1 safety notice
Genetic variations that may affect drug response
1 known genetic variation may influence how your body responds to Celecoxib 400mg capsules.Gene involved: CYP2C9
These are known genetic variations. They don't mean the medicine won't work for you — speak to your doctor or a pharmacogenomics specialist for personalised advice. Source: DrugBank (CC BY-NC 4.0).
rs1057910
CYP2C9
Patients with this genotype have reduced metabolism of celecoxib.
Official documents, adverse reaction reporting, and safety monitoring
Report a side effect
Submit a Yellow Card report to the MHRA
Official medicine documents
Source: MHRA Products DatabaseOGL 3.0
Updated 6 months ago(16 Jan 2026)Safety monitoring data
Yellow Card reports
MHRA
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
View Drug Analysis Profile
Suspected adverse reactions reported for Celecoxib
Browse all iDAP reports
Interactive Drug Analysis Profiles for all medicines
Report a side effect
Submit a Yellow Card report to the MHRA
Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
EMA
The European Medicines Agency (EMA) collects suspected adverse reaction reports from across the EU/EEA through the EudraVigilance system. Search for safety data on this medicine.
View EudraVigilance report
Suspected adverse reactions reported for Celecoxib
About EudraVigilance
Learn about EU pharmacovigilance and safety monitoring
EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
1 branded products available
WHO defined daily dose (DDD)
200 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via the NHS dm+d supplementary BNF/ATC mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
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Lumiracoxib 100mg tablets
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Same therapeutic group
Lumiracoxib 400mg tablets
Tablet
400mg
Same therapeutic group
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
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Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(1)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
Check stock at pharmacies and supply information
Pharmacy stock checkers
Search for this medicine at major UK pharmacy chains. These links open the retailer's own website — results depend on their current online catalogue.
Supply & safety information
Official UK regulator monitoring and safety alerts
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. Shortage and safety information sourced from MHRA drug safety updates (gov.uk, Crown Copyright under OGL v3.0).
Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF code shown is the factual mapping value distributed by NHS Business Services Authority (NHSBSA) in the dm+d supplementary file under OGL v3.0; it is not affiliated with, nor licensed from, the publishers of the British National Formulary. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Searching UK clinical trials...
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 17 · Randomised trials: 31 · 1999–2026
Showing the 50 most relevant studies, sorted by most relevant.
Efficacy, tolerability, and upper gastrointestinal safety of celecoxib for treatment of osteoarthritis and rheumatoid arthritis: systematic review of randomised controlled trials (opens in a new tab)
Jonathan J Deeks, Lesley A Smith, Matthew D Bradley
BMJ, 2002
Systematic review
Highly cited for its field
Cited by 370- Celecoxib
- Anti-Inflammatory Agents, Non-Steroidal
- Arthritis, Rheumatoid
Cyclooxygenase-2 selective non-steroidal anti-inflammatory drugs (etodolac, meloxicam, celecoxib, rofecoxib, etoricoxib, valdecoxib and lumiracoxib) for osteoarthritis and rheumatoid arthritis: a systematic review and economic evaluation (opens in a new tab)
Yen‐Fu Chen, Paresh Jobanputra, Pelham Barton, et al.
Health Technology Assessment, 2008
Systematic review
Highly cited for its field
Cited by 338- Anti-Ulcer Agents
- Arthritis, Rheumatoid
- Cost-Benefit Analysis
Risk of cardiovascular events and celecoxib: a systematic review and meta-analysis (opens in a new tab)
Brent Caldwell
Journal of the Royal Society of Medicine, 2006
Systematic review
Highly cited for its field
Cited by 226- Celecoxib
- Cardiovascular Diseases
- Prognosis
Tolerability and adverse events in clinical trials of celecoxib in osteoarthritis and rheumatoid arthritis: systematic review and meta-analysis of information from company clinical trial reports (opens in a new tab)
R Andrew Moore, Sheena Derry, Geoffrey Makinson, et al.
Arthritis Research & Therapy, 2005
Systematic review
Highly cited for its field
Cited by 225- Drug Industry
- Celecoxib
- Anti-Inflammatory Agents, Non-Steroidal
Neoadjuvant PD-1 blockade with toripalimab, with or without celecoxib, in mismatch repair-deficient or microsatellite instability-high, locally advanced, colorectal cancer (PICC): a single-centre, parallel-group, non-comparative, randomised, phase 2 trial. (opens in a new tab)
Huabin Hu, L. Kang, Jianwei Zhang, et al.
