Indomethacin sodium, a powerful and orally active inhibitor of COX1/2, exhibits IC50 values of 18 nM and 26 nM for COX-1 and COX-2, respectively. Apart from its potent anti-inflammatory effects, this compound possesses notable anticancer and anti-infective activities. Since it has such versatile attributes, it finds useful applicability in cancer, inflammation, and viral infection research [1] [2] [3].

Indomethacin (Indometacin) sodium, across concentrations ranging from 0 to 150 μM administered over 24 hours, exhibits significant anticancer effects in vitro on 3LL-D122 cells, a highly metastatic variant of mouse Lewis lung carcinoma cells [2]. Additionally, this compound, at concentrations up to 1000 μM, activates PKR leading to phosphorylation of eIF2α. This process halts the translation of viral proteins, effectively inhibiting virus replication with an IC50 value of 2μM, thereby protecting the host cells from viral damage [3]. Cell viability assays on the 3LL-D122 line reveal that cell viability is inhibited at 20 mM, achieving a 50% inhibition rate at 60 nM. Furthermore, cell cycle analysis after 24 hours of exposure to 0, 30, and 80μM concentrations shows a decrease in cells at the G2/M phase and an increase at the G1 phase, indicating significant alterations in cell cycle progression induced by Indomethacin sodium [2].

Administered orally to male Sprague-Dawley rats at dosages ranging from 0.01 to 10 mg/kg for three hours, Indomethacin (Indometacin) sodium dose-dependently mitigated carrageenan-induced paw edema and hyperalgesia, evidencing an inhibition of reactive inflammation and pain sensitivity [1]. Similarly, a daily oral dose of 10 mg/mL Indomethacin (Indometacin) sodium for 29 days in male C57BL/6J mice effectively impeded tumor growth in vivo, indicating its potential anti-tumoral properties [2]. Specifically, in the Sprague-Dawley rat model, the administration led to a significant reduction in both carrageenan-induced edema (Effective Dose, ED50 = 2.0 mg/kg) and hyperalgesia (ED 50 = 1.5 mg/kg), demonstrating dose-responsive therapeutic effects. In the C57BL/6J mouse model, the prolonged treatment notably delayed tumor emergence and slowed the initial rate of tumor expansion in the footpad.