Inhibition of KRAS(G12D) mutant cell lines The promising results for the inhibitory activity and mutant-selectivity from the ITC and KRAS–CRAF interaction assays motivated us to evaluate the potential anti-cancer effects of TH-Z827. The KRAS G12D mutation is the most prevalent mutation form ...
400 179 0116 24小时服务热线 info@ldraft.com; sales@ldraft.com; marketing@ldraft.com销售邮箱 prevnext 货号:ABC-KH8069 价格:¥询价 规格: 1 vial 数量:-+ 产品描述 参考文献 资料下载 相关产品 产品描述/Products Description Human KRAS (G12D/+) LIM1215 Cell lineis Heterozygous knockin of KRAS...
Figure 1. KRAS[G12D] BaF3 细胞的构建原理图 III. Introduction Cell Line Name: KRAS G12D/BaF3 Host Cell: Ba/F3 Stability: 16 passages (in-house test, that not means the cell line will be instable beyond the passages we tested.) Application: Useful for the study of enzyme kinetics,...
将RMC-4998与sotorasib结合使用,抑制了细胞增殖和下游信号转导,对KRAS突变肿瘤的疗效显著。 RMC-7977:靶向KRAS、NRAS和HRAS,在临床前研究中,RMC-7977导致KRAS突变肿瘤的退缩,并在KRAS外显子12改变的肿瘤模型中显示出显著的疗效。最近,RMC-7977已在KRAS突...
Methods Obstruction of KRAS G12D and BRAF V600E expression was evaluated through suppression of cell proliferation and specific mRNA transcription. Tumour reduction was assessed through Xenograft mouse models. Results Exposure of KRAS G12D-dependent cell line to modified PNA-peptide conjugate ...
在PDAC中,KRAS蛋白的12号氨基酸最常突变的位点,其中以KRASG12D突变类型最为常见,其次是KRSAG12V。目前针对KRAS突变靶点的药物甚少,主要的药物靶向策略是设计选择性共价抑制剂,其通过与激活状态的KRAS以及青环素A之间形成稳定的、高亲和力的复合物达到抑制效果,但这些药物都尚未使用等基因癌症模型进行验证,对PDAC患者的...
评估GFH375在携带KRAS G12D 突变的晚期实体瘤患者中的安全性/耐受性、PK 和初步有效性,并确定GFH375 的 MTD 和/或 RP2D。 评估GFH375 在携带KRAS G12D 突变的晚期实体瘤患者中的有效性。 开始日期2024-07-02 申办/合作机构 劲方医药科技(上海)股份有限公司初创企业 ...
KRAS G12C突变是实体瘤的致癌驱动因素和有效的治疗靶点。Glecirasib是一种高选择性、共价口服KRAS G12C抑制剂,在非小细胞肺癌和结直肠癌中显示出有希望的临床活性;然而,glecirasib在KRAS G12C突变PDAC和其他实体瘤中的疗效和安全...
withcetuximabinpatientswithKRASG12D-mutant solidtumors.ThetrialisexpectedtocompleteinApril 2027.Thecompanyreleasedpreclinicaldatainlate 2023,whichshowedthatQTX-3034incombination withEGFRmodulatorsinhibiteddownstreamERK phosphorylationandcellproliferationinKRASG12D ...
Adagrasib能够对肿瘤细胞内的KRAS-G12C形成共价修饰,并显著抑制KRAS下游MAPK信号通路,对携带KRAS-G12C突变肿瘤细胞的IC50介于10～973nmol·L-1之间。研究者在26个不同组织来源的肿瘤细胞系移植瘤(celllinederivedxenograft,CDX)或患者组织移植瘤(patientderivedx...