(E/Z)-BCI

本公司产品仅用于科研实验，不得用于人体或动物的临床与诊断

(E/Z)-BCI 通过激活 Nrf2 信号轴和抑制 NF-κB 通路，减弱巨噬细胞中 LPS 诱导的炎症介质和 ROS 产生。 (E/Z)-BCI 是一种具有抗炎活性的双特异性磷酸酶 6 (DUSP6) 抑制剂。

(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

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15982-84-0

317.432

C22H23NO

>98% (HPLC)

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

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(-20℃)

With Ice Pack

≥ 2 years