5-Amino-1-Methylquinolinium · CD38 Inhibitor · NAD+ Booster
A small molecule CD38 inhibitor that blocks the primary enzyme responsible for NAD+ degradation in the body. By inhibiting CD38, 5-amino-1MQ significantly increases intracellular NAD+ levels — synergising powerfully with direct NAD+ supplementation and providing a complementary approach to NAD+ optimisation.
5-Amino-1-methylquinolinium (5-amino-1MQ) is a small molecule that selectively inhibits CD38 — an enzyme found on the surface of immune cells and other tissues that is the primary consumer of NAD+ in the body. CD38 activity increases dramatically with age and inflammation, and is now understood to be the primary driver of age-related NAD+ decline rather than reduced NAD+ synthesis.
By blocking CD38, 5-amino-1MQ reduces NAD+ degradation — effectively raising intracellular NAD+ levels through a fundamentally different mechanism than NAD+ precursors (NMN, NR) or direct NAD+ injection, which increase supply. Combining both approaches — blocking degradation while increasing supply — produces a synergistic increase in NAD+ availability.
Research from the Brenner laboratory demonstrated that CD38 knockout mice maintain youthful NAD+ levels throughout life and are protected from age-related metabolic decline. The enzyme hydrolyses NAD+ extremely efficiently — a single CD38 molecule can degrade thousands of NAD+ molecules. As CD38 expression increases with age (driven partly by senescent cell SASP), NAD+ levels fall despite continued synthesis.
Animal studies have demonstrated that 5-amino-1MQ administration significantly increases intracellular NAD+ levels, reduces fat mass, improves metabolic function, and produces anti-obesity effects through NAD+-mediated SIRT1 activation. The metabolic improvements are consistent with elevated NAD+ signalling — increased fat oxidation, improved insulin sensitivity and enhanced mitochondrial function.
5-amino-1MQ combined with direct NAD+ injection or NMN/NR supplementation addresses both sides of the NAD+ equation simultaneously — increasing supply while reducing degradation. This dual approach consistently produces greater NAD+ elevation than either intervention alone and represents the most comprehensive NAD+ optimisation strategy currently available.