Martin P. Schwalm

This study identifies cyanoquinoline-based HIPK4 inhibitors with nanomolar potency and reveals their cell-type-specific effects on HIPK4 proteostasis and autophagy.

The paper describes the development of AZ137, a potent and selective HIPK4 inhibitor derived from bosutinib, and validates its utility as a tool for studying HIPK4's biological functions.

This paper compares the effects of USP7 inhibition and degradation in cancer cells, finding distinct phenotypic and proteomic responses.

This paper introduces a miniaturized PROTAC synthesis workflow that bypasses compound purification, enabling rapid screening and degradation assessment of multiple targets.

The paper identifies inhibitor-induced kinase destabilization as a common phenomenon and reveals that it occurs through endogenous proteolytic mechanisms rather than classical ubiquitination.

This study shows that the RNF4 ligand CCW16 induces ferroptosis in AML cells through a RNF4-independent mechanism by causing covalent protein modifications and upregulating ferroptosis markers.

The paper describes the optimization of a macrocyclic scaffold to develop a selective STK10 inhibitor with nanomolar activity and good kinome selectivity.

This study develops a covalent LIMK1 inhibitor that selectively targets a unique cysteine, enabling isoform-specific studies of LIMK1 function.

Hybrid type-II inhibitors RN277 and RN341 target inactive LRRK2 with far fewer kinase off-targets than Rebastinib, preserve S935 phosphorylation, and rescue kinesin motility in vitro.

This study develops heterobifunctional protein binders that selectively kill specific cell types by leveraging the abundance of FKBP12, demonstrating enhanced efficacy through cellular enrichment.

The paper repurposes a benzoxazepinone scaffold originally designed for RIPK1 inhibition to develop a novel type-III LIMK1/2 inhibitor with high selectivity.

The paper evaluates diverse ubiquitin pathway inhibitors as controls for CRBN and VHL-mediated protein degradation, assessing their potency and toxicity using the HiBiT system and high content assays.

The paper evaluates the druggability of LC3/GABARAP for autophagy modulators and identifies ligands that bind to the HP2 pocket of the LIR docking site.

The paper introduces PFI-7, a chemical probe that inhibits GID4 Pro/N-degron interactions, revealing non-degradative roles of the CTLH complex in human cells.

This paper provides a detailed protocol for producing LIR peptides and using ITC to study their interactions with LC3/GABARAP proteins, including troubleshooting guidance.

This paper develops cell-based assays to monitor PROTAC degradation kinetics and ternary complex formation, revealing that ternary complex stability is critical for PROTAC efficiency.