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BCI-215

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Catalog No. T7323Cas No. 1245792-67-9

BCI-215 causes selective cancer cell cytotoxicity in part through non-redox-mediated activation of MAPK signaling

BCI-215

BCI-215

🥰Excellent
Catalog No. T7323Cas No. 1245792-67-9
BCI-215 causes selective cancer cell cytotoxicity in part through non-redox-mediated activation of MAPK signaling
Pack SizePriceAvailabilityQuantity
1 mg$42In Stock
5 mg$98In Stock
10 mg$152In Stock
25 mg$289In Stock
50 mg$455In Stock
100 mg$662In Stock
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Purity:≥95%
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Product Introduction

Bioactivity
Description
BCI-215 causes selective cancer cell cytotoxicity in part through non-redox-mediated activation of MAPK signaling
In vitro
In MDA-MB-231 human breast cancer cells, BCI-215 inhibited cell motility, caused apoptosis but not primary necrosis, and sensitized cells to lymphokine-activated killer cell activity. Mechanistically, BCI-215 induced rapid and sustained phosphorylation of extracellular signal-regulated kinase (ERK), p38, and c-Jun N-terminal kinase (JNK) in the absence of reactive oxygen species, and its toxicity was partially rescued by inhibition of p38 but not JNK or ERK. BCI-215 also hyperactivated MKK4/SEK1, suggesting activation of stress responses[1].
Cell Research
Peripheral blood mononuclear cells were obtained from healthy volunteers. Cells were cultured in RPMI 1640 supplemented with 10% fetal calf serum, 1% glutamine, and 1% penicillin/streptomycin, and stimulated with 6,000 IU of Interleukin 2 for 24 hours. After incubation, cells were washed with PBS and counted. In parallel, MDA-MB-231 cells were pretreated in a 384-well plate with vehicle or BCI-215 (3 μM). After 24 hours in culture, medium was replaced and peripheral blood mononuclear cells (PBMCs) added in 2-fold serial dilutions starting with a 50-fold excess of PBMCs in triplicate. After 24 hours of coculture, cells were fixed with formaldehyde/Hoechst 33342, washed twice with PBS, and imaged on the ArrayScan II. Cancer cells were identified by their larger nuclei compared with PBMCs, setting a size gate in the Hoechst channel. In experiments with chemotherapeutics, cells carrying a biosensor consisting of a mitochondrial targeting sequence derived from cytochrome c oxidase VIII linked to GFP that is a surrogate for cytochrome c release from mitochondria were pretreated for 24 hours with cisplatin (2 μM) or doxorubicin (400 nM), exposed to LAK, and cancer cells were identified and quantified by green fluorescence. Cell densities were normalized to those in the absence of PBMCs. Mean cell densities from multiple independent experiments were averaged and plotted in GraphPad Prism version 7.00[1].
Chemical Properties
Molecular Weight396.32
FormulaC22H22BrNO
Cas No.1245792-67-9
SmilesBrc1ccc2C(=O)\C(=C\c3ccccc3)C(NC3CCCCC3)c2c1
Relative Density.1.37 g/cm3 (Predicted)
Storage & Solubility Information
StoragePowder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice.
Solubility Information
DMSO: 3.96 mg/mL (10 mM), Sonication is recommended.
Solution Preparation Table
DMSO
1mg5mg10mg50mg
1 mM2.5232 mL12.6161 mL25.2321 mL126.1607 mL
5 mM0.5046 mL2.5232 mL5.0464 mL25.2321 mL
10 mM0.2523 mL1.2616 mL2.5232 mL12.6161 mL

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