This topic entry sits beside the senolysis and senolytics entries in the cell-clearance branch, but it describes the opposite intervention strategy. Where senolytics remove the source of SASP signaling by killing the cell, senomorphics interrupt the signaling pathways, NF-kB, mTOR, and JAK/STAT among them, that drive SASP output while the cell remains in tissue.
The compounds with the most research behind a senomorphic effect, rapamycin, metformin, and ruxolitinib, were all approved for other conditions first and studied for senescence effects afterward, which built its evidence differently than a purpose-built senolytic combination like dasatinib plus quercetin. Readers researching either mechanism should keep the two apart: a senolytic claim needs cell-clearance and apoptosis evidence, a senomorphic claim needs SASP and cytokine-suppression evidence.
Summary
Senolytics kill senescent cells. Senomorphics leave the cells alive and quiet the inflammatory SASP they secrete, through drugs like rapamycin, metformin, and ruxolitinib that were approved for other conditions and later studied for this effect.