| Field | Specification |
|---|---|
| CAS no. | |
| Applications | |
| Molecular weight | |
| Molecular formula | C13H16BrNO3 |
| Purity | |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
KRA-533 is a potent KRAS agonist that binds to the GTP/GDP binding pocket of the KRAS protein, preventing GTP cleavage. This results in accumulation of constitutively active, GTP-bound KRAS that triggers both apoptotic and autophagic cell death pathways in cancer cells. It is supplied as an off-white to light brown solid (C13H16BrNO3, MW 314.18) at 98.73% purity.
Physical & Chemical Properties
| CAS Number | 10161-87-2 |
|---|---|
| Molecular Formula | C13H16BrNO3 |
| Molecular Weight | 314.18 g/mol |
| Purity | 98.73% |
| Appearance | Solid |
| Color | Off-white to light brown |
| SMILES | O=C(O)C1=CC=C(CCCCNC(CBr)=O)C=C1 |
| Signaling Pathway | GPCR/G Protein; MAPK/ERK Pathway |
| Solubility | In Vitro: DMSO: 250 mg/mL (795.72 mM; Requires sonication; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO) |
| Storage | Powder: -20°C, 3 years. In solvent: -80°C, 6 months; -20°C, 1 month. |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Literature Cited
Sources cited in this description and in the In Vitro & In Vivo Data tab. Peer-reviewed publications that used this product are listed under References.
Safety
For Research Use Only. Not for use in diagnostic or therapeutic procedures, and not for human or veterinary use. Handle in accordance with the Safety Data Sheet and your institution's chemical hygiene plan.
In Vitro
| Solvent | Solubility | Notes |
|---|---|---|
| DMSO | 250 mg/mL (795.72 mM) | requires sonication; use freshly opened DMSO (absorbed moisture lowers solubility) |
Aliquot the stock solution and store it at -80°C (up to 6 months) or -20°C (up to 1 month); avoid repeated freeze-thaw cycles.
Data provided by the manufacturer.
In Vitro
KRA-533 (10 μM; 48 hours; HCC827 cells) raises KRAS activity to a greater extent[1]. KRA-533 (0~15 μM; 48 hours; H157 cells) raises KRAS activity in a dose-dependent manner, associated with increased levels of pERK, an increased ratio of active caspase 3/procaspase 3, and PARP cleavage, which leads to apoptotic cell death[1]. KRA-533 (10 μM; 10 days; H292 cells) mediates suppression of cell growth, relative to cells without KRAS mutation. KRA-533 (5~15 μM) can bind directly to WT, G12C, G12D and G13D mutant KRAS proteins. WT KRAS is activated by KRA-533, with its activity increasing in a dose-dependent manner. The activities of active KRAS mutants are further enhanced by KRA-533[1].
Western Blot Analysis[1]
| Cell Line | HCC827 cells |
|---|---|
| Concentration | 10 μM |
| Incubation Time | 48 hours |
| Result | Enhanced KRAS activity to a greater extent. |
Apoptosis Analysis[1]
| Cell Line | H157 cells |
|---|---|
| Concentration | 0~15 μM |
| Incubation Time | 48 hours |
| Result | Enhanced KRAS activity in a dose-dependent manner, which was associated increased levels of pERK, ratio of active caspase 3/procaspase 3 and PARP cleavage, leading to apoptotic cell death. |
In Vivo
KRA-533 (0~30 mg/kg; i.p.; 28 days) suppresses tumor growth in xenografts of lung cancer with mutant KRAS and induces apoptosis and autophagy in tumor tissues, both in a dose-dependent manner[1]. The optimal therapeutic index of KRA-533 lies between the 7.5 mg/kg and 30 mg/kg doses[1].
| Animal Model | Nu/Nu nude mice (mutant KRAS xenografts)[1] |
|---|---|
| Dosage | 0~30 mg/kg |
| Administration | i.p.; 28 days |
| Result | Suppressed tumor growth in a dose-dependent manner in lung cancer mutant KRAS xenografts and induced apoptosis and autophagy in tumor tissues in a dose-dependent manner. |
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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