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UC166

Sigma-Aldrich

Sulfaphenazole

≥98% (HPLC)

Synonym(e):

4-Amino-N-(1-phenyl-1H-pyrazol-5-yl)benzenesulfonamide

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About This Item

Empirische Formel (Hill-System):
C15H14N4O2S
CAS-Nummer:
526-08-9
Molekulargewicht:
314.36
EG-Nummer:
208-384-3
MDL-Nummer:
MFCD00057226
UNSPSC-Code:
12352202
PubChem Substanz-ID:
24724643
NACRES:
NA.77

Assay

≥98% (HPLC)

Form

solid

Farbe

white to light yellow

mp (Schmelzpunkt)

179-183 °C

Lagertemp.

2-8°C

SMILES String

Nc1ccc(cc1)S(=O)(=O)Nc2ccnn2-c3ccccc3

InChI

1S/C15H14N4O2S/c16-12-6-8-14(9-7-12)22(20,21)18-15-10-11-17-19(15)13-4-2-1-3-5-13/h1-11,18H,16H2

InChIKey

QWCJHSGMANYXCW-UHFFFAOYSA-N

Angaben zum Gen

human ... CYP2C18(1562) , CYP2C19(1557) , CYP2C9(1559)

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Biochem./physiol. Wirkung

Antibacterial. Specific inhibitor of CYP2C9. Blocks pro-inflammatory and atherogenic effects of linoleic acid (increase in oxidative stress and activation of AP-1) mediated by CYP2C9. Specific inhibitor of CYP2C9. Blocks pro-inflammatory and atherogenic effects of linoleic acid (increase in oxidative stress and activation of AP-1) mediated by CYP2C9. Inhibits bradykinin-induced tPA release.

Verpackung

Bottomless glass bottle. Contents are inside inserted fused cone.

WGK

WGK 2

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable

Persönliche Schutzausrüstung

Eyeshields, Gloves, type N95 (US)

Analysenzertifikate (COA)

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Mahmood Khan et al.
Antioxidants & redox signaling, 11(4), 725-738 (2008-10-16)
The objective of this study was to establish the cardioprotective effect of sulfaphenazole (SPZ), a selective inhibitor of cytochrome P450 2C9 enzyme, in an in vivo rat model of acute myocardial infarction (MI). MI was induced by 30 min ligation
Chengqun Huang et al.
American journal of physiology. Heart and circulatory physiology, 298(2), H570-H579 (2009-12-17)
Previously, we showed that sulfaphenazole (SUL), an antimicrobial agent that is a potent inhibitor of cytochrome P4502C9, is protective against ischemia-reperfusion (I/R) injury (Ref. 15). The mechanism, however, underlying this cardioprotection, is largely unknown. With evidence that activation of autophagy
Vienna E Brunt et al.
The Journal of physiology, 590(15), 3523-3534 (2012-06-08)
While it is accepted that NO is responsible for ∼60% of the plateau in cutaneous thermal hyperaemia, a large portion of the response remains unknown. We sought to determine whether the remaining ∼40% could be attributed to EDHF-mediated activation of
Yasuhiro Ishihara et al.
European journal of pharmacology, 611(1-3), 64-71 (2009-04-10)
The effects of inhibitors of cytochrome P450 on myocardial regional ischemia-reperfusion injury were examined in rats. Ischemia-reperfusion injury was evoked by ligation of the left anterior descending coronary artery for 1 h, followed by reperfusion for 24 h. Injuries were
Agostino Virdis et al.
The Journal of clinical endocrinology and metabolism, 95(2), 920-927 (2009-12-22)
The aim of this study was to assess whether patients with primary hyperparathyroidism (PHPT) show reduced endothelial function and to determine the mechanisms involved. The impact of parathyroidectomy (PTx) on endothelial function was also assessed. Endothelial dysfunction is reported in
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