5-Amino-1MQ is sold for laboratory research use only. Terms of sale apply. Not for human consumption, nor medical, veterinary, or household uses. Please familiarize yourself with our Terms & Conditions prior to ordering.
Store in cool dry environment, away from direct sunlight.
Terms
All products are for laboratory developmental research USE ONLY. Products are not for human consumption.
5-Amino-1MQ is sold for laboratory research use only. Terms of sale apply. Not for human consumption, nor medical, veterinary, or household uses. Please familiarize yourself with our Terms & Conditions prior to ordering.
What Is 5-Amino-1MQ (NNMT Inhibitor) Research Liquid?
5-Amino-1-methylquinolinium (5-Amino-1MQ) is a small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT), the cytosolic enzyme that methylates nicotinamide to 1-methylnicotinamide (1-MNA) using S-adenosyl-L-methionine (SAM) as the methyl donor. Inhibition of NNMT rebalances cellular “methyl economy” and NAD⁺ salvage flux, with downstream effects on adipocyte energetics, lipid handling, and insulin action observed in preclinical systems [1–3]. In diet-induced obesity (DIO) models, NNMT loss-of-function and selective small-molecule inhibitors reduce white adipose mass and improve metabolic parameters without overt toxicity, positioning NNMT as a tractable target for metabolic-disease research [2–4]. CAS: 42464-96-0 (commonly supplied as the iodide salt). Structure, identifiers, and physical data are cataloged in curated chemical databases and supplier technical sheets [5–7].
Why Is It Called 5-Amino-1MQ?
The shorthand “5-Amino-1MQ” describes a quinolinium scaffold bearing a methyl substituent at the ring nitrogen (1-methylquinolinium) and an amino group at the 5-position. In the NNMT literature it appears as “5-amino-1MQ,” “5A-1MQ,” or “NNMTi” when referring to the selective, substrate-site-targeting inhibitor series. Reported biochemical potency against human NNMT is in the low-micromolar range with cellular EC₅₀ values in the low-micromolar range for suppression of 1-MNA and lipogenesis, with selectivity over related methyltransferases and NAD⁺-salvage enzymes [1,6,7].
5 Main Research Findings for 5-Amino-1MQ (and NNMT Inhibition)
Reverses diet-induced obesity phenotypes in mice and reduces white adipose tissue while preserving lean mass [1–4].
Increases cellular NAD⁺ and SAM availability and lowers intracellular 1-MNA, consistent with enhanced NAD⁺ salvage and a favorable “methyl economy” [1–3].
Augments adipocyte energy expenditure and remodels lipid metabolism, with links to polyamine flux and epigenetic marks observed with NNMT knockdown [2].
Combines with dietary improvement in DIO mice to accelerate weight/fat loss and improve composition versus diet alone [3,4].
NNMT dysregulation is implicated across obesity, insulin resistance, liver pathology, and other disorders; selective NNMT inhibitors such as 5-Amino-1MQ are prominent tool compounds for target validation [2,8,9].
Mechanistic Rationale
NNMT consumes nicotinamide and SAM to produce 1-MNA and S-adenosylhomocysteine (SAH). By inhibiting NNMT, 5-Amino-1MQ reduces 1-MNA formation and alleviates the methyl “sink,” increasing SAM availability for other methylation reactions, while freeing nicotinamide for recycling through NAMPT toward NAD⁺. Increased NAD⁺ supports redox and sirtuin-dependent pathways tied to mitochondrial function, lipid oxidation, and insulin action. In adipocytes, NNMT inhibition elevates NAD⁺ and SAM and suppresses de novo lipogenesis in a concentration-dependent manner, consistent with on-target activity [1–3].
Selected Preclinical Data
Study 1: Genetic Proof-of-Concept
A seminal investigation reported elevated NNMT expression in white adipose tissue (WAT) and liver of obese/diabetic mice; targeted NNMT knockdown protected against DIO by increasing energy expenditure. Mechanistically, NNMT suppression increased adipose SAM and NAD⁺, upregulated polyamine flux enzymes (ODC, SSAT), and altered histone methylation consistent with a shift toward oxidative metabolism [2].
Study 2: Selective Small-Molecule Inhibitors (including 5-Amino-1MQ) A selective, membrane-permeable NNMT inhibitor series decreased intracellular 1-MNA, increased NAD⁺ and SAM, suppressed adipocyte lipogenesis, and reversed high-fat-diet obesity in mice. Off-target activity was minimal at active concentrations, supporting on-target engagement [1].
