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5-Amino-1MQ

C
Animal replicated
Research chemicalNNMT InhibitorSmall MoleculeNAD+ Metabolism Modulator
RouteOralGray-market only
C
Evidence grade: Animal replicated

Effect demonstrated in multiple animal studies; human data sparse or extrapolated. Grades summarize evidence quality, not whether a compound is appropriate, legal, or risk-free.

At a glance
What it is
5-Amino-1-Methylquinolinium — NNMT Inhibitor — Oral Small Molecule — NNMT Inhibitor, Small Molecule, NAD+ Metabolism Modulator.
Why people use it
Used primarily for muscle and performance and weight loss.
What the evidence supports
Both 5-Amino-1MQ and NMN/NR raise intracellular NAD+. The mechanisms are fundamentally different and potentially synergistic rather than competing. NMN and NR add NAD+ precursors — they increase the supply side of NAD+ synthesis. 5-Amino-1MQ reduces the catabolic drain — it decreases the rate at which nicotinamide is removed from the NAD+ precursor pool. In metabolic disease states where NNMT is overexpressed, the catabolic drain is accelerated — meaning NAD+ precursor supplementation competes directly with an upregulated disposal system. NNMT inhibition addresses the disposal system; NMN/NR address the supply. The theoretical case for combining them: in NNMT-overexpressed obesity, combine NMN (increases precursor flux) with 5-Amino-1MQ (reduces catabolic drain) for greater NAD+ elevation than either alone. This has not been tested in humans. The mouse data for the combination is encouraging from the 2021 Sampson study (where NNMT inhibition + dietary intervention was synergistic for liver fat).
If you only read one thing

5-Amino-1MQ raises NAD+ not by adding more of anything, but by stopping the body from throwing nicotinamide away. NNMT converts nicotinamide into a metabolic dead-end (1-MNA) that cannot be used for NAD+ synthesis and is simply excreted. Block NNMT, and nicotinamide is redirected toward NAD+ production instead. SAM — consumed in the process — is also spared, potentially improving global cellular methylation capacity. The mouse data is genuinely impressive: fat loss without food restriction, muscle function improvement in aged animals, NAD+ elevation. The human evidence base is zero. The community uses it at doses extrapolated from mouse IP injection data using allometric scaling that does not account for oral vs IP bioavailability differences. Clinics are prescribing it to humans. The FDA has made no ruling on its safety. A 2025 Cell Press review calls for clinical translation. And the molecule being blocked — 1-MNA — has documented protective roles in liver and kidney biology that the community narrative has largely ignored. This is the most enthusiasm-versus-evidence gap of any compound in this reference.

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Published literature
0human trials0human studies4animal3in vitro

No published human trials, Phase 1 safety study, human pharmacokinetic study, or human dose-response data for 5-Amino-1MQ.

Evidence reality check
Human evidence
No human studies
0 observational; RCT evidence not present in corpus.
Preclinical base
7 lab signals
4 animal; 3 in-vitro/mechanistic.
Evidence snapshot
Both 5-Amino-1MQ and NMN/NR raise intracellular NAD+. The mechanisms are fundamentally different and potentially synergistic rather than competing. NMN and NR add NAD+ precursors — they increase the supply side of NAD+ synthesis. 5-Amino-1MQ reduces the catabolic drain — it decreases the rate at which nicotinamide is removed from the NAD+ precursor pool. In metabolic disease states where NNMT is overexpressed, the catabolic drain is accelerated — meaning NAD+ precursor supplementation competes directly with an upregulated disposal system. NNMT inhibition addresses the disposal system; NMN/NR address the supply. The theoretical case for combining them: in NNMT-overexpressed obesity, combine NMN (increases precursor flux) with 5-Amino-1MQ (reduces catabolic drain) for greater NAD+ elevation than either alone. This has not been tested in humans. The mouse data for the combination is encouraging from the 2021 Sampson study (where NNMT inhibition + dietary intervention was synergistic for liver fat).
From the chapter quick-reference block.
Categories
Muscle & PerformanceWeight Loss & MetabolicMitochondrial & Energy
Properties
Active malignancy: cautionNot injectable
Evidence
CAnimal replicated
The Core Mechanism
NNMT consumes SAM (the body's universal methyl donor) to methylate nicotinamide into 1-methylnicotinamide (1-MNA). 1-MNA is irreversible — once made, nicotinamide cannot be recovered for NAD+ synthesis; 1-MNA is further oxidized and excreted. NNMT activity therefore simultaneously: depletes nicotinamide (reducing NAD+ precursor availability); depletes SAM (reducing the cell's capacity for other methylation reactions); produces SAH (a homocysteine precursor). Blocking NNMT with 5-Amino-1MQ reverses all three: nicotinamide is preserved for NAD+ synthesis; SAM is spared for other methyl transfer reactions (DNA methylation, histone methylation, protein methylation); SAH production falls, reducing homocysteine. This is mechanistically distinct from NMN or NR — those add precursors; 5-Amino-1MQ removes a catabolic drain.
The Preclinical Evidence
Neelakantan et al. (2019, Biochemical Pharmacology): diet-induced obese mice; 5-Amino-1MQ; significant reductions in body weight, adipose tissue mass, adipocyte size, elevated NAD+ — without food restriction changes. This was the landmark fat loss study. Dimet-Wiley et al. (2024, Scientific Reports): aged mice; NNMT inhibition mimics and boosts exercise-mediated improvements in muscle function. Sampson et al. (2021, Scientific Reports): NNMT inhibitor + lean diet combination; reduced liver fat content and hepatic steatosis beyond either intervention alone. All evidence is preclinical — mice only. No human data.
The Evidence Status
Zero published human trials. Zero Phase 1 safety data. Zero human pharmacokinetic data. Some clinics have begun prescribing 5-Amino-1MQ to humans. A 2025 Trends in Pharmacological Sciences (Cell Press) review specifically calls for clinical translation of NNMT inhibitors. The community dose of 50-100 mg/day was extrapolated from mouse IP injection doses of 10-20 mg/kg using allometric conversion — a methodology that does not account for the different route of administration (IP vs oral bioavailability is substantially different for most compounds) or human metabolism differences.
The 1-MNA Complication
1-Methylnicotinamide (1-MNA) — the molecule that 5-Amino-1MQ prevents from being produced — is not simply metabolic waste. Emerging evidence shows 1-MNA has protective biological roles: protects against hepatic ischemia-reperfusion injury; ameliorates renal fibrosis by inhibiting TGF-β1/Smad3 signaling; has anti-inflammatory effects in vascular tissue. In cancer, NNMT overexpression promotes tumor progression — so blocking NNMT and 1-MNA is anti-cancer in that context. The NNMT/1-MNA axis is more biologically complex than the community narrative acknowledges. The consequences of chronically suppressing 1-MNA in humans are unknown.
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