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Journal articles on the topic 'Oxaprozin'

Author: Grafiati

Published: 10 September 2021

Last updated: 21 June 2025

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1

S, Bhardwaj, Kalra N, and Khan W. "Development and Evaluation of a Nanogel Formulation of Oxaprozin." INTERNATIONAL JOURNAL OF DRUG DELIVERY TECHNOLOGY 14, no. 04 (2024): 1106–9. https://doi.org/10.25258/ijddt.14.4.49.

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The proposed work was aimed to Development and evaluation of a nanotechnology based formulation of oxaprozin. The preformulation studies for the chosen medication Oxaprozin include IR spectroscopy, melting point determination, and physical appearance analysis as methods of identification. It can be inferred from the Eudragit S-100 DSC overlay thermogram of the physical mixture and the pure drug demonstrates that the drug and excipients do not interact. According to Oxaprozin's UV spectra, the drug exhibits absorbances, with the highest absorbance occurring at 285 nm when the solution is made in methanol. Homogenicity, particle size, pH, drug content, in vitro drug release, skin irritation test, spreadability, extrudability, and viscosity were all optimized in the formulation of the nanogel. The drug content (±SD 98.9 ± 0.02), in vitro drug release (%), and spreadability (g.cm/s) of the optimized F7 formulation are 95.85 ± 0.0658 and 6.5 ± 0.3, respectively. 281 ± 0.5 is the extrudability (g). The viscosity of in cp at 50 (rpm) 9857 were found.

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2

&NA;. "Oxaprozin." Reactions Weekly &NA;, no. 726 (1998): 9–10. http://dx.doi.org/10.2165/00128415-199807260-00028.

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3

&NA;. "Oxaprozin." Reactions Weekly &NA;, no. 757 (1999): 11. http://dx.doi.org/10.2165/00128415-199907570-00033.

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4

&NA;. "Oxaprozin." Reactions Weekly &NA;, no. 537 (1995): 9. http://dx.doi.org/10.2165/00128415-199505370-00033.

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5

Todd, Peter A., and Rex N. Brogden. "Oxaprozin." Drugs 32, no. 4 (1986): 291–312. http://dx.doi.org/10.2165/00003495-198632040-00001.

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6

&NA;. "Oxaprozin." Reactions Weekly &NA;, no. 631 (1996): 10. http://dx.doi.org/10.2165/00128415-199606310-00027.

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7

&NA;. "Oxaprozin." Reactions Weekly &NA;, no. 633 (1997): 10. http://dx.doi.org/10.2165/00128415-199706330-00027.

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8

&NA;. "Oxaprozin." Reactions Weekly &NA;, no. 641 (1997): 9. http://dx.doi.org/10.2165/00128415-199706410-00027.

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9

&NA;. "Oxaprozin." Reactions Weekly &NA;, no. 773 (1999): 12. http://dx.doi.org/10.2165/00128415-199907730-00033.

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10

&NA;. "Oxaprozin." Reactions Weekly &NA;, no. 527 (1994): 9. http://dx.doi.org/10.2165/00128415-199405270-00032.

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11

Bozic, Bojan, Nemanja Trisovic, Natasa Valentic, Gordana Uscumlic, and Slobodan Petrovic. "Oxaprozin: Synthesis, SAR study, physico-chemical characteristics and pharmacology." Chemical Industry 65, no. 5 (2011): 551–62. http://dx.doi.org/10.2298/hemind110426040b.

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Oxaprozin (3-(4,5-difeniloksazol-2-yl)propanoic acid) is a nonsteroidal anti-inflammatory drug (NSAID) used in the treatment of numerous inflammatory musculoskeletal diseases, including rheumatoid arthritis, osteoarthritis, tendonitis, ankylosing spondylitis and bursitis. It is the first representative member of the diaryl-substituted heterocyclic compounds, which have found clinical use as selective cyclooxygenase-2 (COX-2) inhibitors. U.S. Food and Drug Administration (FDA) approved its official use in 1992. Both anti-inflammatory and analgesic properties of oxaprozin are mainly due to the potent inhibition of COX. However, oxaprozin-induced benefits might be also regulated by other COX-independent pathways. It has been shown that oxaprozin induced direct proapoptotic effects in CD40L-treated human monocytes independently of COX inhibition. It also has several advantages in the treatment of inflammatory diseases in comparison to other NSAIDs such as aspirin, naproxen, indomethacin and phenylbutazone, which enabled oxaprozin to become one of the most used NSAIDs in America. Oxaprozin, as other members of the group of NSAIDs, can cause gastrointestinal complications, but significantly lower due to relatively high pKa value. In this paper, importance of oxaprozin in the treatment of arthritis and its pharmacokinetic properties were described, therewith its activity and side effects were compared with other commercially available anti-inflammatory drugs.

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12

Santo, J. E., and M. V. Queiroz. "Oxaprozin versus Diclofenac Sodium in the Treatment of Ankylosing Spondylitis." Journal of International Medical Research 16, no. 2 (1988): 150–56. http://dx.doi.org/10.1177/030006058801600210.

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The efficacy and tolerance of 1200 mg/day oxaprozin and 100 mg/day diclofenac sodium were compared in 40 patients with ankylosing spondylitis in a 6-week open study. Overall improvement was seen in the patients in both treatment groups. Oxaprozin-treated patients showed significant improvement in spontaneous pain of the vertebral spine and in morning stiffness after 6 weeks' treatment. There were no statistically significant differences between the treatment groups. Therapy was discontinued in 10 patients; five treated with oxaprozin (three because of intolerance and two because of worsening of symptoms) and five taking diclofenac sodium (four because of intolerance and one because of worsening of symptoms). Five (25%) oxaprozin-treated patients and six (30%) diclofenac sodium-treated patients had side-effects, with gastro-intestinal disturbances and dizziness reported most frequently. There were no statistically significant differences between the groups in the frequency of side-effects. These results indicate that oxaprozin is a promising therapeutic agent for ankylosing spondylitis.

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13

Aitipamula, Srinivasulu, Annie B. H. Wong, Pui Shan Chow, and Reginald B. H. Tan. "Novel solid forms of oxaprozin: cocrystals and an extended release drug–drug salt of salbutamol." RSC Advances 6, no. 41 (2016): 34110–19. http://dx.doi.org/10.1039/c6ra01802e.

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Novel solid forms of an anti-inflammatory drug, oxaprozin, were identified. A drug–drug salt of oxaprozin with salbutamol was proved promising for development of extended release tablet formulations of salbutamol.

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14

Dhuriya, Anubha, and Aaditya Singh. "EVALUATION OF ANTIDEPRESSANT AND ANXIOLYTIC ACTIVITY OF OXAPROZIN IN SWISS ALBINO MICE." International Journal of Advanced Research 11, no. 05 (2023): 295–304. http://dx.doi.org/10.21474/ijar01/16880.

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Depression is a prevalent mental illness. According to estimates, 5 percent of adults worldwide experience depression. Depression affects more women than males. Oxaprozin is a non-narcotic, non-steroidal anti-inflammatory medication (NSAID) used to treat osteoarthritis and rheumatoid arthritis-related inflammation, edoema, stiffness, and joint discomfort. The present study is based on the evaluation of antidepressant and anxiolytic activity of oxaprozin in Swiss albino (either sex) weight 20-25 gm were procured from ICAR-Indian Veterinary Research Institute (ICAR-IVRI), Izzat nagar, Bareilly, Uttar Pradesh. All the mice were divided into 4 groups (n=6) i.e., normal control which was given normal saline, positive control given Imipramine (10mg/kg, i.p.) and diazepam (10mg/kg, subcutaneously), test 1given oxaprozin(10mg/kg, p.o.) and test 2 given Oxaprozin (20mg/kg, p.o.) up to 7 days. The anxiolytic and antidepressant activity were evaluated by parameters i.e., elevated plus maze, FST, rota-rod test and biochemical parameters. It resulted that oxaprozin demonstrates anxiolytic and antidepressant activity. It exhibits antidepressant action probably by facilitating the release of neurotransmitters i. e., serotonin, dopamine. It also increases the release of GABA (Gamma Amino Butyric Acid) and chloride ions influx that leads to hyperpolarization .In conclusion, Oxaprozin is a predominant anxiolytic & anti-depressant drug. It can be effectively used in the treatment of depression, mental agitation and other neurological disorders after successfully evaluating mechanism of action against the same.This study refers, that it might be used in the treatment of depression among human beings after clinical trials.

