Mechanism of action
NAD+ is the universal hydride acceptor that drives mitochondrial oxidative phosphorylation: glycolysis, the TCA cycle, and fatty-acid β-oxidation reduce NAD+ to NADH, which donates electrons at Complex I of the electron-transport chain. Beyond redox, NAD+ is a consumed substrate (not a coenzyme) for three families of NAD+-dependent enzymes — sirtuins (SIRT1–7, lysine deacylases regulating PGC-1α, p53, FOXO, and histone tails), PARPs (DNA-damage-induced poly-ADP-ribose polymerases), and CD38 (an ectoenzyme that hydrolyzes NAD+) — making cellular NAD+ pools rate-limiting for genome maintenance, transcriptional regulation of mitochondrial biogenesis, and circadian metabolism (reviewed in Connell et al.
NAD+ is the universal hydride acceptor that drives mitochondrial oxidative phosphorylation: glycolysis, the TCA cycle, and fatty-acid β-oxidation reduce NAD+ to NADH, which donates electrons at Complex I of the electron-transport chain. Beyond redox, NAD+ is a consumed substrate (not a coenzyme) for three families of NAD+-dependent enzymes — sirtuins (SIRT1–7, lysine deacylases regulating PGC-1α, p53, FOXO, and histone tails), PARPs (DNA-damage-induced poly-ADP-ribose polymerases), and CD38 (an ectoenzyme that hydrolyzes NAD+) — making cellular NAD+ pools rate-limiting for genome maintenance, transcriptional regulation of mitochondrial biogenesis, and circadian metabolism (reviewed in Connell et al., Endocrine Reviews 2024, https://pmc.ncbi.nlm.nih.gov/articles/PMC10692436/). Tissue NAD+ falls with age in humans, and the Sinclair/Imai paradigm posits that this decline contributes to age-related metabolic dysfunction. Oral precursors raise blood NAD+ in humans: NR at 100–2,000 mg/day for up to 12 weeks elevates whole-blood NAD+ safely (Martens et al., Nature Communications 2018, https://www.nature.com/articles/s41467-018-03421-7); NMN at 300–900 mg/day produces dose-dependent NAD+ elevation with the highest functional improvement at 600 mg/day (Yi et al., GeroScience 2023, https://pmc.ncbi.nlm.nih.gov/articles/PMC9735188/). Intravenous NAD+ infusion produces measurable changes in plasma and urinary NAD+ metabolites within 6 hours (Grant et al., Frontiers in Aging Neuroscience 2019, https://pmc.ncbi.nlm.nih.gov/articles/PMC6751327/).
Use & research dosing
NAD+ is not a regulated drug for longevity indications and has no FDA-approved dose. Oral precursor regimens with the strongest human evidence: nicotinamide riboside (NR) 250–1,000 mg/day for 6–12 weeks (Martens et al., 2018) and nicotinamide mononucleotide (NMN) 300–900 mg/day, with 600 mg/day producing the largest functional gains in a multicenter RCT (Yi et al., 2023). IV NAD+ infusion protocols commonly reported in clinics: 250–1,000 mg infused slowly over 2–6 hours, often repeated daily for 5–10 days followed by maintenance (Grant et al., 2019). SC self-administration commonly reported at 50–100 mg/day. All non-supplement parenteral protocols are off-label and lack regulator-validated dose-finding work.
Research-use framing only. SavePeptides sells nothing for human consumption. Doses above reflect reported research / self-experimentation ranges, not clinical recommendations.