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About This Item
Empirical Formula (Hill Notation):
C19H16N8O·CH3SO3H
CAS Number:
Molecular Weight:
468.49
MDL number:
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77
Quality Level
Assay
≥98% (HPLC)
form
powder
color
white to beige
solubility
DMSO: ≥5 mg/mL (warmed)
storage temp.
2-8°C
SMILES string
CS(O)(=O)=O.OCCn1cc(cn1)-c2cnc3nnn(Cc4ccc5ncccc5c4)c3n2
InChI
1S/C19H16N8O.CH4O3S/c28-7-6-26-12-15(9-22-26)17-10-21-18-19(23-17)27(25-24-18)11-13-3-4-16-14(8-13)2-1-5-20-16;1-5(2,3)4/h1-5,8-10,12,28H,6-7,11H2;1H3,(H,2,3,4)
InChI key
HBEMHKVWZJTVOC-UHFFFAOYSA-N
Gene Information
human ... MET(4233)
Related Categories
Application
PF-04217903 has been used as tyrosine-protein kinase Met (C-Met) selective inhibitor in Madin-Darby Canine kidney (MDCK) cells and NT2D1 non-seminoma cells.
Biochem/physiol Actions
PF-04217903 is a c-Met inhibitor.
PF-04217903 is a highly selective, potent inhibitor of the hepatocyte growth factor receptor c-Met. PF-04217903 inhibits endogenous, wild type c-Met in A549 human lung carcinoma cells with an IC50 of 4.8 nM. The compund displays 1000-fold selectivity against a panel of 208 other kinases.
PF-04217903 is an ATP-competitive inhibitor. It elicits antiangiogenic functionality. PF-04217903 inhibits c-Met phosphorylation in xenograft models leading to partial tumor growth suppression.
Features and Benefits
This compound is featured on the Met page of the Handbook of Receptor Classification and Signal Transduction. To browse other handbook pages, click here.
Storage Class Code
11 - Combustible Solids
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
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c-Src Recruitment is Involved in c-MET-Mediated Malignant Behaviour of NT2D1 Non-Seminoma Cells
Leonetti E, et al.
International Journal of Molecular Sciences, 20(2), 320-320 (2019)
c-MET receptor as potential biomarker and target molecule for malignant testicular germ cell tumors
Scheri K, et al.
Testing, 9(61), 31842-31842 (2018)
Sensitivity of selected human tumor models to PF-04217903, a novel selective c-Met kinase inhibitor
Zou HY, et al.
Molecular Cancer Therapeutics, 11(4), 1036-1047 (2012)
Erica Leonetti et al.
International journal of molecular sciences, 20(2) (2019-01-17)
: c-MET pathway over-activation is the signature of malignancy acquisition or chemotherapy resistance of many cancers. We recently demonstrated that type II Testicular Germ Cell Tumours (TGCTs) express c-MET receptor. In particular, we elucidated that the non-seminoma lesions express c-MET
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