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ACBI1 serves as a potent and collaborative degrader for SMARCA2, SMARCA4, and PBRM1. Operating as a PROTAC degrader, ACBI1 exhibits anti-proliferative activity and prompts apoptosis.

SJFα is a PROTAC with a 13-atom linker, designed using a von Hippel-Lindau (VHL) ligand as its foundation.

SIM1 is a highly effective trivalent PROTAC utilizing von Hippel-Lindau (VHL) as its foundation, proficient in degrading all members of the BET family. It exhibits a particular inclination for the degradation of BRD2.

PROTAC ERRα Degrader-3 stands as a powerful and discriminating ERRα degrader formulated around the von Hippel-Lindau ligand. Notably, PROTAC ERRα Degrader-3 displays inactivity against ERRβ and ERRγ proteins, showcasing its specificity in selectively targeting ERRα.

GNE-987 represents a PROTAC that combines ligands for von Hippel-Lindau and BRD4. It demonstrates highly potent cell BRD4 degradation activity at the picomolar level, and it features a robust BET binder/inhibitor, a fragment that binds to VHL, and a spacer moiety with ten methylene units. Additionally, GNE-987 holds applicability in PROTAC-Antibody Conjugate (PAC) approaches.

dTAGV-1 represents a degrader designed to target fusion proteins involving mutant FKBP12F36V. It consists of a ligand specifically tailored for the F36V single-point mutated FKBP12, a linker, and a ligand binding to von Hippel-Lindau (VHL). This compound effectively induces robust and selective degradation of FKBP12F36V fusion proteins, demonstrating its efficacy both in vitro and in vivo.

AGB1 demonstrates robust efficacy as a rapid and highly selective PROTAC degrader specifically targeting BromoTagged proteins. Its pharmacokinetic profile in mice is notably favorable.

PROTAC FLT-3 degrader 1, a von Hippel-Lindau (VHL)-based molecular agent, demonstrates anti-proliferative activity and induces apoptosis by selectively degrading FLT-3 internal tandem duplication (ITD).

ARCC-4 is a potent Androgen Receptor (AR) degrader utilizing the PROTAC mechanism. It functions as an enzalutamide-based von Hippel-Lindau (VHL)-recruiting AR PROTAC and effectively degrades clinically significant AR mutants linked to antiandrogen therapy.