sepantronium bromide (PC-002)

This study presents a novel and effective strategy to induce the abscopal effect through a synergistic combination of targeted drug delivery, radiotherapy, and immunotherapy. The approach offers strong translational potential for improving radioimmunotherapy outcomes in renal and potentially other immunogenic cancers.

However, this was most effective within a specific time window after TIS induction. We suggest that the timely use of senotherapeutics could improve the effectiveness of anticancer drugs in clinical settings.

YM155 enhances imatinib's efficacy against both sensitive and resistant CML cells, overcoming resistance through synergistic inhibition of proliferation, increased apoptosis, and suppression of survivin and BCR::ABL1 expression. These results support further investigation of YM155-Imatinib combination therapy as a potential strategy for resistant CML.

Daporinad, dinaciclib, and sepantronium bromide were predicted as potential drugs for the majority of cancer types. Potential biomarkers had been identified that may predict responses to immunotherapy and improve survival outcomes for cancer patients. This study provided a detailed overview of the functional roles, genetic and epigenetic alterations, and prognostic significance of PRMTs in pan-cancer.

Potency and selectivity of ADT-007 were benchmarked against bortezomib (proteasome inhibitor) and YM155 (survivin inhibitor) using high-content imaging and ATP-based luminescence assays...This study also underscores the translational utility of 3D BEST models for preclinical drug response assessment. Further validation in patient-derived BEST is necessary to evaluate the potential of ADT-007 in clinical settings.

Collectively, these findings identify survivin as a multifaceted oncogenic driver in RCC that integrates cell cycle progression, cytoskeletal organization, and mitochondrial homeostasis. By revealing survivin's dual roles in proliferative and metabolic adaptation, this work highlights survivin as both a prognostic biomarker and a therapeutic vulnerability, supporting future strategies that combine survivin inhibition with metabolic or cell cycle-directed therapies for advanced kidney cancer.

Additionally, our findings revealed that these biomarkers are correlated to chemotherapy drugs, such as vincristine and cyclophosphamide. Furthermore, drug sensitivity analyses identified several candidate drugs, such as dactinomycin, bortezomib, docetaxel, and sepantronium bromide, that may hold therapeutic potential for NB treatment. This study offers novel insights to underlying NB prognosis and therapeutic targets and provides a foundation for developing personalized treatment strategies to improve clinical outcomes.

The prosurvival gene BIRC5 was upregulated in patients with DNMT3A-mutant T-ALL, and these cells were specifically sensitive to the Baculoviral IAP Repeat Containing 5 (BIRC5) inhibitor YM155. Genetic inhibition of BIRC5 in vivo lead to rapid depletion of DNMT3A-mutant T-ALL cells in patient-derived xenografts, positioning BIRC5 as a precision medicine target for these patients.

Initial results showed that omipalisib, verteporfin, CA3, mitoxantrone, navitoclax, venetoclax, and YM155 had significant single-drug activity in either the ALDHlo or both the ALDHlo/ALDHhi cell populations...In vivo, the combination of navitoclax/YM155/carboplatin decreased ovarian cancer metastasis, decreased the percentage of ALDHhi ovarian cancer cells in tumors, and increased survival when compared with carboplatin treatment alone in xenograft models. Our results suggest that the combination of navitoclax/YM155/carboplatin has promise as a therapy for treating ovarian cancer.

The serum starvation-induced ROS-ERK-AP-1 axis is crucial for the up-regulation of TfR1, which contributes to survivin expression and ultimately sustains the viability of NPC cells.

In cancers driven by these proteins, YM155 induces profound cell apoptosis and markedly inhibits tumor growth in xenograft models. Together, these findings demonstrate that YM155 is a broad-spectrum USP inhibitor, and a potential drug candidate for cancers which depend on hyper-active oncogenic proteins that are regulated by the ubiquitin-proteasome pathway.

ADT-007 exhibited high potency and selectivity in KRAS-mutant BOTs, reducing tumor burdens >30% at nanomolar concentrations, and demonstrated superior selectivity over bortezomib and YM155 with minimal cytotoxicity in RAS-WT BOTs...This study also underscores the translational utility of 3D BOT models for preclinical drug response assessment. Further validation in patient-derived BOTs is necessary to evaluate potential of ADT-007 in clinical settings.