The MYC proto-oncogene is a master regulator of transcription with a central role in cancer cell pathophysiology. The expression of MYC is tightly controlled in healthy cells but, in up to 70% of human cancers, MYC expression is elevated or dysregulated. Pharmacological inactivation of the c-Myc oncoprotein is therefore considered an attractive approach as a therapeutic strategy for cancer, with multiple lines of evidence suggesting that MYC inactivation leads to tumour regression. Directly targeting the c-Myc oncoprotein as a therapeutic strategy is challenging, however, due to a lack of a binding pocket amenable to small-molecule inhibitor development. Alternative strategies to target c-Myc indirectly have therefore been pursued, through inhibition or degradation of upstream and downstream proteins including BET bromodomains and the immune cell-specific transcription factor, interferon regulatory factor 4 (IRF4). Knockdown of IRF4 is toxic in multiple myeloma (MM) cell lines, while pharmacological inhibition of the bromodomain histone acetyltransferases CBP/EP300 is reported to lead to direct transcriptional suppression of IRF4 and concomitant reduction in MYC expression. More recent work suggests that MM cell death following treatment with CBP/EP300 inhibitors is not mediated by reduced IRF4 expression, but indirectly through We first explored the phenolic ether exit vector strategy, synthesizing a small panel of analogues to assess feasibility of functionalizing this part of the molecule while retaining balanced binary affinity to both target bromodomains, BRD4 and CBP (Scheme 1). Starting with the amino-nitro analogue 3, known intermediate 5 was subjected to coupling/cyclization procedures previously developed for related analogues. A series of products, 6 -10, were synthesized. The biochemical binary binding affinities of select compounds to both BRD4 and CBP were measured using a FRET assay (Table ) using the broad spectrum bromodomain inhibitor bromosporine as a control. Phenol 6 had similar affinity to both bromodomains as the parent compounds 1 and 2, and affinities towards BRD4 were improved upon incorporation of an acetyl (7), alkyl ester (8), and longer amide-ether linkages (10), the latter two representing model compounds for exit vectors and potential Degraders. Overall, the phenol ether exit vector represented a promising platform for Degrader synthesis because biological activity, in biochemical assays, was not unduly compromised.