Uses
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[1].
Biological Activity
SSK1, a senescence-specific killing compound, is a β-galactosidase-targeted prodrug attenuates inflammation. SSK1 is activated by lysosomal β-galactosidase and selectively killed senescent cells through the activation of p38 MAPK and induction of apoptosis[1].
SSK1 (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[1]. SSK1 (0.01-1 μM; 3 days) selectively and potently eliminates β-galactosidase-positive senescent cells within a wide therapeutic window[1].
SSK1 (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[1].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[1].
in vivo
SSK1 (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[1].
?
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[1].
| Animal Model: | Mice (3-6-month-old) were subjected to transtracheal injection of Bleomycin[1] |
| 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 mice |
storage
4°C, away from moisture and light
References
[1]. Yusheng Cai, et al. Elimination of senescent cells by β-galactosidase-targeted prodrug attenuates inflammation and restores physical function in aged mice. Cell Res. 2020 Jul;30(7):574-589.
