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Arteriosclerosis, Thrombosis, and Vascular Biology
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Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:2414-2416
doi: 10.1161/01.ATV.0000238361.07225.fc
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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:2414.)
© 2006 American Heart Association, Inc.


Letter to the Editor

Mycophenolic Acid Is a Potent Inhibitor of Angiogenesis

Xinrong Wu; Hanbing Zhong; Jianbo Song; Robert Damoiseaux; Zhen Yang; Shuo Lin

From the Liu Hua Qiao Hospital (X.W.), Guangzhou, P.R. China; Shenzhen Graduate School, Peking University (Z.Y., S.L.); and the Department of Molecular, Cell, & Developmental Biology (X.W., H.Z., J.S., S.L.) and MIMG/Pharmacology (R.D.), University of California, Los Angeles.

Correspondence to Shuo Lin, Department of Molecular, Cell, & Developmental Biology, University of California Los Angeles, 621 Charles E. Young Drive South, LS4325, Los Angeles, CA 90095-1606. E-mail shuolin@ucla.edu


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

Angiogenesis is necessary for the vascularization of a tumor, providing essential nourishment for tumor growth, and the progression and metastasis of cancer cells.1

Although tremendous efforts and resources have been dedicated to discovering angiogenesis inhibitors, very few candidates have been approved by FDA for therapeutic applications. Currently, Avastin (bevacizumab), a humanized monoclonal antibody, and Macugen (Pegaptanib), a pegylated oligonucleotide aptamer, both directed against vascular endothelial growth factor (VEGF) pathway, are two of the approved drugs for clinical use. There is still a great need to develop small molecule drugs for antiangiogenesis purpose. One approach to broaden the discovery platform is to identify antiangiogenic activities from existing drugs that have well defined toxicity and pharmacokinetics. Once a known drug is demonstrated to inhibit angiogenesis, it would move into the clinic trails more rapidly. Because most known drugs have well defined structures and defined biological targets, it is also possible to further improve the compound structure or select the target as a new entry point for angiogenesis-based studies and therapies. Currently there are more than 2000 known drugs that can be used for re-purposing applications. It would be desirable to have a single in vivo assay allowing rapid screening of a large number of compounds for new activities such as angiogenesis inhibition. Recently, the zebrafish has been shown to be a useful model organism for this type of approach.2,3 Zebrafish blood vessels form by angiogenic sprouting and appear to use the same pathways necessary for blood vessel growth in mammals.4 Using transgenic . . . [Full Text of this Article]




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