This study aimed to radiolabel finasteride, a novel 5α-reductase inhibitor, to evaluate its cancer targeting potential in experimental model of prostate carcinogenesis. Finasteride was effectively radiolabeled with Tc and showed>90% labeling efficiency. The radiopharmaceutical was found to be stable up to 6 hours in rat serum at 37°C. The blood kinetics of the Tc-finasteride followed a biphasic release pattern, whereby fast-release phase was observed at 15 seconds and a slow-release phase was observed after 30 minutes of administration. The plasma protein binding of the radio complex observed was 83.89%. For biodistribution studies, the rats were divided into two groups. Group I served as normal controls, while group II was subjected to carcinogen N-methyl-N-nitrosourea (MNU) and hormone testosterone propionate (T) for induction of prostate carcinogenesis, which was confirmed histopathologically. The biodistribution studies on control and carcinogen-treated rats revealed a significant percent-specific uptake in prostate, which was found to be increased significantly as a function of time. The most significant finding of the study was an increase in the percent-specific uptake in prostate of carcinogen-treated animals when compared to the percent-specific uptake in prostate of normal rats after 2 and 4 hours postinjection. The study concludes thatTc-finasteride possesses selectively toward prostate cancer tissue and can be explored further for its role in detection of prostate cancer.

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Prostate cancer is the noncutaneous malignancy of the prostate gland in elderly men. Steroid 5α-reductase (5AR) enzyme dictates the cellular availability of dihydrotestosterone to prostatic epithelial cells and consequently modulates its growth. Excessive production of DHT has been implicated in the pathogenesis of Prostate cancer. Finasteride and Dutasteride, clinically available 5AR inhibitors may play an important role in the prevention and treatment of prostate cancer by blocking peripheral conversion of T into DHT. This article gives a brief account of biology of prostate, rationale and efficacy of 5AR inhibitors in prostate cancer management and their associated controversies.