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15

Purdum, Preston P., Stacey L. Shelden, John W. Boyd, and Mitchell L. Shiffman. "Oxaprozin-Induced Fulminant Hepatitis." Annals of Pharmacotherapy 28, no. 10 (1994): 1159–61. http://dx.doi.org/10.1177/106002809402801004.

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OBJECTIVE: To report oxaprozin-induced fulminant hepatic failure. CASE SUMMARY: A 56-year-old woman was admitted with fulminant hepatic failure. Work-up for potential etiologies was negative except for the use of oxaprozin for the preceding two months. Results of premortem liver biopsy were consistent with drug-induced hepatic injury similar to that previously reported with diclofenac. DISCUSSION: Although the literature describes elevation in hepatic transaminase concentrations associated with oxaprozin, fulminant hepatic failure has not been described previously. CONCLUSIONS: Elevations in hepatic transaminase concentrations and now fulminant hepatic failure have been shown to occur with oxaprozin, as previously seen with other nonsteroidal antiinflammatory drugs (NSAIDs). Transaminitis is a known adverse effect of NSAID use, but is usually mild and reversible with discontinuation of drug. Transaminitis may be more likely to occur in the elderly, in patients receiving concurrent potentially hepatotoxic medications, and possibly with the newer long-acting NSAIDs. The existence of fulminant hepatitis, although rare, supports the need for monitoring liver function enzymes during NSAID therapy.

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16

Thangabalan Boovizhikannan, Chandana Ramachandra, Mamatha reddy Meruva, and Naga Srinatha Reddy Nandyala. "A review on analytical methods for estimation of Oxaprozin." World Journal of Biology Pharmacy and Health Sciences 12, no. 2 (2022): 168–75. http://dx.doi.org/10.30574/wjbphs.2022.12.2.0186.

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Oxaprozin is a non-narcotic, non-steroidal, anti-inflammatory drug (NSAID) used to relieve the inflammation, Swelling, stiffness, and joint pain associated with osteoarthritis, and rheumatoid arthritis. Oxaprozin is used to treat rheumatoid arthritis Osteoarthritis, dysmenorrhea and to alleviate moderate pain. This paper explains about the various analytical methods for the estimation of the drug.

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17

Thangabalan, Boovizhikannan, Ramachandra Chandana, reddy Meruva Mamatha, and Srinatha Reddy Nandyala Naga. "A review on analytical methods for estimation of Oxaprozin." World Journal of Biology Pharmacy and Health Sciences 12, no. 2 (2022): 168–75. https://doi.org/10.5281/zenodo.7607175.

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Oxaprozin is a non-narcotic, non-steroidal, anti-inflammatory drug (NSAID) used to relieve the inflammation, Swelling, stiffness, and joint pain associated with osteoarthritis, and rheumatoid arthritis. Oxaprozin is used to treat rheumatoid arthritis Osteoarthritis, dysmenorrhea and to alleviate moderate pain. This paper explains about the various analytical methods for the estimation of the drug.

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18

&NA;. "Nabumetone/naproxen/oxaprozin." Reactions Weekly &NA;, no. 953 (2003): 12. http://dx.doi.org/10.2165/00128415-200309530-00042.

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19

Ingrish, George. "Oxaprozin-lnduced Pseudoporphyria." Archives of Dermatology 132, no. 12 (1996): 1519. http://dx.doi.org/10.1001/archderm.1996.03890360113027.

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20

Ingrish, G. "Oxaprozin-induced pseudoporphyria." Archives of Dermatology 132, no. 12 (1996): 1519–20. http://dx.doi.org/10.1001/archderm.132.12.1519.

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21

Davies, Neal M. "Clinical Pharmacokinetics of Oxaprozin." Clinical Pharmacokinetics 35, no. 6 (1998): 425–36. http://dx.doi.org/10.2165/00003088-199835060-00002.

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22

Kethu, Sripathi R., Sireesha Rukkannagari, and Charles L. Lansford. "Oxaprozin-Induced Symptomatic Hepatotoxicity." Annals of Pharmacotherapy 33, no. 9 (1999): 942–44. http://dx.doi.org/10.1345/aph.18408.

