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술린다크 구조식 이미지
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술린다크 속성

끓는 점
581.6±50.0 °C(Predicted)
1.2581 (estimate)
저장 조건
Sealed in dry,Store in freezer, under -20°C
Very slightly soluble in water, soluble in methylene chloride, sparingly soluble in ethanol (96 per cent). It dissolves in dilute solutions of alkali hydroxides.
물리적 상태
산도 계수 (pKa)
pKa (25°) 4.7
Soluble in water, methanol, ethanol.
최대 파장(λmax)
327nm(0.05mol/L methanolic HCl)(lit.)
CAS 데이터베이스
38194-50-2(CAS DataBase Reference)
1H-Indene-3-acetic acid, 5-fluoro-2-methyl-1-[[4-(methylsulfinyl)phenyl]methylene]-, (1Z)- (38194-50-2)
  • 위험 및 안전 성명
  • 위험 및 사전주의 사항 (GHS)
위험품 표기 Xn
위험 카페고리 넘버 22-63-42/43
안전지침서 -
유엔번호(UN No.) 3249
WGK 독일 3
RTECS 번호 NK8226000
위험 등급 6.1(b)
포장분류 III
HS 번호 29309090
기존화학 물질 KE-17029
신호 어: Danger
유해·위험 문구:
암호 유해·위험 문구 위험 등급 범주 신호 어 그림 문자 P- 코드
H301 삼키면 유독함 급성 독성 물질 - 경구 구분 3 위험 P264, P270, P301+P310, P321, P330,P405, P501
H317 알레르기성 피부 반응을 일으킬 수 있음 피부 과민성 물질 구분 1 경고 P261, P272, P280, P302+P352,P333+P313, P321, P363, P501
H334 흡입 시 알레르기성 반응, 천식 또는 호흡 곤란 등을 일으킬 수 있음 호흡기 과민성 물질 구분 1 위험 P261, P285, P304+P341, P342+P311,P501
H361 태아 또는 생식능력에 손상을 일으킬 것으로 의심됨 생식독성 물질 구분 2 경고 P201, P202, P281, P308+P313, P405,P501
P201 사용 전 취급 설명서를 확보하시오.
P261 분진·흄·가스·미스트·증기·...·스프레이의 흡입을 피하시오.
P280 보호장갑/보호의/보안경/안면보호구를 착용하시오.
P284 호흡 보호구를 착용하시오.
P301+P310 삼켰다면 즉시 의료기관(의사)의 진찰을 받으시오.
P304+P340 흡입하면 신선한 공기가 있는 곳으로 옮기고 호흡하기 쉬운 자세로 안정을 취하시오.
P342+P311 호흡기 증상이 나타나면 의료기관(의사)의 진찰을 받으시오.
P405 밀봉하여 저장하시오.

술린다크 MSDS


술린다크 C화학적 특성, 용도, 생산


Many non-steroidal anti-inflammatory drugs (NSAIDs) are potent but non-selective inhibitors of both COX-1 and COX-2 in humans. Sulindac is one of the older NSAIDs, an isostere of indomethacin developed before the inducible form of COX-2 was discovered. Although a number of NSAIDs have been found to protect against digestive tract cancers, sulindac has an extensive epidemiology documenting reduced human colorectal cancer. In murine models, sulindac was found not only to inhibit the enzymatic activity of polyp-associated COX-2, but also to downregulate the expression of colonic COX-2 protein to control levels.

화학적 성질

Yellow Crystalline Solid


Imbaral,Sharp and Dohme ,W. Germany,1976


Sulindac is used for relieving weak to moderate pain in rheumatoid arthritis and osteoarthritis.


A non-steroidal anti-inflammatory agent. An anti-inflammatory


Sulindac is a non-steroidal anti-inflammatory drug.


ChEBI: A monocarboxylic acid that is 1-benzylidene-1H-indene which is substituted at positions 2, 3, and 5 by methyl, carboxymethyl, and fluorine respectively, and in which the phenyl group of the benzylidene moiety is substituted at the ara position by a methylsulfinyl group. It is a prodrug for the corresponding sulfide, a non-steroidal anti-inflammatory drug, used particularly in the treatment of acute and chronic inflammatory conditions.


Sulindac (Clinoril) is chemically related to indomethacin and is generally used for the same indications. It is a prodrug that is metabolized to an active sulfide metabolite and an inactive metabolite. The most frequently reported side effects are GI pain, nausea, diarrhea, and constipation. The incidence of these effects is lower than for indomethacin, presumably because sulindac is a prodrug and thus the active metabolite is not highly concentrated at the gastric mucosa. As with indomethacin, a rather high incidence of CNS side effects (dizziness, headache) also occurs.

