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F M Giardiello
Cancer metastasis reviews, 13(3-4), 279-283 (1994-12-01)
Sulindac is useful in regression of adenomatous polyps. In addition to orally administered sulindac, rectal preparations also appear to be efficacious [32]. However, further studies are necessary to determine whether regression of adenomas, the precursor of colorectal cancer, will cause
Jigar Pravinchandra Modi et al.
Brain research, 1576, 91-99 (2014-06-27)
The present study analyzed whether administration of sulindac, a non-steroidal anti-inflammatory drug (NSAID) would prevent, attenuate or repair ischemia induced brain injury and reverse functional impairment in a focal ischemia model of stroke. Male Sprague-Dawley rats (weight 250-300 g) were
Stephen P Fink et al.
Carcinogenesis, 36(2), 291-298 (2014-12-17)
Non-steroidal anti-inflammatory drugs prevent colorectal cancer by inhibiting cyclooxygenase (COX) enzymes that synthesize tumor-promoting prostaglandins. 15-hydroxyprostaglandin dehydrogenase (15-PGDH) is a tumor suppressor that degrades tumor-promoting prostaglandins. Murine knockout of 15-PGDH increases susceptibility to azoxymethane-induced colon tumors. It also renders these
The developmental toxicity of indomethacin and sulindac.
A Lione et al.
Reproductive toxicology (Elmsford, N.Y.), 9(1), 7-20 (1995-01-01)
[Sulindac--drug therapy for familial adenomatous polyposis?].
J Zundler et al.
Medizinische Klinik (Munich, Germany : 1983), 88(1), 35-38 (1993-01-15)
W R Waddell
Clinical science (London, England : 1979), 95(3), 385-388 (1998-09-09)
1.Sulindac, cis-5-fluoro-2-methyl-1-(p-methylsulphinylbenzylidene)indene-3-ace tic acid, inhibits growth of colon polyps and cancers. This effect has been attributed to inhibition of prostaglandin synthesis but more recent observations indicate that, in vitro, cells that do not have cyclo-oxygenase nor RNA for synthesis of
R Andrew Moore et al.
The Cochrane database of systematic reviews, (4)(4), CD007540-CD007540 (2009-10-13)
Sulindac is a non-steroidal anti-inflammatory drug (NSAID) licensed for use in rheumatic disease and other musculoskeletal disorders in the UK, and widely available in other countries worldwide. This review sought to evaluate the efficacy and safety of oral sulindac in
Jason L Liggett et al.
Cancer letters, 346(2), 217-224 (2014-02-04)
Non-steroidal anti-inflammatory drugs (NSAIDs) are used extensively for analgesic and antipyretic treatments. In addition, NSAIDs reduce the risk and mortality to several cancers. Their mechanisms in anti-tumorigenesis are not fully understood, but both cyclooxygenase (COX)-dependent and -independent pathways play a
[A case of sulindac induced acute pancreatitis].
M Uchihara et al.
Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology, 89(9), 2073-2076 (1992-09-01)
F Tonelli et al.
Digestive diseases (Basel, Switzerland), 12(5), 259-264 (1994-09-01)
Familial adenomatous polyposis (FAP) is characterized by multiple adenomatous colorectal polyps, some of which progress to adenocarcinoma in the absence of surgery. Colectomy with ileorectal anastomosis still remains much in use, although strict surveillance of the rectal stump is necessary
Arunodoy Sur et al.
Proceedings of the National Academy of Sciences of the United States of America, 111(47), 16754-16759 (2014-11-12)
The retinal pigmented epithelial (RPE) layer is one of the major ocular tissues affected by oxidative stress and is known to play an important role in the etiology of age-related macular degeneration (AMD), the major cause of blinding in the
Yinghua Zhang et al.
International journal of molecular medicine, 35(1), 263-270 (2014-11-12)
Accumulating evidence suggests that anti-inflammatory agents and antioxidants have neuroprotective properties and may be beneficial in the treatment of neurodevelopental disorders, such as autism. In the present study, the possible neuroprotective properties of sulindac, a non-steroidal anti-inflammatory drug (NSAID), were
Brian Leibowitz et al.
Proceedings of the National Academy of Sciences of the United States of America, 111(46), 16520-16525 (2014-11-05)
Colorectal tumorigenesis is driven by genetic alterations in the adenomatous polyposis coli (APC) tumor suppressor pathway and effectively inhibited by nonsteroidal antiinflammatory drugs (NSAIDs). However, how NSAIDs prevent colorectal tumorigenesis has remained obscure. We found that the extrinsic apoptotic pathway
W R Waddell et al.
Journal of surgical oncology, 58(4), 252-256 (1995-04-01)
A putative explanation of the effect of sulindac on adenomatous colon and duodenal polyps from clinical observations and related in vitro experiments is presented. In cells with mutant APC genes, persistent high prostaglandin content of polyps leads to desensitization, downregulation
C Haanen
Current opinion in investigational drugs (London, England : 2000), 2(5), 677-683 (2001-09-25)
It has been repeatedly observed that non-steroidal anti-inflammatory drugs, in particular sulindac and derivatives, may effectively prevent colorectal cancer. It has become apparent that exisulind (sulindac sulfone) induces apoptosis in tumor cells. Cell biological studies provided circumstantial evidence that the
D E Duggan
Drug metabolism reviews, 12(2), 325-337 (1981-01-01)
Sulindac is a prodrug which, following absorption, rapidly attains a metabolic equilibrium with its active pharmacophore, the sulfide metabolite. At the level of the whole body, the reversible interconversion sulindac in equilibrium sulfide, and the differing distributional and excretory properties
L D'Alteroche et al.
