c-FMS inhibitor

C-FMS kinase inhibitor CAS# 885704-21-2

c-FMS inhibitor

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Quality Control of c-FMS inhibitor

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Chemical structure

c-FMS inhibitor

3D structure

Chemical Properties of c-FMS inhibitor

Cas No. 885704-21-2 SDF Download SDF
PubChem ID 11654378 Appearance Powder
Formula C23H30N6O M.Wt 406.52
Type of Compound N/A Storage Desiccate at -20°C
Solubility DMSO : 25 mg/mL (61.50 mM; Need ultrasonic)
H2O : < 0.1 mg/mL (insoluble)
Chemical Name 4-cyano-N-[4-(4-methylpiperazin-1-yl)-2-(4-methylpiperidin-1-yl)phenyl]-1H-pyrrole-2-carboxamide
SMILES CC1CCN(CC1)C2=C(C=CC(=C2)N3CCN(CC3)C)NC(=O)C4=CC(=CN4)C#N
Standard InChIKey DXPSQKSTVIVZLV-UHFFFAOYSA-N
Standard InChI InChI=1S/C23H30N6O/c1-17-5-7-29(8-6-17)22-14-19(28-11-9-27(2)10-12-28)3-4-20(22)26-23(30)21-13-18(15-24)16-25-21/h3-4,13-14,16-17,25H,5-12H2,1-2H3,(H,26,30)
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of c-FMS inhibitor

Descriptionc-FMS inhibitor is a potent, orally active and small-molecule inhibitor of FMS kinase with IC50 value of 0.8 nM.
TargetsFMS kinase    
IC500.8 nM     

c-FMS inhibitor Dilution Calculator

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c-FMS inhibitor Molarity Calculator

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Preparing Stock Solutions of c-FMS inhibitor

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.4599 mL 12.2995 mL 24.599 mL 49.1981 mL 61.4976 mL
5 mM 0.492 mL 2.4599 mL 4.9198 mL 9.8396 mL 12.2995 mL
10 mM 0.246 mL 1.23 mL 2.4599 mL 4.9198 mL 6.1498 mL
50 mM 0.0492 mL 0.246 mL 0.492 mL 0.984 mL 1.23 mL
100 mM 0.0246 mL 0.123 mL 0.246 mL 0.492 mL 0.615 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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Background on c-FMS inhibitor

c-FMS inhibitor, 4-cyano-N-[4-(4-methylpiperazin-1-yl)-2-(4-methylpiperidin-1-yl) phenyl]-1H-pyrrole-2-carboxamide, is a novel FMS kinase inhibitors as anti-inflammatory agents with an IC50 value of 0.8 nM.[1] c-FMS inhibitor resulted in identification of a highly potent series of 2,4-disubstituted arylamides. It served as a proof-of-concept candidate in a collagen-induced model of arthritis in mice.[1] c-FMS inhibitors has a potential to form reactive metabolites which are transformed into a series with equivalent potency by incorporation of carbon-based replacement groups. Structure-based model provides the framework to efficiently effect this transformation and restore potencies to previous levels. This optimization removed a risk factor for potential idiosyncratic drug reactions.[2]

References:
Discovery of novel FMS kinase inhibitors as anti-inflammatory agents.  Bioorg Med Chem Lett. 2008 Mar 1;18(5):1642-8
Structure-based optimization of a potent class of arylamide FMS inhibitors.  Bioorg Med Chem Lett. 2008 Jun 15;18(12):3632-7.

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References on c-FMS inhibitor

Selective inhibition of PGE2 production in cells transfected with c-fms encoded CSF-1 receptor genes by the tyrosine kinase inhibitor, ST638.[Pubmed:1950818]

Agents Actions. 1991 Jul;33(3-4):314-7.

In this study, we investigated the effect of ST638, a novel tyrosine kinase inhibitor, on TPA and ionomycin-stimulated PGE2 production after transfection of c-fms encoded CSF-1 receptor (CSF-1R) DNA (with or without transforming activity) into the myeloid progenitor cell line, 32D. ST638 inhibited prostaglandin E2 (PGE2) production induced after transfection of normal c-fms into 32D cell line, but failed to inhibit PGE2 production induced in 32D cells transformed with c-fms containing a point mutation at tyrosine 969 in the intracellular domain (substitution with phenylalanine) and at leucine 301 in the extracellular domain (substitution with serine). The selective effect on PGE2 production in normal c-fms-bearing cells by ST638 may indicate the presence of different induction pathways, one sensitive to ST638 and the other not. Alternatively, the phosphorylation site at tyr969 in c-fms may be a site of ST638 action, and upon its removal from the transforming c-fms, ST638 loses its inhibitory effect.

A c-fms tyrosine kinase inhibitor, Ki20227, suppresses osteoclast differentiation and osteolytic bone destruction in a bone metastasis model.[Pubmed:17121910]

Mol Cancer Ther. 2006 Nov;5(11):2634-43.

