BRD4 Proteolysis Targeting Chimera (PROTAC®) ARV-825, Causes Sustained Degradation of BRD4 and Modulation of Chemokine Receptors, Cell Adhesion and Metabolic Targets in Leukemia Resulting in Profound Anti-Leukemic Effects
Novel BET Protein Proteolysis Targeting Chimeras (BETP-PROTACs®) Exert Potent Single Agent and Synergistic Activity with Ibrutinib and Venetoclax Against Human Mantle Cell Lymphoma Cells
Superior Lethal Activity of Novel BET Protein Proteolysis Targeting Chimera (BETP-PROTACs®) Versus Betp Bromodomain Inhibitor (BETi) Against Post-Myeloproliferative Neoplasm (MPN) Secondary(s) AML Cells
BRD4 Degradation by PROTACs® Represents a More Effective Therapeutic Strategy than BRD4 Inhibitors in Ovarian Cancer
Hijacking Ubiquitin E3 Ligases Using PROTAC® Technology to Effectively Degrade BRD4 and Achieve Anti-tumor Efficacy
