NAD+
Nicotinamide adenine dinucleotide, a coenzyme central to cellular energy metabolism and DNA repair, studied for age-related decline and its role in sirtuin activation.
Also referenced as: Nicotinamide Adenine Dinucleotide, NAD
Also appears in: Metabolic · Recovery
This name primarily lives in the research market and should not be read like an approved pharmaceutical product.
Primary lane: Longevity. Also surfaces under Metabolic, Recovery for browsing and discovery.
Nicotinamide Adenine Dinucleotide, NAD
FDA label signal · 732 trials · 57592 PubMed results
NAD+ has name-matched human trials with published or reported controlled evidence, but is not FDA-approved. The research is real and ongoing — treat findings as developing rather than settled.
NAD+ has 4 name-matched clinical trials (highest phase: Phase 3) and 57622 PubMed-indexed publications and is not FDA-approved. Human trials are registered but none have posted results yet.
Re-checked nightly against the registries — tracked since 2026-07-09. No band changes yet.
Grades evidence strength, not efficacy or safety. Research-use context; not medical advice. Graded 2026-07-13 from PubMed, ClinicalTrials.gov, ISRCTN, openFDA, Health Canada, and OpenAlex — computed deterministically and refreshed nightly, with a retraction check. How we grade →
What is NAD+?
NAD+ (nicotinamide adenine dinucleotide) is a coenzyme present in every living cell, essential for hundreds of metabolic reactions including glycolysis, the citric acid cycle, and oxidative phosphorylation. It also serves as a substrate for sirtuins (SIRT1–7) and poly(ADP-ribose) polymerases (PARPs), which regulate DNA repair, gene expression, and cellular stress responses.
Why it matters for aging research
NAD+ levels decline with age across multiple tissues. This decline has been linked to:
- Mitochondrial dysfunction — reduced NAD+ impairs the electron transport chain and shifts cells toward less efficient energy production (Gomes et al., Cell, 2013)
- DNA repair deficits — PARPs consume NAD+ during DNA damage repair; chronic low-grade damage depletes the pool (Fang et al., Cell Metabolism, 2014)
- Sirtuin activity — SIRT1 and SIRT3 require NAD+ as a co-substrate; declining NAD+ reduces their deacetylase activity (Imai & Guarente, Trends in Cell Biology, 2014)
Precursor vs. direct supplementation
Most oral NAD+ research uses precursors rather than direct NAD+ because the molecule itself has poor oral bioavailability:
- NMN (nicotinamide mononucleotide) — a direct NAD+ precursor; human trials show it raises blood NAD+ levels (Yoshino et al., Science, 2021)
- NR (nicotinamide riboside) — another precursor; the CHROMADIET trial showed dose-dependent NAD+ increases in humans (Martens et al., Nature Communications, 2018)
- IV NAD+ — bypasses oral absorption; used in clinical settings but not well-studied in controlled trials
- Subcutaneous NAD+ — available from research peptide vendors as injectable formulations (typically 100–500mg vials)
Research status
NAD+ biology is extensively published but injectable NAD+ supplementation specifically has limited clinical trial data. Key references:
- Yoshino et al. (2021) showed NMN supplementation improved muscle insulin sensitivity in prediabetic women (Science, 372(6547):1224–1229)
- Rajman et al. (2018) reviewed therapeutic potential of NAD+-boosting molecules (Cell Metabolism, 27(3):529–547)
- Covarrubias et al. (2021) linked NAD+ decline to age-related inflammation via CD38 upregulation (Nature Metabolism, 3:1–11)
Key considerations
- Injectable NAD+ from research vendors is not pharmaceutical-grade and has no FDA oversight
- The relationship between raising blood NAD+ and functional outcomes in humans is still being established
- Oral precursors (NMN, NR) have more human trial data than injectable NAD+ formulations