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23

Zimmerman, Hyman J. "Hepatic effects of oxaprozin." Seminars in Arthritis and Rheumatism 15, no. 3 (1986): 35–39. http://dx.doi.org/10.1016/s0049-0172(86)80005-1.

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24

Montecucco, Fabrizio, Maria Bertolotto, Luciano Ottonello, Alessandra Quercioli, François Mach, and Franco Dallegri. "Oxaprozin-Induced Apoptosis on CD40 Ligand-Treated Human Primary Monocytes Is Associated with the Modulation of Defined Intracellular Pathways." Journal of Biomedicine and Biotechnology 2009 (2009): 1–9. http://dx.doi.org/10.1155/2009/478785.

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The modulation of CD40L activity might represent a promising therapeutic target to reduce monocyte inflammatory functions in chronic diseases, such as rheumatoid arthritis. In the present study, we investigated the possible influence of nonsteroidal anti-inflammatory drugs (NSAIDs) on CD40L-induced monocyte survival. Monocytes were isolated from buffy coats by using Ficoll-Percoll gradients. Monocyte apoptosis was evaluated by fluorescence microscopy on cytopreps stained with acridine orange or using flow cytometry analysis of Annexin-V and Propidium Iodide staining. Akt and NF-κB activation was assessed using western blot. Caspase 3 activity was determined spectrophotometrically. Among different NSAIDs, only oxaprozin dose-dependently increased apoptosis of CD40L-treated monocytes. Oxaprozin pro-apoptotic activity was associated with the inhibition of CD40L-triggered Akt and NF-κB phosphorylation and the activation of caspase 3. In conclusion, our data suggest that oxaprozin-induced apoptosis in CD40L-treated human monocytes is associated with previously unknown cyclooxygenase (COX)-independent pathways. These intracellular proteins might be promising pharmacological targets to increase apoptosis in CD40L-treated monocytes.

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25

Lewis, Alan J. "The pharmacologic profile of oxaprozin." Seminars in Arthritis and Rheumatism 15, no. 3 (1986): 11–17. http://dx.doi.org/10.1016/s0049-0172(86)80002-6.

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26

Greenblatt, DJ, R. Matlis, JM Scavone, GT Blyden, JS Harmatz, and RI Shader. "Oxaprozin pharmacokinetics in the elderly." British Journal of Clinical Pharmacology 19, no. 3 (1985): 373–78. http://dx.doi.org/10.1111/j.1365-2125.1985.tb02656.x.

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27

Kurowski, M., and H. Thabe. "The transsynovial distribution of oxaprozin." Agents and Actions 27, no. 3-4 (1989): 458–60. http://dx.doi.org/10.1007/bf01972852.

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28

SUWA, TOSHIO, HIDETOSHI URANO, and AKIRA TSUJI. "Pharmacokinetics of Oxaprozin after Multiple Doses." YAKUGAKU ZASSHI 107, no. 6 (1987): 440–48. http://dx.doi.org/10.1248/yakushi1947.107.6_440.

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29

&NA;. "Oxaprozin falsely elevated phenytoin plasma concentrations,." Reactions Weekly &NA;, no. 673 (1997): 4. http://dx.doi.org/10.2165/00128415-199706730-00006.

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30

Mease, Philip J., and Robert F. Willkens. "Treatment of acute gout with oxaprozin." Seminars in Arthritis and Rheumatism 15, no. 3 (1986): 86–89. http://dx.doi.org/10.1016/s0049-0172(86)80013-0.

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31

Ogawa, Makoto, Shiro Ueda, Yuki Hamano, Kazushige Ito, Hiromitsu Saisho, and Bunshiro Akikus. "Membranous Nephropathy Associated with Oxaprozin Treatment." Nephron 74, no. 2 (1996): 439–40. http://dx.doi.org/10.1159/000189356.

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32

Patel, Tejal, Kristine M. Radomski, and Mary Hh Chandler. "Assay Interaction between Oxaprozin and Phenytoin." Annals of Pharmacotherapy 31, no. 2 (1997): 254. http://dx.doi.org/10.1177/106002809703100224.

