(E/Z)-BCI

Research use only, not for human use.

(E/Z)-BCI attenuates LPS-induced inflammatory mediators and ROS production in macrophage cells via activating the Nrf2 signaling axis and inhibiting the NF-κB pathway. (E/Z)-BCI is a dual-specificity phosphatase 6 (DUSP6) inhibitor with anti-inflammatory activities.

(E/Z)-BCI attenuates LPS-induced inflammatory mediators and ROS production in macrophage cells via activating the Nrf2 signaling axis and inhibiting the NF-κB pathway. (E/Z)-BCI is a dual-specificity phosphatase 6 (DUSP6) inhibitor with anti-inflammatory activities.(In Vitro):(E/Z)-BCI hydrochloride (2-10 μM; 72 hours) significantly decreases cell viability in a time and dose-dependent manner in gastric epithelial cell GES1, GC cell lines, and AGS cell lines. (E/Z)-BCI hydrochloride (0.5-4 μM; 24 hours) significantly inhibits DUSP6 expression in LPS-activated macrophages. (E/Z)-BCI hydrochloride inhibits cell proliferation, migration, and invasion in a receptor-independent manner and enhances Cisplatin (CDDP) cytotoxicity (enhances CDDP-induced cell death and apoptosis) at pharmacological concentrations in gastric cancer (GC) cells. (E/Z)-BCI hydrochloride (0.5-2 μM; 24 hours) treatment significantly inhibits the expression of IL-1β, TNF-α, and IL-6 mRNA in LPS-activated macrophages. (E/Z)-BCI hydrochloride decreases ROS production and activates the Nrf2 pathway in LPS-activated macrophages. (In Vivo):(E/Z)-BCI hydrochloride treatment enhances cisplatin efficacy in PDX models.

(E/Z)-BCI hydrochloride (2-10 μM; 72 hours) significantly decreases cell viability in a time and dose-dependent manner in gastric epithelial cell GES1, GC cell lines, and AGS cell lines.(E/Z)-BCI hydrochloride (0.5-4 μM; 24 hours) significantly inhibits DUSP6 expression in LPS-activated macrophages.(E/Z)-BCI hydrochloride (0.5-2 μM; 24 hours) treatment significantly inhibits the expression of IL-1β, TNF-α and IL-6 mRNA in LPS-activated macrophages.(E/Z)-BCI hydrochloride decreases ROS production and activates the Nrf2 pathway in LPS-activated macrophages.(E/Z)-BCI hydrochloride inhibits cell proliferation, migration and invasion in a receptor-independent manner and enhances Cisplatin (CDDP) cytotoxicity (enhances CDDP-induced cell death and apoptosis) at pharmacological concentrations in the gastric cancer (GC) cells. Cell Viability Assay Cell Line:Gastric epithelial cell GES1, GC cell lines (HGC27, SGC7901, MKN45, BGC823, MGC803, SNU216, NUGC4), AGS cell lines Concentration:2 μM, 4 μM, 6 μM, 8 μM, 10 μM Incubation Time:72 hours Result:Cell viability was significantly decreased in a time and dose-dependent manner.Western Blot Analysis Cell Line:RAW264.7 macrophage cells (by LPS-activated macrophages) Concentration:0.5 μM, 1 μM, 2 μM, 4 μMIncubation Time:24 hoursResult:DUSP6 protein was significantly downregulated in LPS-activated macrophages.

(E/Z)-BCI hydrochloride (35 mg/kg; intraperitoneal injection; every 7 days; for four weeks; female BALB/c nude mice) treatment enhances cisplatin efficacy in PDX models. Animal Model:Patient-derived xenograft (PDX) models (4-5-week-old female BALB/c nude mice) Dosage:35 mg/kg Administration:Intraperitoneal injection; every 7 days; for four weeks Result:Tumor weights in the PDX models treated plus CDDP were significantly suppressed compared with tumors from PDX model mice treated with either agent alone.

NSC 150117

Apoptosis

Apoptosis

PEGs

——

——

15982-84-0

317.432

C22H23NO

>98% (HPLC)

——

O=C1\C(=C/c2ccccc2)C(NC2CCCCC2)c2ccccc12

——

(-20℃)

With Ice Pack

≥ 2 years