cdk9-in-9

CDK9-IN-9 is a potent and selective CDK9 inhibitor (IC50: 1.8 nM) with anti-cancer activity. It inhibits CDK2 (IC50: 155 nM).

CDK9-IN-10 is a potent inhibitor of CDK9 and serves as the ligand for the PROTAC CDK9 degrader-2.

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-8 is a highly potent and selective CDK9 inhibitor (IC50: 12 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).

CDK9-IN-1 is a selective and potent CDK9 inhibitor with antiviral activity used in the study of PRRSV infections.

CDK9-IN-11 is a potent CDK9 inhibitor and serves as the ligand for the PROTAC CDK9 Degrader-1 [1].

PROTAC CDK9 degrader-9 (compound 29) is a highly efficient, selective degrader of CDK9 based on PROTAC technology. It is utilized in cancer research.

Zotiraciclib (also known as TG02 and SB1317) is an innovative small-molecule compound with potent inhibitory effects on CDK, JAK2, and FLT3. By inhibiting cyclin-dependent kinase 9 (CDK9) and depleting Myc, it serves as a treatment for cancers that can penetrate the blood-brain barrier. Zotiraciclib is one of the numerous CDK inhibitors under investigation; other compounds targeting CDK9, utilized for treating acute myeloid leukemia, include alvocidib and atuveciclib. Myc overexpression is a known factor in many cancers, with 80% of glioblastomas exhibiting this characteristic.

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

CDK4 9-IN-1 (Compound 29) is a selective dual inhibitor of CDK4 and CDK9, exhibiting IC50 values of 23 nM and 12 nM, respectively. It holds potential for use in cancer research.

CDK7 9 tide is a peptide substrate for CDK7 or CDK9[1].

CDK9-IN-12 is a highly selective CDK9 inhibitor, which is commonly used in leukemia research to regulate oncogene expression, inhibit oncogenic proliferation, and induce apoptosis by targeting CDK9-dependent transcription processes.

CDK6 9-IN-1 (compound 66) is a potent, orally administered dual inhibitor of CDK6 and CDK9, with IC50 values of 40.5 nM and 39.5 nM, respectively.

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.

Zotiraciclib, also known as TG02 and SB1317, is a novel small molecule potent CDK JAK2 FLT3 inhibitor. Zotiraciclib may be useful for the treatment of cancer that crosses the blood brain barrier and acts by depleting Myc through the inhibition of cyclin-dependent kinase 9 (CDK9). It is one of a number of CDK inhibitors under investigation; others targeting CDK9 for the treatment of acute myeloid leukemia include alvocidib and atuveciclib. Myc overexpression is a known factor in many cancers, with 80 percent of glioblastomas characterized by this property.

Ibulocydine is a potent CDK inhibitor. Ibulocydine has high activity against Cdk7 cyclin H Mat1 and Cdk9 cyclin T. Ibulocydine inhibited the growth of HCC cells more effectively than other Cdk inhibitors, including olomoucine and roscovitine, whereas ibulocydine as well as the other Cdk inhibitors and BMK-Y101 minimally influenced the growth of normal hepatocyte cells. Ibulocydine induced apoptosis in HCC cells, most likely by inhibiting Cdk7 and Cdk9. In vitro treatment of HCC cells with ibulocydine rapidly blocked phosphorylation of the carboxyl-terminal domain (CTD) of the large subunit of RNA polymerase II, a process mediated by Cdk7 9. Anti-apoptotic gene products such as Mcl-1, survivin, and X-linked IAP (XIAP) are crucial for the survival of many cell types, including HCC. Following the inhibition of RNA polymerase II phosphorylation, ibulocydine caused rapid down-regulation of Mcl-1, survivin, and XIAP, thus inducing apoptosis. Furthermore, ibulocydine effectively ind......

CDK9-IN-26, also known as compound 1, is a potent inhibitor of Cyclin-Dependent Kinase 9 (CDK9) with an IC50 value of 0.18 μM.[1]

LH2-051 is a lysosomal-enhancing lead compound that stimulates lysosomal biosynthesis and the clearance of Aβ aggregates through the dopamine transporter-cell cycle protein dependent kinase 9-transcription factor EB (DAT-CDK9-TFEB) pathway. Demonstrating favorable pharmacokinetic properties in mouse models, LH2-051 has the potential to improve Alzheimer's disease outcomes.