TL;DR
The design and synthesis of SHP2 PROTACs that recruit the DCAF16 E3 ligase for targeted SHP2 degradation are reported that support the potential of SHP2-targeted protein degradation as an alternative strategy to enzymatic inhibition and provide a promising starting point for the further development of SHP2 degraders.
This work describes the design, synthesis, and biological evaluation of a series of JNK1-targeting PROTACs that recruit either CRBN or VHL E3 ligases that demonstrates excellent degradation potency and selectivity for JNK1, highlighting its potential as a valuable chemical probe for EMT-associated pathologies.
Emerging evidence has expanded the functional repertoire of SKP2 beyond cell cycle control to encompass metabolism, DNA repair, stemness, tumor microenvironment and immunotherapy response, positioning it as an increasingly attractive target for intervention.
KLHL12 is identified as a potentially tumor-selective E3 ligase and the development of the first-in-class KLHL12-recruiting PROTACs are reported, which established KLHL12 as a promising tumor‑selective E3 ligase and provided a KLHL12-recruiting PROTAC platform for cancer therapy.
This review systematically synthesizes the mechanistic roles of USP2 across various cancers, highlighting its function as a double-edged sword, and comprehensively evaluates the landscape of emerging USP2 inhibitors.
These studies establish selective inhibition of the PLK1 Polo-box domain as a viable therapeutic strategy, provide in vivo proof-of-concept for the REPLACE approach, and identify abbapolins as promising leads for advanced prostate cancer.
This study validates stapled peptide-based CMA degraders as a powerful strategy to target "undruggable" intracellular drivers, highlighting MAX-7 as a promising therapeutic lead.
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