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- 详细信息
- 文献和实验
- 技术资料
- 英文名:
N'-[3-[[5-(2-Cyclopropyl-5-pyrimidinyl)-1H-pyrrolo[2,3-b]pyridin-3-yl]carbonyl]-2,4-difluorophenyl]-N-ethyl-N-methylsulfamide
- 供应商:
上海安毕达生物科技有限公司
- CAS号:
1393465-84-3
- 规格:
50μL/1mL/2mg/5mg/10mg/25mg/50mg
| 规格: | 50μL | 产品价格: | ¥129.0 |
|---|---|---|---|
| 规格: | 1mL | 产品价格: | ¥663.0 |
| 规格: | 2mg | 产品价格: | ¥472.0 |
| 规格: | 5mg | 产品价格: | ¥672.0 |
| 规格: | 10mg | 产品价格: | ¥1072.0 |
| 规格: | 25mg | 产品价格: | ¥2256.0 |
| 规格: | 50mg | 产品价格: | ¥3600.0 |
PLX7904 hinders the in vitro proliferation of two melanoma cell lines (A375 and COLO829) and an additional human colorectal cancer cell line COLO205 expressing BRAFV600E, with IC50 values of 0.17 μM, 0.53 μM, and 0.16 μM, respectively, comparable to the IC50 values of vemurafenib in the same assays (0.33 μM, 0.69 μM, and 0.25 μM, respectively)1. PLX7904 and PLX8394 effectively suppress ERK1/2-driven GAL4-Elk1 reporter activity in PRT cells as well as parental cells. Treatment with PLX7904 and PLX8394 at a concentration of 1 μM reduces colony formation and viability in parental cells to a similar extent as PLX47202. PLX7904 strongly inhibits ERK1/2 phosphorylation in mutant BRAF melanoma cells without inducing paradoxical activation in wild-type BRAF or mutant NRAS melanoma cells. It also inhibits ERK1/2 in PLX470-resistant cell lines. Treatment with PLX7904 promotes apoptosis and suppresses anchorage-independent growth of vemurafenib-resistant cells3.
PLX7904 hinders the in vitro proliferation of two melanoma cell lines (A375 and COLO829) and an additional human colorectal cancer cell line COLO205 expressing BRAFV600E, with IC50 values of 0.17 μM, 0.53 μM, and 0.16 μM, respectively, comparable to the IC50 values of vemurafenib in the same assays (0.33 μM, 0.69 μM, and 0.25 μM, respectively)1.
PLX7904 and PLX8394 effectively suppress ERK1/2-driven GAL4-Elk1 reporter activity in PRT cells as well as parental cells. Treatment with PLX7904 and PLX8394 at a concentration of 1 μM reduces colony formation and viability in parental cells to a similar extent as PLX47202.
PLX7904 strongly inhibits ERK1/2 phosphorylation in mutant BRAF melanoma cells without inducing paradoxical activation in wild-type BRAF or mutant NRAS melanoma cells. It also inhibits ERK1/2 in PLX470-resistant cell lines. Treatment with PLX7904 promotes apoptosis and suppresses anchorage-independent growth of vemurafenib-resistant cells3.
溶解方案(细胞实验)
DMSO 中的溶解度 : ≥ 30 mg/mL (58.53 mM; 吸湿的 DMSO 对产品的溶解度有显著影响,请使用新开封的 DMSO)|* "≥" means soluble, but saturation unknown.
溶解方案(动物实验)
"方案 一": "请依序添加每种溶剂:10% DMSO 40% PEG300 5% Tween-80 45% SalineSolubility: ≥ 2.5 mg/mL (4.88 mM); 澄清溶液 此方案可获得 ≥ 2.5 mg/mL(饱和度未知)的澄清溶液。以 1 mL 工作液为例,取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中,混合均匀;再向上述体系中加入 50 μL Tween-80,混合均匀;然后再继续加入 450 μL 生理盐水 定容至 1 mL。生理盐水的配制:将 0.9 g 氯化钠,溶解于 ddH₂O 并定容至 100 mL,可以得到澄清透明的生理盐水溶液。"
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文献和实验Basile KJ, et al. Inhibition of mutant BRAF splice variant signaling by next-generation, selective RAF inhibitors. Pigment Cell Melanoma Res. 2014 May;27(3):479-84
Le K, et al. Selective RAF inhibitor impairs ERK1/2 phosphorylation and growth in mutant NRAS, vemurafenib-resistant melanoma cells. Pigment Cell Melanoma Res. 2013 Jul;26(4):509-17
plx96 请教细胞凋亡信号转导通路共有哪几条? plx96 这个问题好大~,都不知道如何回答 请问你是研究信号转导的吗 要不我把我做了芯片后的凋亡信号传导图发给你 你帮我看看 好不 我看得好晕 可以告诉我你的邮箱不 我的plx96@163.com plx96 哦 那也是啊 我怎么没想到你的得分呢 呵呵 我试试传上来吧 看看这两张凋亡转导图 有什么差别 怎么评价 黄色
域连接在Cas9的末端,但效果并不理想。张锋团队意识到,RNA从Cas9复合体伸出的两个小环是更好的连接位点,这样活化结构域在招募转录机器时就更加灵活。他们用改造后的CRISPR系统成功激活了十个基因。这些基因的转录都得到了两倍以上的增涨,许多基因的活性甚至有了几个数量级的增加。随后,研究人员建立了70, 290个引导RNA的文库,来靶标人类基因组超过两万个基因。他们由此鉴定了让黑色素瘤抵抗药物PLX-4720的基因。PLX-4720对于携带BRAF突变的患者疗效比较好,残存下来的癌细胞会长成新的
芯空一号快讯 | 空间多组学助力发现儿童脑肿瘤DMG的新免疫开关
11-VISTA轴在IUE小鼠DMG模型中高度保守 4.靶向IGSF11-VISTA轴唤醒小胶质细胞可实现肿瘤清除 验证实验显示,敲除或阻断IGSF11-VISTA后,肿瘤体积显著缩小,正常免疫小鼠的生存期大幅延长(对照组平均仅存活38天)。即使肿瘤已经形成后再启动敲除,仍能有效控制肿瘤进展。进一步实验表明,即使在完全没有T细胞的NSG免疫缺陷小鼠中,敲除IGSF11-VISTA仍能让肿瘤明显缩小;而当用药物(PLX3397)特异性耗竭小胶质细胞后,敲除就完全失去了效果,证明
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