NAD+
Also known as: NAD+
A molecule your body needs for hundreds of essential processes — making energy, repairing DNA, and regulating genes. Your NAD+ levels drop by about half between ages 40 and 60, which may contribute to aging and mitochondrial decline. People supplement with IV infusions, oral pills (NMN or NR), or injections to try to restore levels toward what they had when younger.
Dosage
IV: 250-1000 mg per session. Oral NMN/NR: 250-1000 mg daily
Dosages shown are for research reference only. Always consult a qualified healthcare provider.
Half-Life
IV: effects persist 48-72 hours (2-3 days) | Oral precursors (NMN/NR): 2-4 hours
Half-Life Calculator →Administration
Intravenous infusion, intramuscular injection, or oral (NMN/NR precursors)
Get Research-Grade NAD+
99%+ purity · US-based · third-party lab tested
Getting Started — Here's What You'll Need
Effects
Cellular Energy
Required for 500+ enzymatic reactions including all mitochondrial ATP production.
Sirtuin Activation
Essential substrate for SIRT1/SIRT3 — master regulators of aging and metabolism.
DNA Repair
Required by PARP enzymes for DNA damage repair.
Anti-Aging
Restoring NAD+ levels addresses a fundamental driver of cellular aging.
Mechanism of Action
Nicotinamide Adenine Dinucleotide (NAD+) is a dinucleotide coenzyme consisting of nicotinamide mononucleotide (NMN) joined to adenosine monophosphate (AMP) through a pyrophosphate bond. It exists in oxidized (NAD+) and reduced (NADH) forms and participates in over 500 enzymatic reactions, making it one of the most central molecules in cellular metabolism.
As a redox cofactor, NAD+ accepts hydride ions (H-) during catabolic reactions. In glycolysis, the TCA cycle, and fatty acid beta-oxidation, NAD+ is reduced to NADH, which then donates electrons to Complex I of the mitochondrial electron transport chain, driving oxidative phosphorylation and ATP production. Without adequate NAD+, the entire energy production machinery of the cell grinds to a halt.
Equally important are NAD+'s roles as a consumed substrate for three families of signaling enzymes. Sirtuins (SIRT1-7) are NAD+-dependent protein deacylases and ADP-ribosyltransferases that use NAD+ as a co-substrate, cleaving it to nicotinamide and O-acetyl-ADP-ribose during the deacetylation reaction. SIRT1 and SIRT3 are particularly important for aging — SIRT1 deacetylates PGC-1α (activating mitochondrial biogenesis), FOXO transcription factors (activating stress resistance), and NF-κB (suppressing inflammation). SIRT3 in the mitochondrial matrix activates SOD2 and other mitochondrial enzymes. PARPs (poly-ADP-ribose polymerases) consume NAD+ during DNA damage repair, adding chains of ADP-ribose to histones near DNA breaks to recruit repair machinery. CD38, an NAD+-consuming glycohydrolase on immune cells, regulates calcium signaling and immune activation.
NAD+ levels decline 40-60% between ages 40 and 70, driven by increased CD38 expression (with chronic low-grade inflammation), increased PARP activity (from accumulated DNA damage), and reduced synthesis (decreased NAMPT enzyme activity). This decline impairs sirtuin function, reduces ATP production, compromises DNA repair, and contributes to virtually every hallmark of aging. Supplementation strategies aim to restore NAD+ levels either directly (IV infusion) or through biosynthetic precursors: NMN enters the salvage pathway one step from NAD+, while NR (nicotinamide riboside) requires an additional phosphorylation step.
Regulatory Status
Oral precursors (NMN, NR) sold as dietary supplements. IV/IM NAD+ available through wellness clinics and compounding pharmacies. Not FDA approved as a drug.
Risks & Safety
Common
flushing, nausea, chest tightness, anxiety during IV infusion, mild stomach upset with oral forms.
Serious
theoretical concern that NAD+ could fuel growth of existing cancers; rapid infusion can cause significant chest pressure and anxiety.
Rare
severe infusion reaction, irregular heartbeat with rapid IV push.
Compare NAD+ With
Research Papers
30Published: December 5, 2026
AI Summary
Abstract too short to summarize.
Published: February 4, 2026
AI Summary
Blocking NAMPT with FK866 reduced liver fibrosis in mice by lowering NAD+ and dampening inflammation. The drug may be a useful treatment for chronic liver disease.
Published: February 2, 2026
AI Summary
Abstract too short to summarize.
Published: January 28, 2026
AI Summary
Culture conditions for parasite larvae were optimized to support drug screening. Gentamicin improved development, and protease activity was used as a marker of metabolic function.
Published: March 29, 2026
AI Summary
Ginkgolide C slowed atherosclerosis in mice by activating Nrf2 to curb oxidative stress and block NLRP3 inflammasome activation. It may support new cardiovascular treatments.
Published: December 31, 2025
AI Summary
Prostate cancer cells that depend on YAP and NNMT are more sensitive to NAMPT inhibition. NNMT may help identify patients who can benefit from NAD+-targeting therapies.
