NAD+ (nicotinamide adenine dinucleotide) is the coenzyme every cell uses to move electrons through energy metabolism, and the fuel that sirtuins, PARPs and CD38 consume. The big shift in recent research is about where it sits inside the cell. In 2020, Nature identified SLC25A51 as the transporter that carries intact NAD+ into mammalian mitochondria, and it opened a new line of work on the mitochondrial NAD+ pool. That's why labs buy the NAD peptide, as people often search for it, to study the molecule directly.
Here's how NAD+ fails. The powder is hygroscopic, and moisture, heat or the wrong pH hydrolyzes it into nicotinamide and ADP-ribose, while a partly degraded vial can still look like clean white powder. Solutions decompose rapidly in acid or alkali. Mix-ups happen too: reduced NADH differs by just two hydrogens, so a label alone can't be trusted. Titan Core labels this compound for what it is, a coenzyme with no amino-acid sequence. It's made in the USA, measured by HPLC at an independent lab, which separates intact NAD+ from its breakdown products, and packed to keep moisture out. The report carries the same LOT as your vial. It's sold for laboratory research, not as a supplement, and isn't for human or animal use.
Research Highlights
- Mitochondrial import found — Loss of SLC25A51 lowered mitochondrial but not whole-cell NAD+, impaired respiration and blocked NAD+ uptake into isolated mitochondria (Nature, 2020).
- How the pump works — SLC25A51 uses mitochondrial membrane potential and charged pore residues to import NAD+ against its gradient (Science Advances, 2025).
- Liver regeneration — In male mice, the rate of liver regeneration tracked hepatocyte mitochondrial NAD+, and heterozygous SLC25A51 loss impaired it (Nature Metabolism, 2025).
- Brain ischemia models — Cerebral ischemia-reperfusion unbalanced NAD+ between cytoplasm and mitochondria; raising SLC25A51 restored the mitochondrial pool and cut oxidative lipid damage (Antioxidants & Redox Signaling, 2026).
- Flux tracing in colitis — Isotope-labeled precursors in mouse colitis showed salvage-pathway flux rising while de novo NAD+ synthesis fell (Cell Reports, 2026).
- CD38 as consumer — In mouse endometrium, CD38 from myeloid cells was the main driver of NAD+ depletion (Aging Cell, 2026).