The lancet. Gastroenterology & hepatology, 2021
Randomised trial
Cited by 224Risk of Cardiovascular Events in Patients Receiving Celecoxib: A Meta-Analysis of Randomized Clinical Trials (opens in a new tab)
William B. White, Christine R. West, Jeffrey Borer, et al.
The American Journal of Cardiology, 2006
Meta-analysis
Highly cited for its field
Cited by 186- Celecoxib
- Anti-Inflammatory Agents, Non-Steroidal
- Cardiovascular Diseases
Efficacy of adjunctive celecoxib treatment for patients with major depressive disorder: A meta-analysis (opens in a new tab)
Kyoung‐Sae Na, Kang Joon Lee, Ji Sung Lee, et al.
Progress in Neuro-Psychopharmacology and Biological Psychiatry, 2013
Meta-analysis
Highly cited for its field
Cited by 177- Celecoxib
- Anti-Inflammatory Agents, Non-Steroidal
- Depressive Disorder, Major
Minocycline and celecoxib as adjunctive treatments for bipolar depression: a multicentre, factorial design randomised controlled trial (opens in a new tab)
Muhammad Ishrat Husain, Imran B. Chaudhry, Ameer B. Khoso, et al.
The Lancet Psychiatry, 2020
Randomised trial
Highly cited for its field
Cited by 165- Celecoxib
- Anti-Inflammatory Agents, Non-Steroidal
- Anti-Bacterial Agents
Gastrointestinal toxicity with celecoxib vs nonsteroidal anti-inflammatory drugs for osteoarthritis and rheumatoid arthritis: the CLASS study: A randomized controlled trial. Celecoxib Long-term Arthritis Safety Study. (opens in a new tab)
F. Silverstein, G. Faich, J. Goldstein, et al.
JAMA, 2000
Randomised trial
Highly cited for its field
Cited by 3,356- Celecoxib
- Analysis of Variance
- Anti-Inflammatory Agents, Non-Steroidal
Anti-inflammatory and upper gastrointestinal effects of celecoxib in rheumatoid arthritis: a randomized controlled trial. (opens in a new tab)
L. Simon, A. Weaver, D. Y. Graham, et al.
JAMA, 1999
Randomised trial
Highly cited for its field
Cited by 816- Celecoxib
- Analysis of Variance
- Anti-Inflammatory Agents, Non-Steroidal
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
155 found
Half-life
11 hours
Mechanism
Unlike most NSAIDs, which inhibit both types of cyclooxygenases (COX-1 and COX-2…
Food interactions
3 warnings
Human targets
7 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
200 mg
Celecoxib is absorbed rapidly in the gastrointestinal tract.
[A34124]
When a single oral dose of 200 mg was given to healthy research subjects,…
[A34124]
When a single oral dose of 200 mg was given to healthy research subjects,…
Half-life
11 hours
The effective half-life of celecoxib is approximately 11 hours when a single 200 mg dose is given to healthy subjects.
[L3296][L7646]…
[L3296][L7646]…
Protein binding
97%
The protein binding of celecoxib is 97%, and it is primarily bound to albumin.
[A4983][L7646]
[A4983][L7646]
Volume of distribution
429 L
The apparent volume of distribution of celecoxib at steady state (Vss/F) is about 429 L[L3296], which suggests wide distribution into various tissues.…
Metabolism
A large part of celecoxib metabolism is mediated by cytochrome P450 2C9 in the liver with some contribution from CYP3A4 and CYP2C8 and possible contributions from CYP2D6.[A34124,A181379,A38563,T647]…
Elimination
3%
Celecoxib is primarily eliminated by hepatic metabolism with small amounts (<3%) of the unchanged drug found in both the urine and feces.
[A4983]
About 57% of an oral dose of celecoxib is excreted in the feces and 27% is found to be excreted into the urine in the form of metabolites. The main metabolite in urine and feces is identified as the carboxylic acid metabolite (73%). The amount of glucuronide in the urine is reported to be low.
[L7646]
[A4983]
About 57% of an oral dose of celecoxib is excreted in the feces and 27% is found to be excreted into the urine in the form of metabolites. The main metabolite in urine and feces is identified as the carboxylic acid metabolite (73%). The amount of glucuronide in the urine is reported to be low.
