| 包装 | 价格(元) |
| 10mg | 电议 |
| 50mg | 电议 |
Cell experiment: | T56-LIMKi can induce inhibition of cofilin phosphorylation and Panc-1 tumor shrinkage in vivo. Mice treated with T56-LIMKi (60 mg/kg) shows a significant decrease in tumor volume compared to control[1]. |
Animal experiment: | Mice: T56-LIMKi is dissolved in 0.5% carboxymethylcellulose solution. Mice are implanted with xenografted Panc-1 cells. Treatment is started 7 days later. Mice in the two experimental groups are each treated with a daily oral non-toxic dose of T56-LIMKi (30 or 60 mg/kg in gavage) and mice in the control group receives only the vehicle (0.5% CMC) in the gavage[1]. |
| 产品描述 | T56-LIMKi is a selective inhibitor of LIMK2; inhibits the growth of Panc-1 cells with an IC50 of 35.2 μM. T56-LIMKi efficiently inhibits the growth of ST88-14, U87, Panc-1 cells, A549 lung cancer cells with IC50 values of 18.3, 7.4, 35.2 and 90 μM, respectively. T56-LIMKi decreases phosphorylated cofilin (p-cofilin) levels and thus inhibits growth of several cancerous cell lines, including those of pancreatic cancer, glioma and schwannoma[1]. It blocks the phosphorylation of cofilin which leads to actin severance and inhibition of tumor cell migration, tumor cell growth, and anchorage-independent colony formation in soft agar. T56-LIMKi (10-50 μM) reduces p-cofilin in a dose-dependent manner in NF1–/–MEFs with an IC50 of 30 μM. Notably, the inhibitor does not affect the amounts of total cofil. 50μM T56-LIMKi causes a statistically significant reduction in the number of cells exhibiting stress fibers[2]. T56-LIMKi can induce inhibition of cofilin phosphorylation and Panc-1 tumor shrinkage in vivo. Mice treated with T56-LIMKi (60 mg/kg) shows a significant decrease in tumor volume compared to control[1]. References: |
m.cnreagent.com