celecoxib oral

P3, N=53, Completed, Ferring Ventures Limited | Active, not recruiting --> Completed

These findingssuggest that LDRT combined with ICB is safe and may contribute to immunomodulatory activity in immune-excluded tumors. CD8⁺ TIL dynamics, DNA repair responsiveness, and TME composition may predict response and merit further validation in controlled larger studies.

One group received an intra-articular saline injection as the normal control (NC), while the remaining five groups were injected with monosodium iodoacetate (MIA) and consisted of an MIA control group (MC), a positive control group treated with celecoxib (PC, 3 mg/kg), and three groups treated with CP (31.25, 62.5, or 125 mg/kg)...Furthermore, CP decreased the activation of nuclear factor kappa B (NF-κB) signaling. These findings suggest that CP may be a promising functional agent for osteoarthritis, demonstrating beneficial effects on pain-related outcomes and cartilage integrity, potentially mediated by its anti-inflammatory activity.

ADME and ProTox-3.0 predictions suggested favorable drug-likeness and low acute oral toxicity, while molecular docking indicated that the lead compound 7b established stable interactions with voltage-gated calcium channels and cyclooxygenase-2, exhibiting binding modes comparable to sodium valproate and celecoxib, respectively. Remarkable anticonvulsant efficacy was observed in both the pentylenetetrazole (PTZ) induced seizure model and pilocarpine-induced seizure model, where 7b afforded 90% seizure protection with complete prevention of mortality, delayed seizure onset by 156.43%, reduced seizure severity by 70.53%, and achieved 100% survival, surpassing sodium valproate. Mechanistically, 7b markedly attenuated hippocampal neuroinflammation and excitotoxicity, reducing TNF-α, IL-6, and glutamate levels while suppressing glial activation markers glial fibrillary acidic protein and ionized calcium-binding adapter molecule 1, confirming pronounced neuroprotective and anti-neuroinflammatory effects.

Combined treatment with celecoxib (10 µM) and doxorubicin (1 µM) in claudin-low cells not only significantly inhibited Notch signaling and claudin expression, but also suppressed viability, proliferation, migration, and BCSC populations. Since Notch signalling may be an essential factor in these latter events, our findings suggest that Notch1/N1ICD can serve as therapeutic targets for the better management of claudin-low BCs. However, validation of the same requires detailed functional studies involving modulation of each type of Notch receptor or other players involved in Notch signaling using more robust approaches.

P3, N=140, Active, not recruiting, Amsterdam UMC, location VUmc | Recruiting --> Active, not recruiting

Either the depletion of aHSCs or pharmacological inhibition of the PGE2-synthesizing enzyme Cyclooxygenase-2 (COX-2) with Celecoxib (CLX) restored NK cell function and suppressed LM. Notably, CLX treatment synergized with anti-NKG2A-based immunotherapy, significantly boosting its efficacy against LM in the fibrotic liver. Our findings unveil a critical "aHSC-PGE2-NK cell" axis in liver fibrosis-induced immunosuppression and provide a compelling therapeutic strategy for the clinical management of LM.

Micrographs of the ear's tissue clearly showed a decrease in thickness and infiltration of neutrophils, which correlates with the reduction of MPO and cytokines. Finally, molecular docking suggested that the series could inhibit cyclooxygenases and displayed a binding mode like that of celecoxib, though the enzymatic assay will be performed in future work.

Crucially, the addition of exogenous PGE2 restored VM formation in celecoxib-treated cells, confirming that celecoxib-mediated VM suppression is dependent on the reduction of PGE2 levels. These findings establish the COX-2/PGE2 signaling axis as a key regulator of VM in D17 canine osteosarcoma cells and that celecoxib warrants further preclinical evaluation as a strategy to target both tumor growth and alternative vascularization.

P2, N=60, Not yet recruiting, Sun Yat-sen University

P3, N=140, Recruiting, Amsterdam UMC, location VUmc | Not yet recruiting --> Recruiting