SU-11752 is a potent and selective DNA-PK inhibitor. Inhibition kinetics and a direct assay for ATP binding showed that SU11752 inhibited DNA-PK by competing with ATP. SU11752 inhibited DNA double-strand break repair in cells and gave rise to a five-fold sensitization to ionizing radiation. At concentrations of SU11752 that inhibited DNA repair, cell cycle progression was still normal and ATM kinase activity was not inhibited.
CAS 688036-19-3 MFCD88036193
化学结构图
SMILES: CCc1[nH]c(/C=C2\C(=O)Nc3ccc(S(=O)(=O)Nc4ccccc4)cc32)c(CC)c1CCC(=O)O
化学属性
| Mol. Weight | 493.57468 |
|---|---|
| Appearance | Yellow solid powder |
| Solubility | Soluble in DMSO, not in water |
别名和识别编码
| Chemical Name | SU-11752 is a potent and selective DNA-PK inhibitor. Inhibition kinetics and a direct assay for ATP binding showed that SU11752 inhibited DNA-PK by competing with ATP. SU11752 inhibited DNA double-strand break repair in cells and gave rise to a five-fold sensitization to ionizing radiation. At concentrations of SU11752 that inhibited DNA repair, cell cycle progression was still normal and ATM kinase activity was not inhibited. |
|---|---|
| Formula | C26H27N3O5S |
| Synonym | SU11752; SU11752; SU11752. |
| IUPAC Name | (Z)-3-(2,4-diethyl-5-((2-oxo-5-(N-phenylsulfamoyl)indolin-3-ylidene)methyl)-1H-pyrrol-3-yl)propanoic acid |
| InChIKey | QUYIGDGKOSEELL-QNGOZBTKSA-N |
| InChI | InChI=1S/C26H27N3O5S/c1-3-18-19(11-13-25(30)31)22(4-2)27-24(18)15-21-20-14-17(10-12-23(20)28-26(21)32)35(33,34)29-16-8-6-5-7-9-16/h5-10,12,14-15,27,29H,3-4,11,13H2,1-2H3,(H,28,32)(H,30,31)/b21-15- |
| Canonical SMILES | O=C(O)CCC1=C(CC)NC(/C=C2C(NC3=C\2C=C(S(=O)(NC4=CC=CC=C4)=O)C=C3)=O)=C1CC |
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- SU-11752 is a potent and selective DNA-PK inhibitor. Inhibition kinetics and a direct assay for ATP binding showed that SU11752 inhibited DNA-PK by competing with ATP. SU11752 inhibited DNA double-strand break repair in cells and gave rise to a five-fold sensitization to ionizing radiation. At concentrations of SU11752 that inhibited DNA repair, cell cycle progression was still normal and ATM kinase activity was not inhibited.