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33

Bucolo, Claudio, and Adriana Maltese. "Pharmacological Profile of Oxaprozin Eye Drops." Journal of Ocular Pharmacology and Therapeutics 18, no. 1 (2002): 75–81. http://dx.doi.org/10.1089/108076802317233234.

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34

Rainsford, K. D., H. Omar, A. Ashraf, et al. "Recent pharmacodynamic and pharmacokinetic findings on oxaprozin." InflammoPharmacology 10, no. 3 (2002): 185–239. http://dx.doi.org/10.1163/156856002321168204.

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35

Goldfarb, Stanley, Barry R. Walker, and Zalman S. Agus. "The Uricosuric Effect of Oxaprozin in Humans." Journal of Clinical Pharmacology 25, no. 2 (1985): 144–48. http://dx.doi.org/10.1002/j.1552-4604.1985.tb02815.x.

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36

Ugrinovic, Vukasin, Maja Markovic, Bojan Bozic, Vesna Panic, and Djordje Veljovic. "Poly(methacrylic acid) hydrogels crosslinked by poly(ethylene glycol) diacrylate as pH-responsive systems for drug delivery applications." Chemical Industry, no. 00 (2023): 18. http://dx.doi.org/10.2298/hemind221228018u.

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Hydrogels are attractive materials for drug delivery applications due to biocompatible, porous structure with the possibility to load and deliver drugs in a controllable manner. In this paper, poly(methacrylic acid) (PMAA) hydrogels are described, which are synthesized by free-radical polymerization, using poly(ethylene glycol) diacrylate (PEGDA) as a crosslinker. Influence of the PEGDA content on hydrogel properties was investigated and compared to commonly used crosslinker - N,N?-methylenebisacrylamide (MBA). The increasing concentration of crosslinkers led to a higher degree of crosslinking, which was demonstrated by a higher degree of conversion, lower swelling capacity, and improved thermal stability and mechanical properties. Also, the PEGDA-crosslinked hydrogels demonstrated a higher degree of crosslinking than the corresponding MBA-crosslinked hydrogels. Potential application of the synthesized hydrogels for controlled drug delivery was investigated by using two model drugs - oxaprozin and ciprofloxacin. In vitro drug release tests indicated that the interactions between drug, polymer and medium have a key influence on the drug release behavior, rather than the swelling rate. Drug release tests in simulated gastrointestinal conditions indicated that PEGDA-crosslinked PMAA hydrogels are suitable for colon-targeted delivery of oxaprozin.

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37

Desilets, Alicia, Kristine C. Willett, Dustin Waller, and Ann Barry. "Risk of Spontaneous Bruising with Concomitant Use of Nonsteroidal Antiinflammatory Drugs and Citalopram." Journal of Pharmacy Technology 28, no. 5 (2012): 204–7. http://dx.doi.org/10.1177/875512251202800506.

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Objective: To report a case of spontaneous bruising with concomitant use of nonsteroidal antiinflammatory drugs (NSAIDs) and citalopram. Case Summary: A 34-year-old white woman with a history of chronic thrombocytopenia (baseline platelet count 120–130 × 103/μL) presented to the emergency department (ED) after noticing an increase in bruising on her upper and lower extremities. When the patient was interviewed, it was found that her dose of citalopram had been recently increased from 20 to 40 mg/day and she had started ibuprofen (dose unknown) on her own to manage rib pain approximately 1 month after the citalopram dosage increase. The patient was advised to discontinue ibuprofen and was discharged. Shortly thereafter, she was started on oxaprozin 600 mg twice daily for management of trochanteric bursitis. She returned to the ED stating that bruising occurred 1 week after she was given oxaprozin. At this visit, the patient was told to discontinue oxaprozin and naproxen 440 mg twice daily was prescribed. One week later, the patient again returned to the ED with complaints of spontaneous bruising. At this point citalopram and naproxen were discontinued and she was started on acetaminophen (dose not documented) and buspirone 10 mg twice daily. No other episodes of ecchymosis have occurred in the 8 months since this change to her drug regimen. Discussion: Medications that increase the risk of bleeding should be carefully administered in patients who have a low platelet count. This patient experienced bruising when her dose of citalopram was increased and an increase in bruising when she combined an NSAID with citalopram. Selective serotonin reuptake inhibitors (SSRIs) may increase antiplatelet activity of NSAIDs and could therefore increase the risk of bruising. Use of the Horn Drug Interaction Probability Scale indicated a possible interaction with concomitant use of NSAIDs and citalopram. Conclusions: Patients who experience NSAID- and/or SSRI-related bruising should consult their providers and alternative treatments should be considered.

