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Biology subjects

Thoma, N.

Publications and source records attributed to Thoma, N..

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↗

BMAL1-HIF2α heterodimers contribute to ccRCC

Circadian disruption enhances cancer risk, and many tumors exhibit disordered circadian gene expression. We show rhythmic gene expression is unexpectedly robust in clear cell renal cell carcinoma (ccRCC). Furthermore, the clock gene BMAL1 is higher in ccRCC than in healthy kidneys, unlike in other tumor types. BMAL1 is closely related to ARNT, and we show that BMAL1-HIF2 regulates a subset of HIF2 target genes in ccRCC cells. Depletion of BMAL1 reprograms HIF2 chromatin association and target gene expression and reduces ccRCC growth in culture and in xenografts. Analysis of pre-existing data reveals higher BMAL1 in patient-derived xenografts that are sensitive to growth suppression by a HIF2 antagonist (PT2399). We show that BMAL1-HIF2 is more sensitive than ARNT-HIF2 to suppression by PT2399, and increasing BMAL1 sensitizes 786O cells to growth inhibition by PT2399. Together, these findings indicate that an alternate HIF2 heterodimer containing the circadian partner BMAL1 contributes to HIF2 activity, growth, and sensitivity to HIF2 antagonist drugs in ccRCC cells.

cancer biology↗