Big news in the medical world! Chinese researchers have made a groundbreaking advancement in treating hypertrophic cardiomyopathy (HCM), a heart condition that's been a global challenge since the 1950s.
For almost 40 years, treatments for HCM mainly focused on managing symptoms rather than tackling the root cause. But things are changing! Professor Xie Xiaojie from Zhejiang University shares that young patients, especially adolescents, have faced severe symptoms and a higher risk of sudden cardiac death.
The silver lining? This year, China's State Food and Drug Administration approved Mavaket capsules, the world's first selective cardiac myosin allosteric inhibitor. This innovative drug offers new hope for adults in China battling obstructive HCM (HOCM).
So, how does it work? Mavaket acts similarly to targeted cancer therapies by selectively decreasing the ATPase activity of cardiac myosin heavy chain. This reduces excessive myosin-actin cross-bridge formation, shifts myosin to an energy-conserving state, and ultimately helps the heart relax better and use energy more efficiently.
Professor Xie emphasizes that this approval is a monumental step forward. Mavaketel is now included in several leading clinical guidelines, making it a preferred treatment option for HOCM patients.
With symptoms like shortness of breath, chest pain, and fainting often mimicking other heart conditions, Mavaketel's approval could lead to better diagnosis and treatment, significantly improving the lives of many.
NewspaperAmigo – Your Global News Buddy 
Chinese researchers have made a groundbreaking advancement in treating hypertrophic cardiomyopathy (HCM), a heart condition that's been a global challenge since the 1950s.
Professor Xie Xiaojie from Zhejiang University shares that young patients, especially adolescents, have faced severe symptoms and a higher risk of sudden cardiac death.
This innovative drug offers new hope for adults in China battling obstructive HCM (HOCM).
Mavaket acts similarly to targeted cancer therapies by selectively decreasing the ATPase activity of cardiac myosin heavy chain. This reduces excessive myosin-actin cross-bridge formation, shifts myosin to an energy-conserving state, and ultimately helps the heart relax better and use energy more efficiently.