In bone metastatic lesions, osteoclasts play a key role in the development of osteolysis. Previous studies have shown that macrophage colony-stimulating factor (M-CSF) is important for the differentiation of osteoclasts. In this study, we investigated whether an inhibitor of M-CSF receptor (c-Fms) suppresses osteoclast-dependent osteolysis in bone metastatic lesions. We developed small molecule inhibitors against ligand-dependent phosphorylation of c-Fms and examined the effects of these compounds on osteolytic bone destruction in a bone metastasis model. We discovered a novel quinoline-urea derivative, Ki20227 (N-{4-[(6,7-dimethoxy-4-quinolyl)oxy]-2-methoxyphenyl}-N'-[1-(1,3-thiazole-2-yl)e thyl]urea), which is a c-Fms tyrosine kinase inhibitor. The IC(50)s of Ki20227 to inhibit c-Fms, vascular endothelial growth factor receptor-2 (KDR), stem cell factor receptor (c-Kit), and platelet-derived growth factor receptor beta were found to be 2, 12, 451, and 217 nmol/L, respectively. Ki20227 did not inhibit other kinases tested, such as fms-like tyrosine kinase-3, epidermal growth factor receptor, or c-Src (c-src proto-oncogene product). Ki20227 was also found to inhibit the M-CSF-dependent growth of M-NFS-60 cells but not the M-CSF-independent growth of A375 human melanoma cells in vitro. Furthermore, in an osteoclast-like cell formation assay using mouse bone marrow cells, Ki20227 inhibited the development of tartrate-resistant acid phosphatase-positive osteoclast-like cells in a dose-dependent manner. In in vivo studies, oral administration of Ki20227 suppressed osteoclast-like cell accumulation and bone resorption induced by metastatic tumor cells in nude rats following intracardiac injection of A375 cells. Moreover, Ki20227 decreased the number of tartrate-resistant acid phosphatase-positive osteoclast-like cells on bone surfaces in ovariectomized (ovx) rats. These findings suggest that Ki20227 inhibits osteolytic bone destruction through the suppression of M-CSF-induced osteoclast accumulation in vivo. Therefore, Ki20227 may be a useful therapeutic agent for osteolytic disease associated with bone metastasis and other bone diseases.

SB1578, a novel inhibitor of JAK2, FLT3, and c-Fms for the treatment of rheumatoid arthritis.[Pubmed:22962687]

J Immunol. 2012 Oct 15;189(8):4123-34.

SB1578 is a novel, orally bioavailable JAK2 inhibitor with specificity for JAK2 within the JAK family and also potent activity against FLT3 and c-Fms. These three tyrosine kinases play a pivotal role in activation of pathways that underlie the pathogenesis of rheumatoid arthritis. SB1578 blocks the activation of these kinases and their downstream signaling in pertinent cells, leading to inhibition of pathological cellular responses. The biochemical and cellular activities of SB1578 translate into its high efficacy in two rodent models of arthritis. SB1578 not only prevents the onset of arthritis but is also potent in treating established disease in collagen-induced arthritis mice with beneficial effects on histopathological parameters of bone resorption and cartilage damage. SB1578 abrogates the inflammatory response and prevents the infiltration of macrophages and neutrophils into affected joints. It also leads to inhibition of Ag-presenting dendritic cells and inhibits the autoimmune component of the disease. In summary, SB1578 has a unique kinase spectrum, and its pharmacological profile provides a strong rationale for the ongoing clinical development in autoimmune diseases.

The orally-active and selective c-Fms tyrosine kinase inhibitor Ki20227 inhibits disease progression in a collagen-induced arthritis mouse model.[Pubmed:18085662]

Eur J Immunol. 2008 Jan;38(1):283-91.

Macrophage colony-stimulating factor (M-CSF) is important in the development of macrophages and osteoclasts. Previous studies have also shown that CD11b(+) myeloblasts and osteoclasts play key roles during inflammation and bone destruction in arthritic lesions. In this study, we investigated whether N-{4-[(6,7-dimethoxy-4-quinolyl)oxy]-2-methoxyphenyl}-N'-[1-(1,3-thiazole-2-yl)et hyl] urea (Ki20227), an inhibitor of the M-CSF receptor (c-Fms), suppressed disease progression in a type II collagen (CII)-induced arthritis (CIA) mouse model. We found that Ki20227 inhibited M-CSF-dependent reactions, such as lipopolysaccharide-induced tumor necrosis factor-alpha production, which were enhanced by M-CSF in vitro. Oral administration of Ki20227 in vivo prevented inflammatory cell infiltration and bone destruction, and consequently suppressed disease progression. In addition, the number of CD11b(+), Gr-1(+), and Ly-6G(+) cells in the spleen decreased in the Ki20227-treated mice, and the CII-induced cytokine production in splenocytes isolated from the Ki20227-treated arthritic mice was also reduced. These observations indicate that Ki20227 might exert its therapeutic effects in the CIA mouse model by suppressing the M-CSF-dependent accumulation of both inflammatory and osteoclast cells, as well as by inhibiting inflammatory cytokine production. Hence, inhibitors of the c-Fms tyrosine kinase might act as anti-inflammatory or anti-osteolytic agents against arthritis.

Description

c-Fms-IN-3 is a novel c-Fms kinase inhibitor with a potential as anti-inflammatory agent and antirheumatic agent.

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