dBET1 is a hybrid molecule that combines (+)-JQ1 and thalidomide. It induces cereblon-dependent BET protein degradation in vitro (EC50: 430 nM) and induces apoptosis.

ARV-393 HCl is an orally active and potent PROTAC targeting BCL6 with antitumor activity for the study of non-Hodgkin's lymphoma.

ACBI1 is a potent PROTAC degrader of BAF ATPase subunits SMARCA2 and SMARCA4, also degrades the polybromo-associated BAF (PBAF) complex member PBRM1, with DC50s of 6 nM, 11 nM and 32 nM for SMARCA2, SMARCA4 and PBRM1 in MV-4-11 cells, respectively. ACBI1 is composed of a bromodomain ligand, a linker, and the E3 ubiquitin ligase VHL. ACBI1 can induce anti-proliferative effects and apoptosis.

Gefitinib-based PROTAC 3, which connects an EGFR binding element to a VHL ligand via a linker, induces EGFR degradation with DC50s of 11.7 nM and 22.3 nM in HCC827 (exon 19 del) and H3255 (L858R mutation) cells, respectively[1].

ARV-825, a heterobifunctional PROTAC (Proteolysis Targeting Chimera) that recruits BRD4 to the E3 ubiquitin ligase cereblon leading to fast, efficient, and prolonged degradation of BRD4 in all BL cell lines tested.

GMB-475 is a BCR-ABL1 tyrosine kinase degrader based on PROTAC, overcoming BCR-ABL1-dependent drug resistance. GMB-475 targets BCR-ABL1 protein and recruits the E3 ligase Von Hippel Lindau (VHL).resulting in ubiquitination and subsequent degradation of th

dBET57 is heterobifunctional degrader of BRD4 based on the PROTAC technology, exhibits significant degradation of BRD4BD1 with a DC50/5h of 500 nM ,and inactive on BRD4BD2

NH2-PEG2-C6-Cl hydrochloride is a PROTAC linker belonging to the PEG class and can be used to synthesize PROTAC molecules.