Therapeutic and Diagnostic Application of Epicatechin in the Treatment of Cardiovascular and Inflammatory Disorders
These findings can potentially be used in the treatment of heart failure, acute myocardial infarction, atrial fibrillation, and inflammations in the nervous system such as neurovascular and neurological disorders. In addition, epicatechin can be used to improve the exercise capacity in patients. Lastly, genetic testing can potentially be developed, using biomarkers such as B-type natriuretic peptide, myeloperoxidase, tumor necrosis factor, uric acid, ST2, choline, interleukin-6 or fatty acid proteins, to assess individual response to epicatechin treatment.
UC San Diego researchers have discovered that flavanols, epicatechin in particular, protect the heart from ischemia-mediated injury by the way of reducing infarct size. Epicatechin has also demonstrated the capacity to ameliorate various indicators of tissue damage/inflammation in injured myocardium, as well as to limit the development of late adverse ventricular remodeling. Epicatechin is potentially the first compound to be able to reduce infarct size in the acute as well as chronic stage.
Patent Number: US8648059B2
Application Number: US2010922170A
Inventor: Villarreal, Francisco | Yamazaki, Katrina Go | Taub, Pam Rajendran | Maisel, Alan
Priority Date: 13 Mar 2008
Priority Number: US8648059B2
Application Date: 15 Oct 2010
Publication Date: 11 Feb 2014
IPC Current: A61K003165
US Class: 514152 | 514154
Assignee Applicant: The Regents of the University of California
Title: Use of epicatechin and derivatives and salts thereof for cardiac protection of ischemic myocardium and to ameliorate adverse cardiac remodeling
Usefulness: Use of epicatechin and derivatives and salts thereof for cardiac protection of ischemic myocardium and to ameliorate adverse cardiac remodeling
Summary: The method for reducing infarct size in the heart following or during permanent ischemia or an ischemia/reperfusion event. The method is also used for reducing myocardial infarct size following myocardial infarction; for treating subarachnoid hemorrhage; for treating atrial fibrillation; and for delaying, attenuating or preventing adverse cardiac remodeling; for enhancing or preserving migration, seeding, proliferation, differentiation and/or survival of stem cells in injured heart tissue; for treating induced injury to heart or suffering from disease that results from insufficient growth and/or differentiation of stem cells and/or that compromises engraftment of cells in the heart; for treating or preventing ischemic/reperfusion injury; for inducing proliferation and/or survival of stem cells in a tissue; and for treating organ or tissue ischemia. The permanent ischemia or ischemia/reperfusion event is myocardial infarction, unstable angina, or acute coronary syndrome. The adverse cardiac remodeling comprises hypertrophy, thinning of myocardium, scar formation of myocardium, atrophy of myocardium, and/or heart failure progression. The subject suffers from Kawasaki disease, chronic hypertension, congenital heart disease with intracardiac shunting, congestive heart failure or valvular heart disease. The remodeling stems from coronary artery bypass surgery, cardiac transplant or receipt of a mechanical support device (preferably heart). The disease is ischemic injury, myocardial infarction, muscle ischemia, heart disease, congenital heart failure, and congestive heart failure. The organ or tissue ischemia event is acute/reperfusion event. The organ tissue ischemia event is caused by a condition of myocardial infarction, renal injury, total coronary occlusion, myocardial ischemia, stroke, aortic aneurysm, atrial fibrillation, and medical intervention causing temporary acute ischemia. The organ or tissue ischemia event is caused by coronary artery bypass graft surgery, aneurysm repair, angioplasty, or administering a radiocontrast agent. (all claimed).
生物醫學
醫藥成分
8648059
State Of Development The above-mentioned findings have been validated in the murine model and confirmed in a preliminary human study. Related Materials Taub PR, Ramirez-Sanchez I, Ciaraldi TP, Gonzalez-Basurto S, Coral-Vazquez R, Perkins G, Hogan M, Maisel AS, Henry RR, Ceballos G, Villarreal F. “Perturbations in skeletal muscle sarcomere structure in patients with heart failure and Type 2 diabetes: restorative effects of (-)-epicatechin rich cocoa.” Clin Sci (Lond). 2013 Oct 1;125(8):383-9. doi: 10.1042/CS20130023. Tech ID/UC Case 23365/2008-197-0 Related Cases 2008-197-0
Ramirez-Sanchez I, Nogueira L, Moreno A, Murphy A, Taub P, Perkins G, Ceballos GM, Hogan M, Malek M, Villarreal F. “Stimulatory effects of the flavanol (-)-epicatechin on cardiac angiogenesis: additive effects with exercise.” J Cardiovasc Pharmacol. 2012 Nov; 60(5):429-38. doi: 10.1097/FJC.0b013e318269ae0d.
Yamazaki KG, Taub PR, Barraza-Hidalgo M, Rivas MM, Zambon AC, Ceballos G, Villarreal FJ. “Effects of (-)-epicatechin on myocardial infarct size and left ventricular remodeling after permanent coronary occlusion.” J Am Coll Cardiol. 2010 Jun 22; 55(25):2869-76. doi: 10.1016/j.jacc.2010.01.055.
Yamazaki KG, Romero-Perez D, Barraza-Hidalgo M, Cruz M, Rivas M, Cortez-Gomez B, Ceballos G, Villarreal F. Short- and long-term effects of (-)-epicatechin on myocardial ischemia-reperfusion injury. Am J Physiol Heart Circ Physiol. 2008 Aug; 295(2):H761-7. doi: 10.1152/ajpheart.00413.2008. Epub 2008 Jun 20.
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