NAD+ 500mg Cellular senescence

This vial delivers 500 mg of high-purity NAD+ (>98 %, HPLC), type I glass, fluorinated butyl stopper, inert seal. Lyophilisation protects the molecule from hydrolysis: as anhydrous solid at -20 C, stability exceeds 24 months. After reconstitution in bacteriostatic water, the solution remains usable for 14 days refrigerated at 4-8 C, provided warming-cooling cycles and light exposure are minimised. In accordance with European regulations, this product is intended exclusively for in vitro research and preclinical studies on non-human models: it is neither a medicinal product, a food supplement, nor a medical device.

This product is not intended for human use. The protocols described are examples drawn from scientific literature and documented clinical practices, provided strictly for informational purposes for research work on non-human models.

Sealed unreconstituted vialStorage in the fridge (+2 to +8 °C); a -20 °C freezer is an option for long-term storage (over 3 months). At room temperature (20-25 C), do not store beyond 30 days; beyond, NAD+ oxidation to ADP-ribose accelerates.

If in doubt, discard the vial. The cost of a reconstituted vial is negligible compared to research time lost on data corrupted by degraded product. Rigorously document reconstitution date, lot, draws performed and storage conditions in a laboratory logbook.

NAD+ participates in four major families of enzymatic reactions. First, as a redox coenzyme: glycolysis, the Krebs cycle and beta-oxidation convert NAD+ into NADH, whose reducing equivalents feed the mitochondrial respiratory chain (complex I) to generate ATP. The cytoplasmic and mitochondrial NAD+/NADH ratio is a real-time metabolic sensor: a high ratio signals efficient energy status, a low ratio indicates metabolic saturation or relative hypoxia.

Second, NAD+ is the obligatory substrate of sirtuins (SIRT1 to SIRT7), deacetylases and ADP-ribosyltransferases described by Shin-ichiro Imai in 2000 (Nature). SIRT1 deacetylates PGC-1alpha (mitochondrial biogenesis), FOXO3 (longevity, autophagy), p53 (senescence) and numerous histones. SIRT3 is the major mitochondrial sirtuin: it deacetylates SOD2 (antioxidant defence), the respiratory chain and several Krebs cycle enzymes. When NAD+ falls, sirtuin activity collapses in cascade, accelerating the epigenetic and metabolic drift associated with ageing.

Third, NAD+ is consumed by PARPs (Poly-ADP-Ribose Polymerases) during DNA break repair. PARP1 can consume up to 100 NAD+ molecules per second during massive genotoxic stress, literally depleting the cellular pool. The PARP/sirtuin competition for NAD+ explains why chronic inflammatory states or radiation exposure accelerate NAD+ decline.

Fourth, NAD+ is hydrolysed by CD38, an ectonucleotidase expressed on immune cells and senescent tissues. CD38 increases with age (Camacho-Pereira 2016 Cell Metabolism), to the point of becoming the main driver of NAD+ decline in older subjects. CD38 inhibitors (apigenin, 78c) are studied as complementary strategies to NAD+ precursors.

The NAD+ and precursors literature exceeds 15,000 PubMed-indexed publications. Pivotal studies have established three data layers: NAD+ decline with age, precursor efficacy, and human clinical trials.

Massudi 2012 PLoS One first quantified human tissue NAD+ decline: skin biopsies from 30 subjects aged 20-60, mean 50 % drop, negative correlation r = -0.65 with age. Zhu 2015 PNAS showed by in vivo 31P MRS that brain NAD+ falls with age in healthy humans.