Gastroenterologie clinique et biologique, 22(12), 1098-1101 (1999-03-03)
We report the case of a 22-year-old-man having a familial adenomatous polyposis coli treated by total colectomy with ileo-rectal anastomosis. Two years after the operation, an asymptomatic mesenteric fibromatosis appeared which was nonresectable due to mesenteric vessels infiltration. Nine years
N M Davies et al.
Clinical pharmacokinetics, 32(6), 437-459 (1997-06-01)
Sulindac is a nonsteroidal anti-inflammatory drug (NSAID) of the indene acetic acid class. The absorption of sulindac is rapid when given orally. Sulindac is reversibly metabolised to sulindac sulphide which has anti-inflammatory and analgesic properties and is irreversibly metabolised to
Makiko Shimizu et al.
Drug metabolism and pharmacokinetics, 30(1), 70-74 (2015-03-12)
Human flavin-containing monooxygenase 3 (FMO3) in the liver catalyzes a variety of oxygenations of nitrogen- and sulfur-containing medicines and xenobiotic substances. Because of growing interest in drug interactions mediated by polymorphic FMO3, benzydamine N-oxygenation by human FMO3 was investigated as
Beena D Kamath-Rayne et al.
American journal of obstetrics and gynecology, 212(1), 96-96 (2014-08-05)
Most studies of tocolytics are underpowered to assess drug effects on rare adverse neonatal outcomes. Our aim was to optimize statistical power to assess the influence of sulindac on the rare but severe outcome of necrotizing enterocolitis (NEC) by performing
W R Waddell
Journal of surgical oncology, 55(1), 52-55 (1994-01-01)
Sulindac suppresses the growth of colon polyps in Gardner syndrome and familial adenomatous polyposis. The mechanism of action is not known. The problems are to ascertain the significance of high prostaglandin concentrations in transformed cells, colon polyps and cancers and
Elizabeth Guadalupe Sánchez-González et al.
Pharmaceutical development and technology, 20(3), 306-313 (2014-01-15)
Drug polymorphism could affect drug product dissolution, manufacturability, stability and bioavailability/bioequivalence. The impact of polymorphism on the manufacturability and in vitro dissolution profiles of sulindac capsules has not been studied yet. To evaluate the impact of polymorphism on the manufacturability
Alexander Apschner et al.
Disease models & mechanisms, 7(7), 811-822 (2014-06-08)
In recent years it has become clear that, mechanistically, biomineralization is a process that has to be actively inhibited as a default state. This inhibition must be released in a rigidly controlled manner in order for mineralization to occur in
Aldona Majcher et al.
Analytica chimica acta, 855, 51-59 (2014-12-30)
We determine the association constants for ligand-protein complex formation using the flow injection method. We carry out the measurements at high flow rates (F=1 mL min(-1)) of a carrier phase. Therefore, determination of the association constant takes only a few
N Awaya et al.
Ryumachi. [Rheumatism], 33(5), 432-436 (1993-10-01)
Nineteen-year-old woman with mixed connective tissue disease developed Stevens-Johnson syndrome following treatment of arthritis using sulindac. Involvements of infectious and malignant diseases have been ruled out and sulindac has strongly been suspected as a causative agent for Stevens-Johnson syndrome. Ten
A G Gallanosa et al.
Journal of toxicology. Clinical toxicology, 23(2-3), 205-238 (1985-01-01)
A 44 year old female, previously on propranolol, phenytoin and phenobarbital, developed hepatotoxicity while on sulindac and acetaminophen containing analgesic. A limited review of hepatotoxicity and drug interactions of sulindac is presented. The possible mechanism of hepatotoxicity and its treatment
A novel COX-independent mechanism of sulindac sulfide involves cleavage of epithelial cell adhesion molecule protein.
Liggett JL, Min KW, Smolensky D, et al.
Experimental Cell Research, 326(1), 1-9 (2014)
Drugs in R&D, 5(4), 220-226 (2004-07-03)
Exisulind [Aptosyn trade mark, FGN 1 trade mark, Prevatac trade mark, sulindac sulfone], the sulfone derivative of sulindac, is the lead compound in a series of selective apoptotic antineoplastic drugs (SAANDs) being developed by OSI Pharmaceuticals. The compounds were originally
Ziao Fu et al.
Biochemistry, 53(50), 7893-7903 (2014-11-26)
Aβ42 peptides associate into soluble oligomers and protofibrils in the process of forming the amyloid fibrils associated with Alzheimer's disease. The oligomers have been reported to be more toxic to neurons than fibrils, and have been targeted by a wide
Zhengli Wu et al.
Journal of immunology (Baltimore, Md. : 1950), 192(11), 5130-5139 (2014-04-25)
Mast cells play a central role in allergy through secretion of both preformed and newly synthesized mediators. Mast cell mediator secretion is controlled by a complex network of signaling events. Despite intensive studies, signaling pathways in the regulation of mast
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