Study 3: Combination With Diet Independent work showed that NNMT inhibition plus a lean/low-fat diet accelerated weight and fat loss beyond diet alone, improved the lean-mass-to-body-weight ratio, and ameliorated obesity-linked liver pathologies; diet alone failed to normalize the liver readouts to the same degree [3,4].
Representative Figure
Fig. 1 — NNMT vs NAD⁺ salvage schematic
Fig. 1. Pathway map of NNMT and NAD⁺ salvage in adipocytes, highlighting nicotinamide → NAMPT → NMN → NAD⁺ and the competing NNMT branch to 1-MNA; 5-Amino-1MQ blocks the NNMT node to favor salvage flux [1–3].
Fig. 2 — Body composition in DIO mice – NNMTi
Fig. 2. Body composition in DIO mice with/without NNMT inhibition showing reduced WAT mass with preserved lean mass relative to diet-matched controls [1,3,4].
Fig. 3 — Cellular readouts in 3T3-L1 adipocytes
Fig. 3. Cellular readouts in 3T3-L1 adipocytes: decreased 1-MNA, increased NAD⁺ and SAM, and reduced lipogenesis after 5-Amino-1MQ exposure [1,6,7].
In-Vitro Pharmacology and Selectivity
Biochemical profiling places 5-Amino-1MQ potency for research NNMT in the low-micromolar IC₅₀ range under standardized assay conditions, with cell-based EC₅₀ values in the low micromolar range for lowering 1-MNA and suppressing lipogenesis. Vendor technical sheets and primary studies report selectivity over related methyltransferases and enzymes of the NAD⁺ salvage pathway [1,6,7].
Translational Considerations and Safety
NNMT has emerged as a systems-level regulator linking methylation capacity, NAD⁺ biology, and adipocyte energetics; reviews connect NNMT overexpression to obesity, insulin resistance, fatty-liver progression, and other conditions [2,8,9]. To date, efficacy and safety of 5-Amino-1MQ remain preclinical; there are no peer-reviewed human interventional trials of 5-Amino-1MQ. Research use therefore focuses on mechanism, target validation, and combinatorial experiments (e.g., with dietary change or NAD⁺ precursors) [1–4,8,9].
Formulation and Stability Considerations (Research Use)
5-Amino-1MQ is commonly supplied as the crystalline iodide salt. For stock solutions, many laboratories dissolve in DMSO or ethanol before aqueous dilution for in-vitro work; solubility, pH, and ionic strength should be validated per assay. Light, oxygen, and moisture can impact small-molecule stability; opaque containers, dry storage, minimized headspace, and low temperature are typical practices in analytical labs. Lot-specific COAs should be followed, and stability confirmed by standard QC (e.g., HPLC) [6,7].
Discussion
Across rodent and cell models, NNMT inhibition acts as a metabolic “re-allocator,” simultaneously relieving a methyl sink and diverting nicotinamide back to NAD⁺ salvage. The phenotypic outcome is a shift toward higher energy expenditure and improved adipose/lipid profiles without the catabolic loss of lean tissue commonly seen with severe caloric restriction. Combination data with diet suggest complementary mechanisms, and reviews highlight continued medicinal-chemistry work to tune potency, selectivity, and exposure for future translational studies. Open questions include tissue-selective delivery, chronic dosing effects on one-carbon metabolism, and interactions with NAD⁺ precursor strategies [1–4,8,9].
Selected Preclinical Findings
NNMT knockdown protects against DIO via increased energy expenditure and remodeled polyamine flux; adipose epigenetic marks favor oxidative metabolism [2].
Selective NNMT inhibitors (including 5-Amino-1MQ) lower 1-MNA, increase NAD⁺ and SAM, suppress adipocyte lipogenesis, and reverse HFD-induced obesity in mice [1].
NNMT inhibition plus a lean diet accelerates weight/fat loss, improves body-composition indices, and normalizes several liver pathologies versus diet alone [3,4].
Contemporary reviews consolidate evidence that 5-Amino-1MQ is a potent, selective NNMT inhibitor with broad utility as a research tool in metabolic biology [8,9].
FAQs
What is 5-Amino-1MQ?
A quinolinium-based, selective NNMT inhibitor used to interrogate NNMT biology in cells and animal models of obesity, insulin resistance, and related metabolic phenotypes (commonly as the iodide salt; CAS 42464-96-0).
