NAD⁺ is a vital coenzyme involved in more than 500 redox reactions and plays crucial roles in non-redox enzymatic processes, including cell signaling (CD38), DNA repair (PARPs), and epigenetic modifications (sirtuins). The decline of NAD⁺ levels has been linked to various health issues, such as aging and obesity-related metabolic disorders like non-alcoholic fatty liver disease and type 2 diabetes. Replenishing NAD⁺ levels, often through NAD⁺ precursors like NR or NMN, has shown promise in extending lifespan and improving metabolic disorders. Our research has uncovered a remarkable NR derivative compound called NRH, which exhibits unparalleled efficacy in augmenting NAD⁺ levels, surpassing the increase achieved by NR in cell and animal models. Additionally, we have elucidated the NRH-induced NAD⁺ biosynthesis pathway, involving the phosphorylation of NRH into NMNH by adenosine kinase, followed by conversion to NAD⁺. Importantly, by administering adenosine kinase inhibitors, we successfully inhibited the NRH-induced NAD⁺ increases in cells and animal tissues. Presently, our investigation aims to further characterize the physiological effects of NRH and other novel NAD⁺ precursors in aging models, examining their potential to prevent aging and metabolic diseases associated with obesity.