Osteoporosis drugs may halt asthma

Drugs used in fighting osteoporosis may have a key role to play in controlling asthma, according to a new report.

Osteoporosis drugs may halt asthma

Drugs used in fighting osteoporosis may have a key role to play in controlling asthma, according to a new report.

Scientists found that the drugs, known as calcilytics, can reverse all symptoms associated with the condition, which affects 300 million people worldwide.

Researchers at Cardiff University, working with others at King’s College, London and the Mayo Clinic in the United States, found that the calcium sensing receptor (CaSR) had a role in causing the disease.

The team used mouse models of asthma and human airway tissue from asthmatic and non-asthmatic people to reach their findings, which were described as “incredibly exciting” by the principal investigator, Professor Daniela Riccardi from Cardiff University School of Biosciences.

“For the first time we have found a link between airways inflammation, which can be caused by environmental triggers – such as allergens, cigarette smoke and car fumes – and airways twitchiness in allergic asthma,” she said.

“Our paper shows how these triggers release chemicals that activate CaSR in airway tissue and drive asthma symptoms like airway twitchiness, inflammation, and narrowing. Using calcilytics, nebulised directly into the lungs, we show that it is possible to deactivate CaSR and prevent all of these symptoms.”

Dr Samantha Walker, director of research and policy at Asthma UK, which helped fund the research, said: “This hugely exciting discovery enables us, for the first time, to tackle the underlying causes of asthma symptoms. Five per cent of people with asthma don’t respond to current treatments so research breakthroughs could be life changing for hundreds of thousands of people.

“If this research proves successful we may be just a few years away from a new treatment for asthma, and we urgently need further investment to take it further through clinical trials. Asthma research is chronically underfunded; there have only been a handful of new treatments developed in the last 50 years so the importance of investment in research like this is absolutely essential.”

While asthma is well controlled in some people, around one in 12 patients respond poorly to current treatments. This significant minority accounts for around 90% of healthcare costs associated with the condition.

Cardiff University professor Paul Kemp, who co-authored the study, said the identification of CaSR in airway tissue means the potential for treatment of other inflammatory lung diseases beyond asthma is immense.

These include chronic obstructive pulmonary disease (COPD) and chronic bronchitis, for which currently there exists no cure. It is predicted that by 2020 these diseases will be the third biggest killers worldwide.

Prof Riccardi and her collaborators are now seeking funding to determine the efficacy of calcilytic drugs in treating asthmas that are especially difficult to treat, particularly steroid-resistant and influenza-exacerbated asthma, and to test these drugs in patients with asthma.

Calcilytics were first developed for the treatment of osteoporosis around 15 years ago with the aim of strengthening deteriorating bone by targeting CaSR to induce the release of an anabolic hormone. Although clinically safe and well tolerated in people, calcilytics proved unsuccessful in treating osteoporosis.

But this latest breakthrough has provided researchers with the unique opportunity to re-purpose these drugs, potentially accelerating the time it takes for them to be approved for use by asthma patients. Once funding has been secured, the group aim to be trialling the drugs on humans within two years.

“If we can prove that calcilytics are safe when administered directly to the lung in people, then in five years we could be in a position to treat patients and potentially stop asthma from happening in the first place,” Prof Riccardi said.

The findings are published in the journal Science Translational Medicine.

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