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Research peptides at >99% HPLC-verified purity, third-party tested by Janoshik Analytical & Freedom Diagnostics, with Certificates of Analysis published per released batch. Supplied strictly for laboratory research use.
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Research use only (RUO). All products are sold strictly for laboratory and research purposes — not for human or veterinary consumption. Purchasers must be 21 or older.
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NAD+
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Lab-direct quality — full packs or single-vial samples
Every batch ships straight from the lab that synthesises it — sealed, tamper-evident, and HPLC-verified to >99% purity . Buying direct means you pay the lab-direct rate on every vial, with nothing stacked on top.
Order a full sealed 10-vial research pack for a complete study supply, or add a single-vial sample alongside your pack to trial a new compound first. Same lab, same batch, same verified purity — scaled to whatever your research needs.
What It's Researched For
In plain terms, NAD+ is the molecule cells use to move energy around and to switch repair machinery on. Here is what that looks like across the research.
Mitochondrial function
Studied as the carrier that hands electrons to the mitochondria — the step that makes ATP, the cell’s energy currency.
Cellular-ageing models
Tissue NAD+ falls with age in model organisms, so restoring it is one of the most-tested ideas in longevity biology.
DNA-repair signalling
PARP enzymes burn through NAD+ when they detect DNA damage, linking genome maintenance directly to metabolic supply.
Circadian biology
NAD+ levels oscillate on a daily cycle and feed back onto the clock machinery through SIRT1 — a standard readout in chronobiology.
Overview
In short: NAD+ is the cell’s central redox coenzyme and the fuel for the sirtuin, PARP and CD38 signalling enzymes — the single molecule that links energy metabolism to DNA repair, gene regulation and cellular ageing.
Key research facts
Research use only. These points summarise lab themes, not human outcomes.
Nicotinamide adenine dinucleotide is a dinucleotide: an adenine nucleotide and a nicotinamide nucleotide joined through a pair of phosphates. That nicotinamide ring is the working end. It accepts a hydride ion to become NADH and gives it back to become NAD+ again, and this one reversible reaction underpins glycolysis, the tricarboxylic-acid cycle, fatty-acid oxidation and — via complex I of the electron-transport chain — the bulk of mitochondrial ATP production. In this role NAD+ is a catalyst: it is recycled, not used up.
The second role is what makes it interesting to ageing research. Three enzyme families cleave NAD+ and consume it outright. The sirtuins (SIRT1–SIRT7) use it to remove acetyl and other acyl groups from histones and metabolic enzymes, coupling gene regulation to metabolic state. The poly(ADP-ribose) polymerases use it to build ADP-ribose chains at sites of DNA damage. CD38 and CD157 hydrolyse it into cyclic ADP-ribose, a calcium-mobilising second messenger. Because these reactions destroy the molecule, the cell must constantly rebuild it — mostly through the salvage pathway, where the enzyme NAMPT recycles nicotinamide, and to a lesser extent from the dietary precursors nicotinamide riboside and nicotinamide mononucleotide or de novo from tryptophan.
Those two roles collide with age. NAD+ concentrations fall measurably in the tissues of ageing model organisms, at the same time as CD38 expression rises and PARP activity increases with accumulated DNA damage — more demand, less supply. Whether raising NAD+ changes any downstream outcome in humans remains an open research question rather than a settled result. It is supplied here as a research-grade lyophilised powder for in-vitro and preclinical use only, and nothing on this page is medical advice.
Mechanism of Action
NAD+ works two ways at once: as a recycled redox carrier shuttling electrons into the mitochondrial electron-transport chain, and as a consumed substrate for the sirtuin, PARP and CD38 enzyme families that couple metabolic state to gene regulation, DNA repair and calcium signalling.
