FDA approves iberdomide for multiple myeloma based on minimal residual disease negativity, marking the first such approval for the disease.
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Protein Degradation and Inhibitors
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SAGA and ATAC co-activator complexes use distinct strategies to regulate gene transcription, with implications for cancer therapy.
- Open access
Ziftomenib combined with venetoclax and azacitidine achieves a 46% composite complete remission rate in relapsed/refractory NPM1-mutated AML patients at the 600 mg dose.
CLEO4-88 acts as a molecular glue with an EC50 of 12.5 nM to inhibit ACAA1 thiolase by inducing binding to GID4 in vitro and in cells.
- 1 cites
Menin-MLL inhibitors increase JUND activity in MLL-rearranged leukemic cells, contributing to tumor growth and therapy resistance.
- Open access
Venetoclax-controlled DROP-CAR T cells effectively regulate tumor targeting and reduce off-tumor toxicity through dose-dependent cell-cell interaction modulation.
- Open access
- 2 cites
Monovalent degraders can recruit two E3 ligases simultaneously to degrade SMARCA2/4, with tunable dependency on DCAF16 or FBXO22.
- Open access
- 2 cites
MutationProjector, a cancer genotype foundation model, accurately predicts therapeutic resistance and sensitivity across multiple cancer types, surpassing existing methods in all tested contexts.
- Open access
TRI-611 is the first clinical-stage molecular glue degrader targeting ALK fusion proteins, achieving tumor regression in ALK-positive NSCLC models.
Small molecule V20 inhibits SAL phosphatase activity, increasing PAP levels and stress tolerance in Arabidopsis thaliana with 3-fold greater potency than existing inhibitors.
- Open access
- 2 cites
Degrading NSD2 with a targeted ligand degrader reverses oncogenic chromatin changes and improves survival in t(4;14) multiple myeloma models.
Bitopic kinase inhibitors designed with optimized parameters can surpass existing drugs like ponatinib in potency and safety, especially against resistant ABL1 mutants.
- Open access
Heterobifunctional protein binders achieve cell-type-specific targeting with subnanomolar potency via FKBP12-dependent enrichment.
- Open access
Off-target drug repurposing offers a promising therapeutic strategy for rare cancers, with evidence supporting its potential in 20-50% of anticancer agents.
- Open access
HUWE1-HAPSTR1-USP7 complex amplifies ubiquitin chains on nuclear proteins, regulating stress-responsive degradation with a key role in neurodevelopmental disorders and cancer.
RAS-pathway activation, through diverse genetic and nongenetic mechanisms, drives resistance to FLT3 and BCL2 inhibitors in AML, with resistance linked to monocytic differentiation.
- Open access
11.3% of randomly modified ligands across six targets improved potency tenfold or more, revealing a surprising baseline for ligand optimization success.
- Open access
BRD9 degradation enhances GBAF chromatin remodeling activity in synovial sarcoma, undermining therapeutic efforts with minimal impact on tumor proliferation.
- Open access
SMARCB1-deficient tumors are highly sensitive to H3K27 demethylase inhibitors, with GSK-J4 suppressing tumor growth in patient-derived models.
Epigenetic plasticity driven by genomic and cytogenetic changes enables therapy resistance and disease progression in multiple myeloma, with nearly 900 patient samples revealing key transitions.
- Open access
Single-molecule genomics (SMG) enables detailed, genome-wide analysis of regulatory mechanisms on individual DNA molecules, revealing complex interactions and heterogeneity.
Novel CRBN molecular glues induce selective VAV1 degradation via a unique non-canonical RT-loop degron, with potency enhanced by conformational restriction strategies.
- Open access
- 4 cites
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