5-amino-1MQ 50mg – 30 capsules (preorder) Product Information
5-Amino-1MQ 50 mg — 30 oral research capsules. 5-Amino-1-methylquinolinium iodide is the lead first-in-class small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT) — an enzyme overexpressed in white adipose tissue of obese individuals where it consumes the methyl-donor pool and depletes tissue NAD⁺. In landmark mouse studies, oral 5-amino-1MQ produced robust reductions in adipocyte size, body fat and inflammatory adipokines while leaving food intake unchanged — pointing to a fundamentally novel “metabolic-rejuvenation” mechanism that operates entirely on the methylation–NAD axis. The 50 mg per-capsule format mirrors the daily oral dose used in published rodent pharmacology. RESEARCH USE ONLY · Not for human or veterinary use. For laboratory and collector purposes only. Purity ≥ 99 % (HPLC) — third-party tested, CoA on file Form Research capsules Content 50 mg 5-amino-1MQ (iodide salt) per capsule Total 30 capsules per bottle (1.5 g total) Packaging Sealed bottle with tamper-evident closure Storage Room temperature, dry, protected from light Molecular formula C₁₀H₁₁IN₂ (iodide salt) Molecular weight ≈ 286.11 g·mol⁻¹ IUPAC name 5-amino-1-methylquinolin-1-ium iodide CAS number 1374828-69-9 Synonyms 5A1MQ; NNMT inhibitor; MS1812 Research Overview Nicotinamide N-methyltransferase (NNMT) catalyzes the transfer of a methyl group from S-adenosyl-L-methionine (SAM) to nicotinamide, producing 1-methylnicotinamide and S-adenosyl-L-homocysteine [1]. In white adipose tissue of obese, insulin-resistant and aged mammals, NNMT is dramatically upregulated — and because it consumes both the universal methyl donor (SAM) and the NAD⁺ precursor (nicotinamide), its hyperactivity simultaneously depletes the cellular methylation reserve and the NAD-salvage pool [1,2]. 5-Amino-1MQ is the lead potent, selective small-molecule inhibitor of NNMT identified to date. Oral administration to diet-induced-obese mice for ~10 days reduces fat mass without altering food intake, decreases adipocyte size, restores insulin sensitivity, and increases adipose NAD⁺ and SAM levels [2]. In aged rodents, the same pharmacology has been extended to skeletal-muscle pathology, where it preserves muscle stem cell function and mitigates sarcopenia [3]. The molecule has become the canonical chemical probe for the entire NNMT–methylation–NAD axis and is the foundation for a growing field of “methylation-rejuvenation” research. Primary Research Areas NNMT enzymology and pharmacology — the lead first-in-class selective small-molecule NNMT inhibitor used to validate the entire target class [1,2]. Adipose biology and obesity research — robust reductions in adipocyte size and white-adipose mass in DIO mice without changes in food intake — a phenotype distinct from any approved anti-obesity mechanism [2]. Cellular methylation and NAD⁺ pool dynamics — the only well-characterized chemical probe that simultaneously raises tissue NAD⁺ and SAM, enabling clean studies of the methyl-donor / NAD-salvage interface [1,2]. Muscle aging and sarcopenia — preserves quiescent muscle-stem-cell pool and ameliorates aged-muscle dysfunction in rodent studies of sarcopenia [3]. Metabolic-rejuvenation and longevity research — central to an emerging research framework that connects methylation tone, NAD⁺ availability and tissue-specific aging [1,3]. References Kraus D, Yang Q, Kong D, et al. Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity. Nature. 2014;508(7495):258–262. Neelakantan H, Vance V, Wetzel MD, et al. Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Biochem Pharmacol. 2018;147:141–152. Neelakantan H, Brightwell CR, Graber TG, et al. Small molecule nicotinamide N-methyltransferase inhibitor activates senescent muscle stem cells and improves regenerative capacity of aged skeletal muscle. Biochem Pharmacol. 2019;163:481–492.
