Update on treatments for premature ejaculation.

Current and upcoming treatment options for premature ejaculation (PE) are of global clinical interest. In 2008, the International Society for Sexual Medicine published an evidence-based definition for PE. While there are no US Food and Drug Administration-approved therapies for PE, the American Urological Association 2004 guidelines state the serotonergic antidepressants paroxetine, sertraline, fluoxetine and clomipramine and the topical lidocaine-prilocaine cream are effective treatment options. However, there are limitations associated with their use, which may be overcome by PE-specific therapies currently in development. Two agents that are in advanced stages of clinical development include: (i) dapoxetine, an on-demand short-acting selective serotonin reuptake inhibitor, and (ii) PSD502, a metered-dose aerosol containing lidocaine and prilocaine, also for on-demand treatment. Another on-demand agent in development is tramadol, a weak opioid that is currently approved for treating pain. Coupled with efficient diagnosis, it is hoped that these newer agents will improve the quality of life for patients who suffer from PE.

Hellstrom WJ 《-》

Available and future therapies for premature ejaculation.

Hellstrom WJ 《DRUGS OF TODAY》

PSD502 improves ejaculatory latency, control and sexual satisfaction when applied topically 5 min before intercourse in men with premature ejaculation: results of a phase III, multicentre, double-blind, placebo-controlled study.

Dinsmore WW ，Wyllie MG 《-》

The link between penile hypersensitivity and premature ejaculation.

To investigate the correlation between penile hypersensitivity and premature ejaculation (PE), as defined by the criteria identified by the International Society of Sexual Medicine (ISSM). Penile hypersensitivity as a cause of PE is based on historical clinical neurophysiological data and clinical efficacy of the topical desensitizing agent PSD502 in the treatment of PE. PSD502 is a eutectic-like mixture of two local anaesthetics, lidocaine and prilocaine, whose primary action is to reduce neuronal conduction in sensory afferents. Historical neurophysiological data was reviewed, together with data from the recent PSD502 clinical trials, including the first published double-blind clinical trial data evaluating a topical desensitizing agent in a population of men with PE, as per the new ISSM definition. The clinical profile of PSD502, based on its local anaesthetic properties, is used as a surrogate index of the role of sensory afferents in the ejaculatory reflex. The published data does not support unequivocally penile hypersensitivity as the cause of PE. Interpretation of the data is hampered by the variability of the populations described as having PE across studies. Data from the PSD502 clinical trials clearly shows that PSD502 increases ejaculatory latency, and improves control and sexual satisfaction when applied topically to men with PE 5 min before intercourse, enabling subjects to delay ejaculation up to six times longer than those who used a placebo. The clinical profile of PSD502 lends credibility to the penile hypersensitivity hypothesis for PE. The predominant action of local anaesthetics is to reduce neuronal firing in sensory afferents; the clinical profile of PSD502, which shows improvement of ejaculatory function in the absence of a generalized reduction in penile sensitivity, can most readily be explained based on an underlying hypersensitivity in patients with PE.

Wyllie MG ，Hellstrom WJ 《-》

Clinical inquiries. What's the best drug treatment for premature ejaculation?

Mercado MG ，Kimmer SL ，Holman JR ，Wanserski G ，Lo V ... -  《-》