Product Details
| Product Name:
Sulindac sodium |
CAS No.:
63804-15-9 |
| Supply Ability:
10g |
Release date:
2025/10/27 |
Product Introduction
Bioactivity
| Name | Sulindac sodium |
| Description | Sulindac (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 vitro | Sulindac (sodium) (MK-231 (sodium)) effectively counteracts TGF-β1-induced epithelial-mesenchymal transition (EMT), as demonstrated by the upregulation of the epithelial marker E-cadherin and the downregulation of mesenchymal markers and transcription factors. It also inhibits the TGF-β1-enhanced migration and invasion of A549 cells. The modulation of SIRT1 levels plays a crucial role, where its downregulation enhances sulindac’s (sodium) effectiveness in reversing TGF-β1-induced EMT, while its upregulation promotes this process. Western Blot Analysis and Immunofluorescence studies, conducted on A549 cells treated with 500 μM of sulindac (sodium) for 48 hours, showed inhibition of TGF-β1-induced EMT and a reversal of SIRT-1 expression influenced by TGF-β1, including an inhibited cadherin switch. Additionally, Cell Migration and Invasion Assays revealed that sulindac (sodium) treatment reduced cell migration and effectively decreased the TGF-β1-induced increase in cell invasion, highlighting its potential as a therapeutic agent against lung cancer progression. |
| In vivo | Sulindac (sodium) (MK-231 (sodium)), administered orally at doses of 15 mg/kg alone and 7.5 mg/kg in combination with PD-L1 blockade twice daily, was found to significantly decrease tumor volume and enhance CD8+ T lymphocyte infiltration in tumor tissues in a CT26 syngeneic mouse tumor model. The combination therapy notably downregulated Programmed Death-Ligand 1 (PD-L1) by inhibiting NF-κB signaling, leading to a reduction in exosomal P and increasing the availability of PD-L1 antibodies. Despite these effects, Sulindac (sodium) (MK-231 (sodium)) at low doses did not exhibit a systemic inhibitory impact on prostaglandin E2 (PGE2). This indicates Sulindac’s potential to modulate the response of pMMR colorectal cancer (CRC) to anti-PD-L1 immunotherapy without significant systemic toxicity. |
| Storage | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature. |
| Inhibitors Related | Ethyl palmitate | Naringin dihydrochalcone | Kojic acid | Fumaric acid | Myristic acid | Diethylmaleate | Glucosamine | sodium lauroyl-α-hydroxyethyl sulfonate | N,N-Dimethylacetamide | Anethole | Diallyl disulfide | Sodium salicylate |
Company Profile Introduction
TargetMol Chemicals Inc. is headquartered in Boston, MA, and specializes in products and services that serve the research needs of chemical and biological scientists worldwide. With a client base in 40+ countries, TargetMol has evolved into one of the biggest global research suppliers for compound libraries and small molecule compounds.
170+ Compound Libraries， 10000+ Noval Small Molecucles，16000+ Nature Compounds
TargetMol diligently updates and offers over 170 types of compound libraries and a wide range of high-quality research chemicals, including inhibitors, activators, natural products, peptides, antibodies , and novel life-science kits for laboratory and scientific use. In addition, our lab allows us to conduct CADD (computer-aided drug design) and chemical synthesis to meet the customization needs of our clients.
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