bortezomib

P=N/A, N=12, Not yet recruiting, Zhejiang Xiaoshan Hospital; Hainan Dermavon Pharmaceutical Technology Co., Ltd.

P4, N=117, Not yet recruiting, Peking Union Medical College Hospital; Peking Union Medical College Hospital

SRT-1720 induces oxidative stress and apoptosis in leukemic lymphocytes through SIRT1-independent pathway(s). In contrast, it enhances antioxidant defense in normal lymphocytes through a SIRT1-dependent pathway. These findings highlight the potential of SRT-1720 as an adjuvant to chemotherapy in T-ALL, particularly in drug combinations demonstrating strong synergism, which may allow dose reduction and decreased toxicity.

The combination of rosuvastatin and bortezomib exerts a synergistic effect by inhibiting CCL3, thereby rebalancing bone remodeling and promoting osteogenesis. This strategy represents a promising novel therapeutic approach for mitigating MBD.

P3, N=292, Recruiting, Sinocelltech Ltd. | Not yet recruiting --> Recruiting

We then focus on hematological malignancies, especially multiple myeloma, where recent reports implicate the autophagy-related protein GABARAP in bortezomib-induced ICD. Finally, we discuss the translational implications, including rational combinations of autophagy modulators with ICD-inducing chemotherapies, targeted drugs, and cellular immunotherapies, and outline the remaining challenges for safely harnessing the autophagy-ICD axis in the clinical setting.

Factors related to MM may influence systemic cytokine levels in BIPN patients, limiting conclusions on their role in BIPN pathophysiology and their utility as drug targets.

P2, N=52, Active, not recruiting, Massachusetts General Hospital | Trial completion date: Jun 2026 --> Dec 2027 | Trial primary completion date: Dec 2025 --> Dec 2026

P2, N=36, Recruiting, National University Hospital Singapore

P2, N=50, Active, not recruiting, PETHEMA Foundation | Trial completion date: Dec 2025 --> Jun 2026

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.

Serial assessments were performed before and during treatment with bortezomib and dexamethasone for MM, and later with daunorubicin/cytarabine for AML. It demonstrates the earliest events in pDC-AML evolution. Furthermore, the immature immunophenotype raises the question of appropriate treatment, since a diagnosis of acute undifferentiated leukemia can be established.