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Endonovo Reports Pre-Clinical Data Demonstrating Immunotronics™ Reduced Infarct Size and Inhibited Fibrosis following Myocardial Infarction
Endonovo Reports Pre-Clinical Data Demonstrating Immunotronics™ Reduced Infarct Size and Inhibited Fibrosis following Myocardial Infarction.
About this update from Endonovo Therapeutics, Inc.
[{"type":"text","content":"\n\n LOS ANGELES, Feb. 01, 2018 (GLOBE NEWSWIRE) -- Endonovo Therapeutics, Inc. (OTCQB: ENDV) (\"Endonovo\" or the \"Company\"), a commercial-stage developer of non-invasive wearable Electroceutical™ devices, today announced positive results from a study of post-myocardial infarction remodeling in mice.\n In the study, animals treated with the Company's non-invasive medical device one or two times per day for 28 days had significantly smaller (by 36.4%, p<0.01) infarcts versus the controls. Furthermore, animals treated with Pulsed Electromagnetic Fields (PEMF) one or two times per day for 28 days demonstrated significantly less cardiac fibrosis than the controls. Blood levels of Brain Natriuretic Peptide (BNP), a hormone secreted by cardiomyocytes in the heart in response to volume expansion and pressure overload, were significantly higher in animals treated two times per day with PEMF versus the controls. Natriuretic peptides have been shown to be Cardioprotective, anti-fibrotic and paracrine regulators of vascular regeneration. The Company is currently conducting a follow-up study to elucidate a possible mechanism of action of PEMF treatment. Specifically, the Company is examining if PEMF treatment promotes cardiomyocyte survival and wound repair (angiogenesis), and inhibits excessive inflammation in the infarcted heart. The Company had previously announced initial pre-clinical data demonstrating Immunotronics™ significantly improved cardiac function, including ejection fraction and fractional shortening, and reduced ventricular remodeling in infarcted animals following myocardial infarction. Left ventricular (LV) remodeling after myocardial infarction (MI) includes infarct expansion and hypertrophy of the non-infarcted myocardium, fibrosis, LV chamber dilatation, LV functional deterioration and progression to heart failure. Treatments targeting the remodeling process, such as beta-blockers and angiotensin converting enzyme inhibitors have been shown to improve LV function as well as long term survival. However, a slow progression to chronic heart failure continues with large transmural MI as the loss of infarcted tissue and volume overload (chamber dilation) is often out of proportion to the hypertrophic response. Therefore, new treatments that can further improve the remodeling process are critical for prevent...