mpo-in-3

MPO-IN-3, a powerful inhibitor of myeloperoxidase (MPO), is described as such in example 191 of WO2013068875A1. MPO, a heme-containing enzyme, is classified under the peroxidase superfamily.

2-chloro Palmitic acid is a monochlorinated form of palmitic acid . It is produced in a myeloperoxidase (MPO) and time-dependent manner in neutrophils stimulated by phorbol 12-myristate 13-acetate . 2-chloro Palmitic acid (10 μM) induces neutrophil extracellular trap (NET) formation (NETosis) in human neutrophils, increasing DNA release from neutrophils, colocalization of MPO with extracellular DNA (ecDNA), and trapping of E. coli. It increases COX-2 protein levels in human coronary artery endothelial cells (HCAECs) when used at a concentration of 50 μM and increases production of P-selectin, von Willebrand factor, and angiopoietin-2 in HCAECs, as well as neutrophil and platelet adherence, when used at a concentration of 10 μM. 2-chloro Palmitic acid (10-50 μM) also induces apoptosis in THP-1 cells and primary human monocytes and increases caspase-3 activity in THP-1 cells.

Olsalazine-13C6 is intended for use as an internal standard for the quantification of olsalazine by GC- or LC-MS. Olsalazine (T20615) is an orally bioavailable prodrug form of the anti-inflammatory agent 5-aminosalicylic acid that is cleaved by bacterial azo reductases in the gut to generate active 5-ASA.1

Bivalirudin TFA is a hirudin analog and belongs to the class of specific, reversible direct thrombin inhibitors. Bivalirudin TFA exhibits high selectivity, with Ki values of 2.56 nM and 1.84 nM for α-thrombin and ζ-thrombin, respectively, and shows no significant activity against trypsin or γ-thrombin. Bivalirudin TFA also exhibits antiviral and anti-inflammatory activities. Bivalirudin TFA can be used in research on thrombotic diseases and other conditions.

PMX-53, a macrocyclic complement 5a (C5a) peptidomimetic and C5a receptor antagonist (IC50 = 0.3 µM), effectively inhibits the C5a-induced secretion of myeloperoxidase (MPO) in isolated human polymorphonuclear leukocytes (PMNs). Administered orally at 10 mg/kg, PMX-53 mitigates vascular leakage, PMN infiltration, and the production of TNF-α and IL-6 in a rat peritoneal Arthus reaction model. Additionally, in a 3-nitropropionic acid (3-NP)-induced Huntington's disease rat model, it alleviates body weight loss, anorexia, and striatal degeneration. Furthermore, at a dose of 3 mg/kg, PMX-53 decreases atherosclerotic lesion size and lipid content in ApoE-/- mice.