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- CAS号:
180002-83-9
- 规格:
1mLx10mM(inDMSO)/1mg/5mg/10mg/25mg/50mg
| 规格: | 1mLx10mM(inDMSO) | 产品价格: | ¥652.0 |
|---|---|---|---|
| 规格: | 1mg | 产品价格: | ¥278.0 |
| 规格: | 5mg | 产品价格: | ¥662.0 |
| 规格: | 10mg | 产品价格: | ¥984.0 |
| 规格: | 25mg | 产品价格: | ¥1784.0 |
| 规格: | 50mg | 产品价格: | ¥2712.0 |
Product Introduction
Bioactivity
| 名称 | GW 405833 |
| 描述 | GW 405833 (L-768242) is an agonist of cannabinoid-2 (CB(2)) receptor-selective |
| 动物实验 | Baseline mechanical paw withdrawal thresholds were measured in each paw for each animal before performing either PSNL or injecting CFA.?Another predrug baseline was then taken after painful peripheral neuropathy or inflammatory pain was fully established.?GW405833 was administered (i.p.) 30 minutes before evaluation of the impact of drug manipulations on mechanical paw withdrawal thresholds.?Different doses of GW405833 were injected (i.p.) within subjects in the order of vehicle (0), 3, 10, and 30 mg/kg.?Sufficient time was allowed to lapse between each dose to verify that mechanical paw withdrawal thresholds returned to the predrug levels before dose escalation. .?In the groups where CB1 or CB2 antagonists were tested, rimonabant or SR144528 (10 mg/kg i.p.) was administered 20 minutes before GW405833 injection[1]. |
| 体内活性 | GW405833 (3、10及30 mg/kg i.p.) 在WT小鼠的两种疼痛模型中剂量依赖性地逆转了已建立的机械性痛觉过敏;然而,GW405833的抗痛觉过敏效果在CB2KO小鼠中完全保留,而在CB1KO小鼠中则完全缺失。此外,GW405833(30 mg/kg i.p.)的抗痛觉过敏效能被CB1拮抗剂rimonabant(10 mg/kg i.p.)完全阻断,但不被CB2拮抗剂SR144528(10 mg/kg i.p.)阻断。因此,GW405833的抗痛效果依赖于CB1受体。在测量CB1激活的四项主要征象的测试中,GW405833(30 mg/kg i.p.)也显示无活性。此外,与rimonabant(10 mg/kg i.p.)不同,GW405833(10 mg/kg, i.p.)在体内不作为CB1拮抗剂,不会在经Δ9-tetrahydrocannabinol长期处理的小鼠中引发撤回症状。 |
| 存储条件 | Keep away from moisture Powder: -20°C for 3 years | In solvent: -80°C for 1 year Shipping with blue ice/Shipping at ambient temperature. |
| 溶解度 | DMSO : 10 mg/mL (22.35 mM), Sonication is recommended. |
| 关键字 | neuropathic pain | L768242 | L 768242 | Inhibitor | inhibit | GW-405833 | GW405833 | GW 405833 | CB2 | CannabinoidReceptor | Cannabinoid Receptor | anti-inflammatory |
| 相关产品 | Drinabant | AM281 | CB1 inverse agonist 1 | CB2 receptor agonist 2 | β-Caryophyllene | AM-1235 | Pregnenolone acetate | 2,3-Butanediol | CB1 antagonist 2 | Pregnenolone | CB2 modulator 1 | RTICBM-189 |
| 相关库 | Bioactive Compound Library | Anti-Cancer Compound Library | Bioactive Compounds Library Max | Neurotransmitter Receptor Compound Library | Neuronal Signaling Compound Library | NO PAINS Compound Library | GPCR Compound Library | Membrane Protein-targeted Compound Library |
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相关实验
酸吸收细胞的百分比增加,碳水化合物吸收细胞的百分比减少,表明 HLF 在肠道脂质吸收中具有关键作用。接着作者构建了高脂饮食(HFD)诱导的小鼠 MAFLD 模型和杂合肠道特异性表达的 HLF 敲除小鼠(Hlf+/−)模型,结果发现高脂饮食影响肠道脂质吸收。敲除 Hlf 通过增加能量代谢来减轻 HFD 引起的代谢变化,Hlf+/−可降低氧化应激,抑制了铁细胞凋亡,在纯合 Hlf 敲除小鼠中获得了表明肠特异性 Hlf 敲除改善 MAFLD 的结果。腹腔注射脂肪酶抑制剂后再灌胃橄榄油,结果显示 Hlf
发展历史 1976年德国马普生物物理化学研究所Neher和Sakmann首次在青蛙肌细胞上用双电极钳制膜电位的同时,记录到ACh激活的单通道离子电流,从而产生了膜片钳技术。 1980年Sigworth等在记录电极内施加5-50 cmH2O的负压吸引,得到10-100GW10-100G?的高阻封接 (Giga-seal),大大降低了记录时的噪声实现了单根电极既钳制膜片电位又记录单通道电流的突破。 1981年Hamill和Neher等对该技术进行了改进,引进了膜片游离技术和全细胞记录技术,从而使该技术更趋完善
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化合物 GW 405833【180002-83-9】
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