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  • ||||||||||  sulindac / Generic mfg.
    Analysis on the Prevention of NASH Progression by NSAIDs () -  Feb 19, 2025 - Abstract #APASL2025APASL_2451;    
    In summary, current research results on whether NSAIDs can prevent the progression of NASH are inconsistent and somewhat controversial. Although certain NSAIDs, such as sulindac, may have potential anti-NASH activity, the overall safety issues of NSAIDs and the differences in results among studies make their effectiveness in practical application uncertain.
  • ||||||||||  aspirin / Generic mfg.
    Journal:  Aspirin-based PROTACs as COX-2 degraders for anti-inflammation. (Pubmed Central) -  Feb 15, 2025   
    Moreover, we show AspPROTACs could significantly affect proteasome degradation and inflammatory signaling pathways through quantitative proteomic data analysis. These COX-2 degraders offer valuable chemical tools and novel insights for research in anti-inflammatory drugs.
  • ||||||||||  Acomplia (rimonabant) / Sanofi, MJN110 / Scripps Research Institute, LY2828360 / Eli Lilly
    Journal:  Combined Endocannabinoid and Cyclooxygenase Inhibition Additively Attenuates Post-Surgical Pain. (Pubmed Central) -  Feb 14, 2025   
    The dose-dependent anti-allodynic effects of the MAGL inhibitors (irreversible MAGL inhibitor [JZL184] and selective MAGL inhibitor [MJN110]) and the NSAID diclofenac, as well as the additive potential of combined MAGL and cyclooxygenase (COX) inhibition, were assessed...Similarly, the anti-allodynic effects of the CB2-selective agonist (LY2828360) were tested...The anti-allodynic effects of JZL184 (40 mg/kg) were blocked by pre-treatment of the CB2 antagonist SR144528 (3 mg/kg) but not the CB1-selective antagonist rimonabant (SR141716A; 3 mg/kg), suggesting a CB2-mediated mechanism of anti-allodynia via MAGL inhibition...Finally, HPI per se increased pro-inflammatory cytokine levels, which were unaltered by MAGL inhibition despite the anti-allodynia assessed behaviorally. These data support simultaneously targeting endocannabinoids and COX enzymes as a potential post-operative pain management approach.
  • ||||||||||  napabucasin (BBI608) / Sumitomo Pharma, celecoxib oral / Generic mfg.
    Journal, PD(L)-1 Biomarker, IO biomarker:  Crosstalk Between nNOS/NO and COX-2 Enhances Interferon-Gamma-Stimulated Melanoma Progression. (Pubmed Central) -  Feb 13, 2025   
    Cotreatment with celecoxib effectively diminished these changes induced by PGE2...STAT3 inhibitor napabucasin also inhibited COX-2 expression both in the presence and absence of IFN-?...HH044 treatment also significantly reduced tumor PGE2 levels in vivo. Our study demonstrates the positive feedback loop linking nNOS-mediated NO signaling to the COX-2/PGE2 signaling axis in melanoma, which further potentiates the pro-tumorigenic activity of IFN-?.
  • ||||||||||  Review, Journal:  Significance of non-steroidal anti-inflammatory drugs in the prevention and treatment of cervical cancer. (Pubmed Central) -  Feb 7, 2025   
    Nonsteroidal anti-inflammatory drugs (NSAIDs) have demonstrated the capability to significantly inhibit COX activity, playing a crucial preventive and therapeutic role in various tumors. This paper explores the therapeutic value and potential clinical applications of NSAIDs in cervical cancer by examining the mechanistic interactions between HPV and COX and the carcinogenic effects of COX in cervical cancer.
  • ||||||||||  obatoclax (GX 15-070) / Teva
    Journal:  Relocating NSAIDs into the endoplasmic reticulum induces ER stress-mediated apoptosis in cancer cells. (Pubmed Central) -  Feb 6, 2025   
    The resulting ER stress triggered autophagy by upregulating Beclin and LC3-II/LC3-I as autophagy markers, followed by apoptosis, culminating in significant cancer cell death, particularly when combined with bafilomycin A, 10-hydroxycamptothecin and obatoclax. This NSAID-based ER stress inducer provides a powerful tool for exploring the chemical biology of NSAIDs in the ER and holds great potential for advancing ER-targeted cancer therapies in combination with other anti-cancer drugs.
  • ||||||||||  Journal:  Inhibition of PDT-induced PGE2 surge for enhanced photo-immunotherapy. (Pubmed Central) -  Feb 2, 2025   
    In a word, we developed an in-situ tumor vaccination strategy based on COX-Is enhanced PDT, which could alleviate intra-tumoral immune suppression and boost immune system activation. Our study offers a promising modality for advancing clinical treatment strategies for metastatic malignant tumors.
  • ||||||||||  Journal:  Experimental Research Progress of mPGES-1 Inhibitor 2,5-Dimethylcelecoxib in Various Diseases. (Pubmed Central) -  Jan 16, 2025   
    DMC has the ability to address illnesses through the stimulation of autophagy and apoptosis, as well as the regulation of the immune microenvironment and intestinal flora. This study provides a comprehensive overview of the advancements in DMC within experimental research and offers suggestions for potential avenues of future investigation.
