BAM15 vs NAD+

Metabolic

Metabolic

Research Only

Research Only

BAM15 increases proton permeability of the inner mitochondrial membrane, letting protons leak back into the matrix independent of ATP synthase — dissipating the proton-motive force and uncoupling electron transport from ATP synthesis, which raises substrate oxidation and heat production. Unlike DNP/FCCP it does not depolarize the plasma membrane at fully-uncoupling doses and is less cytotoxic than FCCP; downstream it activates AMPK (Kenwood et al., 2014). All data are cell/animal.

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.

No human dose established

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

Oral (rodent studies)

IV, SubQ