Phase I trial by the Melman group has now concluded with successful demonstration of the safety of the hMaxi-K gene therapy. The next phase is to administer at a higher dose regime in order to determine the efficacy of the treatment. To date the group has not reported results on this phase.

There are several other gene therapy strategies which will be briefly summarized. The urology department group at the University of Pittsburgh have published a study on treating ED using neurotrophic gene therapy [4]. They used a viral vector derived from the herpes simplex virus(HSV) and reported that in rats, a significant increase in neuronal growth and electrical activity was observed. This might be useful in patients who experience ED due to nerve damage brought on by diabetes. Further studies need to be taken to see if this result holds true in humans. There is also a safety concern with using an HSV viral vector.

Another group at UCLA have investigated the treatment of ED using gene transfer of Nitric Oxide Synthase (NOS) cDNA constructs in the corpora cavernosa to increase NOS concentration. [6]. Cavernosa smooth muscle relaxation is primarily a nitric oxide (NO)-cGMP-mediated response,and NO is synthesized by the neuronal nitric oxide synthase. They managed to show that rats treated with gene therapy using the NOS cDNAs were effective in raising the mean arterial pressure in the corpora cavernosa. Again no studies on humans were planned at this time.

Finally there is the potential of using stem cell therapy to treat ED where the underlying tissue has degenerated or severely compromised,such as that which frequently occurs after a radical prostatectomy. A group from the Deparment of Urology at UCSF have injected embryonic neuronal stem cells into the corpus cavernosa of rats with nerve crush damage and reported improved intracavernosa arterial pressures [5].



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