Bay 11-7821
(Synonyms: BAY 11-7082) 目录号 : GC13035
Bay 11-7821(BAY 11-7082)是一种IκBα磷酸化和NF-κB抑制剂，选择性且不可逆地抑制TNF-α诱导的IκB-α磷酸化（IC50值约为10μM），并减少NF-κB和粘附分子的表达。Bay 11-7821抑制泛素特异性蛋白酶USP7和USP21，IC50分别为0.19、0.96μM。
Cas No.:19542-67-7
Sample solution is provided at 25 µL, 10mM.
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Related Biological Data
Concentrations of IL-8, IL-1β and TNF-α in supernatants of IPEC-J2 cells. IPEC-J2 cells added with DMSO were regarded as the vehicle control and L. salivarius-involved IPEC-J2 cells were supplemented with (a) 10 μmol/L SB-203580, (b) 10 μmol/L SCH772984 and (c) 10 μmol/L BAY11-7082, respectively.
BAY11–7082 (GlpBio) were first employed in IPEC-J2 cells for 1 h [19–21], followed by L. salivarius involvement for 3 h. After 3 times washes with PBS, IPEC-J2 cells were infected with ETEC K88 for 3, 6, 12 and 24h,respectively.
J Anim Sci Biotechno 11.1 (2020): 1-13. PMID: 32774852 IF: 5.034 -
Related Biological Data
Effects of AFR on the expression of the BDNF-MEK/ERK signalling pathway in the hippocampus (D) Effects of AZD6244 and BAY11-7082 inhibitors on cell viability after AFR treatment and CORT induction.
In vitro, HT-22 cells were treated with corticosterone (CORT) solution (0.35 mg/mL), then AFR (0.05mg/mL) solution and inhibitor AZD6244 (14 μM/mL) or BAY11-7082 (10 μM/mL) (GlpBio) were added, respectively.
Pharmaceutical Biology 60.1 (2022): 1436-1448. PMID: 35938494 IF: 3.8892
Quality Control & SDS
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- Datasheet
| Cell experiment [1]: | |
Cell lines | HGC-27、NCI-N87、AGS、MGC80-3 cells |
Preparation Method | Cells were treated with Bay 11-7821 (0-30μM), and cell viabilities were detected at 6 and 24 h. |
Reaction Conditions | 0-30μM; 6、24h |
Applications | BAY 11-7082 inhibited cell viability in a dose-dependent manner. |
| Animal experiment [2]: | |
Animal models | Sprague-Dawley rats |
Preparation Method | Rats were treated with Bay 11-7821 (1mg/kg and 3mg/kg) intraperitoneally after STZ injection and for the next 4 weeks. |
Dosage form | 1、3mg/kg; i.p. |
Applications | Bay 11-7821-treated rats showed significant improvements in the levels of the enzymatic antioxidant SOD, the non-enzymatic antioxidant GSH, and the increased levels of lipid peroxidation and nitric oxide. Bay 11-7821 treatment significantly restored the renal histological structure of diabetic rats. |
References: [1] Chen L, Ruan Y, Wang X, et al. BAY 11-7082, a nuclear factor-κB inhibitor, induces apoptosis and S phase arrest in gastric cancer cells[J]. Journal of gastroenterology, 2014, 49: 864-874. [2] Kolati S R, Kasala E R, Bodduluru L N, et al. BAY 11-7082 ameliorates diabetic nephropathy by attenuating hyperglycemia-mediated oxidative stress and renal inflammation via NF-κB pathway[J]. Environmental Toxicology and Pharmacology, 2015, 39(2): 690-699. | |
Bay 11-7821(BAY 11-7082) is an inhibitor of IκBα phosphorylation and NF-κB, selectively and irreversibly inhibits TNF-α-induced IκB-α phosphorylation (IC50 value is approximately 10μM), and reduces the expression of NF-κB and adhesion molecules [1]. Bay 11-7821 inhibits ubiquitin-specific proteases USP7 and USP21 with IC50 values of 0.19 and 0.96μM, respectively [2]. Bay 11-7821 inhibits the formation of pores in liposomes by the pore-forming protein gasdermin D (GSDMD), as well as inflammasome-mediated apoptosis and IL-1β secretion [3].
In vitro, Bay 11-7821 (0-30μM) treated gastric cancer cells (HGC-27, NCI-N87, AGS and MGC80-3) for 24h, inhibited cell viability in a dose-dependent manner, Bcl-2 (total and phosphorylated forms) were significantly downregulated, while Bax was upregulated, and induced S phase arrest by inhibiting cyclin A and CDK-2 expression [4]. Bay 11-7821 (3μM) treated HBL-1 cells for 24-72h, inhibited IκB-α phosphorylation and NF-κB activation, and induced cell death [5]. Bay 11-7821 (30μM) treated KMS-12-BM and MM.1S MM cells rapidly induced cell death, with decreased viability detected within 1h, and complete inhibition of cell viability was achieved within 2-4 hours [6].
