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longevity

NAD+

Also known as: Nicotinamide Adenine Dinucleotide, NAD Plus, NAD
FDA: Not FDA-approved as drug WADA: Not prohibited

Nicotinamide adenine dinucleotide (NAD+) is a coenzyme found in every living cell, essential for over 500 enzymatic reactions including energy metabolism, DNA repair, gene expression regulation, and cellular signaling. While not technically a peptide, NAD+ is commonly included in peptide therapy protocols due to its central role in anti-aging medicine. NAD+ levels decline ~50% between ages 40 and 60, and this decline is implicated in age-related metabolic dysfunction, neurodegeneration, and reduced cellular repair capacity. Supplementation strategies include direct NAD+ administration (IV or SubQ), oral precursors (NMN, NR), and combination approaches. With 301,000 monthly search volume and 1,350+ PubMed publications on

This content is for educational and research purposes only. VialBase does not provide medical advice. Consult a healthcare professional before using any peptide.

Molecular weight 663.43 Da
Half-life ~30-45 minutes IV
CAS number —
Route Intravenous · Subcutaneous · Oral (NMN/NR precursors) · Transdermal intravenous preferred
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Mechanism

Essential coenzyme for 500+ enzymatic reactions — activates sirtuins (SIRT1-7), fuels PARP-mediated DNA repair, maintains mitochondrial electron transport chain, regulates NAD+/NADH redox balance

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Dosing

DOSE RANGE 50000–500000 mcg
FREQUENCY 1-2x weekly (SubQ) or monthly (IV)
CYCLE LENGTH Ongoing / maintenance protocol

IV infusions typically 250-500mg over 2-4 hours (can cause flushing, nausea at higher rates). SubQ injections 50-100mg 1-3x weekly. Oral precursors: NMN 250-1000mg daily or NR 300-600mg daily.

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Research summary

Study Type Year Key Finding
NAD+ supplementation attenuates hypoxia-exacerbated oral mucosal inflammation via lactate metabolic reprogramming Preclinical (mouse + in vitro) 2026 Acute hypoxia activates Wnt/beta-catenin --> HIF-1alpha --> LDHA --> accelerated lactate synthesis
NAD+ deficiency from tacrolimus-suppressed IDO1 promotes M1 macrophage polarization and kidney injury Preclinical (mouse + in vitro) 2026 Tacrolimus suppresses IDO1, blocking tryptophan-to-kynurenine conversion
NAD+ Decline in Aging: Sirtuin, PARP, and Mitochondrial Mechanisms Mechanism summary 2018-2025 NAD+ declines ~50% between ages 40-60 in humans
NAD+ / Nicotinamide Riboside (NR) for Age-Related Functional Decline — — —
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Stacking & interactions

Comprehensive longevity — mitochondrial + telomere

Anti-aging — cellular energy + tissue repair/collagen

Cognitive + mitochondrial support

Tissue repair + cellular energy restoration

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Sourcing

Also vetted at
What bloodwork do I need?

Reference ranges are general guidelines. Consult your physician for interpretation.

PRE-CYCLE
  • CMP
  • CBC
  • Fasting Glucose
  • Lipid Panel
  • Uric Acid
DURING CYCLE
  • CMP
  • Uric Acid
POST-CYCLE
  • CMP
  • Lipid Panel
  • Uric Acid
Safety & Regulatory Status
FDA STATUS Not FDA-approved as drug. NAD+ precursors (NMN, NR) available OTC as dietary supplements. IV/SubQ NAD+ available through clinics and compounding pharmacies
WADA STATUS Not prohibited

Regulatory status for NAD+ may change. Verify current status with your jurisdiction before use. This is not legal or medical advice.

References

  1. Various. NAD+ supplementation attenuates hypoxia-exacerbated oral mucosal inflammation via lactate metabolic reprogramming. J Dent (2026). PMID: 41921651
  2. Ye, Zhang, Guo, Zhou, et al.. NAD+ deficiency from tacrolimus-suppressed IDO1 promotes M1 macrophage polarization and kidney injury. Front Immunol (2026). PMID: 41929248
  3. Compiled from Rajman et al. 2018, Yoshino et al. 2018, and others. NAD+ Decline in Aging: Sirtuin, PARP, and Mitochondrial Mechanisms. Cell Metab and various (2018-2025).
  4. NAD+ / Nicotinamide Riboside (NR) for Age-Related Functional Decline.