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Amphista announced the first patient dose in BRAMLIE, a Phase 1 study of AMX-883 in acute myeloid leukemia and high-risk myelodysplastic syndrome. The oral candidate recruits DCAF16 to degrade BRD9. The study will evaluate safety, pharmacokinetics, and preliminary activity, moving a non-cereblon, non-VHL degradation approach beyond preclinical models and into patients.
A Nature Chemical Biology study used high-throughput proteomics and machine learning to investigate toxicity in experimental androgen receptor degraders. Researchers linked off-target effects to mitochondrial complex I inhibition and identified small linker changes that reduced hepatotoxicity signals. Optimized compounds retained target degradation and showed improved activity in prostate cancer xenografts, providing preclinical evidence for a safer design workflow.
Roche entered a research collaboration and licensing agreement with Hangzhou-based Defand Therapeutics to discover molecular glue degraders for oncology and immunology targets. Defand will contribute its screening platform, with Roche taking responsibility for subsequent development and exclusive global commercialization. The announcement did not disclose upfront payment amounts, milestone thresholds, or royalty rates.
Nurix announced the first patient enrollment in NX-5948-203, a Phase 1b/2 trial combining the investigational BTK degrader bexobrutideg with venetoclax in chronic lymphocytic leukemia. Initial enrollment focuses on relapsed or refractory disease. Conducted under the Roche collaboration, the study will assess safety, tolerability, and clinical activity to inform potential combination development across treatment settings.
Arvinas presented final Phase 1 findings for its brain-penetrant LRRK2 degrader ARV-102 in 24 patients with Parkinson’s disease treated for 28 days. Exploratory changes in eye movement measurements correlated with reductions in cerebrospinal fluid LRRK2 and changes in pathway biomarkers. The trial was not designed to establish clinical efficacy or effects on disease progression.
Researchers characterized PSIRC3, an irreversible covalent BTK PROTAC that produced rapid, selective degradation in cellular experiments and target reduction in vivo. Activity required engagement of BTK Cys481 and was lost against the C481S mutant. Modeling supported a balance between target and E3 ligase affinities, challenging the assumption that catalytic turnover is required for potent degradation.
Nurix and Gilead agreed to extend research on an undisclosed oncology program by another two years, marking the program’s second extension. Their collaboration uses E3 ligases to induce degradation of selected targets. Nurix retains options, subject to restrictions, to share development, commercialization, and profits and losses equally in the United States for up to two programs.
In the randomized phase 3 VERITAC-2 trial, vepdegestrant improved progression-free survival versus fulvestrant in the ESR1-mutated subgroup, but not significantly in the overall population. The trial enrolled 624 patients with previously treated ER-positive, HER2-negative advanced breast cancer. Grade 3 or higher adverse events occurred more often with vepdegestrant.
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