SCH 79797 dihydrochloride - CAS 1216720-69-2
Category: Inhibitor
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Molecular Formula:
C23H25N5.2HCl
Molecular Weight:
444.41
COA:
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Targets:
Protease-Activated Receptors (PARs)
Description:
SCH 79797 dihydrochloride is a potent and selective non-peptide PAR1 receptor antagonist (IC50 = 70 nM). SCH 79797 blocks haTRAP-induced human platelet aggregation. It also inhibits PAR1 agonist- or thrombin-induced increases in cytosolic Ca2+ in vascular smooth muscle cells.
Brife Description:
PAR1 receptor antagonist
Purity:
≥99% by HPLC
Synonyms:
SCH 79797 dihydrochloride; SCH79797 dihydrochloride; SCH-79797 dihydrochloride; N3-Cyclopropyl-7-[[4-(1-methylethyl)phenyl]methyl]-7H-pyrrolo[3,2-f]quinazoline-1,3-diamine dihydrochloride
MSDS:
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InChIKey:
NNJTXSQXGHYXAJ-UHFFFAOYSA-N
InChI:
InChI=1S/C23H25N5.2ClH/c1-14(2)16-5-3-15(4-6-16)13-28-12-11-18-20(28)10-9-19-21(18)22(24)27-23(26-19)25-17-7-8-17;;/h3-6,9-12,14,17H,7-8,13H2,1-2H3,(H3,24,25,26,27);2*1H
Canonical SMILES:
CC(C)C1=CC=C(C=C1)CN2C=CC3=C2C=CC4=C3C(=NC(=N4)NC5CC5)N.Cl.Cl
1.SCH 79797, a selective PAR1 antagonist, limits myocardial ischemia/reperfusion injury in rat hearts.
Strande JL;Hsu A;Su J;Fu X;Gross GJ;Baker JE Basic Res Cardiol. 2007 Jul;102(4):350-8. Epub 2007 Apr 30.
Myocardial ischemia/reperfusion (I/R) injury is partly mediated by thrombin. In support, the functional inhibition of thrombin has been shown to decrease infarct size after I/R. Several cellular responses to thrombin are mediated by a G-protein coupled protease-activated receptor 1 (PAR1).However, the role of PAR1 in myocardial I/R injury has not been well characterized. Therefore, we hypothesized that PAR1 inhibition will reduce the amount of myocardial I/R injury. After we detected the presence of PAR1 mRNA and protein in the rat heart by RT-PCR and immunoblot analysis,we assessed the potential protective role of SCH 79797, a selective PAR1 antagonist, in two rat models of myocardial I/R injury. SCH 79797 treatment immediately before or during ischemia reduced myocardial necrosis following I/R in the intact rat heart. This response was dose-dependent with the optimal dose being 25 microg/kg IV. Likewise, SCH 79797 treatment before ischemia in the isolated heart model reduced infarct size and increased ventricular recovery following I/R in the isolated heart model with an optimal concentration of 1 microM. This reduction was abolished by a PAR1 selective agonist. SCH 79797-induced resistance to myocardial ischemia was abolished by wortmannin, an inhibitor of PI3 kinase; L-NMA, a NOS inhibitor; and glibenclamide, a nonselective K(ATP) channel blocker.
2.Induction of tumor necrosis factor (TNF) release from subtypes of T cells by agonists of proteinase activated receptors.
Yang H;Li T;Wei J;Zhang H;He S Mediators Inflamm. 2013;2013:165453. doi: 10.1155/2013/165453. Epub 2013 Dec 16.
Serine proteinases have been recognized as playing an important role in inflammation via proteinase activated receptors (PARs). However, little is known about the influence of serine proteinases and PARs on TNF secretion from highly purified T cells. We challenged T cells from human peripheral blood with serine proteinases and agonist peptides of PARs and measured the levels of TNF in culture supernatants by ELISA. The results showed that thrombin and trypsin, but not tryptase, stimulated approximately up to 2.5-fold increase in TNF release from T cells following 16 h incubation. Proteinase inhibitors and PAR-1 antagonist SCH 79797 almost completely abolished thrombin- and trypsin-induced TNF release from T cells. Agonist peptides of PAR-1, but not PAR-2 induced TNF release from T cells. Moreover, trypsin- and thrombin-induced upregulated expression of TNF was observed in CD4+, IL-4+, or CD25+ T cells, but not in IFN+ or IL-17+ T cells. The signaling pathways MAPK/ERK and PI3K/Akt are involved in the thrombin- and trypsin-induced TNF release from T cells. In conclusion, thrombin and trypsin can induce TNF release from IL-4+ and CD25+ T cells through activation of PAR-1 and therefore contribute to regulation of immune response and inflammation of the body.
3.Thrombin-induced expression of endothelial CX3CL1 potentiates monocyte CCL2 production and transendothelial migration.
Popovic M;Laumonnier Y;Burysek L;Syrovets T;Simmet T J Leukoc Biol. 2008 Jul;84(1):215-23. doi: 10.1189/jlb.0907652. Epub 2008 Apr 24.
CX3CL1 (fractalkine, neurotactin) is the sole CX3C chemokine. It induces monocyte locomotion in its cleaved form, but in its membrane-anchored form, it also acts as an adhesion molecule. The expression of CX3CL1 is up-regulated in endothelial cells by proinflammatory cytokines such as IL-1 or TNF-alpha. Here, we studied the effect of the serine protease thrombin on endothelial CX3CL1 induction and its putative relevance for monocyte function. In HUVEC, thrombin triggered a time- and concentration-dependent expression of CX3CL1 at the mRNA and the protein level as shown by RT-PCR, Western immunoblotting, and flow cytometric analysis. Thrombin induced CX3CL1 by activating protease-activated receptor 1 (PAR1) as demonstrated by the use of PAR1-activating peptide and the PAR1-specific antagonist SCH 79797. The thrombin-induced CX3CL1 expression was NF-kappaB-dependent, as shown by EMSA, ELISA, and by inhibition of the NF-kappaB signaling pathway by the IkappaB kinase inhibitor acety-11-keto-beta-boswellic acid or by transient overexpression of a transdominant-negative form of IkappaBalpha. Upon cocultivation of human monocytes with HUVEC, the thrombin-dependent induction of membrane-anchored CX3CL1 in HUVEC triggered monocyte adhesion and an enhanced release of the MCP-1/CCL2 by monocytes and potentiated the monocyte transendothelial migration.
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CAS 1216720-69-2 SCH 79797 dihydrochloride

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