Columbia University Medical Centre researchers found that low doses of the drug stopped sperm production with no apparent side effects.
And crucial for a contraceptive, normal fertility was restored soon after the drug’s administration was stopped.
Tests of low doses of a compound that interferes with retinoic acid receptors (RARs) showed that it caused sterility in male mice. Scientists have known for almost 100 years that depriving an animal of dietary vitamin A causes male sterility.
Senior study author Debra J. Wolgemuth, professor of genetics, obstetrics and gynaecology, while investigating male infertility, ran across a paper by Bristol-Myers Squibb on a compound that was being tested for the treatment of skin and inflammatory diseases.
The compound seemed to cause changes in the test similar to the mutation that she and Sanny S. W. Chung were probing in Wolgemuth’s lab. Chung is an associate research scientist at Columbia University, according to a Columbia statement.
The company Bristol-Myers dropped its interest when it found that the compound also was in the company’s words – "a testicular toxin".
"We were intrigued," said Wolgemuth. "One company’s toxin may be another person’s
contraceptive." Accordingly, they wanted to investigate whether the compound prevented conception at even lower levels than those cited in the company’s study.
Wolgemuth and her team placed the treated male mice with females and found that reversible male sterility occurred with doses as low as 1.0 mg per kg of body weight for a four-week dosing period.
"We have seen no side effects, so far, and our mice have been mating quite happily," said Wolgemuth.