| Literature DB >> 33142063 |
Pethaiah Gunasekaran1, Min Su Yim1,2, Mija Ahn1, Nak-Kyun Soung3, Jung-Eun Park4, Jaehi Kim1, Geul Bang5, Sang Chul Shin6, Joonhyeok Choi1, Minkyoung Kim7, Hak Nam Kim1, Young-Ho Lee1,2, Young-Ho Chung8, Kyeong Lee7, Eunice EunKyeong Kim6, Young-Ho Jeon9, Min Ju Kim10, Kyeong-Ryoon Lee10, Bo-Yeon Kim3, Kyung S Lee4, Eun Kyoung Ryu1,2, Jeong Kyu Bang1,2.
Abstract
Polo-like kinase-1 (Plk1) plays a key role in mitosis and has been identified as an attractive anticancer drug target. Plk1 consists of two drug-targeting sites, namely, N-terminal kinase domain (KD) and C-terminal polo-box domain (PBD). As KD-targeting inhibitors are associated with severe side effects, here we report on the pyrazole-based Plk1 PBD inhibitor, KBJK557, which showed a remarkable in vitro anticancer effect by inducing Plk1 delocalization, mitotic arrest, and apoptosis in HeLa cells. Further, in vivo optical imaging analysis and antitumorigenic activities in mouse xenograft models demonstrate that KBJK557 preferentially accumulates in cancer cells and selectively inhibits cancer cell proliferation. Pharmacokinetic profiles and partition coefficients suggest that KBJK557 was exposed in the blood and circulated through the organs with an intermediate level of clearance (t1/2, 7.73 h). The present investigation offers a strategy for specifically targeting cancer using a newly identified small-molecule inhibitor that targets the Plk1 PBD.Entities:
Mesh:
Substances:
Year: 2020 PMID: 33142063 PMCID: PMC8919061 DOI: 10.1021/acs.jmedchem.0c01451
Source DB: PubMed Journal: J Med Chem ISSN: 0022-2623 Impact factor: 7.446