Manufacturing Process

The following process sequence is described in US Patent 3,654,349:
p-Fluoro-α-Methylcinnamic Acid: 200 grams (1.61 mols) pfluorobenzaldehyde, 3.5 grams (2.42 mols) propionic anhydride and 155 grams (1.61 mols) sodium propionate are mixed in a 1 liter three-necked flask which had been flushed with nitrogen. The flask is heated gradually in an oilbath to 140°C. After 20 hours the flask is cooled to 100°C and the contents are poured into 8 liters of water. The precipitate is dissolved by adding 302 grams potassium hydroxide in 2 liters of water. The aqueous solution is extracted with ether, and the ether extracts washed with potassium hydroxide solution. The combined aqueous layers are filtered, acidified with concentrated HCl, filtered and the collected solid washed with water, thereby producing pfluoro- α-methylcinnamic acid which is used as obtained.p-Fluoro-α-Methylhydrocinnamic Acid: To 177.9 grams (0.987 mol) p-fluoro-α- methylcinnamic acid in 3.6 liters ethanol is added 11.0 grams of 5% Pd/C and the mixture reduced at room temperature under a hydrogen pressure of 40 psi. Uptake is 31/32 pounds (97% of theoretical). After filtering the catalyst, the filtrate is concentrated in vacuo to give the product p-fluoro-α- methylhydrocinnamic acid used without weighing in next step.
6-Fluoro-2-Methylindanone: To 932 grams polyphosphoric acid at 70°C on the steam bath is added 93.2 grams (0.5 mol) p-fluoro-α-methylhydrocinnamic acid slowly with stirring. This temperature is gradually raised to 95°C and the mixture kept at this temperature for 1 hour. The mixture is allowed to cool and added to 2 liters of water. The aqueous layer is extracted with ether, the ether solution washed twice with saturated sodium chloride solution, 5% Na2CO3 solution, water, and then dried. The ether filtrate is concentrated with 200 grams silica-gel, and added to a five pound silica-gel column packed with 5% ether-petroleum ether. The column is eluted with 5 to 10% etherpetroleum ether and followed by TLC to give 6-fluoro-2-methylindanone.
5-Fluoro-2-Methylindene-3-Acetic Acid: A mixture of 18.4 grams (0.112 mol) of 6-fluoro2-methylindanone, 10.5 grams (0.123 mol) cyanacetic acid, 6.6 grams acetic acid and 1.7 grams ammonium acetate in 15.5 ml dry toluene is refluxed with stirring for 21 hours, as the liberated water is collected in a Dean Stark trap. The toluene is concentrated and the residue dissolved in 60 ml of hot ethanol and 14 ml of 2.2 N aqueous potassium hydroxide solution. 22 grams of 85% KOH in 150 ml of water is added and the mixture refluxed for 13 hours under N2. The ethanol is removed under vacuum, 500 ml water added, the aqueous solution washed well with ether and then boiled with charcoal. The aqueous filtrate is acidified to pH 2 with 50% hydrochloric acid, cooled and the precipitate collected in this way dried 5-fluoro-2-methylindenyl- 3-acetic acid (MP 164° to 166°C) is obtained.
5-Fluoro-2-Methyl-1-(p-Methylthiobenzylidene)-3-Indenylacetic Acid: 15 grams (0.072 mol) 5-fluoro-2-methyl-3-indenylacetic acid, 14.0 grams (0.091 mol) p-methylthiobenzaldehyde and 13.0 grams (0.24 mol) sodium methoxide are heated in 200 ml methanol at 60°C under nitrogen with stirring for 6 hours. After cooling the reaction mixture is poured into 750 milliliters of ice-water, acidified with 2.5 N hydrochloric acid and the collected solid triturated with a little ether to produce 5-fluoro-2-methyl-1-(p-methylthiobenzylidene)-3- indenylacetic acid (MP 187° to 188.2°C).
5-Fluoro-2-Methyl-1-(p-Methylsulfinylbenzylidene)-3-Indenylacetic Acid: To a solution of 3.4 grams (0.01 mol) 5-fluoro-2-methyl-1-(pmethylthiobenzylidene)- 3-indenylacetic acid in a 250 ml mixture of methanol and 100 ml acetone is added a solution of 3.8 grams (0.018 mol) of sodium periodate in 50 ml water with stirring.
450 ml water is added after 18 hours and the organic solvents removed under vacuum below 30°C. The precipitated product is filtered, dried and recrystallized from ethyl acetate to give 5-fluoro-2-methyl-1-(pmethylsulfinylbenzylidene)- 3-indenylacetic acid. Upon repeated recrystallization from ethylacetate there is obtained cis-5-fluoro-2-methyl-1- (p-methylsulfinylbenzylidene)-3-indenylacetic acid (MP 184° to 186°C).


Clinoril (Merck).

