NAD+ in clinic

No. The vial is a freeze-dried cofactor for laboratory assays. The clinic plan is an in-person injection of a prepared solution under eLIVEate's governance. We sell the first. We don't take a cut of the second.

Intact NAD+ crosses membranes poorly and is a substrate for ecto-NADases, CD38 among them — chopping enzymes sitting on the outside of cells. Precursor salvage (NR, NMN, nicotinamide) is how most restoration papers actually raise the intracellular pool. Injection is a different pharmacokinetic experiment, which is why the clinic protocol and the oral-precursor literature don't substitute for each other.

Human skin NAD+ has been measured at roughly half, in older adults, of young-adult levels, with CD38 as a major age-related drain. That's the budget Massudi and Camacho-Pereira were pointing at. It isn't a dosing instruction.

Lyophilised β-NAD+, ≥98% HPLC, for in-vitro assays, standard curves and isolated-organelle work. Cofactor assays are hungry; that is why the aliquot is a gram. It is not a human serving and not a reconstitution of JP's syringe.

No. NR and NMN are precursors with published human metabolomes (Trammell 2016; Yoshino, Science 2021). Intact NAD+ is the charged dinucleotide, a poor membrane passenger, hydrolysed by ecto-enzymes. Three rungs, three experiments, three files.

Consumption outruns salvage in specific tissues. PARP1 can drain the pool after DNA damage; CD38 is an age- and inflammation-associated NADase (Camacho-Pereira, Verdin, Cell Metab 2016); NAMPT, the kinetic bottleneck of salvage, often falls. Supply and demand, not a vitamin-deficiency story.

Yes. SIRT1–7 are NAD+-dependent lysine deacylases. One NAD+ is spent per lysine; nicotinamide and O-acyl-ADP-ribose are released. That is Imai and Guarente, Nature 2000, still the sentence. They do not redox-cycle the cofactor. They spend it.

The metabolome often moves (Trammell, Brenner, 2016 for NR). Clinical endpoints are mixed: a vascular signal in one NR cohort (Martens, 2018); muscle insulin sensitivity, modest, in prediabetic women on NMN with a clamp (Yoshino, Science 2021). An intramuscular NAD+ visit is not those trials.

Neighbourhood, not identity. MOTS-c is a 16-mer (MRWQEMGYIFYPRKLR) translated from mitochondrial 12S rRNA (Lee, Cohen, Cell Metab 2015) and sits on AMPK. NAD+ is the hydride coin Complex I and SIRT3 spend. The appointment is a clinic object. Three jobs, not a bundle.

The listing is a characterised laboratory solid for the assays on this page. The appointment is an in-person medical-aesthetic service on eLIVEate's diary. Pellagra was a niacin-deficiency disease; ageing is not pellagra. Neither object on this page is a vitamin-deficiency cure.