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ut that effectively altering mitochondrial antioxidant capacity as a monotherapeutic approach to slow key histopathological and molecular drivers of FCAVD remains biologically and therapeutically challenging.Rheumatic heart disease (RHD), the principal long-term sequel of acute rheumatic fever (ARF), has been a major contributor to cardiac-related mortality in general population, especially in developing countries. With improvement in health and sanitation facilities across the globe, there has been almost a 50% reduction in mortality ra