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编 号：F759371
分子式：C20H16FNaO3S
分子量：378.39
分子式：C20H16FNaO3S
分子量：378.39
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CAS No: 63804-15-9
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生物活性：
Sulindac (MK-231) is an orally active nonsteroidal anti-inflammatory agent. Sulindac also is an immunomodulatory agent. Sulindac can be used for the research of arthritis of the spine, gouty arthritis and kinds of cancer including colorectal cancer (CRC) and lung cancer.
体内研究：
Sulindac (MK-231) sodium (15 mg/kg, p.o., bid (sulindac alone); 7.5 mg/kg p.o., bid (sulindac combination with PD-L1)) shows a significant reduction in tumor volume and increases infiltration of CD8+ T lymphocytes in the tumor tissues when treated with combination therapy. Sulindac sodium (15 mg/kg, p.o., bid (sulindac alone); 7.5 mg/kg p.o., bid (sulindac combination with PD-L1)) can downregulate PD-L1 by blocking NF-κB signaling, which in turn led to a decrease in exosomal P. Sulindac sodium (15 mg/kg, p.o., bid (sulindac alone); 7.5 mg/kg p.o., bid (sulindac combination with PD-L1)) leads to increased availability of PD-L1 Ab by downregulating PD-L1 in combination therapy. Sulindac sodium has not a systemic inhibitory effect on prostaglandin E2 (PGE2) in low-dose does.Animal Model:CT26 syngeneic mouse tumor model
Dosage: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.
Animal Model:CT26 syngeneic mouse tumor model
Dosage: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.
体外研究：
Sulindac (MK-231) (500 μM, 48 h) sodium is effective in preventing TGF-β1-induced EMT, as indicated by upregulation of the epithelial marker, E-cadherin, and downregulation of mesenchymal markers and transcription factors. Sulindac sodium (500 μM, 48 h) can inhibit TGF-β1-enhanced migration and invasion of A549 cells. Sulindac sodium (500 μM, 48 h) enhances the reversal of TGF-β1-induced EMT by sulindac (sodium) and SIRT1 upregulation promoted TGF-β1-induced EMT.
Sulindac (MK-231) is an orally active nonsteroidal anti-inflammatory agent. Sulindac also is an immunomodulatory agent. Sulindac can be used for the research of arthritis of the spine, gouty arthritis and kinds of cancer including colorectal cancer (CRC) and lung cancer.
体内研究：
Sulindac (MK-231) sodium (15 mg/kg, p.o., bid (sulindac alone); 7.5 mg/kg p.o., bid (sulindac combination with PD-L1)) shows a significant reduction in tumor volume and increases infiltration of CD8+ T lymphocytes in the tumor tissues when treated with combination therapy. Sulindac sodium (15 mg/kg, p.o., bid (sulindac alone); 7.5 mg/kg p.o., bid (sulindac combination with PD-L1)) can downregulate PD-L1 by blocking NF-κB signaling, which in turn led to a decrease in exosomal P. Sulindac sodium (15 mg/kg, p.o., bid (sulindac alone); 7.5 mg/kg p.o., bid (sulindac combination with PD-L1)) leads to increased availability of PD-L1 Ab by downregulating PD-L1 in combination therapy. Sulindac sodium has not a systemic inhibitory effect on prostaglandin E2 (PGE2) in low-dose does.Animal Model:CT26 syngeneic mouse tumor model
Dosage: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.
Animal Model:CT26 syngeneic mouse tumor model
Dosage: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.
体外研究：
Sulindac (MK-231) (500 μM, 48 h) sodium is effective in preventing TGF-β1-induced EMT, as indicated by upregulation of the epithelial marker, E-cadherin, and downregulation of mesenchymal markers and transcription factors. Sulindac sodium (500 μM, 48 h) can inhibit TGF-β1-enhanced migration and invasion of A549 cells. Sulindac sodium (500 μM, 48 h) enhances the reversal of TGF-β1-induced EMT by sulindac (sodium) and SIRT1 upregulation promoted TGF-β1-induced EMT.
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