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Biological Activity for Centrinone B
Centrinone B is a high affinity and selective PLK4 inhibitor (Ki = 0.6 nM). Exhibits >2000-fold selectivity for PLK4 over Aurora A and Aurora B. Depletes centriole and centrosome levels in vitro. Induces cell cycle arrest in normal human cell lines in a p53-dependent manner.
Sold with the permission of the Ludwig Institute for Cancer Research Ltd
Technical Data for Centrinone B
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Solubility Data for Centrinone B
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions for Centrinone B
The following data is based on the product molecular weight 631.67. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|0.5 mM||3.17 mL||15.83 mL||31.66 mL|
|2.5 mM||0.63 mL||3.17 mL||6.33 mL|
|5 mM||0.32 mL||1.58 mL||3.17 mL|
|25 mM||0.06 mL||0.32 mL||0.63 mL|
References for Centrinone B
References are publications that support the biological activity of the product.
Wong et al (2015) Reversible centriole depletion with an inhibitor of Polo-like kinase 4. Science 348 1155 PMID: 25931445
If you know of a relevant reference for Centrinone B, please let us know.
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Keywords: Centrinone B, Centrinone B supplier, LCR323, high, affinity, selective, PLK4, inhibitors, inhibits, centriole, centrosome, LCR, 323, Polo-like, Kinase, Mitosis, 5690, Tocris Bioscience
8 Citations for Centrinone B
Citations are publications that use Tocris products. Selected citations for Centrinone B include:
Dong et al (2020) Prolonged mitosis results in structurally aberrant and over-elongated centrioles. J Cell Biol 219 PMID: 32271878
Minji et al (2020) FAM46C/TENT5C functions as a tumor suppressor through inhibition of Plk4 activity. Commun Biol 3 448 PMID: 32807875
Chen et al (2017) Human microcephaly protein RTTN interacts with STIL and is required to build full-length centrioles. Nat Commun 8 247 PMID: 28811500
Anna et al (2021) Centriole and Golgi microtubule nucleation are dispensable for the migration of human neutrophil-like cells. Mol Biol Cell 32 1545-1556 PMID: 34191538
Kazazian et al (2017) Plk4 Promotes Cancer Invasion and Metastasis through Arp2/3 Complex Regulation of the Actin Cytoskeleton. Cancer Res 77 434 PMID: 27872092
Péter et al (2022) Centrosome function is critical during terminal erythroid differentiation. EMBO J 41 e108739 PMID: 35678476
Carol J et al (2022) Investigating the mechanisms of peritoneal metastasis in gastric adenocarcinoma using a novel ex vivo peritoneal explant model. Sci Rep 12 11499 PMID: 35798764
Mues et al (2019) High-Complexity shRNA Libraries and PI3 Kinase Inhibition in Cancer: High-Fidelity Synthetic Lethality Predictions. Cell Rep 27 631 PMID: 30970263
Do you know of a great paper that uses Centrinone B from Tocris? Please let us know.
Reviews for Centrinone B
Average Rating: 5 (Based on 1 Review.)
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
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Cell Cycle and DNA Damage Research Product Guide
This product guide provides a review of the cell cycle and DNA damage research area and lists over 170 products, including research tools for:
- Cell Cycle and Mitosis
- DNA Damage Repair
- Targeted Protein Degradation
- Ubiquitin Proteasome Pathway
- Chemotherapy Targets
Cell Cycle & DNA Damage Repair Poster
In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the stages of the cell cycle and DNA repair. It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death.