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NNMT Inhibitor  //  NAD+ Salvage Modulator

Small-Molecule
5-Amino-1MQ Protocol

A selective nicotinamide N-methyltransferase inhibitor investigated in research models for preservation of intracellular SAM and NAD+ pools — with downstream signalling implications for adipocyte energetics, white-fat browning and muscle stem-cell rejuvenation.

NNMT Inhibition Mechanism

How a single small-molecule blockade is studied across three downstream metabolic axes in laboratory research.

01 — NNMT Blockade

Enzymatic Inhibition

Selectively binds the NNMT active site, attenuating methylation of nicotinamide and conserving the methyl-donor pool — a primary upstream node studied in metabolic and longevity models.

02 — SAM & NAD+

Cofactor Preservation

Investigated for its capacity to spare S-adenosylmethionine and increase NAD+ salvage flux, supporting sirtuin-related signalling and mitochondrial bioenergetics in cellular research.

03 — Adipose & Muscle

Tissue-Level Studies

Examined in adipocyte models for energy expenditure and white-fat browning, and in muscle stem-cell research for satellite-cell function and regenerative capacity with age.

Research Applications

Where 5-Amino-1MQ sits within the broader NAD+ and longevity research landscape.

01 — Adipocyte Energetics

Metabolic Models

Used in adipose-tissue research to investigate basal energy expenditure, lipid mobilisation and white-to-beige adipocyte transition under chronic NNMT-suppressed conditions.

02 — NAD+ Salvage

Cofactor Pathway Studies

Studied alongside NMN and NR as an upstream regulator rather than a direct precursor — preserving endogenous NAD+ via methyl-donor conservation rather than substrate loading.

03 — Muscle Rejuvenation

Stem-Cell Research

Featured in investigations of aged muscle satellite-cell quiescence, self-renewal capacity and regenerative output following injury in preclinical longevity research.

Compound Profile

Identity at a glance.

PropertyDetail
Chemical name5-amino-1-methylquinolinium — a small molecule, not a peptide
Formula & weightCation C10H11N2+, 159.2 g/mol; commonly supplied as the iodide salt (C10H11IN2, 286.1 g/mol, CAS 42464-96-0)
TargetNicotinamide N-methyltransferase (NNMT)
Human dataNone published
Regulatory statusNot an approved medicine or dietary ingredient

Published Research

The studies behind NNMT inhibition as a research strategy.

StudyWhat it found
2014 — NNMT knockdownReducing NNMT expression in adipose tissue and liver protected mice against diet-induced obesity by increasing energy expenditure, establishing NNMT as a metabolic target.1
2018 — Small-molecule inhibitorsMembrane-permeable NNMT inhibitors, including 5-amino-1MQ, reduced body weight, white fat mass and adipocyte size in diet-induced obese mice without changing food intake.2
2019 — Aged muscleAn NNMT inhibitor activated senescent muscle stem cells and improved regenerative capacity after injury in aged mice.3
2024 — Exercise in aged miceNNMT inhibition mimicked and enhanced exercise-induced improvements in muscle function in aged mice.4

Evidence Quality & Limitations

All 5-amino-1MQ efficacy data come from mouse and cell studies, largely from one research group, and there are no published human pharmacokinetic or safety studies. Effects on SAM and NAD+ pools are inferred from NNMT biology and animal measurements. Because it is a small molecule rather than a peptide, its solubility, stability and handling differ from the peptides in these guides.

References

  1. Kraus D, et al. Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity. Nature. 2014;508:258–62. PubMed
  2. Neelakantan H, et al. Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Biochem Pharmacol. 2018;147:141–52. PubMed
  3. Neelakantan H, et al. Small molecule nicotinamide N-methyltransferase inhibitor activates senescent muscle stem cells and improves regenerative capacity of aged skeletal muscle. Biochem Pharmacol. 2019;163:481–92. PubMed
  4. Dimet-Wiley AL, et al. Nicotinamide N-methyltransferase inhibition mimics and boosts exercise-mediated improvements in muscle function in aged mice. Sci Rep. 2024;14:15554. PubMed

Technical FAQ

Questions researchers ask most often.

Q · 01

How does 5-Amino-1MQ differ from NMN or NR?

NMN and NR act as direct NAD+ precursors, loading the salvage pathway with substrate. 5-Amino-1MQ instead inhibits NNMT upstream, conserving the methyl-donor SAM and indirectly preserving NAD+ pools — a distinct mechanism studied in parallel rather than in competition.

Q · 02

What is the stability and storage profile?

5-Amino-1MQ is typically handled as a lyophilised small-molecule powder for maximum molecular stability. Store the dry vial in a cool, dark environment. Once reconstituted with an appropriate research-grade diluent, refrigerate and use within the validated stability window for the protocol.

Q · 03

What dosing protocol is used in research?

Preclinical research protocols typically employ once-daily administration in rodent metabolic and muscle-regeneration models, with dose ranges titrated against NNMT activity readouts and downstream NAD+/SAM measurements. Strictly for laboratory research use only.

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