Sulindac

Research use only, not for human use.

Sulindac is a nonsteroidal anti-inflammatory agent (NSAIA) of the arylalkanoic acid class that is marketed in the U.S. by Merck as Clinoril.

Sulindac is a nonsteroidal anti-inflammatory agent (NSAIA) of the arylalkanoic acid class that is marketed in the U.S. by Merck as Clinoril. Like other NSAIAs, it may be used in the treatment of acute or chronic inflammatory conditions. Sulindac is a prodrug, derived from sulfinylindene, that is converted in vivo to an active sulfide compound by liver enzymes. The sulfide metabolite then undergoes enterohepatic circulation; it is excreted in the bile and then reabsorbed from the intestine. This is thought to help maintain constant blood levels with reduced gastrointestinal side effects. Some studies have shown sulindac to be relatively less irritating to the stomach than other NSAIA’s except for drugs of the cyclooxygenase-2 (COX-2) inhibitor class. The exact mechanism of its NSAIA properties is unknown, but it is thought to act on enzymes COX-1 and COX-2, inhibiting prostaglandin synthesis.

Western Blot Analysis Cell Line:A549 cells Concentration:500 μM Incubation Time:48 h Result:Inhibit transforming growth factor (TGF)-β1-induced epithelial-mesenchymal transition in A549 cells.Immunofluorescence Cell Line:A549 cells Concentration:500 μM Incubation Time:48 h Result:Reversed SIRT-1 expression by TGF-β1 and inhibited the TGF-β1-induced cadherin switch.Cell Migration Assay Cell Line:A549 cells Concentration:500 μM Incubation Time:48 h Result:Inhibited migration, decreased resistance co-treatment with TGF-β1.Cell Invasion Assay Cell Line:A549 cells Concentration:500 μM Incubation Time:40 h; 48 h Result:Could effectively inhibit the TGF- β1-induced increase in invasion by lung cancer cells.

Animal Model:CT26 syngeneic mouse tumor modelDosage:15 mg/kg; 7.5 mg/kg Administration:15 mg/kg, p.o., bid (sulindac alone); 7.5 mg/kg p.o., bid (sulindac combination with PD-L1)Result:Downregulated PD-L1 through the blockade of NF-κB signaling and modulate the response of pMMR CRC to anti-PD-L1 immunotherapy. Cound effectively inhibit PD-L1 with no significant systematic toxicity.

MK-231 | MK231 | MK 231 | Sulindac | Aflodac | Algocetil

Chromatin/Epigenetic

COX

COX

Inflammation/Immunology

——

38194-50-2

356.41

C20H17FO3S

>98% (HPLC)

Ethanol: 9 mg/mL (25.25 mM); DMSO: 71 mg/mL (199.2 mM)

O=C(O)CC(C1=C/2C=CC(F)=C1)=C(C)C2=C\C3=CC=C(S(C)=O)C=C3

(Z)-2-(5-fluoro-2-methyl-1-(4-(methylsulfinyl)benzylidene)-1H-inden-3-yl)acetic acid

(-20℃)

With Ice Pack

≥ 2 years