HDAC6 and neoplasm: Scheme 9 illustrates how N-hydroxyamide 51 was made by hydrolyzing 1 [120]. Compound 51 inhibited angiogenesis and suppressed tumor cell proliferation by targeting VEGFR2 signaling. In addition, HDAC6-induced Hsp90 hyperacetylation, and HDAC6-enhanced cyclin D1 and CDK4 degradation may be mediated by N-hydroxyamide 52-induced G1 growth arrest [121].