New Drug Eases Asthma Symptoms

Blocks inflammatory activity of two immune system molecules, researchers report

By Ed Edelson
HealthDay Reporter

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THURSDAY, Oct. 18 (HealthDay News) -- A new twist on an old theory of drug treatment for asthma has shown promise in a small, early trial, a California company reports.

The idea is to block the activity of cytokines, immune system molecules believed to play a major role in asthma by causing allergic inflammation.

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A number of cytokines have been implicated in asthma, among them interleukin-4 and interleukin-13. A number of drugs aimed at blocking one or the other have met with little success.

The new approach is a single drug, called pitrakinra, which blocks the receptors for both interleukins simultaneously, said Malinda Longphre, director of the clinical department of Aerovance Inc. in Berkeley.

"It has been shown that IL-4 shares receptors with IL-13," Longphre added. "They produce the same response. Our drug blocks the shared receptors, and it appears from the two clinical trials we report that we are able to intervene and inhibit the allergic response throughout."

Results of the two trials are reported in the Oct. 19 issue of The Lancet. In one trial, 12 people with asthma were given daily injections of pitrakinra and then inhaled allergens. One major measure of lung function, forced expiratory volume, was reduced by only 17.1 percent in those taking the drug, compared to a decrease in lung function of 23.1 percent in a group taking a placebo.

In the second study, 16 people with asthma inhaled pitrakinra. The decrease in lung function when exposed to allergens averaged a mere 4.4 percent, compared to a 15.9 percent decrease in lung function for a comparable group that was given placebo.

"The drug itself is human IL-4, with a couple of amino acid substitutions that allow it to bind to the receptors," Longphre explained. The company hopes to market the drug as an inhalant, but that prospect is years away and will require a long series of successful trials, she added.

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