Health and Prostate

Naftopidil (Asahi Kasei’s Flivas, Kanebo’s Avishot) is an alphai -adrenergic receptor antagonist that was originally in development by Boehringer Mannheim for antihypertension. Roche acquired Boehringer Mannheim and integrated naftopidil into its development pipeline. Roche subsequently discontinued development for the treatment of hypertension in Germany and Japan because research indicated that the drug was no more effective than already marketed therapies. Asahi Kasei and its development partner, Kanebo (now merged with Nippon Organon), licensed naftopidil, and it was launched in Japan in 1999 for benign prostatic hyperplasia-related dysuria.

Using cloned human alphai -adrenergic-receptor subtypes, naftopidil has been shown to have a threefold and 17-fold higher affinity for the alphaio subtype than for the alphaiA and alphas subtypes, respectively. Furthermore, in addition to blocking the alpha1adrenergic receptor, naftopidil inhibits platelet aggregation and antagonizes the effect of calcium on smooth muscle.

Researchers conducted a study in China to test the clinical efficacy and safety of naftopidil in treating benign prostatic hyperplasia. The 42-day, randomized, double-blind study consisted of two groups of 40 patients receiving either naftopidil (25 mg/day) or tamsulosin (0.2 mg/day). At the end of the study, statistical analysis was conducted for 77 patients. The changes in International Prostate Symptom Scores, Qmax, and QoL measures differed significantly between the two groups before and after treatment (p < 0.05). No significant differences were noted in residual urine and prostate volumes (p > 0.05), and adverse reactions in both groups were mild. In conclusion, naftopidil was found to be safe and effective in treating benign prostatic hyperplasia.

Another comparative study, in Japan, assessed the clinical effects of naftopidil and tamsulosin on symptomatic benign prostatic hyperplasia. In this crossover study, patients whose QoL scores did not improve after four weeks of treatment with naftopidil or tamsulosin were switched to the alternative drug: patients who failed naftopidil treatment (85) were dosed with 0.1-0.2 mg/day of tamsulosin for eight weeks; patients who failed treatment with tamsulosin (89) were dosed with 50-75 mg/day of naftopidil. Patients who switched from naftopidil to tamsulosin experienced significant improvement in symptoms of urgency, weak stream, and straining; patients who switched from tamsulosin to naftopidil demonstrated significant improvement in incomplete emptying, intermittency, and nocturia.