fluphenazine

P=N/A, N=168, Completed, University of Liverpool | Recruiting --> Completed | N=125 --> 168 | Trial completion date: Jun 2026 --> Nov 2025 | Trial primary completion date: Jun 2026 --> Nov 2025

P=N/A, N=125, Recruiting, University of Liverpool | Trial primary completion date: Dec 2025 --> Jun 2026

The TNBC prognostic signature comprising four interferon genes (STXBP1, LAMP3, CD276, and POLR2F) was identified, with their expression significantly correlated with the infiltration abundance of multiple immune cells and the drug sensitivity of 30 diverse drugs (ARQ-680, Fluphenazine, and Chelerythrine, etc.). In the prognostic signature and the ceRNA axes, STXBP1, RBPMS-AS1, and FAM198B-AS1 were first reported as potential biomarkers of TNBC. These findings have the potential to provide new insights into the mechanisms driving TNBC tumorigenesis and development.

P=N/A, N=125, Recruiting, University of Liverpool | Trial primary completion date: Jul 2025 --> Dec 2025 | Trial completion date: Aug 2025 --> Jun 2026

The feature gene TGFB2 could inhibit the efficacy of drugs such as XAV-939, Staurosporine, and Dasatinib, but promote the efficacy of drugs such as CUDC-305 and by-product of CUDC-305. Similarly, RBL1 could inhibit the drug action of Fluphenazine and Imiquimod but promote that of Irofulven. A CRC risk prognostic signature was developed on basis of TGF-β-related genes, which provides a reference for risk and further therapeutic selection of CRC patients.

These findings suggest that fluphenazine has the potential to be used as an anti-breast cancer drug by inducing cuproptosis. Therefore, this research provides an insight for the development of novel cuproptosis-dependent anti-cancer agents.

The research emphasizes the significance of SUSD3 as a potential marker for BC, providing insights into the underlying molecular mechanisms implicated in tumorigenesis. SUSD3 holds promise in helping the classification of breast cancer pathological groups, predicting prognosis, and facilitating targeted therapy.

These findings provide a foundation for the potential clinical application of CNS drugs in GBM treatment. Additionally, this work offers critical insights into the mechanisms and determinants of cytotoxicity for drugs currently undergoing clinical trials as repurposing agents for various cancers, including Fluoxetine, Sertraline, Thioridazine, Chlorpromazine, and Fluphenazine.

P=N/A, N=125, Recruiting, University of Liverpool

KLF14 acts as a tumor suppressor which inhibits the proliferation of HCC cells by modulating cellular iron metabolism via the repression of IRP2. We identified Fluphenazine, as an activator of KLF14, could be a potential compound for HCC therapy. Our findings therefore provide an innovative insight into the pathogenesis of HCC and a promising therapeutic target.

Some studies also refer this drug causes DNA alterations and interferes with cell invasion and migration ability as well as with ROS generation. Collectively, these results imply that fluphenazine may be a favorable compound for further research in oncologic therapy.

We demonstrated the combinations of doxorubicin (DOX) + artesunate, DOX + chloroquine, paclitaxel (PTX) + fluoxetine, PTX + fluphenazine, and PTX + benztropine induce significant cytotoxicity in Michigan Cancer Foundation-7 (MCF-7) breast cancer cells. Furthermore, it was found that 5-FU + thioridazine and 5-fluorouracil (5-FU) + sertraline can synergistically induce a reduction in the viability of human colorectal adenocarcinoma cell line (HT-29)...Furthermore, it is also demonstrated that PPT1 may have an important role in the mechanism of action of these combinations, as demonstrated by their ability to decrease PPT1 expression. These results support the use of antimalarial and central nervous system (CNS) drugs in combination regimens with chemotherapeutic agents; nevertheless, additional studies are recommended to further explore their complete mechanisms of action.