Sulindac sulfide

그림문자(GHS)

• 그림문자(GHS)

  

• 신호 어

  Danger

• 유해·위험 문구

  H302：삼키면 유해함

  H317：알레르기성 피부 반응을 일으킬 수 있음

  H334：흡입 시 알레르기성 반응, 천식 또는 호흡 곤란 등을 일으킬 수 있음

  H361：태아 또는 생식능력에 손상을 일으킬 것으로 의심됨

• 예방조치문구

  P201：사용 전 취급 설명서를 확보하시오.

  P280：보호장갑/보호의/보안경/안면보호구를 착용하시오.

  P301+P312：삼켜서 불편함을 느끼면 의료기관(의사)의 진찰을 받으시오.

  P302+P352：피부에 묻으면 다량의 물로 씻으시오.

  P308+P313：노출 또는 접촉이 우려되면 의학적인 조치· 조언를 구하시오.

Sulindac sulfide 화학적 특성, 용도, 생산

• 개요

  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.

• 화학적 성질

  Yellow Solid

• 용도

  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.

• Pharmaceutical Applications

  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.

• Toxicology

  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.

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