QuickView for Piroxicam (compound)

Summary
General Info

PubChem

PubChem Compound 10830762

Name:	Piroxicam
PubChem Compound ID:	10830762
Description:	A cyclooxygenase inhibiting, non-steroidal anti-inflammatory agent (NSAID) that is well established in treating rheumatoid arthritis and osteoarthritis and used for musculoskeletal disorders, dysmenorrhea, and postoperative pain. Its long half-life enables it to be administered once daily.
Molecular formula:	C₁₅H₁₃N₃O₄S
Molecular weight:	337.372 g/mol

DrugBank

Identification

Name:	Piroxicam
Name (isomeric):	DB00554
Drug Type:	small molecule
Description:	A cyclooxygenase inhibiting, non-steroidal anti-inflammatory agent (NSAID) that is well established in treating rheumatoid arthritis and osteoarthritis and used for musculoskeletal disorders, dysmenorrhea, and postoperative pain. Its long half-life enables it to be administered once daily.
Synonyms:	AK1015
Brand:	Pipoxicam, Reudene, piroxicam usp, Riacen, Pirkam, Artroxicam, Flogobene, Piroflex, Zunden, Apo-Piroxicam, Improntal, Bruxicam, Baxo, Sasulen, Solocalm, Larapam, Akten, Roxicam, Caliment, Geldene, Erazon, Feldene, Roxiden
Category:	Cyclooxygenase Inhibitors
CAS number:	36322-90-4

Pharmacology

Indication:	For treatment of osteoarthritis and rheumatoid arthritis.
Pharmacology:	Piroxicam is in a class of drugs called nonsteroidal anti-inflammatory drugs (NSAIDs). Piroxicam works by reducing hormones that cause inflammation and pain in the body. Piroxicam is used to reduce the pain, inflammation, and stiffness caused by rheumatoid arthritis and osteoarthritis.
Mechanism of Action:	The antiinflammatory effect of Piroxicam may result from the reversible inhibition of cyclooxygenase, causing the peripheral inhibition of prostaglandin synthesis. The prostaglandins are produced by an enzyme called Cox-1. Piroxicam blocks the Cox-1 enzyme, resulting into the disruption of production of prostaglandins. Piroxicam also inhibits the m... show more » The antiinflammatory effect of Piroxicam may result from the reversible inhibition of cyclooxygenase, causing the peripheral inhibition of prostaglandin synthesis. The prostaglandins are produced by an enzyme called Cox-1. Piroxicam blocks the Cox-1 enzyme, resulting into the disruption of production of prostaglandins. Piroxicam also inhibits the migration of leukocytes into sites of inflammation and prevents the formation of thromboxane A2, an aggregating agent, by the platelets. show less «
Absorption:	Well absorbed following oral administration.
Biotransformation:	Renal
Route of elimination:	Piroxicam and its biotransformation products are excreted in urine and feces, with about twice as much appearing in the urine as in the feces. Approximately 5% of a piroxicam dose is excreted unchanged. However, a substantial portion of piroxicam elimination occurs by hepatic metabolism. Piroxicam is excreted into human milk.
Half Life:	30 to 86 hours
Toxicity:	Symptoms of overdose include drowsiness, nausea, stomach pain, and/or vomiting.
Affected organisms:	Humans and other mammals

Interactions

Food interaction:

Take with food. Avoid alcohol.

Drug interaction:

Carteolol	Risk of inhibition of renal prostaglandins
Tamoxifen	Piroxicam may reduce clearance rate of Tamoxifen. Monitor for changes in therapeutic/adverse effects of Tamoxifen if Piroxicam is initiated, discontinued or dose changed.
Atenolol	Risk of inhibition of renal prostaglandins
Triflusal	The metabolite of triflusal, 2-hydroxy-4-trifluoro-methyl-benzoic acid (HTB), impairs the serum protein binding of glisentide to the same extent as acetylsalisylic acid. Thus, the free fraction of glisentide may be increased. A dosage reduction may be required if used in combination.
Penbutolol	Risk of inhibition of renal prostaglandins

