For research use only. Not for therapeutic Use.
KRA-533 is a potent KRAS agonist. KRA-533 binds to the GTP/GDP binding pocket in the KRAS protein to prevent GTP cleavage, resulting in the accumulation of constitutively active GTP-bound KRAS that triggers both apoptotic and autophagic cell death pathways in cancer cells.
KRA-533 (10 μM; 48 hours; HCC827 cells) enhances KRAS activity to a greater extent[1].
KRA-533 (0~15 μM; 48 hours; H157 cells) enhances KRAS activity in a dose-dependent manner, which is associated increased levels of pERK, ratio of active caspase 3/procaspase 3 and PARP cleavage, leading to apoptotic cell death[1].
KRA-533 (10 μM; 10 days; H292 cells) mediates cell growth suppression than those without KRAS mutation. KRA-533 (5~15 μM) can directly bind to WT, G12C, G12D and G13D mutant KRAS proteins. KRA-533 activates WT KRAS to increase its activity in a dose-dependent manner. KRA-533 further enhances the activities of active KRAS mutants[1].
KRA-533 (0~30 mg/kg; i.p.; 28 days) suppresses tumor growth in a dose-dependent manner in lung cancer mutant KRAS xenografts and induces apoptosis and autophagy in tumor tissues in a dose-dependent manner[1].
KRA-533 shows optimal therapeutic index between 7.5 mg/kg and 30 mg/kg doses[1].
Catalog Number | I030151 |
CAS Number | 10161-87-2 |
Synonyms | 4-[4-[(2-bromoacetyl)amino]butyl]benzoic acid |
Molecular Formula | C13H16BrNO3 |
Purity | ≥95% |
InChI | InChI=1S/C13H16BrNO3/c14-9-12(16)15-8-2-1-3-10-4-6-11(7-5-10)13(17)18/h4-7H,1-3,8-9H2,(H,15,16)(H,17,18) |
InChIKey | WZQJLTLURXNPQG-UHFFFAOYSA-N |
SMILES | C1=CC(=CC=C1CCCCNC(=O)CBr)C(=O)O |
Reference | [1]. Xu K, et al. Small Molecule KRAS Agonist for Mutant KRAS Cancer Therapy [published correction appears in Mol Cancer. 2020 May 20;19(1):93]. Mol Cancer. 2019;18(1):85. Published 2019 Apr 10. |