Sulindac

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^[1][2]. IC50 & Target: COX-2^[1] In Vitro: Sulindac (MK-231) (500 μM, 48 h) 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 (500 μM, 48 h) can inhibit TGF-β1-enhanced migration and invasion of A549 cells^[1].
Sulindac (500 μM, 48 h) enhances the reversal of TGF-β1-induced EMT by sulindac and SIRT1 upregulation promoted TGF-β1-induced EMT^[1]. In Vivo: Sulindac (MK-231) (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 (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 (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 (15 mg/kg, p.o., bid (sulindac alone); 7.5 mg/kg p.o., bid (sulindac combination with PD-L1)) has not a systemic inhibitory effect on prostaglandin E2 (PGE2) in low-dose does^[2].