Therapeutic Function


일반 설명

Sulindac, (Z)-5-fluoro-2-methyl-1-([p-(methylsulfinyl)phenyl]methylene)-1H-indene-3-acetic acid (Clinoril), isan NSAID prodrug that contains a chiral sulfoxide moietybut is marketed as the racemate because it undergoes invivo reduction by the hepatic enzymes into its achiral, activemetabolite, methyl sulfide that exhibits potent andnonselective COX inhibition similar to indomethacin.
The parent sulfoxide has a plasma half-life of 8 hours, andthe active methyl sulfide metabolite is 16.4 hours. The morepolar and inactive sulfoxide is virtually the only form excretedinto the renal tubules, thus sulindac is believed to haveminimal nephrotoxicity associated with indomethacin. Thelong half-life of sulindac is caused by the extensive enterohepaticcirculation and reactivation of the inactive sulfoxideexcreted. Coadministration of aspirin is contraindicated becauseit considerably reduces the sulfide blood levels. Carefulmonitoring of patients with a history of ulcers is recommended.Gastric bleeding, nausea, diarrhea, dizziness, andother adverse effects have been noted with sulindac, but witha lower frequency than with aspirin. Sulindac is recommendedfor RA, OA, and ankylosing spondylitis.

생물학적 활성

Prodrug. Metabolizes to sulindac sulfide, a cyclooxgenase inhibitor that represses ras signaling, and sulindac sulfone, an antitumor agent, following oral administration in vivo . Widely used anti-inflammatory agent.

Biochem/physiol Actions

Nonsteroidal anti-inflammatory; preferential inhibitor of COX-1.


Sulindac is well absorbed on oral administration (90%), reaches peak plasma levels within 2 to 4 hours, and being acidic (pKa = 4.5), is highly bound to serum proteins (93%). The metabolism of sulindac plays a major role in its actions, because all of the pharmacological activity is associated with its major metabolite. Sulindac is, in fact, a pro-drug, the sulfoxide function being reduced to the active sulfide metabolite. Sulindac is absorbed as the sulfoxide, which is not an inhibitor of prostaglandin biosynthesis in the GI tract. Prostaglandins exert a protective effect in the GI tract, and inhibition of their synthesis here leads to many of the GI side effects noted for most NSAIDs. Once sulindac enters the circulatory system, it is reduced to the sulfide, which is an inhibitor of prostaglandin biosynthesis in the joints. Thus, sulindac produces less GI side effects, such as bleeding, ulcerations, and so on, than indomethacin and many other NSAIDs. In addition, the active metabolite has a plasma half-life approximately twice that of the parent compound (~16 hours versus 8 hours), which favorably affects the dosing schedule. In addition to the sulfide metabolite, sulindac is oxidized to the corresponding sulfone, which is inactive. A minor product results from hydroxylation of the benzylidene function and the methyl group at the 2-position. Glucuronides of several metabolites also are found. Sulindac as well as the sulfide and the sulfone metabolites are all highly protein-bound. Despite the fact that the sulfide metabolite is a major activation product and is found in high concentration in human plasma, it is not found in human urine, perhaps because of its high degree of protein binding.

Clinical Use

Sulindac is indicated for long-term use in the treatment of rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, and acute gouty arthritis. The usual maximum dosage is 400 mg/day, with starting doses recommended at 150 mg twice a day. It is recommended that sulindac be administered with food.


Whereas the toxicity of sulindac is lower than that observed for indomethacin and other NSAIDs, the spectrum of adverse reactions is very similar. The most frequent side effects reported are associated with irritation of the GI tract (e.g., nausea, dyspepsia, and diarrhea), although these effects generally are mild. Effects on the CNS (e.g., dizziness and headache) are less common. Dermatological effects are less frequently encountered.

Chemical Synthesis

Sulindac, 5-fluoro-2-methyl-1-[n-(methylsulfinyl)benzyliden]inden-3-acetic acid (3.2.67) is synthesized in a multi-step synthesis from n-fluorobenzaldehyde, which upon condensation with propionic acid anhydride in the presence of sodium acetate gives 4-fluoro-α- methylcinnamic acid (3.2.62). Reduction of the double bond by hydrogene using a palladium on carbon catalyst gives 4-fluoro-α-methyldihydrocinnamic acid (3.2.63). In the presence of polyphosphoric acid, the resulting product undergoes cyclization to 5-fluoro-2-methyl-3- indanone (3.2.64). The resulting ketone undergoes a Knoevenagel reaction with cyanoacetic acid and is further decarboxylated into 5-fluoro-2-methyliden-3-acetic acid (3.2.65). Condensation of the product with n-mercaptobenzaldehyde in the presence of sodium methoxide gives 5-fluoro- 2-methyl-1-(4-methylthiobenzyliden)-3-indenacetic acid (3.2.66), and the sulfur atom is oxidized by sodium periodate into the desired sulfoxide (3.2.67), sulindac [119–122].

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