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Zielinski, K.

Publications and source records attributed to Zielinski, K..

2 recordsLinked to original sources

A Unified 3D Generative Model for Synthesizable Structure-Based Drug Design

Traditional screening-based drug discovery is inherently limited by the astronomical scale of the chemical space. Generative modelling offers a compelling alternative to the classical search paradigm and enables rational, bottom-up design of novel and target-specific small molecules. However, its impact has been hampered by challenges in synthetic accessibility of the designed compounds and lack of large-scale experimental validation. Here, we introduce LDDM (Large Drug Discovery Model), a generative framework that supports a range of drug discovery tasks, including constrained and unconstrained docking, fragment linking and growing, and de novo design. We further introduce a programmable design algorithm that enables accurate design of synthetically accessible compounds satisfying various fine-grained objectives. We experimentally validated the designed or optimised ligands for five therapeutically relevant protein targets. In all cases, LDDM achieved high success rates, allowing us to identify molecules with confirmed binding affinity while synthesizing only a small number of generated compounds. The best designs were structurally characterised through NMR spectroscopy and X-ray crystallography, demonstrating high prediction accuracy. Overall, LDDM provides a scalable and flexible platform for the rapid and tailored design of small molecules and non-natural peptides for therapeutic applications.

bioinformatics↗

Toward a Random Background for Ligand Optimization

Ligand optimization is central to drug discovery as hundreds of analogs might be designed and synthesized between an initial hit and a therapeutic candidate. The efficiency of this process is unclear, at least partly because there is no random background for optimization against which to compare. Such a random background might emerge from synthetically accessible but otherwise systematic random small substitutions across starting ligands, measuring likelihood of achieving a substantial improvement in affinity/potency or other property by any single perturbation. Recent literature and ligand-affinity/potency databases suggest that perhaps 10% of analogs with minor modifications improve upon a parents potency substantially (by [≥]10-fold), but this number is clouded by reporting bias, intentional improvement, and inter-group reproducibility. To begin to establish a background expectation for ligand optimization, we comprehensively and systematically modified 18 lead molecules across six targets with single atom changes; 257 compounds were synthesized. Unexpectedly, 11.2% of these random small perturbation analogs improved potency by [≥]10-fold over their parents. Conversely, these more potent analogs typically had worse in vitro pharmacokinetics (e.g. reduced metabolic stability, lower plasma free fraction). While it was possible to find analogs where the potency increase compensated for inferior exposure and half-life, resulting in more potent compounds in vivo, overall a frustrated landscape for ligand optimization is revealed. This study begins to establish a background expectation for ligand potency optimization and offers a simple strategy to do so. It also begins to quantify the challenges confronting the field in moving beyond in vitro potency.

pharmacology and toxicology↗