cdk9 in 7

CDK9-IN-7 is a highly selective and orally active CDK9 cyclin T inhibitor (IC50: 11 nM), which exhibits more potent over other CDKs (CDK4 cyclinD: 148 nM; CDK6 cyclinD: 145 nM).

CDK9-IN-2 is a specific CDK9 inhibitor with an IC50 of 5 nM in the A2058 skin cell line (72 hours) and 7 nM in the H929 multiple myeloma cell line (72 hours).

PROTAC CDK9 degrader-2 (compounds 11c) is a potent and selective CDK9 degrader based on PROTAC, with an IC50 of 17 μM in MCF-7 cell lines. Natural product Wogonin binds ubiquitin E3 ligase cereblon (CRBN) via a linker to form PROTAC[1].

CDK9 Antagonist-1 (compounds 11c) is a potent and selective CDK9 degrader based on PROTAC, with an IC50 of 17 μM in MCF-7 cell lines. Natural product Wogonin binds ubiquitin E3 ligase cereblon (CRBN) via a linker to form PROTAC[1]. CDK9|17 μM (IC50, MCF-7 cells) [1]. Bian J , et al. Discovery of Wogonin-based PROTACs against CDK9 and capable of achieving antitumor activity. Bioorg Chem. 2018 Dec;81:373-381.

CDK7 9-IN-1 is a specific inhibitor of cyclin-dependent kinases 7 9 (CDK7 9), targeting CDK7 with IC50 values of 0.0656 μM without pre-incubation and 0.00574 μM after 3 hours pre-incubation, and displaying inhibitory activity against CDK9 with an IC50 of 2.14 μM after 3 hours pre-incubation, making it valuable for cancer research.

BAY 61-3606 HCl is a cell-permeable, reversible inhibitor of spleen tyrosine kinase. BAY 61-3606 HCl can inhibit degranulation and block cytokine release from mast cells. Oral administration of BAY 61-3606 to rats was shown to suppress antigen-induced passive cutaneous anaphylactic reaction, bronchoconstriction, and bronchial edema. It can also sensitize MCF-7 breast cancer cells to TNF-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis by inhibiting Cdk9. This compound has been used in a pre-clinical model to explore the feasibility of targeting Syk in the treatment of retinoblastoma.

CDK7-IN-20 is a potent, selective, and irreversible inhibitor of Cyclin-Dependent Kinase 7 (CDK7) with an IC50 value of 4 nM, exhibiting over 206-fold selectivity against related kinases [CDK1, CDK2, CDK3, CDK5, CDK6, CDK9, and CDK12]. It holds potential for research into autosomal dominant polycystic kidney disease (ADPKD).

CDK9-IN-27 (Compound 6a), a CDK9 inhibitor with an IC50 of 0.424 μM, induces apoptosis and S-phase cell cycle arrest. It exhibits cytotoxicity against HepG2, HCT-116, and MCF-7 cell lines, with IC50 values ranging from 10.31 to 40.34 μM, rendering it applicable in cancer research [1].

LL-K9-3, a selective hydrophobic tagging technology (HyT)-based degrader, specifically targets the CDK9-cyclin T1 complex, displaying DC50 values of 589 nM for cyclin T1 and 662 nM for CDK9. This compound consists of the CDK9 inhibitor, SNS 032, linked to a hydrophobic tag via a glycol linker. Notably, LL-K9-3 does not affect the degradation of other CDKs (CDK1, 2, 4, 5, 6, and 7). Tested in 22RV1 cells, it effectively reduces androgen receptor (AR) and cMyc expression by inducing the selective and synchronous degradation of CDK9 and cyclin T1.