Stanford Research Institute (SRI) International, USA
Sudhakar Yakkanti, Associate Director/Senior Scientist at Center for Cancer & Metabolism, Cell Signaling Laboratory, Bioscience Division, Stanford Research Institute (SRI) International, Menlo Park, California. Earlier he was founder Director of Cell Signaling, Retinal and Tumor Angiogenesis Laboratory at BTNRH, Omaha, NE, USA (2004-2012). He did his postdoctoral training at Harvard Medical School, Boston, MA, USA (2003). He received President’s fellowship (1992), GATE (1996) and CSIR (2007-2000) fellowships from Government of India. He received Mahindra & Mahindra Educational Award (2000) and Young Clinical Scientist Awards from Flight Attendant Medical Research Institute (FAMRI) in 2007 and 2010. He also received Bio-Bio Young Scientist Award from OMICS publishing group; Michael A. O’Connor Young Investigator Award; RO1 grant Award from NIH/NCI and Research Scholar Grant Award from ACS (2010). He was served as AIBS/NIH-RO1 Grant reviewer for DT study section. He has published more than 40 research articles in several top journals including Science, Cancer Cell, JCI, Blood, PNAS, Gastroenterology, Cancer Research, JBC, IOVS, PLOS ONE etc. He is serving as an Editor-in-Chief and Editorial board member of reputed journals and is serving as a reviewer for many scientific journals including JCI, Blood, Circulation, Circulation Research, Cancer research, Clinical Cancer research, IOVS etc. He was honored as honorable gust, keynote speaker, session chair and organizing committee member for many national and international conferences.
Choroidal Neovascularization (CNV) leads to loss of vision in Age Related Macular Degeneration (AMD) that affects approximately 1 in 3 individuals over the age of 65. CNV of AMD is as common as cancer and one of the most prevalent causes of blindness in the world. It has long been recognized that drugs targeting neovascularization may provide new and useful tools for the treatment of patients with CNV of AMD. The present available therapies in clinical trials come in the form of antibodies or antibody fragments that inhibit VEGF, which can only slow the progression of this eye disease. A renewed effort must therefore be made to identify efficient endogenous molecules that could be exploited as therapeutic agents. Thus, the present study identified angioinhibitory signalling mechanism(s) of endogenous metabolite, whose mechanism of actions is yet to be deciphered