To convert the CRBN-utilizing PROTAC into one that recruits DCAF11, we replaced the thalidomide-based ligand (red, A6) with a DCAF11 ligand (orange, 1i, Figure ). We retained the vorinostat-like pan-HDACi to and C7 linker, to trace back any possible effects to the exchange of the E3 ligase. The initial PROTAC 1i, which represents the direct DCAF11-recruiting analog of A6, was complemented by a set of nine degraders, bearing a broad range of different spacers to introduce diversity in regards to chain length, lipophilicity, and rigidity. In detail, two short and rigid cyclic spacers (1a, b, Figure ), three more flexible PEG spacers (1c-e), and some alkyl spacers ranging from C1-C11 (1f-j) were selected. As the line between PROTACs and molecular glues is becoming increasingly blurred, we also designed a compound that can be considered as a spacer-less PROTAC (2). In total, we decided to synthesize eleven PROTACs to study the effect of DCAF11 recruitment on HDAC degradation.