bicalutamide

The results suggest that latent improved outcome of high-risk BCR patients (mean PSA doubling time 4.4 months) on combined MK-2206+Bic versus Bic alone was attributable to a subgroup identified by crosstalk AR activation secondary to inhibition of AKT. Toxicity may affect tolerance of sustained AKT-AR inhibition.

We provide a thorough examination of the landmark clinical trials with antiandrogen agents, including not only enzalutamide but also other first- and second-generation compounds, and discuss the emerging data on their efficacy. Furthermore, we will explore the critical challenges that hinder their widespread clinical adoption, such as primary and acquired resistance mechanisms, the need for robust predictive biomarkers, and the heterogeneity of AR expression. Finally, we outline future research directions, focusing on novel combination therapies and the development of next-generation agents and predictive tools to optimize patient selection and improve clinical outcomes.

P1/2, N=37, Active, not recruiting, Kari Wisinski | Recruiting --> Active, not recruiting | Trial completion date: Sep 2025 --> Oct 2026 | Trial primary completion date: Sep 2025 --> Oct 2026

P3, N=1313, Completed, SWOG Cancer Research Network | Active, not recruiting --> Completed | Trial completion date: Oct 2027 --> Sep 2025

P=N/A, N=36, Active, not recruiting, Insel Gruppe AG, University Hospital Bern | Recruiting --> Active, not recruiting | Trial completion date: Aug 2027 --> Nov 2027 | Trial primary completion date: Sep 2025 --> Nov 2027

Using the GSE211781 dataset from the Gene Expression Omnibus database, the present study analyzed RNA-sequencing data from lymph node carcinoma of the prostate (LNCaP) cell lines resistant to three antiandrogen drugs: Bicalutamide, enzalutamide and apalutamide. Functional assays in C4-2 and LNCaP cells further indicated that MYH11 modulates sensitivity to bicalutamide and enzalutamide. Collectively, the present study findings suggest that MYH11 may serve as a potential predictive biomarker of PCa development and antiandrogen drug resistance in the future.

P2, N=160, Recruiting, CHU de Quebec-Universite Laval | Trial primary completion date: Jul 2025 --> Sep 2026

P2/3, N=612, Completed, NRG Oncology | Active, not recruiting --> Completed | Trial completion date: May 2026 --> Oct 2025 | Trial primary completion date: May 2026 --> Oct 2025

We report the case of a 38-year-old male with unresectable intra-abdominal DSRCT treated with the VAC-IE regimen (vincristine, doxorubicin, and cyclophosphamide, alternating with ifosfamide and etoposide) as first-line therapy...As second-line therapy, he received gemcitabine and docetaxel...Alternative regimens include temozolomide plus irinotecan or gemcitabine plus doxorubicin. In patients with androgen receptor positivity, hormonal blockade with leuprolide and bicalutamide may be a therapeutic option, particularly in frail patients...DSRCT is a challenging and aggressive malignancy requiring a multidisciplinary and individualized approach. The combination of systemic therapy and local control measures remains critical for improving patient outcomes.

The low-risk group exhibited improved survival outcomes and increased sensitivity to immunotherapy, whereas the high-risk group showed heightened sensitivity to to bexarotene, bicalutamide, embelin, FH535, and pazopanib. Quantitative PCR results indicated that ILF3-DT and PPP1R14B-AS1 were downregulated in CC tissues, whereas RUSC1-AS1 was upregulated. In conclusion, we developed a novel prognostic risk signature based on 9 disulfidptosis-related lncRNAs, which may serve as an independent predictor of immunotherapy response and chemotherapy sensitivity in CC.

P3, N=504, Completed, Alliance Foundation Trials, LLC. | Active, not recruiting --> Completed | Trial completion date: Jan 2026 --> Jun 2025

Flow cytometry evaluated immune infiltration in bicalutamide-treated mice, and anti-PD1 was combined with degarelix/bicalutamide in preclinical mouse model. NHT enhances TLS formation, maturation, and immune cell infiltration, suggesting a synergistic role for androgen deprivation in shaping the tumor immune microenvironment. The improved anti-tumor response with combined anti-PD1 and ADT highlights the potential of immunotherapy-endocrine therapy combinations as a promising treatment strategy for PCa.