NAMPT activator SBI-0802162 plus nicotinamide in aged mice: an abstract
In this abstract, the NAMPT activator SBI-0802162 selectively reduced senescent cell viability in cells; in aged mice, combining it with dietary nicotinamide raised tissue NAD+, lowered some age-associated inflammatory and senescence markers, and preserved physical performance. [1]
Automatic summary · not editorially reviewed
The key findings
Senescent cells had elevated NAMPT, yet isotope tracing showed decreased NAD+ biosynthesis and consumption, so NAMPT abundance did not match NAD+ flux. [1]
SBI-0802162 produced a sustained rise in intracellular NAD+ that selectively reduced the viability of senescent cells but not proliferating cells. [1]
In aged mice, SBI-0802162 plus dietary NAM increased tissue NAD+ and preserved physical performance, with lower food intake and body weight. [1]
The source at a glance
- Study type / format
- Preclinical abstract (cell experiments and mouse studies).
- Population / context
- Senescent and proliferating cells in culture and aged mice.
- Summary based on
- Study abstract
- Publication status
- Preprint · peer-review status not confirmed
- Original publication
- August 7, 2026
Senescent cells, NAMPT and NAD+ flux
The abstract describes aging as driven by several interacting processes, so it proposes targeting more than one mechanism at once. Senescent cells showed higher intracellular levels of NAMPT, the rate-limiting enzyme of the nicotinamide salvage pathway for NAD+ production. Yet isotope-tracing studies found decreased NAD+ production and consumption, so the higher NAMPT amount did not come with a matching rise in NAD+ metabolic flux.
Supporting source [1]
SBI-0802162 in cells and NAM levels in mice
Treatment with the NAMPT activator SBI-0802162 used the spare enzymatic capacity of NAMPT in senescent cells. This produced a marked rise in intracellular NAD+ that, when sustained, disrupted their transcriptional program and selectively reduced the viability of senescent cells but not proliferating cells. In mice, SBI-0802162 reduced circulating NAM levels, which the authors read as a possible limit set by substrate availability.
Supporting source [1]
Combination with dietary NAM in aged mice
This observation prompted a combination approach: SBI-0802162 together with dietary NAM supplementation. Co-administration robustly increased tissue NAD+ and suppressed select age-associated inflammatory signatures and markers of cellular senescence in a tissue-specific manner. Alongside these molecular effects, aged mice showed preserved physical performance and reductions in food intake and body weight, whether SBI-0802162 was in the chow or given by oral gavage. The abstract presents this as support for a combined strategy, not as evidence of longer lifespan.
Supporting source [1]
How to interpret this
This is an abstract; the full text was not reviewed. It reports cell experiments and mouse work, not human outcomes, and gives no sample sizes, follow-up durations or effect sizes. The abstract does not report lifespan data, and the described effects are associations within the experiments, not proof that people would benefit.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Alcaraz M, Ramachandra R, Arnold R, Garcia-Teneche M, Rajesh A, Haddadin L, Taing M, Lei X, Gandhi A, Tzaridis T, Miller K, Proulx J, Rad AN, Davis A, Liou A, Tanaka H, Dutta T, Poritt R, Cracan V, Loweth C, Olson S, Gardell SJ, Jackson M, Adams PD. · europepmc.org · August 7, 2026