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Glafenine (Glafenin) Sale

(Synonyms: 格拉非宁; Glafenin) 目录号 : GC31841

格拉芬宁 (Glafenin) 是一种非甾体抗炎药 (NSAID),是一种非麻醉性镇痛剂,广泛用于治疗各种来源的疼痛。

Glafenine (Glafenin) Chemical Structure

Cas No.:3820-67-5

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100mg
¥446.00
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产品描述

Glafenine is a non-steroidal anti-inflammatory drug (NSAID), is a non-narcotic analgesic agent, widely used for the treatment of pains of various origins.

Chemical Properties

Cas No. 3820-67-5 SDF
别名 格拉非宁; Glafenin
Canonical SMILES O=C(OCC(O)CO)C1=CC=CC=C1NC2=CC=NC3=CC(Cl)=CC=C23
分子式 C19H17ClN2O4 分子量 372.8
溶解度 DMSO: 100 mg/mL (268.24 mM) 储存条件 Store at -20°C
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1 mM 2.6824 mL 13.412 mL 26.824 mL
5 mM 0.5365 mL 2.6824 mL 5.3648 mL
10 mM 0.2682 mL 1.3412 mL 2.6824 mL
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Research Update

Bioactivation of glafenine by human liver microsomes and peroxidases: identification of electrophilic iminoquinone species and GSH conjugates

Glafenine (Privadol; 2,3-dihydroxypropyl 2-[(7-chloro-4-quinolinyl) amino]benzoate) is a non-narcotic analgesic agent widely used for the treatment of pains of various origins. Severe liver toxicity and a high incidence of anaphylaxis were reported in patients treated with glafenine, eventually leading to its withdrawal from the market in most countries. It is proposed that bioactivation of glafenine and subsequent binding of reactive metabolite(s) to critical cellular proteins play a causative role. The study described herein aimed at characterizing pathways of glafenine bioactivation and the metabolic enzymes involved. Two GSH conjugates of glafenine were detected in human liver microsomal incubations using liquid chromatography tandem mass spectrometry. The structures of detected conjugates were determined as GSH adducts of 5-hydroxyglafenine (M3) and 5-hydroxy glafenic acid (M4), respectively. GSH conjugation took place with a strong preference at C6 of the benzene ring of glafenine, ortho to the carbonyl moiety. These findings are consistent with a bioactivation sequence involving initial cytochrome P450-catalyzed 5-hydroxylation of the benzene ring of glafenine, followed by two electron oxidations of M3 and M4 to form corresponding para-quinone imine intermediates that react with GSH to form GSH adducts M1 and M2, respectively. Formation of M1 and M2 was primarily catalyzed by heterologously expressed recombinant CYP3A4 and to a lesser extent, CYP2C19 and CYP2D6. We demonstrated that M3 can also be bioactivated by peroxidases, such as horseradish peroxidase and myeloperoxidase. In summary, these findings have significance in understanding the bioactivation pathways of glafenine and their potential link to mechanisms of toxicity of glafenine.

Glafenine-induced intestinal injury in zebrafish is ameliorated by μ-opioid signaling via enhancement of Atf6-dependent cellular stress responses

Beside their analgesic properties, opiates exert beneficial effects on the intestinal wound healing response. In this study, we investigated the role of μ-opioid receptor (MOR) signaling on the unfolded protein response (UPR) using a novel zebrafish model of NSAID-induced intestinal injury. The NSAID glafenine was administered to zebrafish larvae at 5 days post-fertilization (dpf) for up to 24 hours in the presence or absence of the MOR-specific agonist DALDA. By analysis with histology, transmission electron microscopy and vital dye staining, glafenine-treated zebrafish showed evidence of endoplasmic reticulum and mitochondrial stress, with disrupted intestinal architecture and halted cell stress responses, alongside accumulation of apoptotic intestinal epithelial cells in the lumen. Although the early UPR marker BiP was induced with glafenine-induced injury, downstream atf6 and s-xbp1 expression were paradoxically not increased, explaining the halted cell stress responses. The μ-opioid agonist DALDA protected against glafenine-induced injury through induction of atf6-dependent UPR. Our findings show that DALDA prevents glafenine-induced epithelial damage through induction of effective UPR.

Anaphylaxis to glafenine

[Shock caused by glafenine. Apropos of 7 complications]

Glafenine-induced shock. Seven cases. Glafenine is a widely prescribed analgesic drug, and shock is one of its severe side-effects. We report six documented and one highly probable cases of such accidents. From these seven cases and a review of the literature, we have extracted the clinical characteristics of glafenine-induced shock. Shock usually occurs about 30 minutes on average after taking one single tablet. Previous use of the drug is found in more than 50 per cent of the patients, and it was often followed by a neglected side-effect. A series of cutaneous and respiratory manifestations precedes or accompanies the shock. Two physiopathological mechanisms of glafenine-induced shock have been postulated: either anaphylaxis or idiosyncratic reaction involving the prostaglandins. In vitro tests give highly variable results and therefore are of limited value. Glafenine-induced shock is rare; its incidence, probably underestimated, is about 0.7 in 10(5) treatments. Prevention is essential, cure relies on adrenaline.

Epithelial delamination is protective during pharmaceutical-induced enteropathy

Intestinal epithelial cell (IEC) shedding is a fundamental response to intestinal damage, yet underlying mechanisms and functions have been difficult to define. Here we model chronic intestinal damage in zebrafish larvae using the nonsteroidal antiinflammatory drug (NSAID) Glafenine. Glafenine induced the unfolded protein response (UPR) and inflammatory pathways in IECs, leading to delamination. Glafenine-induced inflammation was augmented by microbial colonization and associated with changes in intestinal and environmental microbiotas. IEC shedding was a UPR-dependent protective response to Glafenine that restricts inflammation and promotes animal survival. Other NSAIDs did not induce IEC delamination; however, Glafenine also displays off-target inhibition of multidrug resistance (MDR) efflux pumps. We found a subset of MDR inhibitors also induced IEC delamination, implicating MDR efflux pumps as cellular targets underlying Glafenine-induced enteropathy. These results implicate IEC delamination as a protective UPR-mediated response to chemical injury, and uncover an essential role for MDR efflux pumps in intestinal homeostasis.