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化合物 Sulindac sodium,Sulindac sodium

化合物 Sulindac sodium|T61585|TargetMol

價格 10600 17500 13800
包裝 25mg 100mg 50mg
最小起訂量 1mg
發(fā)貨地 上海
更新日期 2024-12-02
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產(chǎn)品詳情

中文名稱:化合物 Sulindac sodium英文名稱:Sulindac sodium
CAS:63804-15-9品牌: TargetMol
產(chǎn)地: 美國保存條件: Shipping with blue ice.
產(chǎn)品類別: 抑制劑
貨號: T61585
2024-12-02 化合物 Sulindac sodium Sulindac sodium 25mg/10600RMB;100mg/17500RMB;50mg/13800RMB 10600 TargetMol 美國 Shipping with blue ice. 抑制劑

Product Introduction

Bioactivity

NameSulindac sodium
DescriptionSulindac (sodium) (MK-231) is an orally active nonsteroidal anti-inflammatory agent. Sulindac (sodium) is used to reduce pain, swelling, and joint stiffness from arthritis. Sulindac is also used for the research of arthritis of the spine, gouty arthritis. Sulindac (sodium), as an immunomodulatory agent, can downregulate PD-L1 through the blockade of NF-κB signaling and modulates the response of pMMR colorectal cancer (CRC) to anti-PD-L1 immunotherapy, inhibits the development and progression of colorectal cancer CRC. Sulindac (sodium) also inhibits TGF-β1- induced epithelial-mesenchymal transition (EMT) and suppresses lung cancer cell migration and invasion via downregulation of SIRT1 [1] [2].
In vitroSulindac (sodium) (MK-231 (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) (MK-231 (sodium)) can inhibit TGF-β1-enhanced migration and invasion of A549 cells. SIRT1 downregulation 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.
In vivoSulindac (sodium) (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) (MK-231 (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) (MK-231 (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. SulindacSulindac (sodium) (MK-231 (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.
StorageShipping with blue ice.
關鍵字: Sulindac sodium|TargetMol

公司簡介

TargetMol Chemicals Inc. 總部位于馬薩諸塞州波士頓,致力于為全球生化領域科學家的研究提供專業(yè)的產(chǎn)品和服務。TargetMol?品牌的客戶群分布于40多個國家和地區(qū),已發(fā)展成為全球知名的化合物庫和小分子化合物研究供應商。 TargetMol?可提供160多種滿足不同需求的化合物庫,以及多種類型的生化試劑產(chǎn)品,包括12000多種抑制劑、16000多種天然產(chǎn)物和各類多肽、抗體、生命科學試劑盒等,此外,我們還建設有CADD(計算機輔助藥物設計)研究中心、藥理實驗室、藥化合成平臺三大技術中心,全方位滿足客戶的定制需求。 憑借我們優(yōu)質的產(chǎn)品和服務、快速高效的全球供應鏈和專業(yè)的技術支持,我們將有效幫助您縮短研發(fā)周期,取得更成功的結果。
成立日期 2013-04-18 (12年) 注冊資本 589.8595萬人民幣
員工人數(shù) 100-500人 年營業(yè)額 ¥ 1億以上
主營行業(yè) 中間體,天然產(chǎn)物,生物化工,化學試劑,生物技術服務 經(jīng)營模式 貿(mào)易,工廠,試劑,定制,服務
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  • 公司成立:12年
  • 注冊資本:589.8595萬人民幣
  • 企業(yè)類型:有限責任公司(自然人投資或控股)
  • 主營產(chǎn)品:抑制劑&激動劑,天然產(chǎn)物,重組蛋白,化合物庫,技術服務
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