JCS-1 is a potent DcpS PROTAC degrader. JCS-1 non-covalently binds DcpS with a RG3039-based warhead and recruits the E3 ligase VHL. JCS-1 promotes ubiquitination and degradation of DcpS at nanomolar concentrations ( DC50 in MOLM-14 cells: 87 nM). JCS-1 can be used for the research of AML and other DcpS-dependent genetic disorders [1]. (Pink: DcpS ligand; Blue: VHL ligand; Black: linker ).
In Vitro, JCS-1 (0.1-10000 nM, 24 h) degrades DcpS in MOLM-14 cells in a dose-dependent manner with a DC50 of 87 nM[1]. JCS-1 (1 μM) degrades DcpS rapidly and continuously in MOLM-14 cells, with degradation occurring rapidly within 2 h of treatment and maximum degradation occurring between 12 and 24 h[1]. JCS-1 (1 μM, every 3 days for 12 days) inhibits the proliferation and viability of MOLM-14 cells with an IC50 value of 1.1 μM[1]. JCS-1 (1 μM, 6 h) influences the mRNA pool of MOLM-14 cells with significant increase in SNORD99 and DDX24 expression[1]. Degradation by JCS-1 is inhibited by the neddylation inhibitor MLN4924 and proteasome inhibitor Epoxomicin [1].
References:
[1]. Swartzel, et al. Targeted Degradation of mRNA Decapping Enzyme DcpS by a VHL-Recruiting PROTAC. ACS chemical biology. 2022, 17(7), 1789–1798.
In Vitro, JCS-1 (0.1-10000 nM, 24 h) degrades DcpS in MOLM-14 cells in a dose-dependent manner with a DC50 of 87 nM[1]. JCS-1 (1 μM) degrades DcpS rapidly and continuously in MOLM-14 cells, with degradation occurring rapidly within 2 h of treatment and maximum degradation occurring between 12 and 24 h[1]. JCS-1 (1 μM, every 3 days for 12 days) inhibits the proliferation and viability of MOLM-14 cells with an IC50 value of 1.1 μM[1]. JCS-1 (1 μM, 6 h) influences the mRNA pool of MOLM-14 cells with significant increase in SNORD99 and DDX24 expression[1]. Degradation by JCS-1 is inhibited by the neddylation inhibitor MLN4924 and proteasome inhibitor Epoxomicin [1].
References:
[1]. Swartzel, et al. Targeted Degradation of mRNA Decapping Enzyme DcpS by a VHL-Recruiting PROTAC. ACS chemical biology. 2022, 17(7), 1789–1798.
















