Fosribnicotinamide

Fosribnicotinamide (β-nicotinamide mononucleotide) is a product of the nicotinamide phosphoribosyltransferase (NAMPT) reaction and a key NAD⁺ intermediate. The pharmacological activities of Fosribnicotinamide include its role in cellular biochemical functions, cardioprotection, diabetes, Alzheimer's disease, and complications associated with obesity^[1]. In Vitro:Fosribnicotinamide (β-nicotinamide mononucleotide) has several beneficial pharmacological activities. Mostly mediated by its involvement in NAD⁺ biosynthesis, the pharmacological activities of NMN include its role in cellular biochemical functions, cardioprotection, diabetes, Alzheimer's disease, and complications associated with obesity^[1].
The intracellular NAD⁺ levels are significantly decreased by knockdown or knockout of Nampt (Nampt KD or Nampt KO) or treatment with Nampt inhibitor FK866, whereas NAD⁺ levels are dramatically increased by supplement of NAD⁺ precursors NAM or NMN (0.5-1 mM). NAD⁺ precursor NMN treatment inhibited CD8⁺ T cells activation and function^[2]. In Vivo:Fosribnicotinamide (β-nicotinamide mononucleotide) (500 mg/kg; i.p.; 3 times per week for 7-10 week) prevents mtDNA damage and Dox-induced cardiac dysfunction^[3].
Nampt KO markedly inhibits tumor progression, whereas Nampt metabolite Fosribnicotinamide (300 mg/kg body weight; i.p.; once every two days for 2 weeks) significantly promotes tumor growth in C57BL/6 mice (bearing wildtype Hepa1-6 cells). The reduction and increase in NAD⁺ level of respective Nampt KO and Fosribnicotinamide-treated tumors are confirmed^[2].
Fosribnicotinamide ameliorates glucose intolerance by restoring NAD⁺ levels in HFD-induced T2D mice.Fosribnicotinamide also enhances hepatic insulin sensitivity and restores gene expression related to oxidative stress, inflammatory response, and circadian rhythm, partly through SIRT1 activation^[4].