[L7646]
Clearance
200 mg
Apparent clearance (CL/F), single oral 200 mg dose, healthy subjects = 27.7…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Status:
Approved
Investigational
Small molecule
About this compound
Celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, is a nonsteroidal anti-inflammatory drug (NSAID) which is known for its decreased risk of causing gastrointestinal bleeding compared to other NSAIDS.[A181544] It is used to manage symptoms of various types of arthritis pain and in familial adenomatous polyposis (FAP) to reduce precancerous polyps in the colon.[A181532] It is marketed by Pfizer under the brand name Celebrex, and was initially granted FDA approval in 1998.[L7604]
Interestingly, selective COX-2 inhibitors (especially celecoxib), have been evaluated as potential cancer chemopreventive and therapeutic drugs in clinical trials for a variety of malignancies.[A34124]
Interestingly, selective COX-2 inhibitors (especially celecoxib), have been evaluated as potential cancer chemopreventive and therapeutic drugs in clinical trials for a variety of malignancies.[A34124]
Properties:
solid
Avg. mass: 381.37 Da
DrugBank indication
Celecoxib is indicated for symptomatic treatment of adult osteoarthritis (OA) and adult rheumatoid arthritis (RA).
[L7646]
Celecoxib is not a substitute for aspirin for cardiovascular event prophylaxis.
[L7646]
It may be also be used to treat acute pain from various sources, juvenile rheumatoid arthritis in children over 2, ankylosing spondylitis, and primary dysmenorrhea.
[L7646]
Celecoxib, in combination with [tramadol], is indicated for the management of acute pain in adults severe enough to require an opioid analgesic and in whom alternative treatments are inadequate.
[L38949]
[L7646]
Celecoxib is not a substitute for aspirin for cardiovascular event prophylaxis.
[L7646]
It may be also be used to treat acute pain from various sources, juvenile rheumatoid arthritis in children over 2, ankylosing spondylitis, and primary dysmenorrhea.
[L7646]
Celecoxib, in combination with [tramadol], is indicated for the management of acute pain in adults severe enough to require an opioid analgesic and in whom alternative treatments are inadequate.
[L38949]
Also known as(116)
Celecoxib
Célécoxib
Celecoxibum
p-(5-p-Tolyl-3-(trifluoromethyl)pyrazol-1-yl)benzenesulfonamide
1.14.99.1
COX-2
COX2
Cyclooxygenase-2
Molecular properties(19)
Drug interactions(1899)
Known interactions with other medications. Always consult a healthcare professional.
Pravastatin
Moderate
Celecoxib may decrease the excretion rate of Pravastatin which could result in a higher serum level.
Celecoxib may decrease the excretion rate of Atropine which could result in a higher serum level.
Fluorescein
Moderate
Celecoxib may decrease the excretion rate of Fluorescein which could result in a higher serum level.
Disulfiram
Moderate
Celecoxib may decrease the excretion rate of Disulfiram which could result in a higher serum level.
Celecoxib may decrease the excretion rate of Ezetimibe which could result in a higher serum level.
Celecoxib may decrease the excretion rate of Ofloxacin which could result in a higher serum level.
Celecoxib may decrease the excretion rate of Glycochenodeoxycholic Acid which could result in a higher serum level.
Prasterone sulfate
Moderate
Celecoxib may decrease the excretion rate of Prasterone sulfate which could result in a higher serum level.
Celecoxib may decrease the excretion rate of Indocyanine green acid form which could result in a higher serum level.
Pilsicainide
Moderate
Celecoxib may decrease the excretion rate of Pilsicainide which could result in a higher serum level.
Dihydroergocristine
Moderate
Celecoxib may decrease the excretion rate of Dihydroergocristine which could result in a higher serum level.
Glycyrrhizic acid
Moderate
Celecoxib may decrease the excretion rate of Glycyrrhizic acid which could result in a higher serum level.
Celecoxib may decrease the excretion rate of Cefaclor which could result in a higher serum level.
Tinidazole
Moderate
Celecoxib may decrease the excretion rate of Tinidazole which could result in a higher serum level.
Fenofibrate
Moderate
Celecoxib may decrease the excretion rate of Fenofibrate which could result in a higher serum level.
Rosuvastatin
Moderate
Celecoxib may decrease the excretion rate of Rosuvastatin which could result in a higher serum level.
Flucloxacillin
Moderate
Celecoxib may decrease the excretion rate of Flucloxacillin which could result in a higher serum level.
