Myocardial Infarction Research

Myocardial infarction (MI) - more commonly referred to as a heart attack - is an acute event caused by the interruption of blood supply to regions of the heart, leading to myocardial necrosis. Infarction of a substantial area of the myocardium can disrupt normal conductance of the heart, leading to cardiac arrest.In the majority of cases, an MI is immediately preceded by the presence of an occlusive thrombus within a coronary artery, blocking blood flow to the downstream tissue. The most common cause of an occlusive thrombus within a coronary artery is the rupture of an atherosclerotic plaque. However, the occlusion of a coronary artery may also result from coronary embolism. This can occur in patients following stent placement, angioplasty, and coronary artery bypass grafting.

Myocardial Infarction Research Products Targets

Products for Myocardial Infarction Research - Page 20

Cat.No. Product Name Information/Activity
BCC6847 TRIM 25371-96-4
BCC7161 2-Chloro-N6-cyclopentyladenosine Potent, selective A<sub>1</sub> agonist
BCC7160 N6-Cyclopentyladenosine N6-Cyclopentyladenosine (CPA) is a selective Adenosine A1 receptor agonist, with Ki values of 2.3 nM, 790 nM and 43 nM for human A1, A2A and A3 receptors, respectively.
BCC7716 (±)-5'-Chloro-5'-deoxy-ENBA Highly selective A<sub>1</sub> agonist
BCC7215 GR 79236 GR79236 is a highly potent and selective adenosine A1 receptor agonist (Ki = 3.1 nM) that has analgesic and anti-inflammatory actions in humans and animals.
BCC7311 2'-MeCCPA 205171-12-6
BCC7374 SDZ WAG 994 130714-47-5
BCC6664 1,3-Dipropyl-8-phenylxanthine 85872-53-3
BCC6649 DPCPX 102146-07-6
BCC6124 KW 3902 Rolofylline (KW-3902) is a potent, selective adenosine A1 receptor antagonist that is under development for the treatment of patients with acute congestive heart failure and renal impairment. Rolofylline is metabolized primarily to the pharmacologically active M1-trans and M1-cis metabolites by cytochrome P450 (CYP450). Rolofylline is alleviating the presynaptic dysfunction and restores neuronal activity as well as dendritic spine levels in vitro, is an interesting candidate to combat the hypometabolism and neuronal dysfunction associated with Tau-induced neurodegenerative diseases.