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5-Amino-1MQ isn’t a peptide—and it isn’t a stimulant, either. It’s a small-molecule NNMT inhibitor that tweaks your cell’s bookkeeping, not your nerves. By blocking nicotinamide N-methyltransferase, it stops niacin (NAM) and methyl groups from being siphoned off into 1-MNA. The result: more NAD⁺ for mitochondrial “housekeeping” and more SAM for healthy methylation—two upstream resources that quietly run everything.
Think of it as a gentle metabolic rebalancer. When NNMT is turned down, lab models show adipocytes shrink, cellular energy expenditure cues rise, and inflammatory noise softens. It’s not flipping a big performance switch; it’s removing sand from the cellular gears so pathways like sirtuin-guided repair and epigenetic tuning can hum the way they’re supposed to.
That’s why 5-Amino-1MQ has researchers’ attention: one precise enzyme target, system-wide ripple effects—from redox status to lipid handling—without acting like a hormone or receptor agonist.
5-Amino-1MQ (5-amino-1-methylquinolinium) is a small-molecule, cell-permeable inhibitor of nicotinamide N-methyltransferase (NNMT) — the enzyme that methylates nicotinamide (NAM) to 1-methylnicotinamide (1-MNA) using S-adenosyl-methionine (SAM) as the methyl donor. By blocking NNMT, 5-Amino-1MQ:
At the enzyme level it binds within NNMT’s substrate pocket with high selectivity; at the cellular level this reprograms metabolic signaling (e.g., sirtuin-dependent pathways) and has been shown in vitro and in rodent studies to lower 1-MNA, reduce adipocyte lipogenesis/size, and increase energy expenditure. In short, 5-Amino-1MQ acts as a metabolic/epigenetic “node” by inhibiting NNMT, thereby impacting NAD⁺ flux and methylation potential rather than directly activating a receptor.
It blocks NNMT, an enzyme that wastes niacin (NAM) and methyl groups, so your cells keep more NAD⁺ for mitochondrial upkeep and more SAM for healthy methylation. That upstream tweak can ripple through energy, fat storage, and cellular stress — less biochemical “drag,” more efficient housekeeping. Most evidence so far is preclinical (cells/animals), but the story is consistent: free up resources – systems run smoother.
What it may do:
Raise usable NAD⁺ – by stopping NAM from being siphoned off, it feeds the NAD⁺ salvage loop, supporting mitochondrial enzymes (e.g., sirtuins).
Preserve methyl donors (SAM) – less NNMT activity means a better SAM:SAH balance, which can steady epigenetic gene regulation.
Shrink fat-cell size – adipocytes tend to store less and burn more, trimming hypertrophy (seen in rodent/adipocyte studies).
Nudge metabolism toward “burn” – downstream of higher NAD⁺/sirtuins, cells often show higher energy expenditure signals.
Tame inflammatory tone – improved redox control and signaling can dial back some pro-inflammatory pathways.
Lower 1-MNA levels – a direct readout of NNMT inhibition; useful as a biochemical “proof it’s working.”
Note: These effects come from early research, not medical claims or dosing advice.
Oral capsules: 50–100 mg/day (often split 25–50 mg BID); some quote 50–150 mg/day and “cycles” of ~8–12 weeks with breaks.
“Injectable” protocols sold online: 150–600 µg/day with step-up schedules over 4–12 weeks (note the microgram units—this conflicts with capsule mg regimens and reflects nonstandard products).
Use our peptide dosage calculator in order to find out the correct dose for your model.
CellPeptides is an EU-based research chemical company who tries to live up to that exciting legacy. We provide pharmacological-grade SLU-PP-332 with the potential to form the basis for brand new discoveries.
With us, you get:
We handle the reliability (our 5-Amino-1MQ is synthesized in an EU-based WHO/GMP and ISO 9001:2015 certified lab), so you get the compound you need to contribute to the future of science. Every time.
Neelakantan H. et al. Selective and membrane-permeable small-molecule NNMT inhibitors reverse high-fat diet–induced obesity in mice.
https://pmc.ncbi.nlm.nih.gov/articles/PMC5826726/
Neelakantan H. et al. Structure–Activity Relationship for Small-Molecule Inhibitors of NNMT. J Med Chem (SAR incl. 5-Amino-1MQ).
https://pubmed.ncbi.nlm.nih.gov/28548833/ PubMed
Sampson C.M. et al. Combined NNMT inhibition and calorie restriction (microbiome & metabolic effects; uses 5-Amino-1MQ).
https://pmc.ncbi.nlm.nih.gov/articles/PMC7952898/
Dimet-Wiley A.L. et al. NNMT inhibition mimics/boosts exercise benefits in aged muscle (5-Amino-1MQ).
https://pmc.ncbi.nlm.nih.gov/articles/PMC11226645/ PMC
Dimet-Wiley A.L. et al. Reduced-calorie diet combined with NNMT inhibition (uses 5-Amino-1MQ).
https://www.nature.com/articles/s41598-021-03670-5 | PubMed: https://pubmed.ncbi.nlm.nih.gov/35013352/
Iyamu I.D. et al. Mechanisms and inhibitors of NNMT (review; potency notes for 5-Amino-1MQ).
https://pmc.ncbi.nlm.nih.gov/articles/PMC8372200/
Gao Y. et al. NNMT: an emerging therapeutic target (review; SAR mentions 5-Amino-1MQ IC₅₀ ≈ 1.2 µM).
https://www.sciencedirect.com/science/article/pii/S1359644621002427
Sun W.D. et al. NNMT: a novel pharmaceutical target (Frontiers review, 2024).
https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2024.1410479/full
Li X.Y. et al. NNMT as biomarker/target in cancer (broad context; inhibitor landscape).
https://pmc.ncbi.nlm.nih.gov/articles/PMC9218565/
Patent (methods & data excerpts): Quinoline-derived small-molecule NNMT inhibitors (incl. 5-Amino-1MQ).
https://patents.google.com/patent/US20200102274A1/en
| Molecular Structure: | Quinolinium core (benzopyridinium), N1-methyl (quaternized N), 5-amino (–NH₂) on the aromatic ring; overall +1 on the ring nitrogen with iodide (I⁻) as the counter-ion. |
|---|---|
| Molecular Weight: | 286.11 g/mol |
| Molecular Formula: | C₁₀H₁₁IN₂ |
| CAS Number: | 42464-96-0 |