Bindarit - CAS 130641-38-2
Catalog number: 130641-38-2
Category: Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
C19H20N2O3
Molecular Weight:
324.37
COA:
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Targets:
Others
Description:
Bindarit treatment inhibits the release of MCP-1 from IL-1 stimulated osteoblast cell line Saos-2.
Purity:
>98%
Synonyms:
AF 2838
MSDS:
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InChIKey:
MTHORRSSURHQPZ-UHFFFAOYSA-N
InChI:
InChI=1S/C19H20N2O3/c1-19(2,18(22)23)24-13-16-15-10-6-7-11-17(15)21(20-16)12-14-8-4-3-5-9-14/h3-11H,12-13H2,1-2H3,(H,22,23)
Canonical SMILES:
CC(C)(C(=O)O)OCC1=NN(C2=CC=CC=C21)CC3=CC=CC=C3
1.Inhibition of protein denaturation by fatty acids, bile salts and other natural substances: a new hypothesis for the mechanism of action of fish oil in rheumatic diseases.
Saso L;Valentini G;Casini ML;Mattei E;Braghiroli L;Mazzanti G;Panzironi C;Grippa E;Silvestrini B Jpn J Pharmacol. 1999 Jan;79(1):89-99.
Natural hydrophobic substances like bile salts (cholate, deoxycholate, chenodeoxycholate, lithocholate and their conjugates with glycine and taurine), fatty acids (caprylic, capric, lauric, myristic, palmitic, stearic, oleic, linoleic, arachidonic, eicosapentaenoic and docosahexaenoic acid) were much more active (EC50 approximately 10(-4)-10(-5) M) than selected amino acids (EC50 > 10(-2) M) and inorganic salts (EC50 approximately 10(-1) M) in inhibiting heat-induced denaturation of human serum albumin in vitro. Fish oil, rich in n-3-polyunsaturated acids such as eicosapentaenoic acid and docosahexaenoic acid, administered p.o. (1 ml/kg) in the rat, protected ex vivo (after 2 hr) serum against heat-induced denaturation more than bendazac, a known antidenaturant drug. Thus, we speculated that the antidenaturant activity of fish oil may be partly (in addition to the known effect on endogenous eicosanoid composition) responsible for its beneficial effects in rheumatoid arthritis and other rheumatic conditions. In this connection, it is of note that the in vitro antidenaturant activity of fish oil fatty acids was higher than that of known antidenaturant drugs such as bendazac and bindarit and nonsteroidal anti-inflammatory drugs like phenylbutazone and indomethacin which could exert beneficial effects in chronic inflammatory conditions by stabilizing endogenous proteins.
2.Bindarit reduces the incidence of acute aortic dissection complicated lung injury via modulating NF-κB pathway.
Wu Z;Chang J;Ren W;Hu Z;Li B;Liu H Exp Ther Med. 2017 Sep;14(3):2613-2618. doi: 10.3892/etm.2017.4830. Epub 2017 Jul 25.
The pathogenesis of acute aortic dissection (AAD) complicated acute lung injury (ALI) is not currently well defined. At present, no effective animal model has been established for AAD complicated ALI, which hinders research and development of an appropriate treatment regimen for the concurrent conditions. The aim of the present study was to evaluate the therapeutic effects of bindarit (Bnd), an indazolic derivative, on the production of monocyte chemoattractant protein (MCP)-1 in angiotensin II (AngII)-induced complicated ALI in rats. An AAD complicated ALI rat model was established using aminopropionitrile (BAPN) and AngII. The pathological features of AAD complicated ALI were assessed via biochemical and histopathological evaluations. AngII-stimulated human pulmonary microvascular endothelial cells (hPMVECs) were used to assess the effects of Bnd on MCP-1 expression. Western blot analysis was performed to analyze the expression of proteins that may be associated with the process. AAD complicated ALI was established following BAPN and AngII interference, and a massive accumulation of macrophages was observed in the lung tissues of the study rats. Bnd was able to significantly attenuate the incidence of AAD complicated ALI (P<0.
3.Advances in the treatment of lupus nephritis.
Zimmerman R;Radhakrishnan J;Valeri A;Appel G Annu Rev Med. 2001;52:63-78.
Systemic lupus erythematosus (SLE) is an autoimmune disease that leads to the formation and deposition of immune complexes throughout the body, which are pathogenic for the disease. Different forms of glomerulonephritis can occur in patients with SLE and can contribute significantly to the associated morbidity and, ultimately, mortality from the disease. Over the past two decades, there have been significant strides in our understanding of the disease and in treatments that attempt to control the formation and deposition of anti-DNA auto-antibodies and immune complexes, as well as the subsequent inflammatory cascade mediated through various cellular and humoral pathways leading to progressive renal damage and end-stage renal disease. In this chapter, we review the current understanding of the pathogenesis and treatment of lupus nephritis in its various stages and discuss the experimental and human data regarding some of the potential newer forms of therapy. We discuss data regarding the use of steroids, azathioprine, cyclophosphamide, cyclosporine A, mycophenolate mofetil, gammaglobulin, plasmapheresis, LJP 394, flaxseed oil, bindarit, anti-CD40 ligand, and CTLA4Ig.
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CAS 130641-38-2 Bindarit

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