DrugLib.com — Drug Information Portal

Rx drug information, pharmaceutical research, clinical trials, news, and more

Active ingredient: Naproxen - Brands, Medical Use, Clinical Data

Brands, Medical Use, Clinical Data

Drug Category

  • Anti-Inflammatory Agents, Non-Steroidal
  • Cyclooxygenase Inhibitors
  • Gout Suppressants

Dosage Forms

  • Suppository
  • Suspension
  • Tablet
  • Tablet (enteric-coated)
  • Tablet (extended-release)

Brands / Synonyms

Aleve; Anaprox; Bonyl; Diocodal; DL Naproxen; DL-Naproxen; Dysmenalgit; Ec-naprosyn; Equiproxen; Floginax; Laraflex; Laser; Mnpa; Naixan; Naprelan; Napren; Naprium; Naprius; Naprosine; Naprosyn; Naprosyne; Naproxen; Naproxen Sodium; Naprux; Naxen; Naxyn; Niaxan; Nycopren; Opipramol; Panoxen; Pranoxen; Prevacid Naprapac; Prexan; Proxen; Proxine; Reuxen; Treximet; Veradol; Vimovo; Xenar

Indications

For the treatment of rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, tendinitis, bursitis, and acute gout. Also for the relief of mild to moderate pain and the treatment of primary dysmenorrhea.

Pharmacology

Naproxen is a member of the arylacetic acid group of nonsteroidal anti-inflammatory drugs (NSAIDs). Naproxen has analgesic and antipyretic properties. As with other NSAIDs, its mode of action is not fully understood; however, its ability to inhibit prostaglandin synthesis may be involved in the anti-inflammatory effect.

Mechanism of Action

The mechanism of action of naproxen, like that of other NSAIDs, is believed to be associated with the inhibition of cyclooxygenase activity. Two unique cyclooxygenases have been described in mammals. The constitutive cyclooxygenase, COX-1, synthesizes prostaglandins necessary for normal gastrointestinal and renal function. The inducible cyclooxygenase, COX-2, generates prostaglandins involved in inflammation. Inhibition of COX-1 is thought to be associated with gastrointestinal and renal toxicity while inhibition of COX-2 provides anti-inflammatory activity.

Absorption

Naproxen itself is rapidly and completely absorbed from the GI tract with an in vivo bioavailability of 95%. Although naproxen itself is well absorbed, the sodium salt form is more rapidly absorbed resulting in higher peak plasma levels for a given dose. Food causes a slight decrease in the rate absorption.

Toxicity

ORAL (LD50): Acute: 248 mg/kg [Rat]. 360 mg/kg [Mouse]. Symptoms of overdose include drowsiness, heartburn, indigestion, nausea, and vomiting.

Biotrnasformation / Drug Metabolism

Naproxen is extensively metabolized to 6-0-desmethyl naproxen and both parent and metabolites do not induce metabolizing enzymes.

Contraindications

All naproxen products are contraindicated in patients who have had allergic reactions to prescription as well as to over-the-counter products containing naproxen. Anaphylactoid reactions may occur in patients without previous known exposure or hypersensitivity to aspirin, naproxen, or other NSAIDs, or in individuals with a history of angioedema, urticaria, bronchospastic reactivity (e.g. asthma), and nasal polyps. Anaphylactoid reactions, like anaphylaxis, may have a fatal outcome. Therefore, careful questioning of patients for such things as asthma, nasal polyps, urticaria, and hypotension associated with NSAIDs before starting therapy is important. In addition, if such symptoms occur during therapy, treatment with Naprelan should be discontinued.

Drug Interactions

The use of NSAIDs in patients who are receiving ACE inhibitors may potentiate renal disease states.

In vitro studies have shown that naproxen anion, because of its affinity for protein, may displace from their binding sites other drugs which are also albumin-bound .

Theoretically, the naproxen anion itself could likewise be displaced. Short-term controlled studies failed to show that taking the drug significantly affects prothrombin times when administered to individuals on coumarin-type anticoagulants. Caution is advised nonetheless, since interactions have been seen with other nonsteroidal agents of this class. Similarly, patients receiving the drug and a hydantoin, sulfonamide or sulfonylurea should be observed for signs of toxicity to these drugs.

Concomitant administration of naproxen and aspirin is not recommended because naproxen is displaced from its binding sites during the concomitant administration of aspirin, resulting in lower plasma concentrations and peak plasma levels.

The natriuretic effect of furosemide has been reported to be inhibited by some drugs of this class. Inhibition of renal lithium clearance leading to increases in plasma lithium concentrations has also been reported. Naproxen and other NSAIDs can reduce the antihypertensive effect of propranolol and other beta-blockers.

Probenecid given concurrently increases naproxen anion plasma levels and extends its plasma half-life significantly.

Caution should be used if naproxen is administered concomitantly with methotrexate. Naproxen, naproxen sodium and other NSAIDs have been reported to reduce the tubular secretion of methotrexate in an animal model, possibly increasing the toxicity of methotrexate.

Drug/Laboratory Test Interactions

Naproxen may decrease platelet aggregation and prolong bleeding time. This effect should be kept in mind when bleeding times are determined. The administration of naproxen may result in increased urinary values for 17-ketogenic steroids because of an interaction between the drug and/or its metabolites with m-dinitrobenzene used in this assay. Although 17-hydroxy-corticosteroid measurements (Porter-Silber test) do not appear to be artifactually altered, it is suggested that therapy with naproxen be temporarily discontinued 72 hours before adrenal function tests are performed if the Porter-Silber test is to be used.

Naproxen may interfere with some urinary assays of 5-hydroxy indoleacetic acid (5HIAA).

-- advertisement -- The American Red Cross
 
Home | About Us | Contact Us | Site usage policy | Privacy policy

All Rights reserved - Copyright DrugLib.com, 2006-2014