Maintain cell quality and reduce cell aging with β-nicotinamide mononucleotide (β-NMN), an intermediate in the biosynthesis of nicotinamide adenine dinucleotide (NAD+) (Bogan & Brenner). β-NMN is a product of the nicotinamide phosphoribosyltransferase (NAMPT) reaction and is converted to NAD+ by nicotinamide-nucleotide adenylyltransferase (Gallí et al.).

β-NMN has been used for:

MAINTENANCE AND SELF-RENEWAL
· Delays apoptosis in HL60 cells with MCT1 and MCT4 inhibition by restoring NAD+ levels and ATP depletion (Benjamin et al.).
· Protects MC3T3-E1 cells from aluminum-induced oxidative stress, and inhibits thioredoxin-interacting protein (TXNIP)-NLRP3 inflammasome pathway and pro-inflammatory cytokine production (Liang et al.).
DISEASE MODELING
· Reported to treat the pathophysiology of diet- and age-induced type 2 diabetes in mice. β-NMN ameliorates glucose intolerance by restoring NAD+ levels in type 2 diabetic mice models. β-NMN also enhances hepatic insulin sensitivity and restores gene expression related to inflammatory response, oxidative stress, and circadian rhythm, partly through SIRT1 (Yoshino et al.).
· Reported to diminish several old age-associated pathologies (decrease body weight gain, enhance energy metabolism, improve insulin sensitivity and eye function) in mouse models of aging (Mills et al.).
· Restores SIRT1 activity and reverses age-related arterial dysfunction by decreasing oxidative stress in mouse models of aging (Picciotto et al.).
· Reported to improve aging-induced cerebrovascular endothelial dysfunction and neurovascular coupling responses in old mice. Restores NAD+ and mitochondrial energetics and reduces mtROS in aged cerebromicrovascular endothelial cells (Tarantini et al.).
· Promotes mesenchymal stromal cell (MSC) expansion in vitro and in aged mice and upregulates SIRT1. Also, it is shown to stimulate osteogenesis of endogenous MSCs and protect bone from aging and irradiation induced damage in mice (Song et al.).