| DC73219 |
Allopole
|
Allopole is the first allosteric, specfic and cell-permeable inhibitor of the noncatalytic polo-box domain (PBD) of PLK1 (Polo-like kinase 1), Allopole is the prodrug of Allopole-A. |
| DC70300 |
CFI-400945
|
CFI-400945 is a potent, highly selective PLK4 inhibitor with Ki of 0.26 nM and IC50 of 2.8 nM, does not significantly inhibits PLK1/2/3 at 50 uM; causes dysregulated centriole duplication, mitotic defects, and cell death in multiple cancer cell lines (A549 GI50=5 nM, OVCAR-3 GI50=18 nM); significantly inhibits human cancer xenografts; causes polyploidy, growth inhibition, and apoptotic death of murine and human lung cancer cells, despite expression of mutated KRAS or p53, produces supernumerary centrosomes and mitotic defects in lung cancer cells. |
| DC9594 |
Poloxin
|
Poloxin is a non-ATP competitive Polo-like Kinase 1 (PLK1) inhibitor that targets the polo-box domain. |
| DC8768 |
HMN-214
|
HMN-214(IVX214) is a potent PLK1 inhibitor an average IC50 of 0.12 μM. |
| DC73221 |
SBE13
|
PLK1 inhibitor SBE13 is a potent, selective PLK1 inhibitor with IC50 of 0.2 nM, with little to no inhibition against PLK2/PLK3 (IC50, 65 uM/875 nM). |
| DC73220 |
Allopole-A
|
Allopole-A is the first allosteric, specfic inhibitor of the noncatalytic polo-box domain (PBD) of PLK1 (Polo-like kinase 1) with IC50 of 2.5 nM in FP-based assays, Allopole-A is the active form of Allopole. |
| DC71736 |
Plogosertib
|
Plogosertib (CYC140) is a selective, potent, and orally active ATP-competitive PLK1 inhibitor (IC50: 3 nM). Plogosertib is an anti-cancer agent with anti-proliferative activity. Plogosertib can be used in the research of several tumors, including esophageal, gastric, leukemia, non–small cell lung cancer, ovarian, and squamous cell cancers. |
| DC70301 |
CFI-400945 fumarate
|
CFI-400945 is a potent, highly selective, orally available PLK4 inhibitor with Ki of 0.26 nM and IC50 of 2.8 nM, does not significantly inhibits PLK1/2/3 at 50 uM; causes dysregulated centriole duplication, mitotic defects, and cell death in multiple cancer cell lines (A549 GI50=5 nM, OVCAR-3 GI50=18 nM); significantly inhibits human cancer xenografts; causes polyploidy, growth inhibition, and apoptotic death of murine and human lung cancer cells, despite expression of mutated KRAS or p53, produces supernumerary centrosomes and mitotic defects in lung cancer cells. |
