BCI-215

Research use only, not for human use.

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

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

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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Others

Other Targets

Others

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1245792-67-9

396.3

C22H22BrNO

>98% (HPLC)

In Vitro:?DMSO : 33.33 mg/mL (84.10 mM)

Brc1ccc2C(=O)\C(C(NC3CCCCC3)c2c1)=C\c1ccccc1

(E)-2-Benzylidene-5-bromo-3-cyclohexylamino-indan-1-one

(-20℃)

With Ice Pack

≥ 2 years