Speaker Biography

Jun Li

Xinjiang Medical University, China

Title: Kinase inhibitor for the treatment and mechanism of cystic echinococcosis

Jun Li
Biography:

Jun Li, B.Sc., Ph.D., is a professor of Xinjiang Medical University and a senior research fellow of State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Xinjiang Medical University, Urumqi, China. He received her B. Sc from Xinjiang Medical University. In 2004, she obtained her PhD at the University of Queensland working on developing diagnosis tool for detecting cystic echinococcosis. She then spent 3 years working on PanBio for developing diagnosis kit for infectious diseases. From 2008-2013, she worked on molecular biology of Echinococcus as a senior research officer in Molecular Parasitology Laboratory, Infectious Diseases Division, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia. She has published more than 30 papers/articles in the international journals in her research career.

 

Abstract:

The metacestode stages of the two cestode species: Echinococcus granulosus sensu lato and E.multilocularis cause cystic echinococcosis (CE) and alveolar echinococcosis (AE). These diseases on the people's health and animal husbandry development caused great harm. The current number of patients treated by surgery only accounted for 3-8% of the total number of patients, the vast majority of patients taking albendazole treatment, but the treatment of the drug is unsatisfactory, the urgent need for new drug development. The completion of the E..g and E.m genome and transcriptome predicted a number of proteins for drug screening, in which the kinase was the primary drug target protein.

The Kinase Inhibitor Library from Medicines for cancer, comprised of 378(include 14 pathways and 59 targets)commercially available chemicals that show in vitro activity against PSC, was repurposed. Primary screening was carried out at 5 μM, and resulted in the identification of 51 compounds(include 9 pathways 29 targets) that caused deth in PSC Seven out of these 7 drugs(Pathway: Angiogenesis、Cell Cycle、Protein Tyrosine Kinaseï¼›Target: Bcr-Abl、CDK、DUB、EGFR、FAK、JAK、VEGFR) were also active at 1 μM. Dose-response assays revealed that only 2 compounds, namely S2243 and S2895, exhibited an LD50 value below 2.5 μM.S2895 and S2243 was carried out at 20 mg/ml resulted in the identification of 60% that caused physical damage in metacestodes.

These results provide evidence for the kinase potential as a growing of Echinococcus granulosus, different kinase pathway is different of resulted. The target Bcr-Abl, CDK, DUB, FAK, JAK for screening ,Drug residues play an important role in the screening of drugs.