bicalutamide

P1/2, N=146, Recruiting, I.F.O. Istituti Fisioterapici Ospitalieri | Not yet recruiting --> Recruiting

A 53-year-old man with metastatic, castration-sensitive prostate cancer (cT3bN1M1b, PSA 9.39 ng/mL, Gleason 4 + 5) underwent androgen deprivation therapy using bicalutamide and leuprorelin. After 73 cycles, chemotherapy was discontinued, and the patient has remained in remission during follow-up. This case highlights the potential efficacy of carboplatin and paclitaxel in treating poorly differentiated CRPC, suggesting the need for further investigation into platinum-based regimens for aggressive prostate cancer variants.

The patient was started on androgen deprivation therapy with goserelin (10.8 mg every 3 months) and bicalutamide (50 mg once daily), and stable disease was achieved for 66 months...Bicalutamide was replaced by enzalutamide (160 mg once daily) in the treatment regimen. Subsequently, based on the identification of CDK12 mutations by genetic testing, treatment with the poly(ADP-ribose) polymerase (PARP) inhibitor olaparib (300 mg twice daily) was initiated. To date, the patient has remained clinically stable with low PSA levels. This case highlights the potential utility of molecular profiling and combined PARP inhibition and androgen receptor-targeting therapy in CDK12-mutated metastatic castration-resistant PCa with rare penile metastasis.

P2, N=23, Not yet recruiting, Martin T. King, MD, PhD

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