PLK2
PLK2 is an evolutionarily conserved serine/threonine kinase with an N-terminal kinase domain and C-terminal polo-box domain[1]. Mechanistically, PLK2 supports mitotic centriole replication, neural homeostasis, and synaptic plasticity[1][2]. In centrosome biology, PLK2 localizes to centrosomes near the G1/S transition, and its polo-box domain enables centrosomal association and centriole duplication[2]. In neurons, PLK2 regulates α-synuclein turnover by phosphorylating α-synuclein at S129 and promoting selective autophagic degradation[3]. In disease models, PLK2 overexpression reduced α-synuclein accumulation, dopaminergic neurodegeneration, and motor impairment in a rat Parkinson disease model[3]. However, PLK2 deletion reduced presynaptic α-synuclein S129 phosphorylation but did not reduce Lewy body phosphorylation, separating physiological phosphorylation from aggregate pathology[4]. Compared with related isoforms, PLK3 can also catalyze α-synuclein phosphorylation and degradation, while PLK1 and PLK4 remain the dominant inhibitor-focused cancer targets[5][6]. For experimental applications, PLK2 inhibition suppressed LPS-induced microglial proinflammatory signaling through the HSP90α/IKKβ/NF-κB pathway[7].
References:
- [1]. Zhang C, et al. Polo-Like Kinase 2: From Principle to Practice. Front Oncol. 2022 Jul 8;12:956225. [Content Brief]
- [2]. Cizmecioglu O, et al. Plk2 regulated centriole duplication is dependent on its localization to the centrioles and a functional polo-box domain. Cell Cycle. 2008 Nov 15;7(22):3548-55. [Content Brief]
- [3]. Oueslati A, et al. Polo-like kinase 2 regulates selective autophagic α-synuclein clearance and suppresses its toxicity in vivo. Proc Natl Acad Sci U S A. 2013 Oct 8;110(41):E3945-54. [Content Brief]
- [4]. Weston LJ, et al. Genetic deletion of Polo-like kinase 2 reduces alpha-synuclein serine-129 phosphorylation in presynaptic terminals but not Lewy bodies. J Biol Chem. 2021 Jan-Jun;296:100273. [Content Brief]
- [5]. Dahmene M, et al. Dissecting the Molecular Pathway Involved in PLK2 Kinase-mediated α-Synuclein-selective Autophagic Degradation. J Biol Chem. 2017 Mar 3;292(9):3919-3928. [Content Brief]
- [6]. Bian S, et al. Progress with polo-like kinase (PLK) inhibitors: a patent review (2018-present). Expert Opin Ther Pat. 2024 Sep;34(9):789-806. [Content Brief]
- [7]. Cheng J, et al. Polo-like kinase 2 promotes microglial activation via regulation of the HSP90α/IKKβ pathway. Cell Rep. 2024 Oct 22;43(10):114827. [Content Brief]
All Product Categories
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PLK2 Related Products (22)
Related Products (22)
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Volasertib
0 ImagesSynonyms: BI 6727Volasertib (BI 6727) is an orally active, highly potent and ATP-competitive Polo-like kinase 1 (PLK1) inhibitor with an IC50 of 0.87 nM. Volasertib inhibits PLK2 and PLK3 with IC50s of 5 and 56 nM, respectively. Volasertib induces mitotic arrest and apoptosis. Volasertib, a dihydropteridinone derivative, shows marked antitumor activity in multiple cancer models.
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Rigosertib
0 ImagesCat. No.: HY-12037ACAS No.: 592542-59-1Synonyms: ON-01910Rigosertib (ON-01910) is a multi-kinase inhibitor and a selective anti-cancer agent, which induces apoptosis by inhibition the PI3 kinase/Akt pathway, promots the phosphorylation of histone H2AX and induces G2/M arrest in cell cycle. Rigosertib is a selective and non-ATP-competitive inhibitor of PLK1 with an IC50 of 9 nM.
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TAK-960
0 ImagesTAK-960 is an orally available, selective inhibitor of polo-like kinase 1 (PLK1), with an IC50 of 0.8 nM. TAK-960 also shows inhibitory activities against PLK2 and PLK3, with IC50s of 16.9 and 50.2 nM, respectively. TAK-960 inhibits proliferation of multiple cancer cell lines and exhibits significant efficacy against multiple tumor xenografts.
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8012–3246
0 Images8012-3246 is a selective PLK2 inhibitor with an IC50 of 774.5 nM. 8012-3246 suppresses GSK3β phosphorylation. 8012-3246 exhibits potent anticancer activity against colorectal cancer.
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Poloppin II
0 ImagesCat. No.: HY-125220CAS No.: 2248068-54-2Poloppin II is an orally active PBD inhibitor that blocks the binding of phosphopeptide substrates to PLK1/PLK2 PBD, with IC50 values of 41 µM and 105 µM for human PLK1/PLK2 PBD, respectively. Poloppin II binds to PLK4 PBD to inhibit PLK4-dependent mitotic functions. Poloppin II can be used in research on kras-mutant colorectal cancer.
