nicotinamide mononucleotide

β-nicotinamide mononucleotide (NMN) is a natural nucleotide and a key intermediate in the synthesis of coenzyme I (NAD+). β-nicotinamide mononucleotide is involved in a number of biochemical reactions in the human body, which are related to immunity and metabolism.

β-Nicotinamide mononucleotide-d4 is the deuterated form of β-Nicotinamide mononucleotide. β-Nicotinamide mononucleotide (β-NM) is the product of the nicotinamide phosphoribosyltransferase (NAMPT) reaction and serves as a critical intermediate in the synthesis of NAD+. It plays roles in cellular biochemical functions, and has implications in cardioprotection, diabetes, Alzheimer's disease, and obesity-related complications.

β-Nicotinamide mononucleotide (Standard) is a reference standard for research and analysis in studies involving β-Nicotinamide mononucleotide. β-nicotinamide mononucleotide (NMN) is a natural nucleotide and a key intermediate in the synthesis of coenzyme I (NAD+). β-nicotinamide mononucleotide is involved in a number of biochemical reactions in the human body, which are related to immunity and metabolism.

β-Nicotinamide mononucleotide, reduced form (NMNH) disodium is the reduced variant of β-Nicotinamide mononucleotide, with oral bioavailability. This compound significantly increases NAD+ and NADH levels while inhibiting glycolysis, the tricarboxylic acid cycle, and cell growth, mechanisms that are dependent on nicotinamide mononucleotide adenylyltransferase (NMNAT).

SBI-797812 is structurally similar to active-site directed inhibitor of NAMPT(NAMPT with EC50 of 0.37 μM).

Sulfo-ara-F-NMN is an analogue of nicotinamide mononucleotide (NMN) with cellular permeability. Sulfo-ara-F-NMN was selective to activate SARM1 and inhibited CD38 with an IC50 of about 10 μM. Activation by Sulfo-ara-F-NMN to Z-48 or NMN, which has a higher cyclase activity, causes conformational changes in SARM1, resulting in cADPR production, NAD depletion, and non-apoptotic cell death.