Ninlaro (ixazomib)

P1, N=21, Completed, M.D. Anderson Cancer Center | Active, not recruiting --> Completed | Trial completion date: May 2027 --> Jun 2026 | Trial primary completion date: May 2027 --> Jun 2026

P3, N=386, Completed, Celgene | Active, not recruiting --> Completed | Trial completion date: Apr 2027 --> Apr 2026 | Trial primary completion date: Apr 2027 --> Apr 2026

P1/2, N=53, Recruiting, Columbia University | Trial completion date: Sep 2026 --> Sep 2027 | Trial primary completion date: Sep 2026 --> Sep 2027

Anti-glioma effects with the lowest drug concentrations were achieved for proteasome inhibitors (carfilzomib, bortezomib, ixazomib), and HDAC inhibitors (panobinostat, romidepsin). The impact of their drug targets PSMB5 and HDAC1/2 on the growth of GBM cells was successfully validated by RNAi experiments. We established an aHTS platform for GBM TOs, and identified proteasome and HDAC inhibitors as promising drugs for the treatment of GBMs.

P1, N=24, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Jun 2026 --> Jun 2028 | Trial primary completion date: Jun 2026 --> Jun 2028

This bibliometric analysis highlights the rapidly evolving field of lenalidomide resistance in MM. Future efforts should focus on developing next-generation agents against resistance, designing rational combination therapies targeting key pathways like signal transducer and activator of transcription 3 (STAT3)/ nuclear factor kappa-B (NF-κB), and establishing evidence-based treatment consensus to improve outcomes.

In LSCC, USP28 stabilizes c-MYC, ΔNp63, and SREBP2; in LUAD, USP22 emerges as an integrative node coupling proliferation, EZH2-mediated MHC-I silencing, PD-L1 stabilization, and ferroptosis resistance; and in SCLC, USP1 mediates NK-cell evasion and MAST1-dependent cisplatin resistance, whereas USP13 sustains FASN-dependent cancer stem cell states. Therapeutic strategies are evolving from small-molecule inhibitors (GNE-6776, AZ1, and SJB2-043) to OTUB1-recruiting deubiquitinase-targeting chimeras (DUBTACs), DCAF-based PROTACs, and repurposed agents (rolapitant, ixazomib, and chidamide). Most evidence remains preclinical; substrate redundancy, validated biomarkers, and selectivity challenges must be addressed before DUB-directed strategies can be translated into biomarker-stratified combination therapies.

As a TSC2 inhibitor, AcTor should not be used alone in cancer. When combined with proteasome inhibitors, the pharmacodynamics of AcTor shifts towards the development of a mitochondrial catastrophe in AML, which is durable, broad range, agnostic to TP53 mutations and to the acquisition of resistance to common clinical anti-AML drugs.

Furthermore, both the CD79B/BTK inhibitor Ibrutinib and the STAT3 agonist GCDA potentiated the cytotoxicity of the clinical MM drug Ixazomib. In summary, our findings establish that the APN inhibitor Bestatin induces MM cell differentiation via the CD79B/BTK-STAT3 signaling axis. Targeting this pathway represents a promising strategy to enhance the efficacy of Ixazomib, providing a compelling rationale for novel combination therapies in MM.

P2, N=55, Terminated, University Hospital, Caen | Recruiting --> Terminated; Early termination (regarding the follow-up of the patients). The required sample size was reached, and the primary endpoint was met.

Extra-CNS metastatic meningiomas pose significant diagnostic and therapeutic challenges. High-grade meningiomas are more likely to metastasize; early detection of metastatic spread is challenging. Our findings highlight the need for a multidisciplinary approach with close follow-up, especially in recurrent or high-grade meningiomas with distinct mutations.

P1, N=24, Active, not recruiting, National Cancer Institute (NCI) | Recruiting --> Active, not recruiting