Published: January 4, 2026
AI Summary
Abstract too short to summarize.
Published: December 24, 2025
AI Summary
The review ties Nrf2 activation to gut health and describes how various agents can activate it to treat intestinal inflammation in people and animals.
Published: January 22, 2026
AI Summary
Eugenol protected rats from acrylamide-induced brain damage by boosting Nrf2 and reducing inflammation and cell death. It may be a useful neuroprotective agent.
Published: February 9, 2026
AI Summary
A nanopore-based method was used to study glycopeptide–peptidoglycan binding at the single-molecule level. The approach could help design new antibiotics.
Published: January 8, 2026
AI Summary
Stevioside weakens Streptococcus pneumoniae by disrupting its capsule via pyruvate metabolism and NAD+/NADH balance. It protected mice from lethal infection and may be a new anti-pneumococcal strategy.
Published: January 6, 2026
AI Summary
Hydrogel microspheres delivering NMN to mitochondria slowed muscle loss in aging mice by restoring NAD+ and reducing senescence. The approach may help treat sarcopenia.
Published: December 23, 2025
AI Summary
Sirtuins remove acetyl groups from SOD3 and restore its cleavage by furin, linking NAD+-dependent metabolism to extracellular antioxidant defense.
Published: January 8, 2026
AI Summary
Estrogen and NMN restored beige fat formation in obese mice by acting through an ERα/NAMPT/IL-33 axis. The pathway could be targeted to treat obesity-related metabolic disease.
Published: February 10, 2026
AI Summary
Melatonin slowed triple-negative breast cancer by reducing glycolysis and DNA repair via YAP1-NAMPT. It enhanced the effect of the PARP inhibitor olaparib.
Published: November 23, 2025
AI Summary
In diabetic kidney disease, CD38 and NAMPT rose with albuminuria while SIRT1 fell. Restoring NAD+ balance may help protect the kidneys.
Published: December 23, 2025
AI Summary
MED23 drives liver cancer by stabilizing NQO1 and raising IGF2. Blocking MED23 reduced tumor growth in mice.
Published: December 18, 2025
AI Summary
Ovarian cancer cells with RAS/PI3K mutations were more sensitive to combined PARP and NAMPT inhibition. The combination reduced tumor growth and prolonged survival in mice.
Published: December 18, 2025
AI Summary
A Chinese medicine capsule improved cognition in an Alzheimer's rat model by modulating nicotinamide metabolism, NAD+, and SIRT1 while reducing oxidative stress and inflammation.
Published: January 15, 2026
AI Summary
NAMPT inhibition made AML cells more sensitive to venetoclax and chemotherapy by targeting metabolic and DNA repair pathways. Combined NAMPT and BCL2 inhibition may be worth testing in AML.
Published: December 30, 2025
AI Summary
NMN protected ovarian granulosa cells from radiation by promoting SIRT3-mediated deacetylation of NLRP3 at lysine 570, thereby limiting pyroptosis and preserving ovarian reserve.
Published: December 13, 2025
AI Summary
Inhalation of 1-bromopropane altered immune and insulin signaling pathways in the hippocampus and liver of rats, suggesting a role in neuro- and hepatotoxicity.
Published: December 13, 2025
AI Summary
Abstract too short to summarize.
Published: December 10, 2025
AI Summary
Elastic nanogels improved delivery of NMN through the skin. The system could help topical NAD+ precursor use for skin aging and related conditions.
Published: January 7, 2026
AI Summary
NAD+ depletion by SARM1 triggers a non-apoptotic death pathway involving BAX activation and APAF1 degradation. The pathway links metabolic stress to neurodegeneration.
Published: December 15, 2025
AI Summary
NAD+ depletion by SARM1 triggers a non-apoptotic death pathway involving BAX activation and APAF1 degradation. The pathway links metabolic stress to neurodegeneration and may inform new therapeutic targets.
Published: December 31, 2025
AI Summary
SENP7 promotes regulatory B cells by activating SIRT1 via deSUMOylation. Blocking SENP7 improved tumor response to anti-PD-1 therapy.
Published: November 19, 2025
AI Summary
Phase II detoxification enzymes and Nrf2 were downregulated in liver disease in mice. Restoring Nrf2 could help protect the liver.
Published: December 4, 2025
AI Summary
SMP30 protected lens cells from high-glucose-induced oxidative damage by regulating the Keap1/Nrf2/NQO1 pathway. It may be relevant for diabetic cataract.
Published: April 24, 2026
AI Summary
Hanseniaspora yeast strains created favorable niches for malolactic bacteria by upregulating nicotinamide metabolism and NAD+ regeneration. The findings support precision winemaking strategies.
Frequently Asked Questions
What is NAD+?
A molecule your body needs for hundreds of essential processes — making energy, repairing DNA, and regulating genes. Your NAD+ levels drop by about half between ages 40 and 60, which may contribute to aging and mitochondrial decline. People supplement with IV infusions, oral pills (NMN or NR), or injections to try to restore levels toward what they had when younger.
What is NAD+ used for?
