PTP1B抑制剂阻断蛋白酪氨酸磷酸酶1B的活性，这是胰岛素和瘦素信号通路负调节的关键因素。分子动力学研究表明，PTP1B抑制剂具有很强的结合力和很高的选择性，这是由于在活性位点周围形成了氢键网络。如果在CHO和HEK293稳定细胞克隆中过表达PTP1B，则会在整个克隆产生和维持过程中产生细胞毒性和低复兴率。研究表明，PTP1B抑制剂可以显着放大PTP1B过表达的CHO细胞中关键葡萄糖转运蛋白Glut4的膜移位。PTP1B抑制剂选择性地增加了胰岛素受体，胰岛素受体底物1和Akt的磷酸化，从而模仿了胰岛素的作 PTP1B Inhibitor blocks the activity of the Protein Tyrosine Phosphatase 1B, which is a key factor in the negative regulation of insulin and leptin signaling pathway. Molecular dynamic studies have shown that PTP1B Inhibitor has strong binding and high selectivity due to the hydrogen bonding networks formed around the active sites. Cytotoxicity and low revival rates throughout clone generation and maintence result if PTP1B is over-expressed in CHO and HEK293 stable cell clones. Studies have shown that PTP1B Inhibitor could dramatically magnify the membrane translocation of the key glucose transporter Glut4 in PTP1B-overexpressed CHO cells. PTP1B Inhibitor selectively increases the phosphorylation of the insulin receptor, insulin receptor substrate 1, and Akt, mimicking the action of insulin. PTP1B Inhibitor is also known as Protein Tyrosine Phosphatase 1B Inhibitor, and 3-(3,5-dibromo-4-hydroxybenzoyl)-2-ethyl-N-[4-[(2-thiazolylamino)sulfonyl]phenyl]-6-benzofuransulfonamide.