Editing Celecoxib (section)

===Anti-inflammatory===
A highly selective reversible inhibitor of the [[COX-2]] isoform of [[cyclooxygenase]], celecoxib inhibits the transformation of arachidonic acid to prostaglandin precursors. Therefore, it has analgesic and anti-inflammatory properties.<ref name="Celebrex FDA label"/> Nonselective NSAIDs (such as aspirin, naproxen, and ibuprofen) inhibit both [[COX-1]] and COX-2. Inhibition of COX-1 (which celecoxib does not inhibit at therapeutic concentrations) inhibits the production of prostaglandins and the production of thromboxane A2, a platelet activator.<ref name="Celebrex FDA label"/> COX-1 is traditionally defined as a constitutively expressed "housekeeping" enzyme and plays a role in the protection of the gastrointestinal mucosa, kidney hemodynamics, and platelet thrombogenesis.<ref name=Mathew>{{cite journal | vauthors = Mathew ST, Devi SG, Prasanth VV, Vinod B | title = Efficacy and Safety of COX-2 Inhibitors in the Clinical Management of Arthritis: Mini Review | journal = ISRN Pharmacology | volume = 2011 | pages = 480291 | date = 2011 | pmid = 22084715 | pmc = 3197256 | doi = 10.5402/2011/480291 | doi-access = free }}</ref><ref name="Katzung">{{cite book| vauthors = Katzung BG |title=Basic & clinical pharmacology |date=2007 |publisher=McGraw-Hill Medical |location=New York |isbn=9780071451536 |page=579 |edition=10th }}</ref> COX-2, on the contrary, is extensively expressed in cells involved in inflammation and is upregulated by bacterial lipopolysaccharides, cytokines, growth factors, and tumor promoters.<ref name=Mathew/><ref name="Shi S and Koltz U">{{cite journal | vauthors = Shi S, Klotz U | title = Clinical use and pharmacological properties of selective COX-2 inhibitors | journal = European Journal of Clinical Pharmacology | volume = 64 | issue = 3 | pages = 233–52 | date = March 2008 | pmid = 17999057 | doi = 10.1007/s00228-007-0400-7 | s2cid = 24063728 }}</ref> Celecoxib is approximately 10-20 times more selective for COX-2 inhibition over COX-1.<ref name="Katzung"/><ref>{{cite journal | vauthors = Conaghan PG | title = A turbulent decade for NSAIDs: update on current concepts of classification, epidemiology, comparative efficacy, and toxicity | journal = Rheumatology International | volume = 32 | issue = 6 | pages = 1491–502 | date = June 2012 | pmid = 22193214 | pmc = 3364420 | doi = 10.1007/s00296-011-2263-6 }}</ref> It binds with its polar [[Sulfonamide (chemistry)|sulfonamide side chain]] to a hydrophilic side pocket region close to the active COX-2 binding site.<ref name="DiPiro_2008">{{cite book | vauthors = Dipiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM |title=Pharmacotherapy A Pathophysiologic Approach |date=2008 |publisher=McGraw-Hill Medical |location=New York |isbn=978-0-07-147899-1 |edition=7th}}</ref> In theory, this selectivity allows celecoxib and other COX-2 inhibitors to reduce [[inflammation]] (and pain) while minimizing gastrointestinal [[adverse drug reaction]]s (e.g. [[stomach ulcer]]s) that are common with nonselective NSAIDs.<ref>{{cite journal | vauthors = Bhatt DL, Scheiman J, Abraham NS, Antman EM, Chan FK, Furberg CD, Johnson DA, Mahaffey KW, Quigley EM, Harrington RA, Bates ER, Bridges CR, Eisenberg MJ, Ferrari VA, Hlatky MA, Kaul S, Lindner JR, Moliterno DJ, Mukherjee D, Schofield RS, Rosenson RS, Stein JH, Weitz HH, Wesley DJ | title = ACCF/ACG/AHA 2008 expert consensus document on reducing the gastrointestinal risks of antiplatelet therapy and NSAID use: a report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents | journal = Journal of the American College of Cardiology | volume = 52 | issue = 18 | pages = 1502–17 | date = October 2008 | pmid = 19017521 | doi = 10.1016/j.jacc.2008.08.002 | doi-access = free }}</ref>