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Catalog No.S2007

6 publications

Sulindac  Chemical Structure

CAS No. 38194-50-2

Sulindac is a non-steroidal COX inhibitor, which potently inhibits prostaglandin synthesis, used in the treatment of acute or chronic inflammatory conditions.

Selleck's Sulindac has been cited by 6 publications

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  • (d) Parental and regorafenib-resistant HCT116 cells were treated with 40 μM regorafenib, 20 μM sorafenib, 1 μM UCN-01, 1 μM YM-155, 10 μM roscovitine, 15 μM sunitinib, 10 μM crizotinib, 10 nM TRAIL, 10 μM VX680, 20 μM etoposide, 20 μM temsirolimus or 120 μM sulindac sulfide for 48 h. Apoptosis was analyzed as in b. (e) Western blotting of Mcl-1 in parental and regorafenib-resistant HCT116 cells treated with indicated agents as in d for 24 h. Results in (b-d) represent the means±s.d. of three independent experiments. NS, P>0.05; *P<0.05; **P<0.01.

    Oncogene, 2016, 36(6):787-796.. Sulindac purchased from Selleck.

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Biological Activity

Description Sulindac is a non-steroidal COX inhibitor, which potently inhibits prostaglandin synthesis, used in the treatment of acute or chronic inflammatory conditions.
COX [1]
In vitro

Sulindac and its metabolites sulindac sulfide and sulindac sulfone can also inhibit the NF-kappaB pathway in both colon cancer and other cell lines, due to sulindac-mediated decreases in IKKbeta kinase activity. [1] Sulindac sulfide significantly reduces cell number in both preconfluent and confluent cultures of HT-29 cells with the sulfide showing approximately 4-fold greater potency. Sulindac sulfide inhibits the growth of a variety of tumor cell lines derived from other tissues, as well as normal epithelial cells and fibroblasts. [2] Sulindac sulphide abrogates beta-catenin/TCF-mediated transcription in the CRC cell lines DLD1 and SW480, and decreases the levels of nonphosphorylated beta-catenin. [3]

In vivo Sulindac not only inhibits tumor formation but decreases small bowel Cox-2 and prostaglandin E(2) to baseline and restored normal levels of apoptosis in a murine modelof familial adenomatous polyposis. [4] Sulindac reduces the tumor number by 95% but does not alter the levels of PGE2 and LTB4 in intestinal tissues in Min/+爉ice. Sulindac reduces tumor number by 82%, whereas eicosanoid levels remained elevates in Min/+ mice. [5] Sulindac causes regression of 70-80% of small intestinal tumors in Min/+ mice within 4 days, but does not have the same impact on colonic lesions. [6]


Solubility (25°C)

In vitro DMSO 71 mg/mL (199.2 mM)
Ethanol 9 mg/mL (25.25 mM)
Water Insoluble

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 356.41


CAS No. 38194-50-2
Storage powder
in solvent
Synonyms N/A
Smiles CC1=C(C2=C(C1=CC3=CC=C(C=C3)S(=O)C)C=CC(=C2)F)CC(=O)O

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT01636128 Withdrawn Drug: difluoromethylornithine|Drug: Sulindac Focus of Study: Drug Response Biomarkers Chemoprevention Neoplasms Cancer Prevention Pharmaceuticals Inc.|University of Arizona March 2014 Phase 2
NCT01843179 Withdrawn Drug: Cytarabine|Drug: Sulindac Acute Myeloid Leukemia Massachusetts General Hospital January 2014 Phase 2

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COX Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID