Dr. JingwuZang received his medical degree in Shanghai JiaoTong University Med school (formerly Shanghai Second Medical University) and took to earn his PhD in Immunology in Belgium, where he started his illustrious search for an end to multiple sclerosis through simple and clinical research. He later received a professional research fellowship award from US National Multiple Sclerosis Society and conducted his postdoctoral research on ms in Harvard Med school and later joined the college at Baylor College of Medicine as a Professor of Immunology and Neurology as well as the research director of International Ms Centre in Houston. He completed a clinical residency at Baylor College of medication and holds an energetic US medical licensure. Dr.Jingwu Zang was the founding father of Opexa Pharmaceuticals, now listed on NASDAQ. As part of his newer career in China, Dr.JingwuZang established the Institute of Health Sciences with Chinese Academy of Sciences as the founding director and co-founded the Institute Pasteur Shanghai, a partnership institute in 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 in 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 then became GSK’s global head of Neurosciences Therapy Area. In 2013, Dr. JingwuZang joined Simcere pharmaceuticals as CSO and President of BioSciKin, a medication innovation commercial entity combining internal R&D capabilities with an investment fund. Dr.JingwuZang founded I-MAB Biopharmain 2014. Jingwu Zang is often a dynamic and fast-growing global player committed to developing innovative biologics in the parts of immuno-oncology and immuno-inflammation through internal R&D capabilities and global partnerships. I-Mab’s pipeline is driven from the company’s development strategy to address unmet needs in China and also to bring innovative assets to everyone. Following recent Series B financing of $150 million and rapid development in internal R&D capabilities, I-Mab is now 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 with a focus 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 ms - 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 multiple sclerosis.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 in the Nas 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 over the NF-kappaB and MAPK pathways in rheumatism.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 effects 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 inside 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 which is inhibited by TNF-? in rheumatoid arthritis symptoms. Nat Med, 19(3):322-8, 2013.