The history of results achieved while trying to extend mouse life span via manipulation of sirtuins with drugs is not particularly impressive, all told, characterized by an inability to replicate early results, a lack of effectiveness, and challenges from the rest of the scientific community. Nonetheless sirtuins play a role in numerous cellular mechanisms of general interest, so research continues in that sense.
Here one of the later drug candidates for sirtuin manipulation is claimed to modestly extend mean mouse life span - but based on the history you should probably not be terribly excited by this news, even if you consider the development of drugs to slow aging by metabolic manipulation to be a useful activity rather than a distraction from better forms of longevity science:
The prevention or delay of the onset of age-related diseases prolongs survival and improves quality of life while reducing the burden on the health care system. Activation of sirtuin 1 (SIRT1), an NAD+-dependent deacetylase, improves metabolism and confers protection against physiological and cognitive disturbances in old age. SRT1720 is a specific SIRT1 activator that has health and lifespan benefits in adult mice fed a high-fat diet.
We found extension in lifespan, delayed onset of age-related metabolic diseases, and improved general health in mice fed a standard diet after SRT1720 supplementation. Inhibition of proinflammatory gene expression in both liver and muscle of SRT1720-treated animals was noted. SRT1720 lowered the phosphorylation of NF-κB pathway regulators in vitro only when SIRT1 was functionally present. Combined with our previous work, the current study further supports the beneficial effects of SRT1720 on health across the lifespan in mice.