Sulindac (MK-231) 是一种口服活性非甾体类抗炎药。 Sulindac 也是一种免疫调节剂。 Sulindac 可用于脊柱关节炎、痛风性关节炎及多种癌症如结直肠癌、肺癌的研究。
| 生物活性 | Sulindac (MK-231) is an orally active nonsteroidalanti-inflammatoryagent. Sulindac also is an immunomodulatory agent. Sulindac can be used for the research of arthritis of the spine, gouty arthritis and kinds ofcancerincluding colorectalcancer(CRC) and lungcancer[1][2]. |
体外研究
(In Vitro) | 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[1].
Sulindac sodium (500 μM, 48 h) can inhibit TGF-β1-enhanced migration and invasion of A549 cells[1].
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[1].
Western Blot Analysis[1] | 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[1] | 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[1] | Cell Line: | A549 cells | | Concentration: | 500 μM | | Incubation Time: | 48 h | | Result: | Inhibited migration, decreased resistance co-treatment with TGF-β1. |
Cell Invasion Assay[1] | 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. |
|
体内研究
(In Vivo) | 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[2].
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[2].
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[2].
Sulindac sodium has not a systemic inhibitory effect on prostaglandin E2 (PGE2) in low-dose does[2].
| Animal Model: | CT26 syngeneic mouse tumor model[2] | | 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[2] | | 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. |
|
| Clinical Trial | |
| 分子量 | |
| Formula | |
| CAS 号 | |
| 中文名称 | |
| 运输条件 | Room temperature in continental US; may vary elsewhere. |
| 储存方式 | Please store the product under the recommended conditions in the Certificate of Analysis. |
m.cnreagent.com