(E/Z)-BCI

Modify Date: 2024-01-20 16:40:35

(E/Z)-BCI Structure
(E/Z)-BCI structure
Common Name (E/Z)-BCI
CAS Number 15982-84-0 Molecular Weight 317.42
Density N/A Boiling Point N/A
Molecular Formula C22H23NO Melting Point N/A
MSDS N/A Flash Point N/A

 Use of (E/Z)-BCI


(E/Z)-BCI (NSC 150117) 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[1].

 Names

Name (E/Z)-BCI

 (E/Z)-BCI Biological Activity

Description (E/Z)-BCI (NSC 150117) 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[1].
Related Catalog
Target

DUSP6[1]

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[2]. (E/Z)-BCI hydrochloride (0.5-4 μM; 24 hours) significantly inhibits DUSP6 expression in LPS-activated macrophages[1]. (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[1]. (E/Z)-BCI hydrochloride decreases ROS production and activates the Nrf2 pathway in LPS-activated macrophages[1].(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[2]. Cell Viability Assay[2] 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[1] Cell Line: RAW264.7 macrophage cells (by LPS-activated macrophages) Concentration: 0.5 μM, 1 μM, 2 μM, 4 μM Incubation Time: 24 hours Result: DUSP6 protein was significantly downregulated in LPS-activated macrophages. RT-PCR[1] Cell Line: RAW264.7 macrophage cells (by LPS-activated macrophages) Concentration: 0.5 μM, 1 μM, 2 μM Incubation Time: 24 hours Result: The expression of IL-1β, TNF-α and IL-6 mRNA was significantly inhibited inLPS-activated macrophages.
In Vivo (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[2]. Animal Model: Patient-derived xenograft (PDX) models (4-5-week-old female BALB/c nude mice)[2] 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.
References

[1]. Zhang F, et al. DUSP6 Inhibitor (E/Z)-BCI Hydrochloride Attenuates Lipopolysaccharide-Induced Inflammatory Responses in Murine Macrophage Cells via Activating the Nrf2 Signaling Axis and Inhibiting the NF-κB Pathway. Inflammation. 2019 Apr;42(2):672-681.

[2]. Wu QN,et al. Pharmacological inhibition of DUSP6 suppresses gastric cancer growth and metastasis and overcomes cisplatin resistance. Cancer Lett. 2018 Jan 1;412:243-255.

 Chemical & Physical Properties

Molecular Formula C22H23NO
Molecular Weight 317.42

 Safety Information

Hazard Codes Xi