Summary: | Emmanuel Deshayes,1,2 Mathieu Roumiguie,3 Constance Thibault,4 Philippe Beuzeboc,5 Florent Cachin,6 Christophe Hennequin,7 Damien Huglo,8 François Rozet,9 Diana Kassab-Chahmi,10 Xavier Rebillard,11 Nadine Houédé1,12 1Radiobiology Unit, INSERM U1194, Institut du Cancer de Montpellier (ICM), 2Department of Nuclear Medicine, Institut du Cancer de Montpellier (ICM), Montpellier, 3Urology Department, Andrology and Renal Transplantation, CHU Rangueil, Toulouse, 4Medical Oncology Department, Hôpital Européen Georges Pompidou, 5Oncology Department, Institut Curie, 6Department of Nuclear Medicine, CHU, Clermont-Ferrand, 7Radiotherapy Department, Hôpital Saint Louis, Paris, 8Department of Nuclear Medicine, CHRU, Lille, 9Urology Department, Institut Mutualiste Montsouris, 10Intergroupe coopérateur francophone de recherche en onco-urologie, Paris, 11Urology Department, Clinique BeauSoleil, Montpellier, 12Medical Oncology Department, Institut de Cancérologie du Gard – CHU Caremeau, Nîmes, France Abstract: Prostate cancer is the most common malignant disease in men. Several therapeutic agents have been approved during the last 10 years. Among them, radium-223 dichloride (Xofigo®) is a radioactive isotope that induces irreversible DNA double-strand breaks and consequently tumor cell death. Radium-223 dichloride is a calcium-mimetic agent that specifically targets bone lesions. Radium-223 dichloride has been approved for the treatment of metastatic castration-resistant prostate cancer with symptomatic bone metastases, without known visceral metastases. In this review, first we summarize the interplay between prostate tumor cells and bone microenvironment; then, we discuss radium-223 dichloride mechanism of action and present the results of the available clinical trials and future developments for this new drug. Keywords: bone metastasis, mCRPC, mechanism, drug, agents, development
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