CDK9 Inhibitor

CDK9/HDAC1/HDAC3-IN-1 is dual-functional inhibitor of CDK9 and HDAC. CDK9/HDAC1/HDAC3-IN-1 inhibits the protein activity of CDK9/HDAC/HDAC3 with IC₅₀ s of 0.17  μM, 1.73  μM and 1.11 μM for CDK9, HDAC1, and HDAC3, respectively. CDK9/HDAC1/HDAC3-IN-1 inhibits cancer cells by inducing cell apoptosis and cell cycle arrest in the G2/M phase, as well as tumor growth in a murine TNBC MDA-MB-231 xenograft model. CDK9/HDAC1/HDAC3-IN-1 has a broad-spectrum anti-cancer activity, such as breast cancer, cervical cancer, and liver cancer.

CDK9-IN-50 is a selective and orally active CDK9 inhibitor with an IC₅₀ of 2.2 nM. CDK9-IN-50 targets a distinct CDK9-specific subpocket to disrupt RNA polymerase II Ser2 phosphorylation and downregulate short-lived oncoproteins, including AR-V7 and Myc. CDK9-IN-50 exhibits antiproliferative activity against cancer cells, induces apoptosis and induces tumor growth inhibition in CRPC orthotopic mice models. CDK9-IN-50 can be used for the research of cancer, such as prostate cancer.

CDK9-IN-19 is a highly potent and selective CDK9 inhibitor with an IC₅₀ value of 2.0 nM. CDK9-IN-19 has excellent cellular antiproliferative activity, moderate pharmacokinetic property and low hERG inhibition. CDK9-IN-19 significantly induces tumour growth inhibition in an MV4-11 xenograft mice model. CDK9-IN-19 can be used for researching acute myeloid leukaemia (AML).

CDK9-IN-22 is a potent CDK9 inhibitor with IC₅₀s of 10.4, 876.2 nM for CDK9, CDK, respectively. CDK9-IN-22 induces apoptosis and cell cycle arrests at G2/M phase. CDK9-IN-22 decreases the expression of p-RNAPII (S2) and CDK9 protein. CDK9-IN-22 shows antiproliferative and aiti-tumor activity.

CDK4/6-IN-14 is a potent and highly selective CDK4 and CDK6 (CDK) inhibitor with IC₅₀s of 10 nM and 16 nM, respectively. CDK4/6-IN-14 exhibits more than 60-fold selectivity over CDKs 1, 2, 7, and 9, and shows high selectivity among other 205 kinases.

CDK9-IN-48 is a CDK9 inhibitor with an IC₅₀ of 1.37 nM. CDK9-IN-48 inhibits the proliferation of various cancer cells. CDK9-IN-48 can be used in the research of cancers such as acute myeloid leukemia and prostate cancer.

BLINK11 is a BBB-penetrant CDK5 inhibitor. BLINK11 lowers CDK5 activity for both complexes CDK5/p35 (IC₅₀ = 17.09 nM) and CDK5/p25 (IC₅₀ = 14.69 nM). BLINK11 offers anti-diabetic and neuroprotective benefits. BLINK11 lowers blood glucose, enhances cognition, and reduces neurodegeneration in T2D mice.

IIIM-290 is a potent and oral CDK inhibitor with IC₅₀s of 90 and 94 nM for CDK2/A and CDK9/T1.

CDK9-IN-46 (Compound Formula I) is a CDK9 inhibitor. CDK9-IN-46 can be used for the research of cancer.

CDK9-IN-42 is a potent and selective CDK9 inhibitor with an IC₅₀of 3.8 nM. CDK9-IN-42 can inhibit the growth of cancer cells and induce apoptosis by downregulating Myc-1 and c-Myc. CDK9-IN-42 can be used for the research of cancer, such as breast and lungcancer.

CDK9-IN-40 is a potent and orally active CDK9 inhibitor with an IC₅₀ of 5.5 nM. CDK9-IN-40 shows high selectivity for CDK9 versus CDK1, CDK2, CDK4, and CDK6, respectively. CDK9-IN-40 can arrest cell cycle, induce cell apoptosis and inhibit tumor growth. CDK9-IN-40 exhibits strong anti-cancer activity.

