c-FMS inhibitor - CAS 885704-21-2
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c-FMS inhibitor is a novel c-Fms kinase inhibitor with a potential as anti-inflammatory agent and antirheumatic agent.
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1H-Pyrrole-2-carboxamide, 4-cyano-N-[4-(4-methyl-1-piperazinyl)-2-(4-methyl-1-piperidinyl)phenyl]-
1.Impact of long-term exposure to the tyrosine kinase inhibitor imatinib on the skeleton of growing rats.
Tauer JT1, Hofbauer LC2, Jung R3, Gerdes S4, Glauche I4, Erben RG5, Suttorp M1. PLoS One. 2015 Jun 24;10(6):e0131192. doi: 10.1371/journal.pone.0131192. eCollection 2015.
The tyrosine kinase (TK) inhibitor imatinib provides a highly effective therapy for chronic myeloid leukemia (CML) via inhibition of the oncogenic TK BCR-ABL1. However, off-target TKs like platelet-derived growth factor receptors (PDGF-R) and colony-stimulating factor-1 receptor (c-fms), involved in bone remodeling, are also inhibited. Thus, pediatric patients with CML on imatinib exhibit altered bone metabolism, leading to linear growth failure. As TKI treatment might be necessary for a lifetime, long-term effects exerted on bone in children are of major concern. Therefore, we studied the skeletal long-term effects of continuous and intermittent imatinib exposure in a juvenile rat model. Four-weeks-old male Wistar rats were chronically exposed to imatinib via drinking water over a period of 10 weeks. Animals were exposed to a standard and high imatinib dosage continuously and to the high imatinib dose intermittently. Bone mass and strength were assessed using pQCT, micro-computed tomography (μCT), and biomechanical testing at the prepubertal, pubertal, and postpubertal age.
2.Targeting c-fms kinase attenuates chronic aristolochic acid nephropathy in mice.
Dai XY1,2,3, Huang XR1, Zhou L3, Zhang L2, Fu P3, Manthey C4, Nikolic-Paterson DJ5, Lan HY1. Oncotarget. 2016 Mar 8;7(10):10841-56. doi: 10.18632/oncotarget.7460.
Aristolochic acid nephropathy (AAN) is a progressive kidney disease caused by some Chinese herbal medicines, but treatment remains ineffective. Macrophage accumulation is an early feature in human and experimental AAN; however, the role of macrophages in chronic AAN is unknown. We report here that targeting macrophages with fms-I, a selective inhibitor of the tyrosine kinase activity of the macrophage colony-stimulating factor receptor, suppressed disease progression in a mouse model of chronic AAN. Treatment with fms-I (10mg/kg/BID) from day 0 to 28 (prevention study) or from day 14 to 28 (intervention study) substantially inhibited macrophage accumulation and significantly improved renal dysfunction including a reduction in proteinuria and tubular damage. Progressive interstitial fibrosis (myofibroblast accumulation and collagen deposition) and renal inflammation (increased expression of MCP-1, MIF, and TNF-α) were also attenuated by fms-I treatment.
3.Deficiency of Lipocalin-2 Promotes Proliferation and Differentiation of Osteoclast Precursors via Regulation of c-Fms Expression and Nuclear Factor-kappa B Activation.
Kim HJ1, Ohk B2, Kang WY2, Seong SJ2, Suk K3, Lim MS4, Kim SY5, Yoon YR2. J Bone Metab. 2016 Feb;23(1):8-15. doi: 10.11005/jbm.2016.23.1.8. Epub 2016 Feb 29.
BACKGROUND: Lipocalin-2 (LCN2), a small glycoprotein, has a pivotal role in diverse biological processes such as cellular proliferation and differentiation. We previously reported that LCN2 is implicated in osteoclast formation induced by receptor activator of nuclear factor-kappa B ligand (RANKL) and macrophage colony-stimulating factor (M-CSF). In the present study, we used a knockout mouse model to further investigate the role of LCN2 in osteoclast development.
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CAS 885704-21-2 c-FMS inhibitor

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