1627580-64-6
Most orderedMOTS-c
A 16-residue mitochondrial-derived peptide encoded in mtDNA. Supplied lyophilised, released at ≥ 99.0% by RP-HPLC.
From
£86.00
In stock
β-Nicotinamide adenine dinucleotide · NAD · Nicotinamide adenine dinucleotide, oxidised form
The oxidised pyridine dinucleotide cofactor, supplied lyophilised for redox, sirtuin and PARP work. Released at ≥ 98.0% by HPLC.
Total, ex VAT
£42.00
For laboratory research use only. Not for human or veterinary use, and not a medicine, food or cosmetic. Sold to qualified researchers and institutions who accept responsibility for safe handling and lawful use.
Compound data
Indicative values for this line. The certificate issued with your batch is the authoritative record and reports the measured figures for the material you receive.
Targets and pathways
Overview
NAD+ is not a peptide. It is the oxidised form of nicotinamide adenine dinucleotide, a pyridine dinucleotide that sits at the centre of cellular metabolism in two distinct roles: as the hydride-accepting half of the NAD+/NADH redox couple, and as a consumed substrate for the sirtuin, PARP and CD38 enzyme families. We list it alongside the mitochondrial peptides because that second role is why most laboratories buying it are buying it.
The distinction matters analytically. Used as a redox cofactor, NAD+ is recycled and a working solution is comparatively forgiving. Used as a sirtuin or PARP cosubstrate, it is consumed stoichiometrically and cleaved to nicotinamide plus ADP-ribose — so cofactor depletion and nicotinamide product inhibition both become variables the experiment has to control for.
It is also one of the most demanding compounds in the catalogue to store correctly. The free acid is strongly hygroscopic and degrades in alkaline aqueous solution, hydrolysing to nicotinamide and ADP-ribose. A vial left open on a bench in a humid room will gain mass measurably within minutes, and that water is the start of the degradation. Ryzen supplies it desiccated and sealed, released at ≥ 98.0% by HPLC with water content reported by Karl Fischer on every certificate.
In short
Where it is used
All seven sirtuins consume NAD+ as a cosubstrate for deacetylation and related deacylation reactions. Cofactor purity directly affects measured kinetics, and residual nicotinamide in a poor preparation inhibits the very reaction being measured.
PARP enzymes consume NAD+ heavily during poly(ADP-ribosyl)ation following DNA strand breaks, making cofactor supply a limiting variable in damage-response models.
As the NAD+/NADH couple, the compound underpins the dehydrogenase assays used across intermediary metabolism, from glycolysis through to the TCA cycle.
Tissue NAD+ declines with age across several species, and the compound is central to work on precursor supplementation, CD38-mediated consumption and the salvage pathway.
Purified NAD+ is used as a calibration standard in LC-MS quantitation of the nucleotide pool alongside NADH, NADP+ and NMN.
Handling
Bring the sealed vial fully to room temperature before opening — opening a cold vial condenses atmospheric moisture directly onto a hygroscopic powder. Weigh quickly, reseal immediately and return to desiccated storage. Dissolve in water or a buffer at or below pH 7; NAD+ solutions are inherently acidic and are stable in that range.
Sealed, desiccated and held at −20 °C, the powder is stable for at least 24 months. In neutral aqueous solution at 2–8 °C, use within 7 days. Above pH 7 degradation is rapid and a solution should be regarded as single-session. Freeze aliquots at −80 °C where longer solution storage is unavoidable.
Laboratory reference
Enter the fill weight on the vial and the diluent volume you intend to add. The calculator returns the resulting solution concentration and the volume that contains a given mass.
Figures are mass-to-volume arithmetic for laboratory preparation of NAD+ and take no account of net peptide content, which is stated on the batch certificate and should be applied to the fill weight before calculating. Nothing here constitutes dosing, administration or clinical guidance of any kind.
Published work
Summaries of published findings, provided as research reference. These describe work done by others in preclinical and clinical settings; they are not claims about this material or outcomes for any reader.
A widely cited review setting out the evidence for age-associated NAD+ decline, the enzymes that consume it, and the precursor strategies studied to restore tissue levels.
Rajman, Chwalek & Sinclair, Cell Metabolism, 2018
A comprehensive treatment of biosynthesis via the salvage and de novo routes, compartmentalisation between cytosol, nucleus and mitochondria, and the consuming enzyme families.
Covarrubias et al., Nature Reviews Molecular Cell Biology, 2021
Work identifying CD38 as a major driver of age-related NAD+ decline established the enzyme as a target of interest and gave the field a mechanism for the decline rather than only an observation of it.
Camacho-Pereira et al., Cell Metabolism, 2016
Foundational enzymology establishing that sirtuin deacetylation is NAD+-dependent and inhibited by nicotinamide, which remains the basis of most sirtuin assay design.
Imai et al., Nature, 2000
Questions
Something not covered here? Ask us directly — technical questions reach someone who runs the assays.
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Important
NAD+ is supplied strictly for laboratory research and analytical use. It is not a medicine, food, cosmetic or veterinary product; it is not for human or animal consumption; and it is not intended to diagnose, treat, cure or prevent any condition. It is not manufactured, tested or released to any standard that would support administration to humans or animals. Information on this page is compiled for research reference and is not medical advice. No dosing, administration or therapeutic guidance is given or implied. By ordering you confirm you are a qualified researcher or institution and accept responsibility for safe handling and lawful use.