How does 5-Amino-1MQ work?
It inhibits NNMT, lowering 1-MNA formation while increasing availability of nicotinamide for NAD⁺ salvage and SAM for other methylation reactions; adipocytes show increased NAD⁺ and altered lipid handling in models.
What is the shelf life of 5-Amino-1MQ?
Shelf life is supplier-specific and formulation-dependent. As general lab practice, intact, unopened solid stored dry, light-protected, and cool is often assigned 24 months by chemical suppliers; solvent stocks are typically prepared fresh, aliquoted, and frozen, with aqueous dilutions used same day. Always follow the COA and confirm by analytical QC.
How should I store it?
Store the solid in a desiccated, light-protected container at low temperature with a tight seal. Prepare small solvent aliquots to minimize freeze–thaw cycles and reduce exposure to air/light during handling.
Is it water-soluble?
The iodide salt is polar, but working stocks are typically prepared in DMSO or ethanol, then diluted into aqueous buffers. Verify solubility and pH compatibility empirically for your assay system.
What concentration should I start with in cells?
Preclinical work commonly screens low-micromolar ranges (e.g., 1–30 μM) for pathway readouts such as 1-MNA reduction and lipogenesis suppression; use a titration series with appropriate vehicle and pathway controls.
Can it be combined with NAD⁺ precursors in research?
Yes. Because NNMT intersects NAD⁺ salvage, pairing with NMN/NR is a common experimental strategy to test additive or synergistic effects on cellular NAD⁺ and metabolic endpoints; design factorial studies and confirm pathway engagement.
Is 5-Amino-1MQ legal to purchase?
For legitimate laboratories, it is generally available under “research use only” terms. It is not approved as a drug or dietary ingredient.
OVERALL CONCLUSIONS
5-Amino-1MQ enables precise interrogation of NNMT’s role at the crossroads of NAD⁺ metabolism, one-carbon biochemistry, and adipocyte energetics. Genetic and pharmacologic NNMT suppression reduces adiposity and improves metabolic readouts in preclinical models, with supportive cellular data showing increases in NAD⁺ and SAM and suppression of lipogenesis. The target is well-validated mechanistically; the compound class is promising as a research platform for metabolic-disease biology and combinatorial strategies with diet or NAD⁺ precursor approaches. Human efficacy and long-term safety data are not yet available, so applications remain strictly within laboratory research.
Regulatory Note
5-Amino-1MQ is sold for laboratory research use only. Terms of sale apply. Not for human consumption, nor medical, veterinary, or household uses. Review all Terms & Conditions prior to ordering.
References
[A] Umbrella Labs product page — 5-Amino-1MQ research liquid: https://umbrellalabs.is/shop/nootropics/nootropic-liquid/5-amino-1mq-liquid/
[1] Neelakantan H, et al. Selective and membrane-permeable small-molecule inhibitors of NNMT reverse high-fat-diet-induced obesity in mice and remodel adipocyte metabolism (open-access). https://pmc.ncbi.nlm.nih.gov/articles/PMC5826726/
[2] Kraus D, et al. Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity by augmenting energy expenditure. Nature Medicine (primary report; open-access). https://pmc.ncbi.nlm.nih.gov/articles/PMC4107212/
[3] Sampson CM, et al. Combined NNMT inhibition and lean-diet substitution improves adiposity and body-composition endpoints in DIO mice. Scientific Reports. https://www.nature.com/articles/s41598-021-85051-6
[4] Dimet-Wiley A, et al. Reduced-calorie diet combined with NNMT inhibition normalizes liver pathologies vs diet alone. Scientific Reports. https://www.nature.com/articles/s41598-021-03670-5
[7] Sigma-Aldrich catalog index for 5-Amino-1-methylquinolinium iodide (lists CAS 42464-96-0). https://www.sigmaaldrich.com/BR/en/search/5-amino-1-mq-iodide-supplier?focus=products
[8] Liu JR, et al. Roles of Nicotinamide N-Methyltransferase in Obesity and Type 2 Diabetes (review). https://pmc.ncbi.nlm.nih.gov/articles/PMC8337113/
[9] Sun WD, et al. Nicotinamide N-methyltransferase: metabolic regulator and emerging therapeutic target (2024 review). https://pmc.ncbi.nlm.nih.gov/articles/PMC11196770/
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