CT52923
CAS No. 205256-55-9
CT52923( —— )
Catalog No. M35387 CAS No. 205256-55-9
CT52923 is a selective, orally active antagonist of platelet-derived growth factor receptor (PDGFR), functioning as an ATP-competitive inhibitor.
Purity : >98% (HPLC)
COA
Datasheet
HNMR
HPLC
MSDS
Handing Instructions
| Size | Price / USD | Stock | Quantity |
| 5MG | 41 | Get Quote |
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| 10MG | 64 | Get Quote |
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| 25MG | 125 | Get Quote |
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| 50MG | 205 | Get Quote |
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| 100MG | 303 | Get Quote |
|
| 500MG | Get Quote | Get Quote |
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| 1G | Get Quote | Get Quote |
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Biological Information
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Product NameCT52923
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NoteResearch use only, not for human use.
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Brief DescriptionCT52923 is a selective, orally active antagonist of platelet-derived growth factor receptor (PDGFR), functioning as an ATP-competitive inhibitor.
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DescriptionCT52923 is a selective, orally active platelet-derived growth factor receptor (PDGFR) antagonist. CT52923 also is an ATP-competitive inhibitor. CT52923 can be used for the research variety of pathological diseases, including atherosclerosis, glomerulonephritis, liver cirrhosis, pulmonary fibrosis, and cancer.
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In VitroCell Migration Assay Cell Line:Rat A10 smooth muscle cells Concentration:0.01-30 μM Incubation Time:24 h Result:Inhibited PDGF-induced cell migration with an IC50 of 64 nM.
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In VivoAnimal Model:Rat carotid artery balloon angioplasty model.Dosage:5, 15, 30, and 50 mg/kg Administration:Oral gavage; twice daily Result:Inhibited PDGF-mediated response to vascular injury.
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Synonyms——
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PathwayAngiogenesis
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TargetPDGFR
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RecptorPDGFR
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Research Area——
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Indication——
Chemical Information
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CAS Number205256-55-9
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Formula Weight467.54
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Molecular FormulaC23H25N5O4S
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Purity>98% (HPLC)
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SolubilityIn Vitro:?DMSO : 50 mg/mL (106.94 mM; Ultrasonic (<60°C)
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SMILESCOc1cc2ncnc(N3CCN(CC3)C(=S)NCc3ccc4OCOc4c3)c2cc1OC
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Chemical Name——
Shipping & Storage Information
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Storage(-20℃)
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ShippingWith Ice Pack
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Stability≥ 2 years
Reference
1. J C Yu, et al. Efficacy of the novel selective platelet-derived growth factor receptor antagonist CT52923 on cellular proliferation, migration, and suppression of neointima following vascular injury. J Pharmacol Exp Ther. 2001 Sep;298(3):1172-8.?
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