CDK9-IN-52 is a CDK9 inhibitor. CDK9-IN-52 exhibits antiproliferative activity against cancer cells. CDK9-IN-52 can be used in studies related to lung cancer, cervical cancer, and breast cancer.

CDK2/9-IN-1 (compound 20a) is an orally active dual inhibitor of CDK2 and CDK9 with IC₅₀ values are 0.004 μM and 0.009 μM respectively. CDK2/9-IN-1 induces apoptosis by regulating G2/M cell cycle arrest. CDK2/9-IN-1 has antitumor activity.

CDK7-IN-20 is a potent, selective and irreversible CDK7 (CDK) inhibitor with an IC₅₀ value of 4 nM. CDK7-IN-20 displays >206-fold selectivity for CDK7 over CDK1, CDK2, CDK3, CDK5, CDK6, CDK9 and CDK12 . CDK7-IN-20 has the potential for autosomal dominant polycystic kidney disease (ADPKD) research.

CDK2-IN-47 is a potent CDK2 inhibitor with an IC₅₀ of 0.21 μM. CDK2-IN-47 exhibits outstanding anticancer activity against MCF-7, HCT-116, and MGC-803 cell lines. CDK2-IN-47 effectively induces G1 cell cycle arrest, retinoblastoma protein (Rb) dephosphorylation, and significant apoptosis. CDK2-IN-47 can be used for the studies of breast cancer, colorectal cancer and gastric cancer.

CDK2-IN-55 (Compound 12c) is a CDK2 inhibitor with an IC₅₀ value of 4.7 nM. CDK2-IN-55 also has a strong inhibitory effect on CDK1 (IC₅₀ = 26.3 nM), moderate inhibitory effects on Aurora A (IC₅₀ = 92.0 nM) and CDK9 (IC₅₀ = 288 nM), and very weak inhibitory activities on CDK4, CDK6, DYRK1A, and GSK3β (IC₅₀ > 1000 nM). CDK2-IN-55 shows strong anti-proliferative activity against various cancer cell lines, inducing cell cycle arrest and apoptosis. CDK2-IN-55 can be used for research on colorectal cancer, lung cancer, and cervical cancer.

CDK8-IN-20 (Compound 67j) is a selective, potent and orally active type I CDK8 inhibitor with an IC₅₀ of 70.5 nM. CDK8-IN-20 shows IC₅₀ values of 147.8, 726.9 and 217.4 nM for homologous kinase CDK19, CDK7 and CDK9. CDK8-IN-20 can inhibit the Wnt/β-catenin pathway and downregulate the expression of β-catenin, Cyclin D1, and c-Myc. CDK8-IN-20 can induce ROS production and cause G2/M and S phase arrest. CDK8-IN-20can be used for the research of cancer, such as colon cancer.

KB-0742 hydrochloride is a potent, selective and orally active CDK9 inhibitor with an IC₅₀ of 6 nM for CDK9/cyclin T1. KB-0742 hydrochloride is selective for CDK9/cyclin T1 with >50-fold selectivity over other CDK kinases. KB-0742 hydrochloride has potent anti-tumor activity.

PROTAC CDK9 degrader-6 is a PROTAC targeting to CDK9 sepcifically. PROTAC CDK9 degrader-6 mediates CDK9 degradation via the proteasome. PROTAC CDK9 degrader-6 degrades CDK9 with DC₅₀s of 0.10 μM and 0.14 μM for the CDK9₄₂ and CDK9₅₅ isoforms, respectively.

KI-ARv-03 is a potent and selective ATP-competitive CDK9 inhibitor with an IC₅₀ of 0.15 μM (at 45 μM ATP), exhibiting over 130-fold selectivity against other CDKs (including CDK1-7). KI-ARv-03 reduces androgen receptor (AR)-driven transcription and proliferation in prostate cancer cells. KI-ARv-03 can be used for leukemia, pancreatic cancer, alveolar rhabdomyosarcoma (ARMS) and castration-resistant prostate cancer (CRPC) research. KI-ARv-03 is a ligand for target protein for PROTAC. KI-ARv-03 can be used to synthesize PROTAC KI-CDK9d-32 (HY-173523)^[1][2].