Description
SSK1, a senescence-specific killing compound, is a β-galactosidase-targeted proagent attenuates inflammation. SSK1 is activated by lysosomal β-galactosidase and selectively killed senescent cells through the activation of p38 MAPK and induction of apoptosis.In VitroSSK1 (0.5 µM; 12-72 hours) activates the phosphorylation levels of both p38 MAPK and MKK3/MKK6 in senescent cells. SSK1 kills senescent cells through the activation of the p38 MAPK signaling pathway. SSK1 is able to induce mitochondrial DNA damage in senescent cells. SSK1 (0.01-1 µM; 3 days) selectively and potently eliminates β-galactosidase-positive senescent cells within a wide therapeutic window. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Cell Proliferation AssayCell Line: Primary mouse fibroblasts Concentration: 0.5 µM Incubation Time: 12 hours, 24 hours, 36 hours, 48 hours, 72 hours Result: Both p38 MAPK and MKK3/MKK6 were activated by phosphorylation in senescent cells.In VivoSSK1 (0.5 mg/kg; i.p.; two days every week; for four weeks) could eliminate senescent cells and decrease senescence-associated markers in lung-injured mice. In aged mice (20-month-old), SSK1 (0.5 mg/kg; 3 days every 2 weeks for 8 weeks) effectively clears senescent cells in different tissues, decreases the senescence- and age-associated gene signatures, attenuates low-grade local and systemic inflammation, and restores physical function. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Mice (3-6-month-old) were subjected to transtracheal injection of Bleomycin Dosage: 0.5 mg/kg Administration: Intraperitoneally injection; two days every week; for four weeks Result: SSK1 significantly reduced the percentage of SA-β-gal-positive cells in lung by 3.8-fold compared with that in vehicle-treated lung-injured miceForm:Solid