1933460-23-1
Chemical Structure
AZM198
- CAS No.: 1933460-23-1
- Formula:C14H13ClN4OS
- Molecular Weight:320.80
InChIKey: MFCVOLWLNXXQFY-UHFFFAOYSA-N
SMILES: O=C1NC(N(CC2=CC=C(C=C2CN)Cl)C3=C1NC=C3)=S
Biological Activity:
AZM198 is an orally active myeloperoxidase (MPO) inhibitor. AZM198 irreversibly inactivates MPO (IC50=0.015 μM) via covalent binding to the heme prosthetic group, preferentially targets extracellular MPO activity, and reduces neutrophil extracellular trap formation, reactive oxygen species production and degranulation. AZM198 increases the fibrous cap thickness of atherosclerotic plaques, reduces lesion area, ameliorates hepatic steatosis and fibrosis in non-alcoholic steatohepatitis, and alleviates proteinuria and inflammatory infiltration associated with glomerulonephritis. AZM198 also decreases circulating levels of high-sensitivity Cardiac Troponin I and IL-1β, and mitigates endothelial cell injury. Therefore, AZM198 is suitable for research on various MPO-related diseases, including atherosclerotic cardiovascular disease, myocardial infarction, ischemic stroke, non-alcoholic steatohepatitis and crescentic glomerulonephritis[1][2][3][4].
| Cat. No. | Product Name | Purity | Description | Pricing | |||||||||||||||||||
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AZM198 | 98.40% | AZM198 is an orally active myeloperoxidase (MPO) inhibitor. AZM198 irreversibly inactivates MPO (IC50=0.015 μM) via covalent binding to the heme prosthetic group, preferentially targets extracellular MPO activity, and reduces neutrophil extracellular trap formation, reactive oxygen species production and degranulation. AZM198 increases the fibrous cap thickness of atherosclerotic plaques, reduces lesion area, ameliorates hepatic steatosis and fibrosis in non-alcoholic steatohepatitis, and alleviates proteinuria and inflammatory infiltration associated with glomerulonephritis. AZM198 also decreases circulating levels of high-sensitivity Cardiac Troponin I and IL-1β, and mitigates endothelial cell injury. Therefore, AZM198 is suitable for research on various MPO-related diseases, including atherosclerotic cardiovascular disease, myocardial infarction, ischemic stroke, non-alcoholic steatohepatitis and crescentic glomerulonephritis. |
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- [1]. Antonelou M, et al. Therapeutic Myeloperoxidase Inhibition Attenuates Neutrophil Activation, ANCA-Mediated Endothelial Damage, and Crescentic GN. J Am Soc Nephrol. 2020;31(2):350-364. [Content Brief]
- [2]. Florez-Barros F, et al. Myeloid expression of the anti-apoptotic protein Mcl1 is required in anti-myeloperoxidase vasculitis but myeloperoxidase inhibition is not protective. Kidney Int. 2023;103(1):134-143. [Content Brief]
- [3]. Shamsuzzaman S, et al. Novel Mouse Model of Myocardial Infarction, Plaque Rupture, and Stroke Shows Improved Survival With Myeloperoxidase Inhibition. Circulation. 2024;150(9):687-705. [Content Brief]
- [4]. Rashid I, et al. Myeloperoxidase is a potential molecular imaging and therapeutic target for the identification and stabilization of high-risk atherosclerotic plaque. Eur Heart J. 2018;39(35):3301-3310. [Content Brief]
Keywords