Treatment of MM cells with the selective AURKA inhibitor LY3295668 induced dose-dependent cytotoxicity, caspase-3/7 activation, and cellular senescence. These findings underscore AURKA expression as a prognostic marker in plasma cell disorders and support the therapeutic potential of combining AURKA inhibition with selinexor for bortezomib-resistant MM and PCL. To explore biomarker-driven strategies for optimizing therapeutic outcomes, future studies are warranted.

A phase II is currently exploring this combination in leiomyosarcoma and malignant peripheral nerve sheath tumors. Trial registration: NCT04595994.

P2, N=129, Active, not recruiting, Canadian Cancer Trials Group | Trial primary completion date: Dec 2025 --> Mar 2026

P=N/A, N=75, Active, not recruiting, iOMEDICO AG | Recruiting --> Active, not recruiting

P=N/A, N=114, Completed, University Health Network, Toronto | Active, not recruiting --> Completed

The XPO1 inhibitor KPT-330 exerts anti-cancer effects through stabilizing p53 and inhibiting the PI3K-AKT pathway, providing a molecular basis for DLBCL treatment. We may provide a potential promising combination therapy for the treatment of DLBCL with p53 mutations.

P1/2, N=56, Terminated, Antengene Corporation | Active, not recruiting --> Terminated; Based on the adjustment of clinical research and development strategy，sponsor decided to terminate the study

Inhibition of XPO1 with selective inhibitors of nuclear export (SINE) compounds, including selinexor, has demonstrated the ability to restore nuclear localization and function of these proteins, thereby enhancing cellular sensitivity to DNA-damaging agents, kinase inhibitors, and immunotherapies. In preclinical NSCLC models, XPO1 inhibition has shown efficacy both as monotherapy and in combination strategies, with particular promise in KRAS- and EGFR-driven tumors. This review explores the role of XPO1 in NSCLC biology and therapy resistance, the rationale for targeting nuclear export, and the current landscape of XPO1-directed clinical development in lung cancer.

Selinexor and azacitidine offer a promising strategy to overcome therapeutic resistance and improve outcomes in TET2/RHOA-mutated PTCL, supporting further clinical evaluation.

P2, N=70, Active, not recruiting, National Cancer Institute (NCI) | Recruiting --> Active, not recruiting

P1, N=22, Active, not recruiting, Mayo Clinic | Trial completion date: Aug 2027 --> Jun 2026

CRM1 inhibition by Selinexor re-establishes nuclear PHD2 residency, increases the degradation of HIF-1α in hypoxia, abrogates P-gp-mediated lysosomal anthracycline trapping, and confers potent in-vitro and in-vivo chemosensitization. These data provide mechanistic rationale for integrating Selinexor into salvage regimens for R/R-AML.