"When that drug screen identified meclizine, it was a bit of a surprise for us, because this compound had been in the market for several years and had never been linked to mitochondrial respiration," Gohil said. "It's a known drug, and was known to target a few of the molecules within the cell."
But unlike other classes of antihistamine, he noted, meclizine has a unique property which allows it to be used for the treatment of nausea and motion sickness, while most other antihistamines cannot.
"So there was this unique thing about this particular antihistamine," Gohil noted. "And it is well-tolerated so the toxicological profile is very acceptable, so it doesn't have to be sold under strict regulations."
"With that kind of profile, when we saw it in our drug screen we got excited about it because we could see that it decreases cellular oxygen consumption or respiration," he said. "We started trying to figure out the mechanism and to see if it could have any clinical benefit and application."
Gohil said for certain diseases like stroke, heart attack and some neurological diseases, previous medical research has shown that if mitochondrial respiration can be turned down, it could be beneficial for treatment.
"The way many of the cells die during the heart attack or stroke is connected to mitochondrial respiration, so the idea was that if you can turn down the respiration, then it will prevent death," he said. "This is exactly what we found when used meclizine in models of heart attack, stroke and even Huntington disease. We have a drug with a known clinical use and have identified a new biochemical target within the cells, so that opens up new applications."
He said when he and colleagues started studying the mechanism of this drug in terms of how it is
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