KRAS G12C inhibitor 20,2640858

肿瘤临床前研究重要工具——自发肺癌动物模型

家族。当 KRAS 基因发生异常时，下游信号传导失调导致肿瘤发生，KRAS 突变也是中国 NSCLC 的患者第二大常见的基因突变，其中 KRAS G12C 在肺腺癌中最为常见。 目前 NSCLC 的小鼠模型主要集中在腺癌亚型上，大多数的研究采用条件性 KRAS 点突变模型进行，在 KRAS-LSL-G12C 或 KRAS-LSL-G12D 小鼠细胞中引入 Cre 重组酶导致内源性水平上突变等位基因的表达，模拟人类肿瘤发展的启动条件。Jackson 等[2] 就采用了这样的方式构建肿瘤模型，他们在 KRASG12

Trypsin Inhibitor

city directed primarily toward trypsin (Kunitz inhibitor), and (2) those that have a molecular weight of only 6000 to 10,000 Da with a high proportion of cystine residues and are capable of inhibiting chymotrypsin as well as trypsin at independent

Methods for Studying the Interaction of Barnase with Its Inhibitor Barstar

complex, with K d =10−14 M , half-life of about 2 d and an association rate constant of 4�108 M −1 /s. The kinetic and thermodynamics of the barnase-barstar interaction were investigated in detail (12 –20 ). High affinity is maintained at pH 7.0–