June 23rd, 2026
The primary scientific impulse is to accumulate data and extract knowledge from that data. Application of that knowledge to the production new technologies is a distant afterthought. So too in the life sciences specifically. When it comes to cellular senescence as a driving mechanism of aging, the primary focus of the research community is to employ modern omics tools to build as great a body of data as possible regarding the burden of cellular senescence in aged tissues. In particular this includes the ways in which the state of senescence differs between cell types, or even within the same cell type. Senescence appears to be much more a collection of distinct subtypes than initially suspected.
None of this changes the potential utility of early senotherapeutics, such as the low cost senolytic combination of dasatinib and quercetin that selectively pushes senescent cells into programmed cell death. Clearing even a third of lingering senescent cells from aged tissues produces dramatic benefits in aged mice, meaning a clear reversal of many different age-related diseases and dysfunctions. Yet relatively little effort has been made to rigorously assess this and other early senolytic drugs in humans. A few small academic clinical trials at a few doses have been undertaken when it comes to dasatinib and quercertin, too small a sample to say anything other than the results seem promising, and one company has made it as far as phase 2 trials for a poor choice of senolytic strategy before failing. One would think that the quality of the animal data demands a greater effort when it comes to dasatinib and quercetin.
