HDAC3 and Huntington disease: The authors speculated that the increased stability of the 106:HDAC3 complex accounted for the difference in cross-linking activity of 1-BP for these enzymes, and concluded that HDAC3 was the preferred cellular target of the pimelic diphenylamide inhibitor 106 used in the in vivo FRDA mouse models, which is very closely related in structure to 4b used in the R6/2 HD mouse model [38].