JUN04542
CAS No. 2367004-54-2
JUN04542( CL-092 )
Catalog No. M24079 CAS No. 2367004-54-2
JUN04542 is an Axl Mer cMet KDR inhibitor for the treatment of Axl and Mer receptor tyrosine kinase- dependent disorders.
Purity : >98% (HPLC)
COA
Datasheet
HNMR
HPLC
MSDS
Handing Instructions
| Size | Price / USD | Stock | Quantity |
| 1 mL x 10 mM in DMSO | 47 | In Stock |
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| 2MG | 29 | In Stock |
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| 5MG | 41 | In Stock |
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| 10MG | 69 | In Stock |
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| 25MG | 129 | In Stock |
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| 50MG | 207 | In Stock |
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| 100MG | 345 | In Stock |
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| 200MG | Get Quote | In Stock |
|
| 500MG | Get Quote | In Stock |
|
| 1G | Get Quote | In Stock |
|
Biological Information
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Product NameJUN04542
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NoteResearch use only, not for human use.
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Brief DescriptionJUN04542 is an Axl Mer cMet KDR inhibitor for the treatment of Axl and Mer receptor tyrosine kinase- dependent disorders.
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DescriptionJUN04542 is an Axl Mer cMet KDR inhibitor for the treatment of Axl and Mer receptor tyrosine kinase- dependent disorders.
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In Vitro——
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In VivoAnimal Model:Rat Dosage:3 mg/kg (Pharmacokinetic Analysis) Administration:IV Result:Had a T1/2 of 5.4 hours, a CL of 43 mL/hr?kg.
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SynonymsCL-092
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PathwayAngiogenesis
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Targetc-Met/HGFR
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RecptorAxl|c-Met|KDR|Mer
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Research Area——
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Indication——
Chemical Information
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CAS Number2367004-54-2
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Formula Weight528.53
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Molecular FormulaC29H25FN4O5
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Purity>98% (HPLC)
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SolubilityDMSO:10 mM
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SMILESCNC(=O)C1=CC2=C(C=CN=C2C=C1OC)OC3=CC=C(C=C3)NC(=O)C4(CC4)C(=O)NC5=CC=C(C=C5)F
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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
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SGX-523
SGX-523 is a potent, selective ATP-competitive inhibitor of MET receptor tyrosine kinase with IC50 of 4 nM.
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c-Met inhibitor 1
c-Met inhibitor 1 is a c-Met receptor signaling pathway inhibitor, used for the treatment of cancer including glioblastoma, gastric, and pancreatic cancer.
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Capmatinib hydrochlo...
Capmatinib hydrochloride is an orally bioavailable inhibitor of the proto-oncogene c-Met (HGFR)with potential antineoplastic activity.Capmatinib was found to be highly selective for MET over other kinases.?It was active against cancer models that are characterized by MET amplification, marked MET overexpression, MET exon 14 skipping mutations, or MET activation via expression of the ligand hepatocyte growth factor (HGF).
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