| Identification | Back Directory | [Name]
5-CHLORO-3-[(3,5-DIMETHYLPYRROL-2-YL)METHYLENE]-2-INDOLINONE | [CAS]
1055412-47-9 | [Synonyms]
SU 5614
CS-1552
AC1NS4RE
(Z)-SU5614
SU 5614;SU-5614
5-CHLORO-3-[(3,5-DIMETHYLPYRROL-2-YL)METHYLENE]-2-INDOLINONE
(Z)-5-Chloro-3-((3,5-dimethyl-1H-pyrrol-2-yl)methylene)indolin-2-one
5-chloro-3-[(3,5-dimethyl-1h-pyrrol-2-yl)methylene]-1,3-dihydro-2 H-indol-2-one
(3Z)-5-Chloro-3-[(3,5-diMethyl-1H-pyrrol-2-yl)Methylene]-1,3-dihydro-2H-indol-2-one
2H-Indol-2-one, 5-chloro-3-[(3,5-dimethyl-1H-pyrrol-2-yl)methylene]-1,3-dihydro-, (3Z)- | [Molecular Formula]
C15H13ClN2O | [MDL Number]
MFCD01868565 | [MOL File]
1055412-47-9.mol | [Molecular Weight]
272.73 |
| Chemical Properties | Back Directory | [Boiling point ]
508.6±50.0 °C(Predicted) | [density ]
1.352±0.06 g/cm3(Predicted) | [storage temp. ]
Sealed in dry,2-8°C | [solubility ]
DMSO: ≥20mg/mL | [form ]
powder | [pka]
11.96±0.20(Predicted) | [color ]
orange |
| Hazard Information | Back Directory | [Uses]
SU5614 is a FMS-like tyrosine kinase 3 (FLT3) inhibitor; selective inhibitor of VEGF and PDGF receptor tyrosine kinases. | [Definition]
ChEBI: SU5614 is a member of the class of oxindoles that is 5-chlorooxindole in which the two hydrogens at position 3 are replaced by a (3,5-dimethylpyrrol-2-yl)methylidene group. It has a role as a vascular endothelial growth factor receptor antagonist. It is a member of pyrroles, a member of oxindoles and an organochlorine compound. | [Biological Activity]
su5614 is a protein tyrosine kinase inhibitor.tyrosine kinases are enzymes for the activation of many proteins by signal transduction cascades. the proteins are activated by adding a phosphate group to the protein. | [in vitro]
previous study found that su5614 could induce growth arrest and apoptosis in c-kit-expressing kasumi-1, m-07e, and ut-7 cells and inhibited the stem cell factor (scf)-induced tyrosine phosphorylation of c-kit. moreover, the sensitivity of kasumi-1 cells towards the growth inhibitory activity of su5614 was mainly caused by an autocrine production of scf, but not by the transforming mutations of c-kit [1]. | [in vivo]
it was found that administration of su5614, a vascular endothelial growth factor (vegf) inhibitor, to mice could reduce the levels of vegf dramatically in bal fluids 72 h after toluene diisocyanate inhalation. moreover, consistent with the results obtained from the enzyme immunoassays, western blot analyses showed that su5614 reduced the levels of vegf in the bal fluid 72 h after toluene diisocyanate inhalation. these results suggested that vegf might be one of the major determinants of toluene diisocyanate -induced asthma and that the inhibition of vegf might be a good therapeutic strategy [2]. | [IC 50]
100 nm for flt3 inhibition | [References]
[1] spiekermann k,faber f,voswinckel r,hiddemann w. the protein tyrosine kinase inhibitor su5614 inhibits vegf-induced endothelial cell sprouting and induces growth arrest and apoptosis by inhibition of c-kit in aml cells. exp hematol.2002 jul;30(7):767-73.
[2] lee yc,kwak yg,song ch. contribution of vascular endothelial growth factor to airway hyperresponsiveness and inflammation in a murine model of toluene diisocyanate-induced asthma. j immunol.2002 apr 1;168(7):3595-600. |
|
|