106359-61-9

Upstream product

• 106359-69-7 4-(naphthalen-1-yl)benzoic acid 
• 229467-26-9 4-naphthalene-1-ylbenzoic acid methyl ester 
• 619-44-3 methyl 4-iodobenzoate 
• 90-11-9 1-Bromonaphthalene 
• 13922-41-3 1-Naphthylboronic acid 
• 586-76-5 4-Bromobenzoic acid 

Relevant academic research and scientific papers

INHIBITORS FOR HDAC8

INHIBITORS FOR HDAC8 ABSTRACT OF THE DISCLOSURE This invention discloses a new HDAC inhibitor scaffold designed to exploit a unique sub-pocket of the HDAC8 active site. These compounds are based on inspection of HDAC8 crystal structures bound to various inhibitors, which showed that the HDAC8 active site is surprisingly malleable and can accommodate inhibitor structures that are distinct from the canonical "zinc-binding group-linker-cap group" structures of SAHA, TSA and similar HDAC inhibitors. Some of the new inhibitors based on this new scaffold are >100 fold selective for HDAC8 over other class I and class II HDACs with IC50 values 1μM against HDAC8. The present invention provides a new type of "linkerless" HDAC8 inhibitors and methods of treating a pathological condition using the same. Treatment of human cells with the new inhibitors of the present invention show a unique pattern of hyperacetylated proteins compared with the broad spectrum HDAC inhibitor TSA.

Design and evaluation of 'Linkerless' hydroxamic acids as selective HDAC8 inhibitors

In this report, we describe new HDAC inhibitors designed to exploit a unique sub-pocket in the HDAC8 active site. These compounds were based on inspection of the available HDAC8 crystal structures bound to various inhibitors, which collectively show that the HDAC8 active site is unusually malleable and can accommodate inhibitor structures that are distinct from the canonical 'zinc binding group-linker-cap group' structures of SAHA, TSA, and similar HDAC inhibitors. Some inhibitors based on this new scaffold are >100-fold selective for HDAC8 over other class I and class II HDACs with IC50 values 1 μM against HDAC8. Furthermore, treatment of human cells with the inhibitors described here shows a unique pattern of hyperacetylated proteins compared with the broad-spectrum HDAC inhibitor TSA.