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].

CLZX-205 (compound C-7) is a selective inhibitor of CDK9 with an IC50 value of 2.9 nM, playing a critical role in cancer research.

VCC972839:01 is an inhibitor of cyclin-dependent kinase (CDK9) with an IC50 value of 7 nM. It inhibits the viability of SCLC cells at nanomolar concentrations and induces apoptosis through the intrinsic pathway. Additionally, VCC972839:01 demonstrates antitumor activity in mouse models.

CDK9-IN-44 (Compound 7) is a selective inhibitor of CDK9 with an IC50 of 7.6 μM. It effectively inhibits CDK9/cyclin T1 kinase activity, impedes transcription elongation, reduces the expression of oncogenic proteins such as MCL1 and c-MYC, and induces apoptosis in tumor cells. CDK9-IN-44 shows potential for research in glioblastoma (GBM) and central nervous system (CNS) diseases.

KI-ARv-03 is a potent and selective ATP-competitive CDK9 inhibitor with an IC50 of 0.15 μM (in the presence of 45 μM ATP), demonstrating over 130-fold selectivity for CDK9 over other CDKs (including CDK1-7). It reduces AR-driven transcription and proliferation in prostate cancer cells and is applicable for research on leukemia, pancreatic cancer, alveolar rhabdomyosarcoma (ARMS), and castration-resistant prostate cancer (CRPC). Additionally, KI-ARv-03 serves as a ligand for target protein for PROTAC and is used in the synthesis of PROTAC KI-CDK9d-32[1][2].

dCDK9-202 is a potent CDK9-PROTAC degrader with a DC50 value of 3.5 nM. It exhibits broad-spectrum antitumor activity and significantly disrupts oncogenic transcriptomes. dCDK9-202 activates Caspase-3/7, increases levels of cleaved PARP, and directly induces tumor cell apoptosis (apoptosis). It effectively inhibits the growth of TC-71 tumors without any observed toxicity in mice. dCDK9-202 is applicable for researching EGFR-driven cancers, such as sarcomas.

Olomoucine II is a potent cyclin-dependent kinase inhibitor with IC50 values of 7.6, 0.1, 19.8, 0.45, and 0.06 μM for CDK1, CDK2, CDK4, CDK7, and CDK9, respectively. Olomoucine II demonstrates high selectivity over numerous other kinases while retaining measurable activity against ERK2 and ABCB1, allowing it to modulate multidrug resistance pathways. Olomoucine II suppresses proliferation across cancer cell lines regardless of p53 status and exhibits synergistic action with daunorubicin in ABCB1-expressing HCT-8 cells.Olomoucine II additionally inhibits replication of HSV-1, HSV-2, vaccinia virus, adenovirus 4, and human CMV, making Olomoucine II an important antiviral and anticancer research tool.

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.

Tricin (Standard) is a reference standard for research and analysis in studies involving Tricin. Tricin can inhibit human cytomegalovirus (HCMV) replication by inhibiting CDK9. Tricin inhibits the proliferation and invasion of C6 glioma cells via the upregulation of focal-adhesion-finase (FAK)-targeting microRNA-7.