KPV vs NAD+

Immune

Metabolic

Research Only

Research Only

KPV enters cells (in part via the di/tripeptide transporter PepT1 in intestinal epithelium and immune cells) and acts intracellularly to inhibit NF-kB activation, reducing pro-inflammatory cytokine production (TNF-α, IL-6, IL-1β). Unlike full-length alpha-MSH, KPV does not meaningfully activate MC1R and does not cause skin pigmentation, differentiating it from melanocortin agonists such as MT-I and MT-II.

NAD+ functions as a primary electron carrier in glycolysis, the TCA cycle, and oxidative phosphorylation. Beyond its redox role, NAD+ serves as a consumable substrate for sirtuin deacetylases (SIRT1-7), poly(ADP-ribose) polymerases (PARPs), and CD38/CD157 ectoenzymes. Sirtuin activation is linked to mitochondrial biogenesis, autophagy, and stress-response gene expression, and PARP activity is central to DNA-damage repair. Oral bioavailability of intact NAD+ is poor, which is why clinics market IV infusion; the best human data for raising tissue NAD+ involve oral precursors NR (nicotinamide riboside) and NMN (nicotinamide mononucleotide) rather than NAD+ itself.

200–500 mcg (SubQ); 500 mcg–1 mg (oral)

IV 500-1500mg per session; SubQ 100-200mg

Oral, SubQ, or Topical

IV, SubQ