Advantages of PROTACs in achieving selective degradation of homologous protein families

• Luxi Yang,
• Xinfei Mao,
• Jingyi Zhang,
• Jing Shu,
• Wenhai Huang,
• Xiaowu Dong,
• Yinqiao Chen and
• Mingfei Wu

Beilstein J. Org. Chem. 2026, 22, 628–661, doi:10.3762/bjoc.22.49

• ; PROTAC; protein–protein interaction; selectivity; ubiquitination; Introduction The cell is the fundamental unit of structure and function in the human body [1][2]. More than 20,000 proteins act in concert to regulate the entire cellular life process [1]. To date, dysregulated protein function has been

• sufficient to trigger rapid ubiquitination [15][16]. Consequently, a PROTAC operates through an event-driven pharmacological paradigm, distinguishing itself from the traditional occupancy-driven model of small-molecule inhibitors [17]. Furthermore, PROTACs function catalytically, requiring only

• isoform-specific selectivity. Furthermore, we examine the influence of PPIs, a factor increasingly recognized for its critical contribution to the refined selectivity of PROTACs. The review also explores potential selectivity variations arising from the spatial distribution of ubiquitination-accessible

Identification and removal of a cryptic impurity in pomalidomide-PEG based PROTAC

• Bingnan Wang,
• Yong Lu and
• Chuo Chen

Beilstein J. Org. Chem. 2025, 21, 407–411, doi:10.3762/bjoc.21.28

• chimera (PROTAC) has made it a popular starting point to develop selective small-molecule degraders [2]. Currently, leveraging ubiquitination by the von Hippel–Lindau (VHL) protein or cereblon (CRBN) is the most successful method to achieve targeted protein degradation [3][4]. For initial studies, a short

Pyridinoacridine alkaloids of marine origin: NMR and MS spectral data, synthesis, biosynthesis and biological activity

• Louis P. Sandjo,
• Victor Kuete and
• Maique W. Biavatti

Beilstein J. Org. Chem. 2015, 11, 1667–1699, doi:10.3762/bjoc.11.183

• containing only one of the motifs such as shermilamine B (67) and lissoclinidine B (27) inhibit TOPO II [42][83] or induce apoptosis via other mechanisms like ubiquitination and degradation of p53 by acting on ubiquitin ligase [44]. Conclusion This review compiles up-to-date information on recently

Regulation of integrin and growth factor signaling in biomaterials for osteodifferentiation

• Qiang Wei,
• Theresa L. M. Pohl,
• Anja Seckinger,
• Joachim P. Spatz and
• Elisabetta A. Cavalcanti-Adam

Beilstein J. Org. Chem. 2015, 11, 773–783, doi:10.3762/bjoc.11.87

• regulate G-proteins involved in filopodia, lamellipodia, and contraction [7]. Moreover, FAK can directly serve to gene regulation. It can transfer from focal adhesions to the nucleus to target ubiquitination of the cell-cycle mediator p53 and act as a transcription co-regulator with the GATA4 zinc-finger