plk2

AAPK-25 is a potent and selective Aurora/PLK dual inhibitor with anti-tumor activity, causing mitotic delay and arresting cells in prometaphase, followed by increased apoptosis. It targets Aurora-A/-B/-C with Kd values ranging from 23-289 nM.

Poloxin is a non-ATP competitive Polo-like Kinase 1 inhibitor targeting the polo-box domain (IC50: appr 4.8 μM).

Rigosertib (ON-01910) is a selective, non-ATP-competitive PLK1 inhibitor (IC50: 9 nM) and multi-kinase inhibitor. As a selective anti-cancer agent, Rigosertib induces apoptosis by inhibiting the PI3 kinase/Akt pathway, promotes histone H2AX phosphorylation, and induces G2/M arrest in the cell cycle.

TC-S 7005 is an effective inhibitor of Polo-like kinases (IC50s: 214 nM, 4 nM and 24 nM for Plk1, Plk2, and Plk3).

ON1231320 (GBO-006) is a Polo-like kinase 2 (PLK2) inhibitor.

SBE13 Hydrochloride (SBE 13 HCl) is an effective and specific PLK1 inhibitor (IC50: 0.2 nM); no inhibition om Aurora A kinase, Plk2/3.

BI2536 is an effective Plk1 inhibitor (IC50: 0.83 nM). It has 4- and 11-fold greater selectivity than Plk2 and Plk3.

Onvansertib (NMS-1286937) is a PLK1 inhibitor (IC50=2 nM) with high selectivity and oral activity. Onvansertib has antitumor activity and inhibits tumor growth.

Dihydrobaicalein is a natural product from Scutellaria baicalensis, a PLK1 inhibitor (IC50:6.3 μM).Dihydrobaicalein inhibits VRK2 and PLK2.

Plogosertib (CYC140) is an orally active, selective, potent, and ATP-competitive PLK1 inhibitor with an IC50 value of 3 nM.Plogosertib exhibits antiproliferative and anticancer activity and can be used for the study of solid and hematologic tumors. and hematologic tumors.

Volasertib (BI 6727) trihydrochloride is a dihydropteridinone derivative that potently and selectively inhibits Polo-like kinase 1 (PLK1), PLK2, and PLK3, acting as an orally active ATP-competitive inhibitor with an IC50 of 0.87 nM against PLK1, 5 nM against PLK2, and 56 nM against PLK3. Its mechanism includes inducing mitotic arrest and apoptosis, with significant antitumor activity observed in various cancer models.

Rigosertib sodium (ON-01910), a non-ATP-competitive inhibitor of PLK1(IC50=9 nM), exhibits 30-fold higher specificity activity over Plk2 and no effect on Plk3.

Volasertib (BI 6727) (BI-6727) is a potent inhibitor of PLK1 (IC50: 0.87 nM), inducing mitotic arrest and apoptosis. It also inhibits PLK2/PLK3 (IC50s: 5/56 nM).

TAK-960 hydrochloride is a potent, selective, orally active inhibitor of polo-like kinase 1 (PLK1) (IC50: 0.8 nM). TAK-960 hydrochloride inhibits the proliferation of a variety of tumour cell lines and significantly treats a variety of tumour xenografts.

TAK-960 is an orally bioavailable, selective inhibitor of Plks with IC50 values of 0.8, 16.9, and 50.2 nM for Plk1, Plk2, and Plk3, respectively.

TAK-960 dihydrochloride is an orally administered, selective polo-like kinase 1 (PLK1) inhibitor with a potent IC50 of 0.8 nM. It also targets PLK2 and PLK3 with IC50 values of 16.9 and 50.2 nM, respectively. This compound effectively inhibits the proliferation of a broad range of cancer cell lines and demonstrates substantial efficacy against various tumor xenografts.

YLT-11 is a potent, selective, and orally active inhibitor of polo-like kinase 4 (PLK4), with dissociation constant (Kd) values of >10000 nM for PLK1, 653 nM for PLK2, >10000 nM for PLK3, and 5.2 nM for PLK4. It demonstrates antiproliferative effects, induces apoptosis, and causes cell cycle arrest at the G2/M phase, highlighting its anticancer activity.

CCB02 is a selective CPAP-tubulin interaction inhibitor (IC50: 689 nM) with anti-tumor activity, showing no inhibition on cell cycle- and centrosome-related kinases, nor affecting the phosphorylation status of Aurora-A, CDK2, Plk1, Plk2, and CHK1.

T521 is a selective inhibitor of the PBD of Plk1 and shows no inhibitory effect on Plk2 and Plk3.

PLK1-IN-12 is a highly selective, orally active PLK1 inhibitor with an IC50 of 20 nM. It demonstrates greater selectivity for PLK1 over PLK2 (IC50: >10000 nM) and PLK3 (IC50: 3953 nM). PLK1-IN-12 exhibits anticancer efficacy across a wide range of cell lines and is applicable to anti-leukemia research.

PLK1-IN-13 is a selective, orally active PLK1 inhibitor with an IC50 of 0.27 nM. It also inhibits PLK2 (IC50: 12.72 nM) and PLK3 (IC50: 4.12 nM). PLK1-IN-13 induces cell cycle arrest at the G2 phase, promotes apoptosis, and downregulates the transcription of the cancer-associated oncogene c-MYC. This compound inhibits tumor growth and is applicable for research in acute myeloid leukemia (AML).

CZL-S092 is a PLK4 inhibitor with exceptional selectivity for other PLK4 family members (PLK1, PLK2, and PLK3), exhibiting an IC50 of 0.9 nM. It demonstrates antineuroblastoma activity in vitro (IMR-32, IC50 = 1.143 μM) and shows good oral bioavailability in vivo (SD rats, F = 22.1%). CZL-S092 is applicable in research on various cancers, including neuroblastoma.

Y207–5465 is a potent and highly selective inhibitor of PLK2 with an IC50 value of 584.3 nM. It exhibits limited anticancer activity in HT-29 and HCT-116 cell lines. Y207–5465 is applicable for cancer research.

8012-3246 is a selective PLK2 inhibitor with an IC50 value of 774.5 nM. It inhibits the phosphorylation of GSK3β and exhibits significant anticancer activity against colorectal cancer.