| 包装 | 价格(元) |
| 5mg | 电议 |
| 10mg | 电议 |
| 25mg | 电议 |
Preparation Method | A549 cells plated. The next day, compound library(including R-7050) prepared were added at a final concentration of 10 μM in 0.2% (v/v) DMSO. Cells were preincubated with compounds for 1 hr prior to a 4 hr stimulation with either TNFα or IL-1β. |
Reaction Conditions | 10 μM R-7050 and cell for 1h |
Applications | In TNFα-induced ICAM-1 expression, R-7050 inhibition potency (EC50 = 0.63 μM) was 2- to 3-fold greater than EC50 for IL-1β-induced ICAM-1 expression (1.45 μM). |
Cell lines | Wild-type RBL-2H3 cells |
Preparation Method | Wherever indicated, 6.7 μM of R-7050 (dissolved in DMSO) or 0.1 μM of bafilomycin A1 was added along with anti-TNP IgE during sensitization. |
Reaction Conditions | 6.7 μM R-7050 |
Applications | R-7050 significantly reduced TNF proliferation when autophagy was also inhibited by Baf-A1. |
Animal models | Male CD-1 mice (8–10 weeks old) |
Preparation Method | R-7050 (6–18 mg/kg) was administered via intraperitoneal route at the time of injury or up to 2 h post-ICH. |
Dosage form | 6–18 mg/kg R-7050 for 0.5-2h |
Applications | R-7050 attenuates neurovascular injury after ICH. |
| 文献引用 | |
| 产品描述 | R-7050 is a novel cell-permeable triazoloquinoxaline compound that selectively inhibited TNF-α induced cellular signaling[2]. In RBL-2H3 cells R-7050 significantly reduced TNF proliferation when autophagy was also inhibited by Baf-A1[7].CA to reduce cell viability in MDA-MB-231 breast cancer cells and tumorigenic HEK 293 cells but not in normal NIH3T3 fibroblast cells. Abundance of TNFA, TNF Receptor 1 (TNFR1) and cleaved caspase-8/-3 proapoptotic proteins to increase with CA treatment. Blocking of TNFA-TNFR1 signalling by small molecule inhibitor, R-7050, reduced the expression of cleaved caspase-8 and caspase-3 at the protein level[3]. TRPA1 channel was positively expressed in the cell bodies and processes of HODs. The expression TRPA1 channel was significantly up-regulated by high concentration of TNF-α, which could be suppressed by R-7050[5]. A single administration of R-7050 reduced neurovascular injury after ICH. In contrast to biologic approaches that directly bind and neutralize TNF-α activity, R-7050 selectively inhibits the association of TNFR with intracellular adaptor molecules, such as TRADD and RIP1, limiting receptor internalization and preventing subsequent cellular responses after TNF-α binding[1]. Capsaicin, a selective TRPV1 agonist, increased ipsilateral afferent renal nerve activity in WT but not TRPV1-/- mice. WD intake increased leptin, IL-6, and TNF-α in adipose tissue, and TNF-α antagonist III, R-7050, decreased leptin in TRPV1-/--WD. The urinary albumin level was higher in TRPV1-/--WD than WT-WD[4]. Treatment with the TNF receptor-1 inhibitor R-7050 during nephrotoxic serum nephritis reduced damage, fibrosis, and necroptosis in wild-type mice and mice with KLF4-deficient macrophages, and abrogated the differences between the two groups in these parameters[6]. References: |
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