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piroxicam (piroxicam, Douglas)

✓ Approved

Douglas Pharmaceuticals Limited · PTGS1 · Small Molecule

What is piroxicam?

piroxicam is a small molecule developed by Douglas Pharmaceuticals Limited. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand Namespiroxicam, Douglas
CompanyDouglas Pharmaceuticals Limited
Drug ClassSmall Molecule
Molecular TargetPTGS1, PTGS2
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Douglas Pharmaceuticals Limited

Mechanism of Action

Molecular Targets

piroxicam acts on 2 molecular targets:

PTGS1prostaglandin-endoperoxide synthase 1 (COX3, PCOX1)
PTGS2prostaglandin-endoperoxide synthase 2 (GRIPGHS, hCox-2)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

piroxicam is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Hepatobiliary disordersHepatitis✓ Approved

Related Research Articles

PubMedJournal of ethnopharmacology2026-10-13

Artemisia vulgaris and sabinene ameliorate gastric ulceration and its recurrence through modulation of acid secretion, oxidative stress, and inflammatory cytokines: an in vivo and in silico study.

Borba Ana Laura Tomaselli ALT, Freschi Khetlyn K, Miorando Daniela D, Maccagnan Juliana Cristina JC et al.

Artemisia vulgaris L., popularly known as mugwort, is traditionally used to treat gastric disturbances, yet the mechanistic basis of its antiulcer effects is largely unexplored. The study evaluated the gastroprotective, healing, and anti-recurrence effects of the hydroalcoholic extract of A. vulgaris (HEAv) and its constituent sabinene, and their underlying pharmacological mechanisms. Phytochemical analysis of HEAv used LC-MS, LC-MS/MS, and LC-ESI-IT-MSn. Gastroprotective activity of HEAv (3, 10, or 30 mg/kg) and sabinene (3 mg/kg) was assessed in ethanol- and piroxicam-induced ulcers, beyond pyloric ligation. Healing and recurrence were assessed via acetic acid-induced and IL-1β-triggered ulcers, the latter monitored by ultrasonography. Oxidative stress, inflammatory markers, histology, network pharmacology, and molecular docking/dynamics were evaluated, along with acute toxicity in mice. Chemical analysis identified 36 compounds in HEAv, predominantly phenolics and flavonoids. HEAv and sabinene showed gastroprotective effects, corroborated by mucosal protection and modulation of oxidative stress and inflammatory parameters. In addition, HEAv increased gastric pH, compared to omeprazole. Moreover, HEAv and sabinene reduced ulceration in both the healing and recurrence models, accompanied by increased GSH and CAT activity, and reduced LPO, MPO, and pro-inflammatory cytokines (IL-6 and IL-17A). No acute toxicity was observed. Network pharmacology identified inflammatory signaling as a key target of HEAv constituents, and docking and dynamic molecular assays confirmed favorable, stable interactions between phenolic compounds and sabinene with H+/K+-ATPase and IKKβ, supported by favorable MM-PBSA/MM-GBSA binding energies. HEAv and sabinene exert gastroprotective and healing effects by modulating acid secretion, oxidative stress, and inflammatory cytokines, as suggested by in silico analyses. Nonetheless, further studies are warranted to validate the predicted molecular targets and to elucidate additional pharmacological pathways.

PMID 42869396
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PubMedCancer biology & therapy2026-10-08

Inhibition of WNT signaling sensitizes CRC cells to anti-tumor effects of retinoids: basis for new drug combinations in oncology.

Hunsu Victoria O VO, Facey Caroline O B COB, Opdenaker Lynn M LM, Boman Bruce M BM

Our Goal is to sensitize human colorectal cancer (CRC) to the differentiation-inducing effects of retinoic acid (RA) agents by suppressing WNT signaling. Previously, we reported that the WNT and RA pathways are functionally linked, and in CRC, APC mutation generates a WNT:RA imbalance leading to incomplete differentiation and stem cell (SC) overpopulation. Hypothesis: Therapeutically inhibiting WNT signaling enhances the ability of retinoid agents to induce growth suppression and differentiation. We tested drug combinations of: (1) anti-WNT agents (Sulindac & Piroxicam) that produce anti-tumor activity in humans and animals harboring germline APC mutations, with (2) RA agents (All-trans-RA, 9-cis RA) and RA metabolism blocking agent (CYP26A1 inhibitors Liarozole and Talarozole), which inhibit proliferation and induce differentiation of CRC cell lines. Results: The combined effect of anti-WNT agents and RA drugs shows additive or synergistic responses in CRC cell lines compared to single agents. Drug combinations decrease the proportion of aldehyde dehydrogenase-positive SCs and increase neuroendocrine cell differentiation in CRC cells that show a synergistic response to treatment. NanoString profiling shows that therapeutically decreasing WNT signaling in CRC cells significantly changes the effect of RA signaling on gene expression. Treating human CRC organoid cultures and PDX mouse models with WNT:RA-based drug combinations led to greater anti-tumor activity as compared to individual agents. Conclusion: Inhibiting WNT signaling effectively sensitizes CRC cells to the anti-tumor effects of retinoids. These findings have important clinical significance for designing new drug combinations against CRC.

