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PROTAC EGFR Degrader 2 is a highly potent compound that effectively targets EGFR for degradation. It demonstrates strong antiproliferative properties and can be utilized in the synthesis of nitroreductase-responsive PROTACs.

HDAC6 Degrader-3 is a selective compound that facilitates HDAC6 degradation through ternary complex formation and the ubiquitin-proteasome system. It shows significant selectivity for HDAC6 over HDAC1 and induces marked hyperacetylation of α-tubulin.

CMP98 is a PROTAC that does not promote VHL degradation and serves as a negative control for CM11. It features two von Hippel-Lindau ligands within its active structure.

NJH-2-056 is a deubiquitinase-targeting chimera (DUBTAC) that connects the OTUB1 recruiter EN523 with the CFTR chaperone lumacaftor. This compound facilitates studies on protein regulation and folding mechanisms associated with cystic fibrosis.

PZ703b is a PROTAC designed to degrade Bcl-xl, promoting apoptosis and suppressing the proliferation of cancer cells. This compound serves as a valuable tool for investigating mechanisms related to bladder cancer.

PROTAC α-synuclein degrader 5 is a selective small-molecule degrader targeting α-synuclein aggregates. It features the probe molecule sery308 along with E3 ligase ligands, facilitating significant degradation activity. This compound is a valuable resource for research in neurological disorders.

PROTAC BRD4 Degrader-9 is a bifunctional compound that utilizes ligands for von Hippel-Lindau and BRD4 to facilitate targeted degradation. It can be conjugated with STEAP1 and CLL1 antibodies, enhancing its effectiveness in degrading BRD4 protein within prostate cancer cell lines.

ARD-2051 is a highly effective orally bioavailable degrader designed to target the androgen receptor (AR) for proteolysis. This compound demonstrates significant potency in degrading AR protein in prostate cancer cell lines such as LNCaP and VCaP, making it valuable for research into AR-related pathways.

INY-05-040 is a selective AKT degrader that targets all three AKT isoforms, effectively disrupting downstream signaling and inhibiting cell proliferation across various cancer cell lines.