NAD+

Overview

NAD+ (nicotinamide adenine dinucleotide, oxidized form) is a 663 Da dinucleotide coenzyme present in every living cell, functioning as an essential electron carrier in over 500 enzymatic redox reactions including glycolysis, the TCA cycle, and oxidative phosphorylation that collectively generate the majority of cellular ATP. Beyond its metabolic role, NAD+ serves as the obligate co-substrate for three critical families of signaling enzymes: sirtuins (SIRT1-7), which are NAD+-dependent deacetylases and ADP-ribosyltransferases that regulate DNA repair, mitochondrial biogenesis, inflammation, and cellular stress resistance; PARPs (poly-ADP-ribose polymerases), which consume NAD+ during DNA damage repair; and CD38/CD157 ectoenzymes involved in calcium signaling and immune cell function. Published peer-reviewed literature demonstrates that NAD+ levels decline by approximately 50% between ages 40 and 60 across multiple human tissue types, driven by increased CD38 expression, elevated PARP activity from accumulating DNA damage, and reduced salvage pathway synthesis. Injectable NAD+ provides direct systemic delivery of the intact coenzyme, bypassing the multi-step enzymatic conversion required for oral precursors (NMN, NR) to generate intracellular NAD+ through the salvage pathway. What distinguishes injectable NAD+ from oral precursor supplementation is its immediate bioavailability and the ability to rapidly elevate circulating and tissue NAD+ levels without rate-limiting enzymatic conversion steps. Current scientific investigation spans metabolic dysfunction, neurodegenerative disease, cardiac ischemia-reperfusion injury, immune aging (immunosenescence), and the broader role of the NAD+ metabolome in the biology of aging.

Research Applications

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