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YLT-11
0 ImagesCat. No.: HY-115589CAS No.: 3040940-49-3
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Rigosertib sodium
0 ImagesSynonyms: ON-01910 sodiumRigosertib sodium (ON-01910 sodium) is a multi-kinase inhibitor and a selective anti-cancer agent, which induces apoptosis by inhibition the PI3K/Akt pathway, promotes the phosphorylation of histone H2AX and induces G2/M arrest in cell cycle. Rigosertib sodium is a selective and non-ATP-competitive inhibitor of PLK1 with an IC50 of 9 nM.
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Poloxin
0 ImagesPoloxin is a non-ATP competitive Polo-like Kinase 1 (PLK1) inhibitor that targets the polo-box domain, with an IC50 of appr 4.8 μM.
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Plogosertib
0 ImagesSynonyms: CYC140Plogosertib (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.
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Volasertib trihydrochloride
0 ImagesSynonyms: BI 6727 trihydrochlorideVolasertib (BI 6727) trihydrochloride is an orally active, highly potent and ATP-competitive Polo-like kinase 1 (PLK1) inhibitor with an IC50 of 0.87 nM. Volasertib trihydrochloride inhibits PLK2 and PLK3 with IC50s of 5 and 56 nM, respectively. Volasertib trihydrochloride induces mitotic arrest and apoptosis. Volasertib trihydrochloride, a dihydropteridinone derivative, shows marked antitumor activity in multiple cancer models.
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PLK1-IN-13
0 ImagesPLK1-IN-13 is a selective and orally active PLK1 inhibitor (IC50: 0.27 nM). PLK1-IN-13 also inhibits PLK2 (IC50: 12.72 nM) and PLK3 (IC50: 4.12 nM). PLK1-IN-13 arrests cell at G2 phase, induces apoptosis and down-regulates the transcription of the proliferation-related oncogene c-MYC. PLK1-IN-13 inhibits tumor growth, and can be used for research of acute myeloid leukemia (AML).
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TAK-960 dihydrochloride
0 ImagesCat. No.: HY-15160BPurity: 99.15%TAK-960 dihydrochloride is an orally available, selective inhibitor of polo-like kinase 1 (PLK1), with an IC50 of 0.8 nM. TAK-960 dihydrochloride also shows inhibitory activities against PLK2 and PLK3, with IC50s of 16.9 and 50.2 nM, respectively. TAK-960 dihydrochloride inhibits proliferation of multiple cancer cell lines and exhibits significant efficacy against multiple tumor xenografts.
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PLK1-IN-12
0 ImagesCat. No.: HY-172364PLK1-IN-12 is a highly selective and orally active PLK1 inhibitor with an IC50 of 20 nM. PLK1-IN-12 shows more selective for PLK1 than PLK2 (IC50: >10000 nM) and PLK3 (IC50: 3953 nM). PLK1-IN-12 exhibits anticancer potency across a broad spectrum of cell lines. PLK1-IN-12 can be used in anti-leukemia research.
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Rucaparib metabolite M324
0 ImagesCat. No.: HY-187971CAS No.: 1577998-89-0Rucaparib metabolite M324 is a metabolite generated from Rucaparib (HY-10617A) via oxidative deamination. Rucaparib metabolite M324 inhibits PLK2 (IC50 591 nM), GSK3A (579 nM), GSK3B (2.0 µM), PARP1, PARP2, TNKS1, and TNKS2. Rucaparib metabolite M324 inhibits the accumulation of α-synuclein in iPSC-derived dopaminergic neurons. Rucaparib metabolite M324 in combination with Rucaparib produces synergistic antitumor effects in prostate cancer cells. Rucaparib metabolite M324 can be used in research related to prostate cancer and Parkinson's disease.
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PLK2-IN-1
0 ImagesCat. No.: HY-189637PLK2-IN-1 is a selective PLK2 inhibitor (IC50 0.78 μM). PLK2-IN-1 induces Apoptosis and cell cycle arrest, reduces AKT and mTOR phosphorylation, and decreases Cyclin E expression as well as downregulates the CDK2/Rb/E2F1 axis. PLK2-IN-1 inhibits tumor growth in colorectal cancer xenograft models. PLK2-IN-1 can be used for research on colorectal cancer.
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PLK1-IN-16
0 ImagesCat. No.: HY-181051CAS No.: 3068378-51-5PLK1-IN-16 is a selective polo-like kinase 1 (PLK1) inhibitor with an IC50 of 0.25 nM. PLK1-IN-16 exhibits lower inhibitory potency against PLK2 and PLK3, induces G2 phase cell cycle arrest, induces apoptosis, and exhibits antiproliferative activity against tumor cells. PLK1-IN-16 can be stable under simulated gastric acid environmental conditions, and acceptable CYP 450 inhibition. PLK1-IN-16 can be used for the study of triple-negative breast cancer (TNBC), breast cancer, leukemia.
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