スリンダックスルフィド

危険有害性情報のコード(GHS)

• 絵表示(GHS)

  

• 注意喚起語

  Danger

• 危険有害性情報

  H302：飲み込むと有害

  H317：アレルギー性皮膚反応を起こすおそれ

  H334：吸入するとアレルギー、喘息または、呼吸困難 を起こすおそれ

  H361：生殖能または胎児への悪影響のおそれの疑い

• 注意書き

  P201：使用前に取扱説明書を入手すること。

  P280：保護手袋/保護衣/保護眼鏡/保護面を着用するこ と。

  P301+P312：飲み込んだ場合：気分が悪い時は医師に連絡する こと。

  P302+P352：皮膚に付着した場合：多量の水と石鹸で洗うこと。

  P308+P313：暴露または暴露の懸念がある場合：医師の診断/手当てを 受けること。

スリンダックスルフィド 価格

スリンダックスルフィド 化学特性,用途語,生産方法

• 外観

  うすい黄色～褐色粉末～結晶

• 説明

  Sulindac sulfide is an aryl sulfide that is a metabolite of sulindac. A non-steroidal anti-inflammatory drug, which also has anticancer activity. It has a role as a non-steroidal anti-inflammatory drug, an apoptosis inducer and an antineoplastic agent. It is an aryl sulfide, an organofluorine compound and a monocarboxylic acid. It derives from a sulindac.

• 化学的特性

  Yellow Solid

• 使用

  Sulindac sulfide is an active metabolite of Sulindac that inhibits for COX. Sulindac is a non-steroidal anti-inflammatory drug. Inhibits cyclooxygenase, but induces apoptosis by a cyclooxygenase-independent mechanism. Inhibition of Ras activation of Ref-1. Impairs nucleotide exchange on Ras by CDC25 and accelerates Ras hydrolysis of GTP b.

• 応用例（製薬）

  Sulindac Sulfide is the active metabolite of sulindac, a sulfinylindene derivative with anti-inflammatory, analgesic and antipyretic properties. Sulindac is a nonsteroidal anti-inflammatory drug (NSAID) which inhibits cyclooxygenase (COX-1 and-2)-mediated conversion of arachidonic acid to pro-inflammatory prostaglandins. This agent may posulindac sulfideesulindac sulfide chemopreventive activity against colorectal tumors through a mechanism that involves the induction of apoptosis. The sulfide metabolite is excreted in the bile and reabsorbed from the intestine, thereby helping to maintain constant blood levels and reduce gastrointestinal side effects.

• 毒性学

  The NSAID sulindac sulfide (SS) inhibits growth of tumors in azoxymethane-induced rat colon models, suppresulindac sulfidees intestinal polyp formation in APCMin+mice, down-regulatesβ-catenin protein apoptosis, and induces apoptosis under a number of experimental conditions. SULINDAC SULFIDE has been shown to change colorectal cancercell morphology, alter cytoskeletal organization, and cause losulindac sulfide of actin stresulindac sulfidefibers. This is probably due to a dose-dependent reduction of tyrosine phosphorylation of focal adhesion kinase. It has also been demonstrated that SULINDAC SULFIDE reduces cell migration and invasion in mouse models and human colorectal cell line[4]. Many, but not all, studies in healthy and diseased states suggest that renal prostaglandin synthesis and sodium excretion are relatively unaffected by conventional doses of sulindac that inhibit nonrenal cycle-oxygenase. The mechanism responsible for the biochemical selectivity of sulindac is not related to a differential sensitivity of the active metabolite of sulindac, sulindac sulfide, on renal cycle-oxygenase. Appropriate clinical use of all nonsteroidal anti-inflammatory drugs, including sulindac, requires careful consideration of risk factors that predispose to nephrotoxicity and careful monitoring when administered to patients at risk.

スリンダックスルフィド 生産企業

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