carfilzomib

P2, N=76, Completed, University of Chicago | Active, not recruiting --> Completed | Trial completion date: Dec 2026 --> Mar 2026

P1, N=0, Withdrawn, Roswell Park Cancer Institute | N=21 --> 0 | Not yet recruiting --> Withdrawn

P1/2, N=37, Not yet recruiting, Glaxosmithkline Research & Development Limited

P3, N=614, Active, not recruiting, Janssen Research & Development, LLC | Trial primary completion date: Feb 2026 --> Oct 2025

P1, N=59, Active, not recruiting, Pfizer | Trial primary completion date: Apr 2026 --> Jul 2025

P1/2, N=70, Not yet recruiting, Assistance Publique Hopitaux De Paris

To explore potential therapeutic candidates, we first performed a screening of an FDA-approved drug library using a cPAC cell line, which identified bortezomib-a proteasome inhibitor-as a potential agent...Drug-interaction analysis showed reproducible synergy between carfilzomib and carboplatin in HDC and LuBi, whereas combinations with vinorelbine were mainly additive or antagonistic effects...In particular, the combination of carfilzomib and carboplatin may represent a promising therapeutic strategy. Further in vivo and clinical investigations are warranted to evaluate therapeutic efficacy, safety, and pharmacokinetics of proteasome inhibitors in cPAC.

Treatment with the KXD regimen (carfilzomib, cyclophosphamide, dexamethasone) resulted in transient disease stabilization for approximately two months, followed by further progression. In addition, infiltration of CD138-positive plasma cell-like tumor cells with λ light chain restriction was observed in the gastric lamina propria, consistent with extramedullary disease (EMD). The final diagnosis was relapsed MM complicated by sPCL, gastric mucosal extramedullary plasmacytic infiltration, and synchronous moderately differentiated intramucosal papillary adenocarcinoma.

P1/2, N=246, Recruiting, BeOne Medicines | Active, not recruiting --> Recruiting

P1, N=15, Recruiting, City of Hope Medical Center | Trial completion date: Mar 2026 --> Nov 2026 | Trial primary completion date: Mar 2026 --> Nov 2026

Our findings highlight ABCB1 promoter hypomethylation as a potential epigenetic driver of CFZ resistance in MM. These results underscore the clinical relevance of epigenetic regulation in drug resistance and the potential of targeting DNA methylation as a therapeutic strategy to overcome resistance in MM.

In vivo experiments confirmed that WYC-209 potentiated the antitumor efficacy of CFZ by upregulating ZMYND8, thereby ameliorating tumor burden in NSG mice. These findings establish that targeting ZMYND8 with the novel retinoid WYC-209 potently enhances the efficacy of CFZ and holds translational promise for improving clinical outcomes in patients with MM.