Carteolol	Risk of inhibition of renal prostaglandins
Tamoxifen	Piroxicam may reduce clearance rate of Tamoxifen. Monitor for changes in therapeutic/adverse effects of Tamoxifen if Piroxicam is initiated, discontinued or dose changed.
Atenolol	Risk of inhibition of renal prostaglandins
Triflusal	The metabolite of triflusal, 2-hydroxy-4-trifluoro-methyl-benzoic acid (HTB), impairs the serum protein binding of glisentide to the same extent as acetylsalisylic acid. Thus, the free fraction of glisentide may be increased. A dosage reduction may be required if used in combination.
Penbutolol	Risk of inhibition of renal prostaglandins
Bisoprolol	Risk of inhibition of renal prostaglandins
Metoprolol	Risk of inhibition of renal prostaglandins
Anisindione	The NSAID, piroxicam, may increase the anticoagulant effect of anisindione.
Methotrexate	The NSAID, piroxicam, may decrease the renal excretion of methotrexate. Increased risk of methotrexate toxicity.
Bevantolol	Risk of inhibition of renal prostaglandins
Colesevelam	Bile acid sequestrants may decrease the absorption of Nonsteroidal Anti-Inflammatory Agents. Monitor for decreased serum concentrations/therapeutic effects of nonsteroidal anti-inflammatory agents (NSAID) if coadministered with bile acid sequestrants. Separating the administration of doses by 2 or more hours may reduce (but not eliminate) the risk of interaction. The manufacturer of colesevelam recommends that drugs should be administered at least 1 hour before or 4 hours after colesevelam.
Acebutolol	Risk of inhibition of renal prostaglandins
Trandolapril	The NSAID, Piroxicam, may reduce the antihypertensive effect of Trandolapril. Consider alternate therapy or monitor for changes in Trandolapril efficacy if Piroxicam is initiated, discontinued or dose changed.
Carvedilol	Risk of inhibition of renal prostaglandins
Labetalol	Risk of inhibition of renal prostaglandins
Warfarin	Piroxicam, a strong CYP2C9 inhibitor, may decrease the metabolism of warfarin. The antiplatelet effect of piroxicam may also increase the bleed risk associated with warfarin. Consider alternate therapy or monitor for changes in the therapeutic and adverse effects of warfarin if piroxicam is initiated, discontinued or dose changed.
Cyclosporine	Monitor for nephrotoxicity
Nadolol	Risk of inhibition of renal prostaglandins
Tolbutamide	Piroxicam, a strong CYP2C9 inhibitor, may decrease the metabolism and clearance of Tolbutamide, a CYP2C9 substrate. Consider alternate therapy or monitor for changes in Tolbutamide therapeutic and adverse effects if Piroxicam is initiated, discontinued or dose changed.
Sotalol	Risk of inhibition of renal prostaglandins
Voriconazole	Piroxicam, a strong CYP2C9 inhibitor, may increase the serum concentration of voriconazole by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of voriconazole if piroxicam is initiated, discontinued or dose changed.
Torasemide	Piroxicam, a strong CYP2C9 inhibitor, may increase the serum concentration of Torasemide, a CYP2C9 substrate, by decreasing Torasemide metabolism and clearance. Consider alternate therapy or monitor for changes in the therapeutic and adverse effects of Torasemide if Piroxicam is initiated, discontinued or dose changed.
Lithium	The NSAID, piroxicam, may decrease the renal excretion of lithium. Increased risk of lithium toxicity.
Oxprenolol	Risk of inhibition of renal prostaglandins
Telmisartan	Concomitant use of Telmisartan and Piroxicam may increase the risk of acute renal failure and hyperkalemia. Monitor renal function at the beginning and during treatment.
Trimethoprim	The strong CYP2C9 inhibitor, Piroxicam, may decrease the metabolism and clearance of Trimethoprim, a CYP2C9 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimethoprim if Piroxicam is initiated, discontinued or dose changed.
Acenocoumarol	The NSAID, piroxicam, may increase the anticoagulant effect of acenocoumarol.
Vilazodone	Increased risk of bleeding with concomitant use of NSAIDs and vilazodone
Ritonavir	Ritonavir increases the toxicity of piroxicam
Betaxolol	Nonsteroidal Anti-Inflammatory Agents such as piroxicam may diminish the antihypertensive effect of Beta-Blockers such as betaxolol. Monitor for increases in blood pressure if a nonsteroidal anti-inflammatory agent (NSAID) is initiated/dose increased, or decreases in blood pressure if a NSAID is discontinued/dose decreased; this is particularly important if NSAID treatment is for extended periods of time. Ophthalmic beta-blockers are likely of little concern.
Practolol	Risk of inhibition of renal prostaglandins
Timolol	Risk of inhibition of renal prostaglandins
Ginkgo biloba	Additive anticoagulant/antiplatelet effects may increase bleed risk. Concomitant therapy should be avoided.
Pindolol	Risk of inhibition of renal prostaglandins
Treprostinil	The prostacyclin analogue, Treprostinil, may increase the risk of bleeding when combined with the NSAID, Piroxicam. Monitor for increased bleeding during concomitant thearpy.
Alendronate	Increased risk of gastric toxicity
Dicumarol	The NSAID, piroxicam, may increase the anticoagulant effect of dicumarol.
Esmolol	Risk of inhibition of renal prostaglandins
Propranolol	Risk of inhibition of renal prostaglandins

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Targets

Prostaglandin G/H synthase 2

Prostaglandin G/H synthase 1

Enzymes

Cytochrome P450 2C9

Cytochrome P450 2C8

Transporters

Solute carrier family 22 member 6

Solute carrier family 22 member 8

Solute carrier family 22 member 11

Carriers

Serum albumin