Why Dutasteride and not Proscar?
There are two papers that Sartor mentions in the abstract which provide the rationale for this approach(2,3). Titus, MA et al(2) concludes: “Expression levels and isozyme activity shifts from S5RII toward S5RI in recurrent prostate cancer. Dual inhibition of S5RI and S5RII should reduce dihydrotestosterone biosynthesis and may prevent or delay growth of recurrent prostate cancer.” In other words, since proscar affects type II and dutasteride affects both I and II 5-alpha reductase inhibitors, then dutasteride is the appropriate drug to use in this study. Stanbrough et al(3) discusses AIPC samples from bone metastases and again finds that the lesions over-express type I, but not type II 5-alpha reductase. The additional fact stated is that many HRPC cancer cells are hypersensitive to androgens and hence inhibition of 5-alpha reductase enzyes along with ketoconazole might affect progression positively. The preliminary Clinical Trial Results Number of patients: 10 (but there is an ongoing