  • ||||||||||  Journal:  Constitutive surface expression of the thromboxane A2 receptor is Pim kinase-dependent. (Pubmed Central) -  Jan 12, 2025   
    This study provides a comprehensive overview of the advancements in DMC within experimental research and offers suggestions for potential avenues of future investigation. Pim kinase inhibition may offer a novel therapeutic approach to limit cellular responses to thromboxane A2, independent of cyclooxygenase inhibition and direct antagonism of the receptor.
  • ||||||||||  indomethacin / Generic mfg.
    Journal:  Calcitonin gene-related peptide promotes epithelial reparative and anti-colitic functions of IL-4 educated human macrophages. (Pubmed Central) -  Dec 17, 2024   
    Moreover, M(IL4,CGRP)s displayed increased cyclooxygenase (COX)-1 and prostaglandin D2 (PGD2), and CM from M(IL4,CGRP)s treated with indomethacin or SC-560 to inhibit COX-1 activity failed to promote repair of wounded CaCo2 cell monolayers...These data confirm the human M(IL4)s' anti-colitic effect that was enhanced by CGRP, and may be partially dependent on macrophage COX1/PDG2 activity. Thus, input from neurone-derived molecules is a local modifier capable of boosting the anti-colitic effect of autologous M(IL4) transfer.
  • ||||||||||  Journal:  Re-design and evaluation of diclofenac-based carborane-substituted prodrugs and their anti-cancer potential. (Pubmed Central) -  Dec 17, 2024   
    Our findings suggest that carborane-based prodrugs could be a promising direction for new anti-cancer therapies. Inhibition assays for COX-1 and COX-2 revealed that while diclofenac had strong COX inhibition, the re-engineered carborane compounds demonstrated a varied range of anti-cancer effects, probably owing to both, COX inhibition and COX-independent pathways.
  • ||||||||||  piroxicam / Generic mfg., indomethacin / Generic mfg.
    Preclinical, Journal:  Optogenetic screening of MCT1 activity implicates a cluster of non-steroidal anti-inflammatory drugs (NSAIDs) as inhibitors of lactate transport. (Pubmed Central) -  Dec 12, 2024   
    Since these molecules form a distinct structural cluster with known NSAID MCT4 inhibitors, such as diclofenac, ketoprofen, and indomethacin, we hypothesize that these newly identified inhibitors may also inhibit both transporters. Consequently, NSAIDs as a class, and piroxicam specifically (IC50 4.4 ?M), demonstrate MCT1 inhibition at theoretically relevant human dosages, suggesting immediate potential for standalone MCT inhibition or combined anticancer therapy.
  • ||||||||||  naproxen / Generic mfg.
    Journal:  Concomitant suppression of COX-1 and COX-2 is insufficient to induce enteropathy associated with chronic NSAID use. (Pubmed Central) -  Dec 9, 2024   
    Here we report that concomitant postnatal deletion of Cox-1 and -2 over 10 months failed to cause intestinal injury in mice unless they were treated with naproxen or its structural analog, phenylpropionic acid, which is not a COX inhibitor...These results show that prostaglandin suppression plays a trivial role in NSAID-induced enteropathy. However, Cox deletion causes dysbiosis of the gut microbiome that amplifies the enteropathic response to NSAIDs.
  • ||||||||||  naproxen / Generic mfg.
    Journal, IO biomarker:  Detouring NSAID into mitochondria to induce apoptosis in cancer cells. (Pubmed Central) -  Dec 3, 2024   
    Herein, we have synthesized a small library of Meclofenamic acid and Naproxen derivatives having ester and amide linkage with substituted triphenylphosphonium cations for mitochondria targeting...This 8A3-mediated mitochondrial impairment triggered apoptosis by inhibiting Cox-2, reduction in Bcl-2/Bcl-xl expression and Caspase-3/9 cleavage leading to remarkable HCT-116 cell death. This novel mitochondrion targeted Meclofenamic acid derivative has the potential to be used as a chemical biology tool to understand the role of NSAIDs in mitochondria towards cancer therapy.
  • ||||||||||  celecoxib oral / Generic mfg.
    Journal:  Early Celecoxib Use in Spontaneous Intracerebral Hemorrhage is Associated with Reduced Mortality. (Pubmed Central) -  Nov 26, 2024   
    There exists a growing interest in using COX-2 as a potential target strategy for neuroprotection in patients with sICH, with some evidence of a mortality benefit in small cohort studies. This study shows that early celecoxib use is associated with decreased mortality in patients with sICH.
  • ||||||||||  Germanin (suramin) / Optimum Therap
    Preclinical, Journal, Tumor cell:  P2Y12 receptor-mediated cyclooxygenase 2 (COX-2) expression enhances tumor cell progression in a mouse model of lymphoma. (Pubmed Central) -  Oct 29, 2024   
    A more comprehensive and personalized treatment plan can be achieved by incorporating dietary changes, lifestyle modifications, and, if necessary, herbal therapies to complement other treatments normally. The broad-spectrum P2 receptor antagonist, suramin, P2X7 receptor-specific antagonist, oATP, P2Y6 receptor-specific antagonist, MRS 2578, and P2Y12 receptor-specific antagonist, AR-C 69931, all showed significant arrest in tumor growth...Disaggregated cells from AR-C 69931-treated tumors, when injected intravenously in na