GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE336nnn/GSE336391/primaryOK200TranscriptomicsHomo sapiensExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE336391GEOGSEfalseEffect of NAMPT modulation in OIS-senescent IMR90 cellsNicotinamide adenine dinucleotide (NAD+) metabolism becomes dysregulated with age and has emerged as a targetable feature of aging and age-related dysfunction, yet the cellular contexts in which altered NAD+ homeostasis creates therapeutic vulnerabilities remain incompletely defined. Here, we identify senescence as one such context. Senescent cells retained elevated levels of nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in the NAM salvage pathway yet exhibited a paradoxical reduction in NAD+ turnover, suggesting a disconnect between protein abundance and enzymatic output. Treatment with SBI-0802162 engaged the spare enzymatic capacity of NAMPT in senescent cells and produced a marked rise in intracellular NAD+ that, when sustained, reinforced their existing stress-associated transcriptional program and selectively reduced senescent cell viability while sparing proliferating cells. Together, these findings identify elevated NAMPT coupled with reduced NAD+ turnover as a metabolic vulnerability in senescent cells and support combined NAMPT activation with dietary NAM as a novel strategy to restore NAD+ homeostasis and improve age-associated inflammation.2026/09/23GSE336391GSM9834090GSM9834080GSM9834091GSM9834083GSM9834094GSM9834084GSM9834095GSM9834081GSM9834092GSM9834093GSM9834082GSM9834087GSM9834077GSM9834088GSM9834096GSM9834085GSM9834086GSM9834097GSM9834089GSM9834078GSM983407930173336391Homo sapiens[42620342]