Description

5-Amino-1MQ Nootropic Liquid

 

CAS Number	42464-96-0
Other Names	5-Amino-1-MQ iodide, 5-Amino-1-methylquinolinium, iodide (1:1), 5-Amino-1MQ iodide
IUPAC Name	1-methylquinolin-1-ium-5-amine
Molecular Formula	C₁₀H₁₁N₂I
Molecular Weight	286.11
Purity	≥99% Pure (LC-MS)
Liquid Availability	30mL liquid (50mg/mL, 1500mg bottle)
Powder Availability	3 grams, 6 grams, 9 grams  60 capsules (50mg/capsule, 3000mg total) 50 milligrams vial (lyophilized/freeze-dried)  100 milligrams vial (lyophilized/freeze-dried)
Storage	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)

1. Reverses diet-induced obesity phenotypes in mice and reduces white adipose tissue while preserving lean mass [1–4].
2. Increases cellular NAD⁺ and SAM availability and lowers intracellular 1-MNA, consistent with enhanced NAD⁺ salvage and a favorable “methyl economy” [1–3].
3. Augments adipocyte energy expenditure and remodels lipid metabolism, with links to polyamine flux and epigenetic marks observed with NNMT knockdown [2].
4. Combines with dietary improvement in DIO mice to accelerate weight/fat loss and improve composition versus diet alone [3,4].
5. 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. 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 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: 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
• [5] PubChem CID 950107 — 5-Amino-1-methylquinolinium (cation entry). https://pubchem.ncbi.nlm.nih.gov/compound/5-Amino-1-methylquinolinium
• [6] Sigma-Aldrich SML2832 — 5-Amino-1-methylquinolinium iodide technical page. https://www.sigmaaldrich.com/US/en/product/sigma/sml2832
• [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/
• [10] Diabetes Obesity & Metabolism (2024) — NNMT inhibition mitigates obesity-linked metabolic imbalance and liver pathology (translational perspective). https://dom-pubs.onlinelibrary.wiley.com/doi/10.1111/dom.15879
• [11] PubChem “NNMTi” (5-Amino-1-methylquinolinium iodide compound listing). https://pubchem.ncbi.nlm.nih.gov/compound/NNMTi

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