In vivo, intraperitoneal injection of Bay 11-7821 (1, 3 mg/kg) in diabetic rats with renal dysfunction significantly improved the decreased levels of SOD and GSH, as well as the increased levels of lipid peroxidation and nitric oxide, and restored the renal histological structure of diabetic rats [7].
References:
[1] Pierce J W, Schoenleber R, Jesmok G, et al. Novel inhibitors of cytokine-induced IκBα phosphorylation and endothelial cell adhesion molecule expression show anti-inflammatory effects in vivo[J]. Journal of Biological Chemistry, 1997, 272(34): 21096-21103.
[2] Ritorto M S, Ewan R, Perez-Oliva A B, et al. Screening of DUB activity and specificity by MALDI-TOF mass spectrometry[J]. Nature communications, 2014, 5(1): 4763.
[3] Hu J J, Liu X, Zhao J, et al. Identification of pyroptosis inhibitors that target a reactive cysteine in gasdermin D[J]. BioRxiv, 2018: 365908.
[4] Chen L, Ruan Y, Wang X, et al. BAY 11-7082, a nuclear factor-κB inhibitor, induces apoptosis and S phase arrest in gastric cancer cells[J]. Journal of gastroenterology, 2014, 49: 864-874.
[5] Strickson S, Campbell D G, Emmerich C H, et al. The anti-inflammatory drug BAY 11-7082 suppresses the MyD88-dependent signalling network by targeting the ubiquitin system[J]. Biochemical Journal, 2013, 451(3): 427-437.
[6] Rauert-Wunderlich H, Siegmund D, Maier E, et al. The IKK inhibitor Bay 11-7082 induces cell death independent from inhibition of activation of NFκB transcription factors[J]. PloS one, 2013, 8(3): e59292.
[7] Kolati S R, Kasala E R, Bodduluru L N, et al. BAY 11-7082 ameliorates diabetic nephropathy by attenuating hyperglycemia-mediated oxidative stress and renal inflammation via NF-κB pathway[J]. Environmental Toxicology and Pharmacology, 2015, 39(2): 690-699.
Bay 11-7821(BAY 11-7082)是一种IκBα磷酸化和NF-κB抑制剂，选择性且不可逆地抑制TNF-α诱导的IκB-α磷酸化（IC50值约为10μM），并减少NF-κB和粘附分子的表达[1]。Bay 11-7821抑制泛素特异性蛋白酶USP7和USP21，IC50分别为0.19、0.96μM[2]。Bay 11-7821抑制脂质体中的成孔蛋白gasdermin D （GSDMD）孔的形成，以及炎性体介导的细胞凋亡和IL-1β的分泌[3]。
在体外，Bay 11-7821（0-30μM）处理胃癌细胞（HGC-27、NCI-N87、AGS和MGC80-3）24h，以剂量依赖性方式抑制了细胞活力，Bcl-2（总形式和磷酸化形式）均显著下调，而Bax则相反上调，还通过抑制细胞周期蛋白A和 CDK-2表达来诱导S期停滞[4]。Bay 11-7821（3μM）处理HBL-1细胞24-72h，抑制了IκB-α的磷酸化和NF-κB的激活，诱导了细胞死亡[5]。Bay 11-7821（30μM）处理KMS-12-BM和MM.1S MM细胞，快速诱导了细胞死亡，1h就检测到活力降低，且在2-4小时内达到完全抑制细胞活力的效果[6]。
在体内，Bay 11-7821（1、3mg/kg）通过腹腔注射治疗肾功能障碍的糖尿病大鼠，显著改善了SOD、GSH水平降低以及脂质过氧化、一氧化氮水平升高，恢复了糖尿病大鼠的肾脏组织学结构[7]。
| Cas No. | 19542-67-7 | SDF | |
| 别名 | BAY 11-7082 | ||
| 化学名 | (E)-3-(4-methylphenyl)sulfonylprop-2-enenitrile | ||
| Canonical SMILES | CC1=CC=C(C=C1)S(=O)(=O)C=CC#N | ||
| 分子式 | C10H9NO2S | 分子量 | 207.25 |
| 溶解度 | ≥ 64 mg/mL in DMSO, ≥ 10.64 mg/mL in EtOH with ultrasonic and warming | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 4.8251 mL | 24.1255 mL | 48.2509 mL |
| 5 mM | 0.965 mL | 4.8251 mL | 9.6502 mL |
| 10 mM | 0.4825 mL | 2.4125 mL | 4.8251 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。