BCI-215

SKU: orb1220473

Description

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

Key Properties

• CAS Number: 1245792-67-9
• MW: 396.3
• Purity: >98% (HPLC)
• Formula: C₂₂H₂₂BrNO
• SMILES: Brc1ccc2C(=O)\C(C(NC3CCCCC3)c2c1)=C\c1ccccc1
• Target: Others
• Solubility: In Vitro: DMSO : 33.33 mg/mL (84.10 mM)

Bioactivity

• In Vitro:
  BCI-215 concentration-dependently increases pERK levels in DUSP-overexpressing cells with IC50 value in the micromolar range. BCI-215 (1-20 μM; 6 hours) retains fibroblast growth factor hyperactivating and cellular DUSP6/MKP-3 and DUSP1/MKP-1 inhibitory activity but is nontoxic to zebrafish embryos and an endothelial cell line. BCI-215 inhibits survival and motility of MDA-MB-231 human breast cancer cells but does not affect viability of cultured hepatocytes. BCI-215 is completely devoid of hepatocyte toxicity up to 100 μM. BCI-215 does not generate ROS in hepatocytes or in developing Zebrafish larvae. BCI-215 (22 μM) has antimigratory and proapoptotic activities in breast cancer cells that correlate with induction of ERK phosphorylation. BCI-215 (20 μM; 1 hour) induces mitogenic and stress signaling in cancer cells without generating ROS. Apoptosis Analysis Cell line: MDA-MB-231 cells. Concentration: 22 μM. Incubation time: Result: Caused apoptotic cell death at concentrations that induce ERK phosphorylation. Western blot analysis. Cell line: MDA-MB-231 cells. Concentration: 20 μM. Incubation time: 1 hour. Result: Induced a stress response that is not dependent on oxidation.
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Storage & Handling

• Storage: Storage temperature: -20°C. Stability: ≥ 2 years
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

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