| Bioactivity | Ki20227 is an orally active and highly selective c-Fms tyrosine kinase (CSF1R) inhibitor with IC50s of 2 nM, 12 nM, 451 and 217 nM for CSF1R, VEGFR2 (vascular endothelial growth factor receptor-2), c-Kit (stem cell factor receptor) and PDGFRβ (platelet-derived growth factor receptor β). Ki20227 suppresses osteoclast differentiation and osteolytic bone destruction[1]. | ||||||||||||
| Target | IC50: 2 nM (CSF1R), 12 nM (VEGFR2), 451 nM (c-Kit) and 217 nM (PDGFRβ) | ||||||||||||
| Invitro | Ki20227 (0.1-1000 nM; 72 hours) with 100 and 1,000 nM almost suppresses M-NFS-60 cell growth and HUVEC cell growth, respectively[1]. Ki20227 (0.1-1000 nM; 1 hour) suppresses M-CSF-dependent c-Fms phosphorylation in a dose-dependent manner[1]. Cell Viability Assay[1] Cell Line: | ||||||||||||
| In Vivo | Ki20227 (orally;10-50 mg/kg/d for 20 days) of 50 mg/kg/d of Ki20227 for 20 days markedly decreases the osteolytic lesion areas[1]. ki20227 during global ischemia led to a significant deficit in microglial density in the CNS in mice, and CSF1R-inhibition led to a significant reduction in the neuronal density of mice[2]. Animal Model: | ||||||||||||
| Name | Ki20227 | ||||||||||||
| CAS | 623142-96-1 | ||||||||||||
| Formula | C24H24N4O5S | ||||||||||||
| Molar Mass | 480.54 | ||||||||||||
| Appearance | Solid | ||||||||||||
| Transport | Room temperature in continental US; may vary elsewhere. | ||||||||||||
| Storage |
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| Reference | [1]. Ohno H, et al. A c-fms tyrosine kinase inhibitor, Ki20227, suppresses osteoclast differentiation and osteolytic bone destruction in a bone metastasis model. Mol Cancer Ther. 2006 Nov;5(11):2634-43. [2]. Boru Hou, et al. Ki20227 influences the morphology of microglia and neurons through inhibition of CSF1R during global ischemia. Int J Clin Exp Pathol. 2016;9(12):12459-12469. |