Indomethacin is an orally active nonsteroidal anti-inflammatory drug (NSAID) that non-selectively inhibits cyclooxygenase enzymes COX-1 and COX-2, with IC₅₀ values of 18 nM and 26 nM, respectively. It exhibits good blood-brain barrier permeability and shows significant anti-inflammatory, anti-tumor, and anti-infective activities. Indomethacin is widely used in research related to cancer, inflammation, and viral infections, and is also commonly used to induce gastric ulcer models in animals.

COX-1:0.28 μM, COX-2:14 μM

METHODS: Human gastric cancer cells AGS were treated with Indomethacin (100-500 µM) for 24 h, and the expression levels of target proteins were detected by Western Blot.
RESULTS: Indomethacin increased LC3-II protein levels in AGS cells, which may be a result of induction of autophagy or inhibition of lysosome-dependent autophagic degradation. [1]
METHODS: Human tumor cells HT29 and A431 were treated with Indomethacin (1-10 µM) and EGF (25 ng/mL) for 24-48 h. Cell migration was detected by wound-healing assay.
RESULTS: Indomethacin inhibited HT29 cell migration. After treating A431 cells with EGF only, the wound closed within 24 h, but the wound remained open after 24 h of treatment with Indomethacin. [2]

METHODS: To test the antitumor activity in vivo, Indomethacin (1 mg/kg) was administered by gavage to CDF1 mice bearing Colon 26 xenografts twice daily for 7-21 days.
RESULTS: Mean tumor weight was significantly lower in both the long-term and short-term Indomethacin administration groups, serum immunosuppressive acidic protein levels were significantly lower, serum IL-6 levels were also significantly lower, and prostaglandin E2 levels in tumor tissues were significantly lower than those in the control group. [3]