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38

Wells, D. S., F. W. Janssen, and H. W. Ruelius. "Interactions between oxaprozin glucuronide and human serum albumin." Xenobiotica 17, no. 12 (1987): 1437–49. http://dx.doi.org/10.3109/00498258709044004.

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39

&NA;. "A first for oxaprozin in the US market." Inpharma Weekly &NA;, no. 865 (1992): 23. http://dx.doi.org/10.2165/00128413-199208650-00049.

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40

Greenblatt, David J., and Joseph M. Scavone. "Pharmacokinetics of oxaprozin and other nonsteroidal antiinflammatory agents." Seminars in Arthritis and Rheumatism 15, no. 3 (1986): 18–26. http://dx.doi.org/10.1016/s0049-0172(86)80003-8.

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41

Dahl, Stephen L., and John R. Ward. "Efficacy and tolerability of oxaprozin in the elderly." Seminars in Arthritis and Rheumatism 15, no. 3 (1986): 40–46. http://dx.doi.org/10.1016/s0049-0172(86)80006-3.

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42

Powell, William R., Jeffrey L. Miller, and William B. Sheldon. "Once-daily oxaprozin and piroxicam compared in osteoarthritis." Seminars in Arthritis and Rheumatism 15, no. 3 (1986): 80–85. http://dx.doi.org/10.1016/s0049-0172(86)80012-9.

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43

Lazou, Marialena, Antonios G. Hatzidimitriou, Athanasios N. Papadopoulos, and George Psomas. "Zinc-oxaprozin compounds: Synthesis, structure and biological activity." Journal of Inorganic Biochemistry 195 (June 2019): 101–10. http://dx.doi.org/10.1016/j.jinorgbio.2019.03.016.

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44

Scavone, J. M., D. J. Greenblatt, R. Matlis, and J. S. Harmatz. "Interaction of oxaprozin with acetaminophen, cimetidine, and ranitidine." European Journal of Clinical Pharmacology 31, no. 3 (1986): 371–74. http://dx.doi.org/10.1007/bf00981141.

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45

Scavone, J. M., H. R. Ochs, D. J. Greenblatt, and R. Matlis. "Pharmacokinetics of oxaprozin in women receiving conjugated estrogen." European Journal of Clinical Pharmacology 35, no. 1 (1988): 105–8. http://dx.doi.org/10.1007/bf00555518.

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46

Pulini, M. "False-positive benzodiazepine urine test due to oxaprozin." JAMA: The Journal of the American Medical Association 273, no. 24 (1995): 1905–6. http://dx.doi.org/10.1001/jama.273.24.1905.

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47

Pulini, Marie. "False-positive Benzodiazepine Urine Test Due to Oxaprozin." JAMA: The Journal of the American Medical Association 273, no. 24 (1995): 1905. http://dx.doi.org/10.1001/jama.1995.03520480023025.

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48

Xu,, Xuetao, Jie Chen,, Zhiqing Lin,, et al. "Synthesis and Anti-inflammatory Effects of Oxaprozin-Paeonol Ester." Chinese Journal of Organic Chemistry 39, no. 10 (2019): 2958. http://dx.doi.org/10.6023/cjoc201903020.

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49

Fraser, A. D., and P. Howell. "Oxaprozin cross-reactivity in the Abbott FPIA benzodiazepine assay." Clinical Biochemistry 30, no. 4 (1997): 379. http://dx.doi.org/10.1016/s0009-9120(97)89015-7.

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50

Matuch-Hite, T., P. Jones, and J. Moriarity. "Interference of Oxaprozin with Benzodiazepines via Enzyme Immunoassay Technique." Journal of Analytical Toxicology 19, no. 2 (1995): 130. http://dx.doi.org/10.1093/jat/19.2.130.

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