JBIR-17, a novel trichostatin analog from Streptomyces sp. 26634

The Journal of Antibiotics
2009.0

Abstract

Histone deacetylases (HDACs) play an important role in the epigenetic regulation of gene expression by catalyzing the removal of acetyl groups from lysine residue of histone protein, stimulating chromatin condensation and promoting transcriptional repression. HDACs are divided into four classes on the basis of their homology to yeast HDACs: class I (HDAC1, 2, 3 and 8), class IIa (HDAC4, 5, 7 and 9), class IIb (HDAC6 and 10), class III (SIRT1, 2, 3, 4, 5, 6 and 7) and class IV (HDAC11). As aberrant epigenetic changes are a hallmark of cancer, HDACs are a promising target for an anticancer drug. The inhibitors of HDACs can induce cell-cycle arrest, promote differentiation and stimulate tumor cell death. In fact, several HDAC inhibitors are currently in clinical trials both for solid and hematological malignancies. Therefore, we attempted to search new HDAC inhibitors. As a result, we isolated a novel compound designated as JBIR-17 (1) from Streptomyces sp. 26634. The structure of JBIR-17, determined by NMR spectral analyses and Marfey's method, consists of a trichostatic acid moiety linked to an L-serine moiety through an amide bond, with a molecular formula of C20H26N2O5. Biological evaluation showed that JBIR-17 selectively inhibits HDAC6 (IC50 4.7 μM) and HDAC4 (IC50 69 μM) but has no activity against HDAC1 at a concentration of 100 μM. These results indicate that JBIR-17 could be a valuable tool for the studies of HDAC6 and enzymatic property among HDAC subtypes.

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