n methylnicotinamide

N-Methylnicotinamide is one of the endogenous metabolites that ameliorates endothelial dysfunction.

TRIA-662 (Nicotinamide Chloromethylate) is a niacin metabolite excreted via the urinary system.

Bisubstrate inhibitor 78 is an inhibitor of nicotinamide N-methyltransferase (NNMT; IC50= 1.41 μM).1It binds the NNMT active site in the binding pockets for the NNMT substrates S-adenosyl-L-methionine (SAM) and nicotinamide . Bisubstrate inhibitor 78 is selective for NNMT over histone-lysine N-methytransferase NSD2 and protein arginine methyltransferase 1 (PRMT1; IC50s = >50 μM for both). It reduces levels of 1-methylnicotinamide in, and inhibits proliferation of, HSC-2 oral cancer cells when used at a concentration of 100 μM.This compound is unstable in powder form and other related salt forms are recommended.

1-Methylnicotinamide is the active metabolite of nicotinamide, formed by nicotinamide N-methyltransferase. 1-Methylnicotinamide induces the secretion of nitric oxide by human umbilical vein endothelial cells (HUVECs) in a concentration-dependent manner. When administered at a dose of 30 mg/kg, it can increase the level of 6-keto-prostaglandin F1α in rat plasma and inhibit collagen-induced thrombosis at the same dose.

NNMTi (5-Amino-1-methylquinolinium) is a substrate site-targeting, selective nicotinamide N-methyltransferase (NNMT) inhibitor (IC50 = 1.2 μM; 50 μM SAM, 100 μM NCA) that reduces 3T3-L1 lipogenesis (EC50 = 30μM) and adipocytes 1-methylnicotinamide level (EC50 = 2.3 μM) without affecting related methyltransferases & enzymes in the NAD+ salvage pathway

N-Methylnicotinamide is one of the endogenous metabolites that ameliorates endothelial dysfunction.