A molecule your body needs for hundreds of essential processes — making energy, repairing DNA, and regulating genes. Your NAD+ levels drop by about half between ages 40 and 60, which may contribute to aging and mitochondrial decline. People supplement with IV infusions, oral pills (NMN or NR), or injections to try to restore levels toward what they had when younger.
What is the dosage for NAD+?
IV: 250-1000 mg infusion over 2-4 hours, once or twice weekly. Oral precursors (NMN/NR): 250-1000 mg once daily. Intramuscular: 50-100 mg once daily. Sublingual: 100-250 mg once daily.
What are the side effects of NAD+?
Common: flushing, nausea, chest tightness, anxiety during IV infusion, mild stomach upset with oral forms. Serious: theoretical concern that NAD+ could fuel growth of existing cancers; rapid infusion can cause significant chest pressure and anxiety. Rare: severe infusion reaction, irregular heartbeat with rapid IV push.
How does NAD+ work?
Nicotinamide Adenine Dinucleotide (NAD+) is a dinucleotide coenzyme consisting of nicotinamide mononucleotide (NMN) joined to adenosine monophosphate (AMP) through a pyrophosphate bond. It exists in oxidized (NAD+) and reduced (NADH) forms and participates in over 500 enzymatic reactions, making it one of the most central molecules in cellular metabolism. As a redox cofactor, NAD+ accepts hydride ions (H-) during catabolic reactions. In glycolysis, the TCA cycle, and fatty acid beta-oxidation, NAD+ is reduced to NADH, which then donates electrons to Complex I of the mitochondrial electron transport chain, driving oxidative phosphorylation and ATP production. Without adequate NAD+, the entire energy production machinery of the cell grinds to a halt. Equally important are NAD+'s roles as a consumed substrate for three families of signaling enzymes. Sirtuins (SIRT1-7) are NAD+-dependent protein deacylases and ADP-ribosyltransferases that use NAD+ as a co-substrate, cleaving it to nicotinamide and O-acetyl-ADP-ribose during the deacetylation reaction. SIRT1 and SIRT3 are particularly important for aging — SIRT1 deacetylates PGC-1α (activating mitochondrial biogenesis), FOXO transcription factors (activating stress resistance), and NF-κB (suppressing inflammation). SIRT3 in the mitochondrial matrix activates SOD2 and other mitochondrial enzymes. PARPs (poly-ADP-ribose polymerases) consume NAD+ during DNA damage repair, adding chains of ADP-ribose to histones near DNA breaks to recruit repair machinery. CD38, an NAD+-consuming glycohydrolase on immune cells, regulates calcium signaling and immune activation. NAD+ levels decline 40-60% between ages 40 and 70, driven by increased CD38 expression (with chronic low-grade inflammation), increased PARP activity (from accumulated DNA damage), and reduced synthesis (decreased NAMPT enzyme activity). This decline impairs sirtuin function, reduces ATP production, compromises DNA repair, and contributes to virtually every hallmark of aging. Supplementation strategies aim to restore NAD+ levels either directly (IV infusion) or through biosynthetic precursors: NMN enters the salvage pathway one step from NAD+, while NR (nicotinamide riboside) requires an additional phosphorylation step.
How is NAD+ administered?
NAD+ is administered via intravenous infusion, intramuscular injection, or oral (nmn/nr precursors).
What is the half-life of NAD+?
The half-life of NAD+ is IV: effects persist 48-72 hours (2-3 days) | Oral precursors (NMN/NR): 2-4 hours.
Is NAD+ legal?
Oral precursors (NMN, NR) sold as dietary supplements. IV/IM NAD+ available through wellness clinics and compounding pharmacies. Not FDA approved as a drug.
Related Peptides
5-Amino-1MQ
A pill that aims to switch fat cells from 'storage mode' to 'burning mode' by blocking an enzyme (NNMT) that is overactive in the fat tissue of overweight people. Not technically a peptide, but commonly sold alongside them. Unlike appetite suppressants, this targets the fat cells directly rather than making you eat less. The science is promising in lab studies, but there are no completed human trials yet.
AEDG Peptide
A tetrapeptide (Ala-Glu-Asp-Gly) identical to Epithalon's core active sequence — effectively the same compound. Studied for telomerase activation and pineal gland regulation, promoting melatonin production and potentially slowing cellular aging through telomere maintenance. Part of the Khavinson bioregulator peptide family developed in St. Petersburg.
AICAR
A natural compound that activates your cells' energy sensor — the same pathway that turns on during exercise. Mimics the metabolic effects of endurance exercise at the cellular level, helping with fat burning, glucose uptake, and building more mitochondria. Banned by WADA as a metabolic modulator after detection in professional cycling.
CJC-1295 (no DAC)
One of the most popular growth hormone peptides, often called Mod GRF 1-29. Instead of injecting growth hormone directly, this tells your pituitary gland to release more of its own GH naturally. This is considered healthier than injecting GH directly because your body keeps its normal feedback systems intact. Usually combined with Ipamorelin for much stronger effects — the two work together better than either alone.