PMID 42845214
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PubMedBMC chemistry2026-09-27

Holistically benchmarked optimization-assisted green spectrophotometric-chemometric approach for simultaneous determination of piroxicam and venlafaxine in pharmaceutical formulations and spiked human plasma.

Alsfouk Bshra A BA, Al-Khatee Lateefa A LA, Al Kamaly Omkulthom O, Tantawy Mahmoud A MA et al.

The recent clinical introduction of the piroxicam (PIR) and venlafaxine hydrochloride (VEN) combination has highlighted the need for analytical methodologies capable of simultaneously quantifying both drugs while minimizing the environmental burden of routine pharmaceutical analysis. To date, only a chromatographic method has been reported for this purpose, which is associated with relatively high organic solvent consumption, greater instrumental complexity, and increased energy requirements. A green UV spectrophotometric platform integrated with chemometric modeling was therefore established for the concurrent determination of PIR and VEN in pharmaceutical formulations and as a proof-of-concept application to spiked human plasma. Spectral measurements were performed using a water-ethanol (1:1, v/v) solvent system, whereas methanol was employed solely for plasma protein precipitation. Experimental design efficiency was enhanced by combining Brereton's multilevel calibration design with a Maximin Distance Design (MMD) for validation sample selection, enabling representative calibration and validation datasets to be generated with a reduced number of experimental mixtures. Severe spectral overlap between the two analytes was effectively resolved using six well-established chemometric approaches: CLS, PCR, PLS, GA-PLS, FA-PLS, and MCR-ALS. Among the investigated models, MCR-ALS showed the best overall numerical performance, achieving correlation coefficients of up to 0.9998 for pharmaceutical formulations and 0.9996 for spiked human plasma. The corresponding limits of detection were 0.125 and 0.029 µg mL⁻¹ for VEN and PIR, respectively, in pharmaceutical formulations, and 0.245 and 0.058 µg mL⁻¹ in spiked human plasma. Across the investigated concentration ranges, the proposed method also exhibited satisfactory accuracy and precision. The sustainability performance of the analytical platform was evaluated using multiple complementary metrics, with the pharmaceutical assay compared with the previously reported chromatographic procedure according to the evaluated criteria. The proposed pharmaceutical spectrophotometric assay showed a more favorable sustainability profile according to the evaluated criteria, including environmental and practical applicability dimensions. The application to spiked human plasma provided a proof-of-concept assessment of matrix applicability. Nevertheless, additional investigations involving incurred clinical specimens and full bioanalytical validation are required before the methodology can be considered suitable for routine clinical practice or pharmacokinetic studies.

PMID 42800863
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PubMedScientific reports2026-09-02

Sorafenib/piroxicam therapy with biomarker-defined survival benefit in canine muscle-invasive urothelial carcinoma.

Maeda Shingo S, Yokota Shohei S, Komori Mao M, Goto-Koshino Yuko Y et al.

Molecular-targeted therapies require biomarker-driven evaluation to optimize precision oncology strategies; however, translational models integrating clinical outcomes with mechanistic biomarkers are limited. Canine urothelial carcinoma shares molecular features with human muscle-invasive bladder cancer, including activation of VEGFR signaling, providing a valuable comparative oncology platform. Sorafenib is a multi-kinase inhibitor targeting VEGFRs, PDGFRβ, BRAF, and related pathways, but its therapeutic mechanisms and clinical benefit in urothelial carcinoma remain incompletely understood. In this study, 43 dogs with naturally occurring urothelial carcinoma received first-line sorafenib and piroxicam therapy. The overall response rate was 62.8%, with median progression-free and overall survival of 175 (range, 31-665) and 407 (range, 103-1,723) days, respectively. The results exceeded outcomes in historical controls treated with piroxicam alone. Treatment was generally well tolerated, with only three grade 3 adverse events and no grade 4-5 toxicities. Biomarker analyses revealed that treatment-induced hypertension and high tumor CX3CL1 mRNA expression were independently associated with improved overall survival, suggesting that effective VEGFR pathway inhibition and modulation of the tumor immune microenvironment contribute to clinical benefit. These findings support sorafenib-based therapy as a promising strategy for canine urothelial carcinoma and highlight the translational potential of biomarker-driven VEGFR-targeted approaches in precision oncology.

PMID 42680778
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PubMedJournal of visualized experiments : JoVE2026-08-18

A Model of Piroxicam-Accelerated Enterocolitis in Interleukin-10 Knockout Mice for Studying Inflammation-Induced Metabolic Alterations.

Ranjan Mihir M, Williams Justin J, Peng Lan L, Burstein Ezra E et al.

Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the digestive tract affecting over 10 million individuals globally. While substantial research has focused on the immunologic mechanisms and consequences underlying IBD, less is understood about how mucosal inflammation contributes to metabolic dysregulation, including weight loss and reduced appetite. Here, the authors describe a mouse model of piroxicam-accelerated enterocolitis in interleukin-10-knockout (IL-10-KO) mice to study inflammation-induced metabolic dysregulation. IL-10-KO mice are known to develop spontaneous enterocolitis and have heightened susceptibility to enterocolitis triggered by infections or drugs. However, vivarium conditions and strain background have been reported as confounders in colitis development in this model. Piroxicam, a non-steroidal anti-inflammatory drug (NSAID), has been demonstrated to trigger or accelerate enterocolitis in animal models by increasing mucosal exposure to luminal bacteria. In this protocol, male and female IL-10-KO mice were fed a piroxicam-fortified diet in place of a regular chow diet. Food intake and body weight were measured daily to reflect whole-body metabolic alterations, along with clinical manifestations of enterocolitis such as diarrhea and rectal bleeding. The protocol is efficient and reproducible, inducing enterocolitis simultaneously in multiple mice, and allows assessment of metabolic dysregulation in an inflammatory bowel disease model. Further studies using this protocol may investigate the effects of enterocolitis on other components of metabolic dysregulation, such as energy expenditure and body composition, revealing broader connections between inflammatory bowel disease and host metabolism.

PMID 42611797
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PubMedInflammopharmacology2026-08-17

Evaluation of anti-arthritic activity of aripiprazole through multi models: new potential of an old drug.

Akber Aroosa A, Alamgeer, Irfan Hafiz Muhammad HM, Nawaz Shoaib S

This study was conducted to investigate the anti-arthritic effect of three different doses of aripiprazole based on its previously reported anti-inflammatory activity. Aripiprazole, an atypical antipsychotic, has been used in the present study in animal models. Histamine model was used to verify the documented property of aripiprazole to treat inflammation. In-silico evaluation included molecular docking that was done by Auto-Dock of Chemical Computing Group. In-vitro studies involved heat evoked BSA protein degradation and egg albumin degradation and maintenance of human RBCs membrane test, whereas in-vivo studies encompassed, formaldehyde evoked arthritis & CFA evoked arthritis. Acute histamine model was carried out for four hours. Formaldehyde provoked arthritic disease in Sprague Dawley rats was studied to appraise anti-arthritic action of three respective doses of aripiprazole at 5 mg/kg, 10 mg/kg and 15 mg/kg oral dose for 10 days while the time period for study of same activity was twenty eight days with Complete Freund adjuvant and diameter of rat hind paw, arthritic index, body weight, radiological and histopathological investigation of ankles joints were performed. Variety of inflammation causing bio-markers (interleukin-1β, interleukin-6, nuclear factor-Kβ, tumor necrosis factor-α, Cox-2, interleukin-4, interleukin-10 and PGE2) had been investigated by real time-polymerase chain reaction and ELISA. Aripiprazole significantly suppressed paw edema in acute inflammatory model of histamine at dose of 15 mg/kg of aripiprazole showed significant (p < 0.0001) prevention of paw edema showing percentage inhibition of (56.10%) and diameter of 3.13 mm (± 0.046). Molecular docking analysis disclosed that aripiprazole shows binding interactions with TNF-alpha, IL6, IL-1β, NF- κB and Cox-2. It was evaluated in this study that aripiprazole showed inhibition of protein degradation and stability of human red blood cell membrane in concentration gradient manner, demonstrating maximum activity at concentration of 6400 µg/ml. Similarly, considerable (****p < 0.0001) prevention in hind paw edema and arthritic score had been shown at dose of 15 mg/kg in arthritic models that was interestingly greater than piroxicam. aripiprazole suppressed increase in paw diameter in dose dependent manner. 15 mg/kg of aripiprazole showed significant (****p < 0.0001) suppression of in paw edema showing percentage inhibition (64.14%) and paw diameter of 2.94 mm (± 0.044) in formaldehyde provoked arthritic model. Administration of 15 mg/kg of aripiprazole in CFA induced arthritic model presented significant (****p < 0.0001) suppression in paw edema showing percentage inhibition (70.58%) that was interestingly greater then piroxicam and paw diameter of 3.5 mm (± 0.105) and aripiprazole 15 mg/kg has significantly (****p < 0.0001) reduced arthritic score with suppression of edema confirmed by arthritic score 1 (± 0.00) recorded on 28th day of model. Aripiprazole had recovered body weight alteration in CFA induced arthritic model (****p < 0.0001), Radiographic and histopathological investigation displayed no substantial architectural variations in joints of rats that were given treatment. Inflammatory genes IL-1β, TNF-α, IL-6, Cox-2, NF-Kβ and PGE2 were down regulated together with remarkable rise in expression of interleukin-4 and interleukin-10 in treated animals had been revealed by aripiprazole. Significant (****p < 0.0001) downregulation of levels of PGE2 of 222.055 ng/ml (± 4.760) was detected at highest dose of aripiprazole 15 mg/kg. Whereas, a significant (****p < 0.0001) down-regulation of fold change of NF- κB, IL-1β, TNF-α, IL-6, Cox-2 in dose dependent manner was shown by aripiprazole. Above stated results strongly claims that aripiprazole is an effective anti-arthritic therapy as verified through molecular docking, in-vitro and in-vivo assessment and via down regulating pro-inflammatory markers and up regulation of anti-inflammatory cytokines and can be thought to be an appropriate option to repurpose the drug as anti-arthritic agent.

PMID 42606646
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