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Klingegard, F.

Publications and source records attributed to Klingegard, F..

2 recordsLinked to original sources

A cell-based degrader assessment platform facilitates discovery of functional NUDT5 PROTACs

Targeted protein degradation (TPD) via PROTACs and molecular glues holds significant therapeutic promise but demands detailed mechanistic evaluation in live cells to fully understand compound behavior and optimize efficacy. Here, we present an integrated, cell-first platform that combines a modular degradation assay with E3 ligase target engagement readouts for comprehensive assessment of TPD molecules in cells and use it to evaluate PROTACs towards NUDT5. To mimic endogenous degradation conditions and TPD amenability, we established a fusion protein expression system consisting of a lysine-free FKBP12 F36V PROTAC handle (FKBPVK0) and used a HiBiT/akaLuc dual luciferase reporter to accurately measure degradation dynamics. This set-up identified a VHL-dependent NUDT5 PROTAC, DDD2, that induced robust NUDT5 degradation, despite impaired NUDT5 binding in vitro and in cellulo, but no CRBN-dependent degraders. NUDT5 lysine availability mapping with DDD2 and FKBP12 F36V-directed PROTACs suggested that the CRL4CRBN complex is more sensitive to target lysine accessibility than CRL2VHL, which may have implications for E3 ligase choice and therapeutic resistance. CeTEAM drug biosensors were also established towards CRBN and VHL to quantitatively monitor degrader engagement in living cells and confirmed that the tested CRBN-directed NUDT5 PROTACs poorly engaged the E3. All together, this platform provides a versatile and scalable framework for TPD molecule discovery in a cellular context.

biochemistry↗

Conformational dynamics in the membrane interactions of bispecific targeted degrader therapeutics

Proteolysis targeting chimeras (PROTACs) offer vast new therapeutic opportunities, however their physicochemical properties are difficult to combine with optimal cell permeability and exposure at the target sites. We have systematically analyzed a dataset of more than 3500 PROTACs to investigate how the choice of ubiquitin E3 ligase ligands, linker design, and global molecular properties can be optimized to achieve the desired cell permeability and intracellular exposure. We find that conformational flexibility leads to environment-dependent shielding of polar functions and improved interactions with cell membranes, but that at the same time extended, linear conformations within the membrane are beneficial. Linker composition was a major factor in determining the folding propensity. Collectively, our results suggest that strategies to rationally design linkers and to shield polarity selectively within the protein-of-interest (POI) ligand and/or E3 ligand domains, rather than more extensive folding, may be beneficial in the design of permeable and effective PROTACs.

pharmacology and toxicology↗