csk

Ibrutinib (PCI-32765) is an irreversible inhibitor of BTK (IC50: 0.5 nM) that selectively blocks B cell activation.

Propargyl-PEG1-acid, a PEG-based PROTAC linker, enables the synthesis of BTK-CRBN PROTACs, specifically Ibrutinib-based PROTAC 4 and PROTAC 5. At a concentration of 10 μM, PROTAC 5 facilitates the degradation of BTK and induces the degradation of CSK, LYN, and LAT2[1].

DB1113 (Example 24) is a bifunctional compound designed for the targeted degradation of various kinases, including ABL1, ABL2, BLK, CDK11B, CDK4, CSK, EPHA3, FER, GAK, LIMK1, MAP3K20, MAP4K1, MAP4K2, MAP4K3, MAP4K5, MAPK14, MAPK7, MAPK8, MAPK9, MAPKAPK2, MAPKAPK3, NLK, PDIK1L, PTK2B, RIPK1, RPS6KA1, RPS6KA3, SIK2, SIK3, STK35, TNK2, and ULK1. This capability positions DB1113 as a valuable tool for research into diseases or disorders associated with aberrant kinase activity [1].

DB0614 (Example 21) is a bifunctional compound designed for the targeted degradation of kinases, effectively breaking down AAK1, AURKA, BMP2K, CAMKK1, CDK16, CML, CDK6, EIF2AK2, FER, GAK, LCK, LIMK2, MAP3KH, MAPK8, MAPK9, NEK9, PLK4, PTK2B, SIK2, STK17A, STK17B, ULK1, ULK3, and WEE1. This compound has potential applications in research on diseases or disorders caused by aberrant kinase activity [1].