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Submit ReviewLIMKi 3
Description: Potent LIM kinase inhibitor; antitumor
Alternative Names: BMS 5
Chemical Name: N-[5-[1-(2,6-Dichlorophenyl)-3-(difluoromethyl)-1H-pyrazol-5-yl]-2-thiazolyl]-2-methylpropanamide
Purity: ≥98% (HPLC)
Biological Activity for LIMKi 3
LIMKi 3 is a potent LIM kinase inhibitor (IC50 values are 7 and 8 nM for LIMK1 and LIMK2 respectively). Inhibits cofilin phosphorylation in MDA-MB-231 breast cancer cells. Reduces MDA-MB-231 tumor cell invasion in a 3D matrigel invasion assay.
Compound Libraries for LIMKi 3
LIMKi 3 is also offered as part of the Tocriscreen 2.0 Max and Tocriscreen Kinase Inhibitor Library. Find out more about compound libraries available from Tocris.
Technical Data for LIMKi 3
| M. Wt | 431.29 |
| Formula | C17H14Cl2F2N4OS |
| Storage | Store at +4°C |
| Purity | ≥98% (HPLC) |
| CAS Number | 1338247-35-0 |
| PubChem ID | 56965901 |
| InChI Key | IVUGBSGLHRJSSP-UHFFFAOYSA-N |
| Smiles | FC(F)C1=NN(C2=C(Cl)C=CC=C2Cl)C(C3=CN=C(NC(C(C)C)=O)S3)=C1 |
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 LIMKi 3
| Solvent | Max Conc. mg/mL | Max Conc. mM | |
|---|---|---|---|
| Solubility | |||
| DMSO | 43.13 | 100 |
Preparing Stock Solutions for LIMKi 3
The following data is based on the product molecular weight 431.29. 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 |
|---|---|---|---|
| 1 mM | 2.32 mL | 11.59 mL | 23.19 mL |
| 5 mM | 0.46 mL | 2.32 mL | 4.64 mL |
| 10 mM | 0.23 mL | 1.16 mL | 2.32 mL |
| 50 mM | 0.05 mL | 0.23 mL | 0.46 mL |
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Product Datasheets for LIMKi 3
References for LIMKi 3
References are publications that support the biological activity of the product.
Ross-Macdonald et al (2008) Identification of a nonkinase target mediating cytotoxicity of novel kinase inhibitors. Mol.Cancer Ther. 7 3490 PMID: 19001433
Scott et al (2010) LIM kinases are required for invasive path generation by tumor and tumor-associated stromal cells. J.Cell Biol. 191 169 PMID: 20876278
Sparrow et al (2012) The actin-severing protein cofilin is downstream of neuregulin signaling and is essential for Schwann cell myelination. J.Neurosci. 32 5284 PMID: 22496574
If you know of a relevant reference for LIMKi 3, please let us know.
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Keywords: LIMKi 3, LIMKi 3 supplier, LIMKi3, potent, lim, kinases, inhibitors, inhibits, antitumor, BMS5, BMS, 5, LIMK, 4745, Tocris Bioscience
5 Citations for LIMKi 3
Citations are publications that use Tocris products. Selected citations for LIMKi 3 include:
Georgouli et al (2019) Regional Activation of Myosin II in Cancer Cells Drives Tumor Progression via a Secretory Cross-Talk with the Immune Microenvironment. Cell 176 757 PMID: 30712866
Michael R et al (2021) The Wdr1-LIMK-Cofilin Axis Controls B Cell Antigen Receptor-Induced Actin Remodeling and Signaling at the Immune Synapse. Front Cell Dev Biol 9 649433 PMID: 33928084
Johannes et al (2021) Arhgef6 (alpha-PIX) cytoskeletal regulator signals to GTPases and Cofilin to couple T cell migration speed and persistence. J Leukoc Biol 110 839-852 PMID: 33527537
William M et al (2018) The actin filament bundling protein α-actinin-4 actually suppresses actin stress fibers by permitting actin turnover. J Biol Chem 293 14520-14533 PMID: 30049798
Marie et al (2019) Cyclosporine A inhibits MRTF-SRF signaling through Na+/K+ ATPase inhibition and actin remodeling. FASEB Bioadv 1 561-578 PMID: 32123851
Do you know of a great paper that uses LIMKi 3 from Tocris? Please let us know.
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Literature in this Area
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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. 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.