Acute & chronic heart failure are still lacking effective therapeutics
Novel therapies in acute and chronic heart failure.
Pharmacology & Therapeutics 135:1-17, 2012.
Despite past advances in the pharmacological management of heart failure, the prognosis of these patients remains poor, and for many, treatment options remain unsatisfactory. Additionally, the treatments and clinical outcomes of patients with acute decompensated heart failure have not changed substantially over the past few decades. Consequently, there is a critical need for new drugs that can improve clinical outcomes.
Heart failure is an abnormality of the structure or function of the heart. Even in a normal environment, the heart is unable to supply enough oxygen for organ metabolism. Typical symptoms of heart failure include shortness of breath (dyspnea), leg swelling, fatigue, an increase in jugular venous pressure, pulmonary edema, and apical impulse movement. Cardiac anomalies may result from abnormalities in left ventricular systolic or diastolic function, the heart valve, the coronary artery, pericardium, endocardium, and rhythm and conduction. In developing countries, 1-2% of adults have heart failure. Among adults above the age of 70, prevalence is as high as 10%. Despite the improved drug therapy for heart failure, prognosis for patients is not improving, and as a result, neither doctor nor patient is satisfied. Particularly in acute decompensated heart failure patients, clinical treatment has not improved in decades. Therefore, new drug development is the key to a turning point in clinical treatment of patients with heart failure.
The major existing heart failure drugs are Angiotensin-converting enzymes, beta blockers, Mineralo-corticoid/aldosterone receptor antagonists, Angiotensin receptor blockers, Ivabradine, digoxin, and diuretics. In the treatment of acute heart failure, there are also new inotrops such as cardiac myosin enhancers and relaxin in development. For chronic heart failure, new drugs such as renin-angiotensin-aldosterone system inhibitors, ryanodine receptor stabilizers, and SERCA enhancers are currently in development. For heart failure-related pulmonary hypertension and anemia, there remains a lack of effective treatments to improve these related conditions. The drugs currently used in clinical trials can potentially either temporarily relieve symptoms of heart failure, or be used as prevention towards the continued deterioration of acute or chronic heart failure. However, their ability to improve the underlying causes of heart failure still remains unclear. As posted in the latest International Journal, heart failure drug development is still facing a bottleneck.
The AcaMed company’s R&D team discovered, in anti-aging medicine from ancient books of traditional Chinese medicine, that almost all non-hematopoietic cells can promote ribosome synthesis and induce hormone production in dimer hemoglobin. Dimer hemoglobin’s ability to carry oxygen is much higher than the tetramer hemoglobin that exists in the red blood cell. Our product uniquely delivers a dual mechanism for supplying your cells with adequate supplies of ATP energy and oxygen that lead to the restoration cell function. This accomplishment has never been achieved so far worldwide. We have used the internationally recognized research model of heart failure in mice, validated by ultrasound and electrocardiogram of the heart, to confirm that our ingredients can allow mice to fully restore previously injured heart function. This result was categorized as addressing an “unmet need” and recognized as an unprecedented therapeutic drug rather than a preventive drug upon the submission to top international academic journals. Our research has been published in British Journal of Pharmacology in 2013. AcaMed will team up with university hospitals to perform clinical trials further.
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