Indomethacin

Indomethacin

Cat. No.: PI53861

Description: Indomethacin is NSAID with anti-inflammatory, analgesic, and antipyretic properties. It is a synthetic nonsteroidal indole derivative with anti-inflammatory activity and chemopreventive properties. Indomethacin inhibits the enzyme cyclooxygenase, thereby preventing cyclooxygenase-mediated DNA adduct formation by heterocyclic aromatic amines. This agent also may inhibit the expression of multidrug-resistant protein type 1, resulting in increased efficacies of some antineoplastic agents in treating multi-drug resistant tumors. In addition, indomethacin activates phosphatases that inhibit the migration and proliferation of cancer cells and downregulates survival, which may result in tumor cell apoptosis.

Indomethacin
Product Details
CAS 53-86-1
Molecular Formula C19H16ClNO4
Molecular Weight 357.8
Standard BP / EP / IP / USP
Uses Oral indomethacin is indicated for symptomatic management of moderate to severe rheumatoid arthritis including acute flares of chronic disease, moderate to severe ankylosing spondylitis, moderate to severe osteoarthritis, and acute painful shoulder (bursitis and/or tendinitis), and acute gouty arthritis. Intravenous indomethacin is indicated to induce closure of a hemodynamically significant patent ductus arteriosus in premature infants weighing between 500 and 1750 g when after 48 hours of usual medical management (e.g., fluid restriction, diuretics, digitalis, respiratory support, etc.) is ineffective.
Mechanism Of Action The anti-inflammatory, analgesic, and antipyretic effects of indomethacin and other NSAIDs, including selective inhibitors of cyclooxygenase-2 (COX-2) (e.g., celecoxib), appear to result from the inhibition of prostaglandin synthesis. While the precise mechanism of the anti-inflammatory and analgesic effects of NSAIDs continues to be investigated, these effects appear to be mediated principally through inhibition of the COX-2 isoenzyme at sites of inflammation with subsequent reduction in the synthesis of certain prostaglandins from their arachidonic acid precursors. This effect may be related to the inhibition of the synthesis of prostaglandins that are believed to play a role in modulating the rate and extent of leukocyte infiltration during inflammation. Indomethacin also inhibits lysosomal enzyme release from polymorphonuclear leukocytes.
Case Study

Indomethacin for Restoring Autophagic Flux in Experimental Acute Pancreatitis Models

Indomethacin alleviates acute pancreatitis by restoring autophagic flux via the AMPK signaling pathway Luo L, et al. Pathology - Research and Practice, 2026, 279, 156377.

Indomethacin was experimentally evaluated for its therapeutic potential in acute pancreatitis (AP) using both in vivo and in vitro models. A cerulein-induced AP mouse model was established to assess pancreatic injury, where indomethacin was administered prior to and during cerulein challenge. Pancreatic tissues were collected for histopathological scoring, while serum amylase and lipase levels were quantified to evaluate exocrine dysfunction. In parallel, AR42J pancreatic acinar cells were treated with cerulein in the presence or absence of indomethacin to investigate cytotoxicity and autophagic activity. Autophagic flux was assessed through LC3-II accumulation, p62 degradation, and transmission electron microscopy. Transcriptomic analysis and pathway enrichment identified AMPK signaling as a key regulatory axis. Pharmacological inhibition using chloroquine and Compound C was employed to validate the dependence on autophagy and AMPK activation. These experimental approaches demonstrate indomethacin's direct application as a modulator of autophagy in AP research models.

Indomethacin for the Synthesis of Poly(ε-caprolactone)-Based Nanocapsules via Emulsion-Diffusion

In vivo immunological evaluation of indomethacin and omega-3 nanocapsules for the treatment of rheumatoid arthritis in the temporomandibular joints of rats Dos Santos VAB, et al. Archives of Oral Biology, 2026, 182, 106456.

This case study highlights the experimental application of indomethacin in the preparation of polymeric nanocapsules designed to enhance therapeutic efficacy. Indomethacin-loaded nanocapsules were synthesized using a modified emulsion-diffusion method. Briefly, mutually saturated ultrapure water and ethyl acetate phases were prepared. Polyvinyl alcohol (2.5%) was dissolved in the aqueous phase, while indomethacin, poly(ε-caprolactone) (2%), and omega-3 fatty acids were co-dissolved in the organic phase. The two phases were emulsified via ultrasonication under controlled amplitude and pulse conditions to generate a stable oil-in-water emulsion. Subsequent diffusion was induced by dropwise addition of excess water, followed by solvent removal under reduced pressure. Polarized light microscopy confirmed the absence of indomethacin crystallization, indicating successful molecular encapsulation. This method demonstrates the suitability of indomethacin for incorporation into nanocarrier systems through precisely controlled formulation processes.

Indomethacin for Acid-Base Supersolubilization-Enabled Amorphous Solid Dispersion via Low-Temperature Hot Melt Extrusion

Development of indomethacin amorphous solid dispersion by applying acid-base supersolubilization (ABS) principle to enhance solubility and enable low-temperature hot melt extrusion Raje V, et al. International Journal of Pharmaceutics, 2026, 687, 126405.

This case study describes the experimental application of indomethacin in developing an amorphous solid dispersion (ASD) using the acid-base supersolubilization (ABS) principle. Indomethacin, a weakly acidic and poorly water-soluble drug, was combined with the weak base tromethamine to induce strong acid-base interactions without salt formation. A 1:2 molar ratio of indomethacin to tromethamine was prepared and incorporated with poloxamer 407 and Kollidon® VA64, followed by hot melt extrusion at a significantly reduced temperature of 80 °C. Differential scanning calorimetry and PXRD confirmed complete amorphization. The ABS approach markedly reduced the melting point of indomethacin, enabling low-temperature processing while preventing thermal degradation. In vitro dissolution testing demonstrated rapid and sustained drug release across physiological pH conditions, validating ABS as an effective formulation strategy.

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