CDK9-IN-2

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).

EGFR HER2 CDK9-IN-2 are potent inhibitors of EGFR HER2 CDK9, and they exhibited significant antitumor effects with IC50s of 145.35, 129.07 and 117.13 nM, respectively.

CDK9-IN-23 (Example 4) is a highly potent CDK9 inhibitor with an IC50 value below 20 nM [1].

CDK9-IN-24 (compound 21a) is a potent and selective CDK9 inhibitor that significantly inhibits tumor proliferation, impedes cell growth, and triggers apoptosis via downregulation of Mcl-1 and c-Myc, making it valuable for acute myeloid leukemia research [1].

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].

CDK9-IN-25 (compound 4a), an imidazopyrazine derivative, functions as a CDK9 inhibitor with an IC50 of 0.24 μM. It also exhibits affinity for the main protease of COVID-19 and demonstrates antiviral activity against human coronavirus 229E, with an IC50 of 63.28 μM [1].

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]

PROTAC CDK9 CycT1 Degrader-1 (compounds 10), a potent CDK9 inhibitor and target protein ligand for PROTAC synthesis, exhibits substantial anti-proliferative activity in solid tumors [1], making it instrumental in the targeted degradation of CDK9 CycT1.

CDK9-IN-29 (compound Z11) is a potent CDK9 inhibitor, demonstrating high kinase selectivity with an IC50 of 3.20 nM, effectively hindering cell proliferation and inducing apoptosis [1].

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

InhA-IN-2 directly inhibits InhA and does not require activation by the catalase peroxidase KatG.

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-IN-40 is an inhibitor of CDK2 (Cyclin-dependent kinase 2). It effectively inhibits CDK2 Cyclin E1, with an IC50 of ≤ 10 nM.

CDK12-IN-2 (CDK12 inhibitor 2) is an effective and selective inhibitor of CDK12 with an IC50 of 52 nM, >100 μM, >10 μM and 16 μM for CDK12, CDK2, CDK7, and CDK9. CDK12-IN-2 can be used in studies about the function of CDK12.

CDK12-IN-4, a pyrazolotriazine compound, exhibits potent inhibition of CDK12 by achieving an IC50 value of 0.641 μM, utilizing high ATP levels (2 mM). Notably, CDK12-IN-4 does not impact CDK2 Cyclin E (IC50 > 20 μM) or CDK9 Cyclin T1 (IC50 > 20 μM) under the influence of high ATP (2 mM) levels (WO2021116178A1).

CDK12-IN-6, a pyrazolotriazine compound, is a powerful inhibitor of CDK12. Its inhibitory activity is significant with an IC50 value of 1.19 μM when tested at high ATP concentration (2 mM). Notably, CDK12-IN-6 does not exhibit any inhibitory effect on CDK2 Cyclin E (IC50 >20 μM) and CDK9 Cyclin T1 (IC50 >20 μM) when tested under the same high ATP conditions (2 mM) (WO2021116178A1).

Riviciclib hydrochloride (P276-00) is a novel inhibitor of CDK1, CDK4, and CDK9, with IC50 values of 79 nM, 63 nM, and 20 nM, respectively, currently in Phase 2 3.

SB-1295, an orally active CDK9 T1 inhibitor with an IC50 of 0.17 μM, exhibits antiproliferative effects on HCT 116 and MIA PaCa-2 cells. It promotes cell death in MIA PaCa-2 by elevating intracellular ROS levels, diminishing mitochondrial membrane potential, and triggering apoptosis. This compound holds potential for 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.

CDK-IN-2 (CDK inhibitor II) is a potent and specific CDK9 inhibitor (IC50: <8 nM).