GE Healthcare Technologies Inc. received U.S. FDA approval for its novel radiotracer, Flyrcado (flurpiridaz F-18), for use in the diagnosis of myocardial ischemia or infarction in patients with known or suspected coronary artery disease.
Ethris GmbH and Heqet Therapeutics srl, a company spun out last year from King’s College London, have entered into a collaboration agreement to harness the potential of non-coding RNA (ncRNA) for heart tissue regeneration following acute myocardial infarction and in heart failure.
The endogenous human protein annexin A1 (ANXA1) is a driver of inflammatory resolution and has shown protective effects in several models of diseases with inflammatory components, including myocardial infarction. Researchers from Resother Pharma A/S and colleagues reported on the preclinical cardioprotective role of RTP-026, a peptide derived from the ANXA1 N-terminal region that acts as N-formyl peptide receptor 2 (FPR2) ligand. In vitro, testing of receptor selectivity and activation in FPR2-HEK-293 cells showed an EC50 value between 10 and 30 nM.
Avertix Medical Inc. signed a definitive merger agreement with Bios Acquisition Corp., a special purpose acquisition company (SPAC), in a deal that will take the company public on the Nasdaq. The deal will establish the combined entity, which will continue under the Avertix name and trade as AVRT, with an estimated enterprise value of $195 million. The transaction is expected to close in the second half of the year.
Shengke Pharmaceuticals (Jiangsu) Ltd. has described proprotein convertase subtilisin/kexin-type 9 (PCSK9) inhibitors reported to be useful for the treatment of atherosclerosis, myocardial infarction, nonalcoholic steatohepatitis, stroke, type 2 diabetes, dyslipidemia, hyperphosphatemia and diabetic nephropathy.
Researchers in Japan may have found a way to repair cardiac damage in patients suffering from chronic heart attack and heart failure by reprogramming cardiac fibroblasts (CFs) to cardiomyocytes (CMs) in a mouse model of chronic myocardial infarction (MI). Published online Dec. 12, 2022, in Circulation, the study showed that by tweaking the expression of a few key genes, researchers could reverse the lasting damage caused by heart attacks.
Recent findings have suggested glycosylated apolipoprotein J (ApoJ-Glyc) levels to be a marker for the diagnosis of myocardial ischemia. Analysis of this marker was performed in a cohort of patients with chest pain suggestive of acute coronary syndrome (ACS) (N=404). ApoJ-Glyc serum levels were analyzed with a novel ELISA assay that targets a specific glycosylated variant of ApoJ (ApoJ-GlycA6). It was found that 291 patients were diagnosed as having a nonischemic event, while 113 were classified as having an ischemic event, 33 as STEMI, 48 as non-STEMI, 27 as unstable angina pectoris and 5 as unclassifiable ACS patients.
Researchers from the International Centre for Genetic Engineering and Biotechnology and colleagues have worked on the systematic identification of cellular proteins that can exert cardioprotective activity after a myocardial infarction (MI).
Angioplasty and stenting have combined to become the standard of care for patients with myocardia that sustained damage due to an infarct, but a new study suggests that some of these patients are no worse off with medical management compared to a trip to the cath lab.
