cdk9/cyct1

CDK9 CycT1-IN-93 is a highly specific, ATP-competitive inhibitor of CDK9 CycT1 with antiviral activity.

PROTAC CDK9 CycT1 Degrader-2 inhibits CDK9 with an IC50 of 45 nM [1].

(R)-Atuveciclib is an isomer of Atuveciclib. Atuveciclib (BAY 1143572) is a potent and highly selective PTEFb CDK9 inhibitor with an IC50 value of 13 nm for CDK9 CycT1 and a selectivity ratio of 100 for CDK2, with highly bioavailable and orally available advantages.

Samuraciclib hydrochloride (ICEC0942 hydrochloride) is a potent, selective, ATP competitive and oral active CDK7 inhibitor with IC50 of 41 nM. The selectivity of Samuraciclib hydrochloride is 45-, 15-, 230- and 30-fold higher than CDK1, CDK2 (IC50 is 578 nM), CDK5 and CDK9 respectively. Samuraciclib hydrochloride inhibits the growth of breast cancer cell lines with GI50 values between 0.2-0.3 μM. Samuraciclib hydrochloride has anti-tumor effects.

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.

Atuveciclib (BAY 1143572) is a potent and highly selective PTEFb CDK9 inhibitor with an IC50 value of 13 nm for CDK9 CycT1 and a selectivity ratio of 100 for CDK2, with highly bioavailable and orally available advantages.

Voruciclib hydrochloride is an orally active and selective CDK inhibitor with a Ki range of 0.626 nM to 9.1 nM.

Atuveciclib S-Enantiomer (BAY-1143572 S-Enantiomer) is a potent and selective CDK9 inhibitor, inhibiting CDK9 CycT1 with an IC50 of 16 nM.

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

TTC-352 is an orally bioavailable selective human estrogen receptor alpha (ERalpha; ESR1; ERa) partial agonist (ShERPA), with potential antineoplastic activity. Upon administration, TTC-352 mimics the naturally-occurring 17beta-estradiol (E2) and targets and binds to ERa located in the nucleus. This causes translocation of ERa to extranuclear sites. Nuclear export of ERa prevents normal ER-mediated signaling and inhibits proliferation of ER-positive tumor cells.

Voruciclib is an orally active and selective CDK inhibitor (Ki: 0.626 nM-9.1 nM) that represses the expression of MCL-1 in multiple models of diffuse large B-cell lymphoma and effectively blocks CDK9, the transcriptional regulator of MCL-1.