The cell keeps NAD+ and NADH in a strongly oxidised ratio — free cytosolic NAD+:NADH is typically several hundred to one — because that gradient is what makes the redox reactions of glycolysis thermodynamically favourable. Compartmentalisation matters: cytosolic, mitochondrial and nuclear pools are regulated separately, and the inner mitochondrial membrane is impermeable to intact NAD+, so shuttles (malate–aspartate, glycerol-3-phosphate) rather than direct transport move reducing equivalents between them. This compartmentalisation is why the route and form of NAD+ used in an experiment change the result. On the consumption side, the picture that has emerged from ageing models is one of competing sinks: PARP activity climbs as DNA damage accumulates, CD38 expression rises with inflammatory ageing, and both draw down the same pool that sirtuins depend on — the mechanistic basis for the widely studied hypothesis that sirtuin activity falls in ageing tissue because its substrate does. Exogenous NAD+ itself is a large, charged molecule with poor cell permeability and is substantially degraded extracellularly by CD38 and the ectoenzyme CD73, which is why much of the field works with the smaller precursors NR and NMN and why route, infusion rate and formulation dominate the experimental literature on intact NAD+.
Common Questions People Are Asking
What is NAD+ used for in research?
NAD+ is studied as the central redox coenzyme of metabolism and as the consumed substrate of the sirtuin, PARP and CD38 enzyme families. Research examines mitochondrial electron transport and ATP production, sirtuin-mediated gene regulation, PARP-dependent DNA-repair signalling, calcium second-messenger generation, circadian oscillation of the NAD+ pool, and the age-related decline of tissue NAD+ in cellular-senescence models. It is supplied here for laboratory research only and is not for human use.
What is the difference between NAD+ and NADH?
They are the two halves of one redox couple. NAD+ is the oxidised form; it accepts a hydride ion (two electrons and a proton) to become NADH, the reduced form, which then donates that hydride elsewhere — most importantly to complex I of the mitochondrial electron-transport chain — regenerating NAD+. Cells hold the free cytosolic pool strongly toward NAD+, and that ratio is what makes the oxidative steps of glycolysis thermodynamically favourable.
How does NAD+ differ from NMN and nicotinamide riboside?
NMN and NR are precursors — smaller molecules that cells convert into NAD+ through the salvage pathway. NAD+ is the finished coenzyme. The practical difference is delivery: NAD+ is large and doubly charged, so it crosses membranes poorly and is broken down extracellularly by CD38 and CD73, which is why most oral human research uses NR or NMN while intact NAD+ research uses parenteral routes.
Why does NAD+ decline with age?
Model-organism data point to both sides of the ledger changing at once. Supply falls as NAMPT salvage-pathway activity decreases, while demand rises: PARP enzymes consume more NAD+ as DNA damage accumulates, and CD38 expression increases with inflammatory ageing. Since sirtuins draw on the same pool, the widely studied hypothesis is that sirtuin activity falls in ageing tissue because its substrate does.
How should NAD+ be stored?
Keep the lyophilised powder frozen at −20 °C, protected from light and moisture. After reconstitution in bacteriostatic water or sterile saline, refrigerate at 1–6 °C and use promptly — NAD+ hydrolyses in solution, and degradation accelerates at alkaline pH and at room temperature. Aliquot after reconstitution and avoid repeated freeze-thaw cycles where the protocol allows.
Where can I buy NAD+?
Right here — NAD+ is supplied directly by New-U Research Compounds on this page. Every batch is independently third-party tested to >99% HPLC purity with a batch-linked Certificate of Analysis, supplied as lyophilised research-grade material, and shipped direct from source worldwide in discreet, tracked packaging. Strictly for laboratory research use only — not for human use.
How much does NAD+ cost?
NAD+ pricing is shown live on this page, per pack size — 10-vial research packs as standard, with single-vial sample options on selected compounds. Larger vial strengths lower the per-mg cost, every order includes the batch Certificate of Analysis, and shipping is free on orders over $300.
Is NAD+ third-party tested?
Yes. Every NAD+ batch is verified by independent laboratories (Janoshik Analytics and Freedom Diagnostics) for identity and purity, with a batch-linked Certificate of Analysis confirming >99% purity by HPLC. Every order ships with its COA, and current batch certificates are published on our COA page.
