Health and Prostate

Benign prostatic hyperplasia is the most common neoplastic disease in men, seen histologically in more than 50% of those over 60 years of age; however, the basic hormonal and cellular processes which lead to its development are still unclear. In the last few decades, there has been a tremendous effort to understand these processes because in some cases, prostatic enlargement can cause bladder outlet obstruction leading to significant voiding dysfunction or even loss of renal function. For a number of years, surgical procedures were the only means available to relieve this obstruction. Although obstruction is but one possible cause of voiding dysfunction, if perhaps we knew why benign prostatic hyperplasia occurred, we may be able to prevent or reverse the process with less invasive medical therapy. Although there has been limited success in this regard, research has led to the development of medical treatments such as 5 a-reductase inhibitors and alpha-adrenergic receptor blockers, both of which are helpful in select patients but are not universally efficacious. What has become clear is that Read more [...]

The possible role of a nonandrogenic factor in the development of benign prostatic hyperplasia has been suggested by the observation that as the testosterone levels decrease in most aging men, the prostate continues to grow in size. Additionally, the exogenous addition of androgens increase the growth of the prostate in vivo but androgens do not act as mitogens to prostatic epithelial cells in culture. When epithelial cells are cultured with stromal cells, however, androgens are able to induce epithelial cell proliferation. Therefore, some other factor (s) must act as the final step in stimulating prostatic growth. Studies involving irradiation of the testicles of beagle dogs found that these animals maintained a normal level of testosterone and estra-diol but sustained a significant decrease in prostatic size and weight, suggesting that a nonandrogenic factor elaborated by the testis is necessary for prostatic growth. Additionally, the exogenous administration of dihydrotestosterone or testosterone to castrated dogs rarely produces significant benign prostatic hyperplasia. On the other hand, if Read more [...]

Overview One approach to reducing lower urinary tract symptoms resulting from benign prostatic hyperplasia is to reduce prostate hyperplasia, which limits the amount of smooth-muscle development and activity associated with dynamic benign prostatic hyperplasia as well as bladder outlet obstruction as a result of static benign prostatic hyperplasia. Development of this type of drug treatment is needed because it would relieve not only urinary symptoms but also the progression of benign prostatic hyperplasia. Nymox Pharmaceuticals is currently researching NX-1207, which has shown ability to reduce prostate size. The company has yet to release details about the exact mechanism of action, but clinical trials have focused on prostate size reduction and symptom relief. Mechanism Of Action Drug development databases suggest that NX-1207 has cytotoxic qualities that contribute to apoptosis within the prostate. However, the specific targets involved in the mechanism of action are unclear. NX-1207 Nymox Pharmaceuticals is currently conducting Phase II clinical trials of its new oral drug, NX-1207, Read more [...]

Overview In benign prostatic hyperplasia, hyperplasia of the prostate gland increases the number of smooth-muscle cells, and smooth-muscle tension causes bladder outlet obstruction leading to lower urinary tract symptoms . Drugs that reduce total prostate volume, either by slowing cell multiplication or inducing cell apoptosis, reduce symptoms of benign prostatic hyperplasia. Emerging therapies, such as hexokinase inhibitors, that can take advantage of this strategy offer a different approach to treatment than drugs that are currently available, and they may avoid associated side effects such as orthostatic hypotention, reverse ejaculation, decreased libido, and impotence. Mechanism Of Action Recent research has shown that hexokinase inhibitors have the ability to disrupt glycolysis. Because prostate cells depend more on glycolysis than the citric acid cycle for energy to maintain and regenerate tissue, hexokinase inhibitors can cause prostate cell death, which relieves bladder outlet obstruction. Reducing prostate size through metabolic targeting is a novel method of treating benign prostatic Read more [...]

AEterna Zentaris recently announced a decision to continue development of cetrorelix, an luteinizing hormone-releasing hormone antagonist, in Japan after making advances in Phase II studies in Germany and completing a broad Phase II program in endometriosis, benign prostatic hyperplasia, and uterine myoma in the United States. This agent is currently the most advanced of the gonadotropin modulators in development for treatment of benign prostatic hyperplasia. AEterna Zentaris's Japanese partners, Shionogi and Nippon Kayaku, planned to begin a Phase Ha clinical trial in 2005. This multicenter, placebo-controlled, randomized study will attempt to extrapolate the results from European studies to the Japanese benign prostatic hyperplasia population. Cetrorelix blocks luteinizing hormone-releasing hormone receptors on the pituitary gland to prevent the release of luteinizing hormone (luteinizing hormone), thereby reducing the production of testosterone. Cetrorelix is different from other agents in the gonadotropin modulator class because of its unique, incomplete suppression of testosterone Read more [...]