Ninlaro (ixazomib)

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

P1/2, N=11, Terminated, University of Michigan Rogel Cancer Center | Active, not recruiting --> Terminated; Lack of accrual

P4, N=141, Terminated, Takeda | Trial completion date: Nov 2026 --> Mar 2026 | Active, not recruiting --> Terminated | Trial primary completion date: Nov 2026 --> Mar 2026; All participants on the study have concluded treatment, core study activities are complete, and the scientific goals of the study have been met.

P1/2, N=300, Active, not recruiting, Karyopharm Therapeutics Inc | Recruiting --> Active, not recruiting

Conclusions 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.

Addition of ixazomib to gemcitabine plus doxorubicin modestly increased radiographic response but did not extend disease control in an all-comer biomarker-unstratified RMC cohort. The integrated correlatives nominate mechanisms and biomarkers to guide future mechanism-directed trials in RMC.

P=N/A, N=482, Completed, Takeda | Active, not recruiting --> Completed

IXZ effectively inhibited LUAD tumor growth and may overcome platinum resistance. These findings warrant further investigation into the clinical role of IXZ alone or in combination with CBP or other chemotherapies in patients with LUAD.

Dual targeting of FLT3/SYK (TAK-659) and the proteasome (Ixazomib) showed strong synergy across genetically defined AML subsets, irrespective of FLT3 mutant status. These findings define a therapeutically targetable axis linking FLT3/SYK/β-catenin signaling to stress adaptation, provide a mechanistic basis for combinatorial targeting in high-risk AML. Trial registration: NCT04079738, Date of registration 03 September 2019.

P2, N=21, Terminated, Mayo Clinic | Trial completion date: Jun 2025 --> Jan 2026

P2, N=25, Completed, Institute of Hematology & Blood Diseases Hospital, China | Recruiting --> Completed | N=55 --> 25