How do I buy NAD+?
Add the NAD+ pack size you need to your cart and check out: enter your shipping details, then choose your payment method — cryptocurrency or card — on the next step. Every order ships with its batch Certificate of Analysis (COA). NAD+ is supplied strictly for laboratory research use only, not for human or veterinary use.
What payment methods can I use to buy NAD+?
At checkout you can pay by cryptocurrency (BTC, ETH, SOL, LTC, USDC, USDT and more) or by card, each handled by a dedicated secure payment provider. You choose your method after confirming your order.
How fast is shipping, and do you ship worldwide?
Yes — we ship worldwide in discreet, unmarked, temperature-stable, tracked packaging. Delivery typically takes 6–14 business days, and shipping is free on orders over $300.
Is it legal to buy NAD+?
In the United States, NAD+ is sold strictly for laboratory and research purposes only. It is not approved by the FDA for human consumption and is not sold for that purpose. Regulatory status varies by jurisdiction — buyers are responsible for compliance in their own region.
Pharmacokinetics
Evidence Tier
Overall: Mixed (human + animal)
The biochemistry of NAD+ is textbook-established: its redox role, its consumption by sirtuins, PARPs and CD38, and the NAMPT salvage pathway are among the best-characterised facts in metabolism, and the age-related decline of tissue NAD+ is reproduced across multiple model organisms. What is not established is the interventional claim. Human trials have largely studied the precursors nicotinamide riboside and nicotinamide mononucleotide rather than intact NAD+, and while they report reliable increases in blood NAD+ metabolites, functional outcomes remain inconsistent. Interventional data on intravenous NAD+ itself is limited to small, mostly uncontrolled studies. As a supplied research compound it is unapproved laboratory material, not an approved drug.
Tier 1 · Human clinical
Tier 2 · Animal
Certificates, databases & peer-reviewed sources
Last reviewed: 5 August 2026 · New-U Research Compounds
Key Characteristics
Specifications
About NAD+ (Nicotinamide Adenine Dinucleotide): Redox Coenzyme and Sirtuin Substrate Research Guide
NAD+ is one of the few molecules that turns up in every chapter of a metabolism textbook. It is a dinucleotide — an adenine nucleotide joined to a nicotinamide nucleotide through a pyrophosphate bridge — and its nicotinamide ring can accept a hydride ion to become NADH and release it again to become NAD+. That single reversible step is the electron-carrying backbone of glycolysis, the tricarboxylic-acid cycle and fatty-acid oxidation, and it is how reducing equivalents reach complex I of the mitochondrial electron-transport chain, where the proton gradient that drives ATP synthesis begins.
What moved NAD+ from textbook biochemistry to the centre of ageing research is its second, non-catalytic role. The sirtuins — SIRT1 through SIRT7 — cannot deacylate histones or metabolic enzymes without consuming NAD+, which makes them direct sensors of the cell’s metabolic state. The poly(ADP-ribose) polymerases consume it to mark DNA strand breaks. CD38 and CD157 hydrolyse it into cyclic ADP-ribose for calcium signalling. All three destroy the molecule, so the cell continuously rebuilds it, chiefly through the NAMPT-driven salvage of nicotinamide and secondarily from the precursors nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN) or de novo from tryptophan. In ageing tissue, supply falls while PARP and CD38 demand rises — the mechanistic core of the NAD+ decline hypothesis.
The honest position on the interventional question is that it is unsettled. Human studies have overwhelmingly used the oral precursors NR and NMN rather than intact NAD+, and although they reliably raise circulating NAD+ metabolites, functional endpoints have been inconsistent across trials. Data on intravenous NAD+ itself is limited to small and largely uncontrolled work. New-U Research Compounds supplies NAD+ as a research-grade lyophilised powder at >99% HPLC purity, strictly for in-vitro and preclinical research use. It is not approved for human therapeutic use in any jurisdiction, and nothing on this page constitutes medical advice or a dosing recommendation.
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