Dr. JingwuZang received his medical degree in Shanghai JiaoTong University Med school (formerly Shanghai Second Medical University) and continued to earn his PhD in Immunology in Belgium, where he soon began his illustrious hunt for get rid of ms through simple and easy clinical research. He later received a professional research fellowship award from US National Ms Society and conducted his postdoctoral research on ms in Harvard School of medicine and later joined the school at Baylor College of drugs being a Professor of Immunology and Neurology as well as the research director of International Multiple Sclerosis Centre in Houston. He completed a clinical residency at Baylor College of Medicine and holds a dynamic US medical licensure. Dr.Jingwu Zang was the founding father of Opexa Pharmaceuticals, now on NASDAQ. In his more modern career in China, Dr.JingwuZang established the Institute of Health Sciences with Chinese Academy of Sciences since the founding director and co-founded the Institute Pasteur Shanghai, a partnership institute of the Chinese Academy of Sciences with Institute Pasteur Paris. Dr.JingwuZang published a lot more than 160 scientific papers including in Science, Nature Medicine, Nature Immunology, and book chapters around immunology and received many awards for the scientific works he led in US and China. He joined GlaxoSmithKline in 2007 as Corporate SVP and founded GSK’s R&D Centre in China and later became GSK’s global head of Neurosciences Therapy Area. In 2013, Dr. JingwuZang joined Simcere pharmaceuticals as CSO and President of BioSciKin, a drug innovation commercial entity combining internal R&D capabilities and an investment fund. Dr.JingwuZang founded I-MAB Biopharmain 2014. MAB Biopharma is often a dynamic and fast-growing global player dedicated to developing innovative biologics in the regions of immuno-oncology and immuno-inflammation through internal R&D capabilities and global partnerships. I-Mab’s pipeline is driven through the company’s development technique to address unmet needs in China and to bring innovative assets around the world. Following recent Series B financing of $150 million and rapid rise in internal R&D capabilities, I-Mab is well positioned to relocate its China portfolio of multiple Phase 2 and Phase 3 innovative clinical assets as well as global portfolio of first-in-class and best-in-class assets in China and/or US in 2018. I-Mab’s long-term commitment is always to deliver transformational medicines to patients globally which has a concentrate on unmet needs in China.
Representative Publications:
1. Zhang JZ, Medaer R, Stinissen P, Hafler D, Raus J. MHC-restricted depletion of human myelinbasic-protein reactive T-cells by T-cell vaccination. Science 261(5127): 1451- 1454, 1993.
2. Zang JingwuYC, Samanta AK, Halder JB, Hong J, Tejada-Simon MV, Rivera VM, Zhang JZ. Aberrant Tcellmigration toward RANTES and MIP-1 alpha in patients with multiple sclerosis - Overexpression ofchemokine receptor CCR5. Brain 123: 1874-1882, 2000.
3. Tejada-Simon MV, Zang YC, Hong J, Rivera VM, Zhang JZ. Cross-reactivity with myelin basic proteinand human herpesvirus-6 in ms.Annals of Neurology 53:189-197, 2003.
4. Sun W, Popat U, Hutton G, Zang YC, Krance R, Carrum G, Land GA, Heslop H, Brenner M, Zhang JZ.Characteristics of T-cell receptor repertoire and myelin-reactive T cells reconstituted from autologoushaematopoietic stem-cell grafts in ms. Brain 127(5):996-1008, 2004.
5. Xu G, Nie H, Li N, Zheng W, Zhang D, Feng G, Ni L, Xu R, Hong J, Zhang JZ. Role of osteopontin inamplification and perpetuation of rheumatoid synovitis.Journal of Clinical Investigation 115(4):1060-1067,2005.
6. Hong J, Li N, Zhang X, Zheng B, Zhang JZ. Induction of CD4+CD25+ regulatory T cells bycopolymer-Ithrough activation of transcription factor Foxp3.Proceedings with the National Academy of Sciences USA102(18): 6449-6454, 2005.
7. Hong J, Zang YC, Nie H, Zhang JZ. CD4+ Regulatory T Cell Responses Induced by T Cell Vaccination inPatients with Multiple Sclerosis. Proceedings from the Nas USA 103:5024-5029,2006.
8. Wang Z, Hong J, Sun W, Xu G, Li N, Chen X, Liu A, Xu L, Sun B, Zhang JZ. Role of Gamma-Interferonin Induction of Foxp3 and Conversion of CD4+CD25- T cells to CD4+ Regulatory T Cells. Journal ofClinical Investigation 116(9):2434-2441, 2006.
9. Chen G, Li N, Zang YC, Zhang D, He D, Feng G, Ni L, Xu R, Wang L, Shen B, Zhang JZ. Vaccinationwith Selected Synovial T Cells in Rheumatoid Arthritis.Arthritis and Rheumatism 56(2), 453-463, 2007.
10. Zhang JZ. Yin and Yang interplay of IFN-gamma in inflammation and autoimmune disease. Journal ofClinical Investigation 117(4):871-3, 2007.
11. Shi Y, Feng Y, Kang J, Liu C, Li Z, Li D, Cao W, Qiu J, Guo Z, Bi E, Lu C, Zhang JZ (Co-correspondingauthor), Pei G. Critical unsafe effects of CD4+ T cell survival and autoimmunity by ?-arrestin 1. NatureImmunology 8: 817-824, 2007.
12. Zheng W, Li R, Pan H,He D, Xu R, Guo TB, Guo Y, Zhang JZ. Role of osteopontin in induction of monocyte chemoattractant protein 1 and macrophage inflammatory protein 1beta through the NF-kappaB and MAPK pathways in arthritis rheumatoid.ArthritisRheum, 60(7):1957-65, 2009.
13. Chen X, Fang L, Song S, Liu A, Zhang JZ. Thymic regulating autoimmune disease by accelerated differentiation of Foxp3+ regulatory T cells through IL-7 signaling pathway.JImmunol, 183(10):6135-44, 2009.
14. Qian G, Qin X, Zang YQ, Ge B, Guo TB, Wan B, Fang L, Zhang JZ. High doses of alpha-galactosylceramide potentiate experimental autoimmune encephalomyelitis by directly enhancing Th17 response. CellRes, 20(4):480-91, 2010.
15. Cao W, Yang Y, Wang Z, Liu A, Fang L, Wu F, Hong J, Shi Y, Leung S, Dong C, Zhang JZ.Leukemia Inhibitory factor inhibits T helper 17 cell differentiation and confers treatment outcomes of neuralprogenitor cell therapy in autoimmune disease. Immunity, 35(2):273-84, 2011.
16. Liu X, Fang L, Guo TB, Mei H, Zhang JZ. Drug targets within the cytokine universe for autoimmune disease. Trends Immunol, 34(3):120-8, 2013.
17. Nie H, Zheng Y, Li R, Guo TB, He D, Fang L, Liu X, Xiao L, Chen X, Wan B, Chin YE, Zhang JZ. Phosphorylation of FOXP3 controls regulatory T cell function and it is inhibited by TNF-? in rheumatoid arthritis symptoms. Nat Med, 19(3):322-8, 2013.