Molecular Formula | C10H9NO2S |
Molar Mass | 207.25 |
Density | 1.237±0.06 g/cm3(Predicted) |
Melting Point | 133-135℃ |
Boling Point | 397.6±42.0 °C(Predicted) |
Solubility | DMSO: 25mg/mL, soluble |
Appearance | solid |
Color | white |
Storage Condition | Keep in dark place,Inert atmosphere,2-8°C |
Stability | Stable for 1 year from date of purchase as supplied. Solutions in DMSO or ethanol may be stored at -20° for up to 3 months. |
Sensitive | Sensitive to heat, light and air |
MDL | MFCD00712162 |
Physical and Chemical Properties | Bioactive BAY 11-7082 (BAY 11-7821) is an NF-κB inhibitor that inhibits TNFα-induced phosphorylation of IκBα with an IC50 of 10 μM in tumor cells. BAY 11-7082 can inhibit the ubiquitin-specific protease USP7 and USP21, and the corresponding IC50 values are 0.19 μM and 0.96 μM respectively. BAY 11-7082 can induce apoptosis and S phase arrest in gastric cancer cells. |
Use | An anti-inflammatory agent and NFκB inhibitor |
In vitro study | BAY 11-7082 completely and specifically abolished NF-κB DNA binding, down-regulated NF-κB-induced cytokine IL-6, and induced apoptosis. BAY 11-7082 (< 8 μm) potently inhibited the intrinsic and TNFα-stimulated NF-κB luciferase activity in a dose-dependent manner. BAY 11-7082 (8 μm) strongly inhibited cell proliferation by NCI-H1703. Bay 11-7082 (5 μm) acts on the T cell line infected with HTLV-I, rapidly and effectively reduces the DNA binding capacity of NF-κB, and down-regulates the expression of anti-apoptotic gene Bcl-x(L), there was no effect on the other transcription factor AP-1 binding to DNA. Bay 11-7082 induced apoptosis in primary ATL cells more significantly than in normal peripheral blood mononuclear cells, and induced apoptosis in these cells was also associated with down-regulation of NF-κB activity. Bay 11-7082 (5 μm) selectively induced apoptosis in T cell lines infected with HTLV-I and down-regulated the expression of cyclin D1, cyclin D2, and Bcl-xL. BAY 11-7082 (100 μm) inhibited the nuclear translocation of p65 induced by NMDA, and also inhibited the enhancement of NF-κB binding induced by NMDA in the hippocampus of mice. The inhibition of NMDA toxicity by BAY 11-7082 occurred in the CA1 region of the hippocampus, 20 μm, which had a protective effect on 40% of the nerves, and 100 of the nerves were protected at 70% μm. Acting on adipose tissue, BAY 11-7082 at all concentrations in the experiment significantly inhibited the DNA binding activity of NF-κB p65, while acting on skeletal muscle, only 50 μm and 100 μm of BAY 11-7082 significantly inhibited NF-κB p65 DNA binding activity. BAY 11-7082 (100 μm) acts on human adipose tissue and skeletal muscle to reduce IKK-β protein. BAY 11-7082 (100 μm) significantly reduced the release of TNF-α from animal adipose tissue, while the release of IL-6 and IL-8 significantly inhibited all concentrations of BAY 11-7082 in the experiment. BAY 11-7082 (50 μm) significantly reduced the release of TNF-α, IL-6, and IL-8 in skeletal muscle. In addition, BAY 11-7082 was also found to inhibit the activity of E2-conjugating enzyme and E3 ligase enzyme, thereby inducing the death of B- and T-lymphoma cells. |
In vivo study | BAY 11-7082 (2.5 mg/kg and 5 mg/kg; intratumoral injection; twice-weekly for 21 days ) significantly suppresses tumor growth in a dose-dependent manner. Animal Model: Four-week-old male BALB/c nude mice with human gastric carcinoma cell lines HGC-27 Dosage: Low-dose (2.5 mg/kg body weight), high-dose (5 mg/kg body weight) Administration: Intratumoral injection; twice-weekly for 21 days Result: Suppressed tumor growth in a dose-dependent manner. |
WGK Germany | 3 |
RTECS | UD1430000 |
WGK Germany | 3 |
RTECS number | UD1430000 |
storage conditions | Keep in dark place,Inert atmosphere,2-8°C |
solubility | DMSO: 25 mg/mL, soluble |
morphology | solid |
color | white |
in vitro study
BAY 11-7082 completely and specifically abolished NF-& kappa;B DNA binding, down-regulation of NF-& kappa;B-induced cytokine IL-6, and induced apoptosis. BAY 11-7082 (< 8 μM) effectively inhibited the original and TNFα-stimulated NF-& kappa;B luciferase activity, which was dose-dependent. BAY 11-7082 (8 μM) strongly inhibited the proliferation of NCI-H1703 cells. Bay 11-7082 (5 μM) acts on T cell line infected with HTLV-I, rapidly and effectively reduces NF-& kappa; The DNA binding capacity of B and down-regulates the expression of anti-apoptosis gene Bcl-x(L), but has no effect on the binding of another transcription factor AP-1 to DNA. Bay 11-7082 induced apoptosis of primary ATL cells more significantly than that of normal peripheral blood mononuclear cells, and the induced apoptosis of these cells was also related to the down-regulation of NF-& kappa;B activity. Bay 11-7082 (5 μM) selectively induces apoptosis in T cell lines infected with HTLV-I and down-regulates the expression of cyclin D1, cyclin D2, and Bcl-xL. BAY 11-7082 (100 μM) acts on the hippocampal brain region of mice, inhibiting nuclear translocation of p65 caused by NMDA, and also inhibiting NF-& kappa induced by NMDA; Enhancement of B binding force. BAY 11-7082 inhibits NMDA toxicity in CA1 region of hippocampus. It has protective effect on 40% nerve at 20 μM and 70% nerve at 100 μM. On adipose tissue, all concentrations of BAY 11-7082 significantly inhibited NF-& kappa;B p65 DNA binding activity, while on skeletal muscle, only 50 μM and 100 μM BAY 11-7082 significantly inhibited NF-& kappa;B p65 DNA binding activity. BAY 11-7082 (100 μM) acts on human adipose tissue and skeletal muscle to reduce IKK-β protein. BAY 11-7082 (100 μM) significantly reduced the release of TNF-α from animal adipose tissue, while the release of IL-6 and IL-8 significantly inhibited all concentrations of BAY 11-7082 in the experiment. BAY 11-7082 (50 μM) acts on skeletal muscle, significantly reducing the release of TNF-α, IL-6, and IL-8. In addition, BAY 11-7082 was also found to inhibit the activities of E2-conjugating enzyme and E3 ligase enzyme, thereby inducing the death of B- lymphoma cells and T-lymphoma cells.
in vivo studies
BAY 11-7082 (2.5 mg/kg and 5 mg/kg; intratumoral injection; twice-weekly for 21 days ) significantly suppresses tumor growth in a dose-dependent manner.
Animal Model: Four-week-old male BALB/c nude mice with human gastric carcinoma cell lines HGC-27
Dosage: Low-dose (2.5 mg/kg body weight), high-dose (5 mg/kg body weight)
Administration: Intratumoral injection; twice-weekly for 21 days
Result: Suppressed tumor growth in a dose-dependent manner.