it depletes two critical metabolic cofactors: nicotinamide (a precursor of NAD+) and SAM (the universal methyl donor). This dual depletion impairs cellular energy metabolism and epigenetic regulation.
By inhibiting NNMT, 5-Amino-1MQ preserves intracellular NAD+ and SAM pools. In preclinical models, this shifts adipocyte metabolism from energy storage toward energy expenditure: lipogenesis decreases, fat oxidation increases, and mitochondrial function improves. The landmark 2017 study by Neelakantan et al. (Biochemical Pharmacology) demonstrated that 5-Amino-1MQ reduced body weight, white adipose mass, and adipocyte size in diet-induced obese mice without affecting food intake or producing observable adverse effects over an 11-day treatment period.
Critical context: 5-Amino-1MQ is entirely a preclinical compound. There are zero published human clinical trials. The longest published animal study is 11 days. Long-term safety data does not exist. Despite this, it is widely available from peptide and research compound suppliers and is used in integrative medicine practices.
5-Amino-1MQ has never been given to a human in a published clinical trial. The only dosing figures that exist for it are animal figures — 20 mg/kg per subcutaneous injection, three times a day, for 11 days in diet-induced obese mice — and milligram-per-kilogram amounts in mice do not scale to people. There is no human amount, no human schedule and no human frequency to chart, and converting the mouse figure into one would be an invention rather than a conversion. The reconstitution figures above are arithmetic and are correct at both strengths; what is missing is a human schedule to apply them to.
5-Amino-1MQ is a small molecule of about 159 Da rather than a peptide, and it is sold both as an oral capsule and as a lyophilised vial. Athena lists two vial strengths, and every figure in the strip above is calculated from the one selected: the 10 mg vial made up with 2 mL comes to 5 mg/mL, and the 50 mg vial made up with 5 mL comes to 10 mg/mL, so the same amount drawn from the 50 mg vial is half the syringe units it would be from the 10 mg vial. As arithmetic and not as a dose, 1 mg is 20 units on a U-100 syringe at 5 mg/mL and 10 units at 10 mg/mL. What that arithmetic has nothing to apply to is a schedule. The published work on this compound is preclinical throughout: cultured adipocytes, an 11-day subcutaneous study in diet-induced obese mice at 20 mg/kg three times daily (about 34 mg/kg a day of parent compound, chosen from an escalation ranging up to 150 mg/kg a day), and a later study in aged mice. Those are body-weight amounts in rodents, they are recorded here rather than charted, and no human course has been derived from them.
What this evidence establishes. No human dosing exists for 5-Amino-1MQ. There are no published human clinical trials, no human safety data and no human pharmacokinetics, so its half-life, clearance and tolerated amounts in people are all unknown. The whole evidence base is cell culture and rodent work, and the longest published treatment period in that work is 11 days. The figures above are reconstitution arithmetic only.
Sources: Neelakantan et al., Biochemical Pharmacology, 147, 141–152 — 11-day subcutaneous dosing study in diet-induced obese mice
For educational and laboratory research purposes only. It does not provide medical advice, dosing recommendations, or instructions for human or veterinary use. Syringe units assume a U-100 syringe, on which 1 mL is 100 units and a 50-unit syringe holds 0.5 mL.
5-Amino-1MQ works by blocking NNMT, an enzyme that sits at the intersection of nicotinamide metabolism, methyl-donor balance, and adipocyte energy regulation:
Selectively blocks NNMT without inhibiting related SAM-dependent methyltransferases or NAD+ salvage pathway enzymes. High selectivity confirmed.
By preventing nicotinamide waste through NNMT, intracellular NAD+ levels increase. Higher NAD+ activates sirtuins (SIRT1/SIRT3) and improves mitochondrial function.
Preserves the universal methyl donor SAM, supporting histone methylation (H3K4me3) and shifting gene expression away from adipogenic programs.
Lipogenesis reduced by >50%. Adipocyte volume decreased ~40%. Fat oxidation increased. All observed in preclinical models without dietary changes.
2024 study: NNMT inhibition enhanced muscle stem cell activation, increased myofiber size 2x, and improved grip strength better than exercise alone in aged mice.
Unlike earlier NNMT inhibitors, 5-Amino-1MQ crosses cell membranes efficiently (confirmed by PAMPA and Caco-2 assays). This is why it works in living systems, not just test tubes.
5-Amino-1MQ has zero published human safety data. All assessments below are from preclinical models:
| Concern | Risk Level | Rationale |
|---|---|---|
| Human safety data | ABSENT | Zero published human clinical trials. All data is from cell culture and 11-day mouse studies. Long-term effects completely unknown. |
| Pregnancy / breastfeeding | UNKNOWN | No reproductive toxicology data. Standard precaution for unstudied compounds. |
| Active malignancy | MODERATE (complex) | NNMT is overexpressed in some cancers. Effects of NNMT inhibition on tumor biology are context-dependent and not well characterized. |
| Drug interactions | UNKNOWN | Zero drug interaction studies. Effects on concurrent medications that depend on methylation pathways are unstudied. |
| Long-term NNMT inhibition | UNKNOWN | 11 days is the longest published animal treatment period. Chronic effects of sustained NNMT blockade on methylation homeostasis, epigenetics, and organ function are entirely unstudied. |
| Selectivity (short-term) | FAVORABLE (preclinical) | 5-Amino-1MQ does not inhibit related methyltransferases or NAD+ salvage enzymes at therapeutic concentrations. Good selectivity profile. |
| Acute toxicity (preclinical) | LOW (short-term) | No cytotoxicity at 10 uM in cell culture. No observable adverse effects in 11-day mouse studies. No food intake changes. |
| Oral bioavailability | FAVORABLE (preclinical) | High membrane permeability confirmed by PAMPA and Caco-2 assays. Oral administration feasible. |
FDA: 5-Amino-1MQ is not FDA-approved for any indication. It is not a peptide; it is a small molecule quinolinium compound. It has not entered formal clinical development (no IND application filed).
Classification: 5-Amino-1MQ is not a controlled substance. It is available from research compound suppliers.
Key distinction: 5-Amino-1MQ represents a genuinely novel mechanism. NNMT inhibition is a different lever than anything else in the metabolic space: it is not an incretin, not a GH secretagogue, not a mitochondrial peptide. It works inside fat cells by preserving their own NAD+ and SAM pools. The 2017 and 2024 preclinical data are published in peer-reviewed journals by legitimate academic groups. However, "legitimate preclinical science" and "ready for human use" are separated by years of clinical development that has not occurred. The entire evidence base is 11-day mouse studies and cell culture.
Test your understanding of NNMT biology, 5-Amino-1MQ's mechanism, and its evidence limitations.
This profile is for educational and research purposes only. It is not medical advice, and nothing on it is a protocol, a recommendation, or an instruction for use in a person or an animal.
Athena Peptides Education does not prescribe, sell, or recommend any compound. Compounds discussed here are for laboratory research only and are not for human consumption. Always consult a qualified physician before making any decision about your health.