Newswire (Published: Monday, April 19, 2021, 11:03:00 AM CDT, Received: Monday, April 19, 2021, 11:23:06 AM CDT)

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Men undergoing surgery for prostate cancer may no longer have to live with erectile dysfunction afterward, thanks to an innovative new treatment, researchers said in a paper published Monday by JCI Insight.

The treatment, developed at Albert Einstein College of Medicine in New York City, involves the surgical implantation of a topical drug that regenerates and restores the function of erectile nerves damaged by radical prostatectomy, they said.

When applied to the nerves immediately after injury sustained during surgery, the drug significantly improved erectile function in rats within three to four weeks, according to the researchers.

The treatment still must undergo clinical trials in humans, which means it could be five to seven years before it is available for use, the researchers said.

"What puts people off to getting radical prostatecomy is the associated side effects, including ED," co-author David J. Sharp told UPI in a phone interview.

"What we found is that we can regenerate these nerves," said Sharp, a professor of physiology and biophysics at Einstein.

Radical prostatectomy, or the surgical removal of the prostate gland, is the most commonly used -- and, to date, most effective -- treatment for prostate cancer, according to the American Cancer Society.

Although "nerve-sparing" procedures have been developed, the procedure can still damage the cavernous nerves, which control erectile function by regulating blood flow to the penis, Sharp and his colleagues said.

About 60% of men who have surgery report having having erectile dysfunction 18 months later, and fewer than 30% have erections firm enough for intercourse within five years, according to Johns Hopkins Medicine in Baltimore.

Viagra and similar ED treatments rarely are effective in these men, as the drugs fail to address the root cause -- the damage to the nerves -- Sharp and his colleagues said.

Just over 10 years ago, the Einstein researchers discovered that, following nerve damage, the enzyme fidgetin-like 2 works to stop skin cells that naturally try to heal the damaged nerves in men who have had radical prostatectomy.

They developed a drug called a small interfering RNA molecule that is designed to restrict the production of fidgetin-like 2 in the body.

For this study, they evaluated the drug in gel form using rats with peripheral nerve injury in which the cavernous nerves were either crushed or severed to replicate the nerve damage associated with radical prostatectomy.

The gel was applied to the nerves immediately after injury and found to enhance cavernous nerve regrowth and restore function, according to the researchers.

At three and four weeks post-treatment, the treated rats had significantly better erectile function compared to untreated ones and, after a month, the blood pressure response of the treated animals was comparable to that of normal animals.

In addition, the penile shafts of treated animals had higher levels of the enzyme nitric oxide synthase compared to controls. The enzyme produces the nitric oxide needed to trigger the sequence of events leading to erections.

If the drug is found to be safe and effective in human clinical trials, an implantable wafer containing it could be implanted in the region surrounding the cavernous nerves before, during or after prostate surgery.

Being able to reverse the nerve damage, and potentially restore erectile function, could "encourage" more men to undergo the procedure, which is still the best treatment for the most common cancer among men, Sharp said.

Based on the success in these experiments, the Einstein researchers are currently studying whether these drugs can promote nerve regeneration after spinal cord injuries, they said.

"This treatment would be ideal for younger men undergoing radical prostatectomy, because they would be the most concerned about erectile function," Sharp said.

"There are also a lot of nerve injuries that this could be useful for," he said.

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