Atorvastatin
Moderate
Celecoxib may decrease the excretion rate of Atorvastatin which could result in a higher serum level.
Belantamab mafodotin
Moderate
Celecoxib may decrease the excretion rate of Belantamab mafodotin which could result in a higher serum level.
Brexpiprazole
Moderate
The metabolism of Brexpiprazole can be decreased when combined with Celecoxib.
Eliglustat
Moderate
The metabolism of Celecoxib can be decreased when combined with Eliglustat.
Isoetharine
Unknown severity
The risk or severity of hypertension can be increased when Isoetharine is combined with Celecoxib.
Zolmitriptan
Unknown severity
The risk or severity of hypertension can be increased when Zolmitriptan is combined with Celecoxib.
Norepinephrine
Unknown severity
The risk or severity of hypertension can be increased when Norepinephrine is combined with Celecoxib.
Phenylephrine
Unknown severity
The risk or severity of hypertension can be increased when Phenylephrine is combined with Celecoxib.
Phenylpropanolamine
Unknown severity
The risk or severity of hypertension can be increased when Phenylpropanolamine is combined with Celecoxib.
Droperidol
Unknown severity
The risk or severity of hypertension can be increased when Droperidol is combined with Celecoxib.
The risk or severity of hypertension can be increased when Celecoxib is combined with Doxapram.
The risk or severity of hypertension can be increased when Celecoxib is combined with Linezolid.
Metaraminol
Unknown severity
The risk or severity of hypertension can be increased when Celecoxib is combined with Metaraminol.
Furazolidone
Unknown severity
The risk or severity of hypertension can be increased when Celecoxib is combined with Furazolidone.
Methoxamine
Unknown severity
The risk or severity of hypertension can be increased when Celecoxib is combined with Methoxamine.
Isoflurane
Unknown severity
The risk or severity of hypertension can be increased when Celecoxib is combined with Isoflurane.
Propiomazine
Unknown severity
The risk or severity of hypertension can be increased when Celecoxib is combined with Propiomazine.
Orciprenaline
Unknown severity
The risk or severity of hypertension can be increased when Celecoxib is combined with Orciprenaline.
Phenmetrazine
Unknown severity
The risk or severity of hypertension can be increased when Celecoxib is combined with Phenmetrazine.
Pseudoephedrine
Unknown severity
The risk or severity of hypertension can be increased when Celecoxib is combined with Pseudoephedrine.
The risk or severity of hypertension can be increased when Celecoxib is combined with Ritodrine.
Remifentanil
Unknown severity
The risk or severity of hypertension can be increased when Celecoxib is combined with Remifentanil.
Bitolterol
Unknown severity
The risk or severity of hypertension can be increased when Celecoxib is combined with Bitolterol.
Oxymetazoline
Unknown severity
The risk or severity of hypertension can be increased when Celecoxib is combined with Oxymetazoline.
Diethylpropion
Unknown severity
The risk or severity of hypertension can be increased when Celecoxib is combined with Diethylpropion.
Naratriptan
Unknown severity
The risk or severity of hypertension can be increased when Celecoxib is combined with Naratriptan.
Frovatriptan
Unknown severity
The risk or severity of hypertension can be increased when Celecoxib is combined with Frovatriptan.
Isoprenaline
Unknown severity
The risk or severity of hypertension can be increased when Celecoxib is combined with Isoprenaline.
Arbutamine
Unknown severity
The risk or severity of hypertension can be increased when Celecoxib is combined with Arbutamine.
Desflurane
Unknown severity
The risk or severity of hypertension can be increased when Celecoxib is combined with Desflurane.
Isocarboxazid
Unknown severity
The risk or severity of hypertension can be increased when Celecoxib is combined with Isocarboxazid.
The risk or severity of hypertension can be increased when Celecoxib is combined with Fenoterol.
Pirbuterol
Unknown severity
The risk or severity of hypertension can be increased when Celecoxib is combined with Pirbuterol.
Showing 50 of 1899 interactions
Food & lifestyle interactions
Avoid Alcohol
Avoid alcohol. Alcohol increases the risk of gastrointestinal irritation.
Advice
Avoid multivalent ions. Separate the administration of aluminum and magnesium containing drugs by several hours.
Advice
Take with or without food. Doses up to 200 mg can be taken without regard to food, but doses of 400mg or higher should be taken with food.
Toxicity & overdose
The oral TDLo in humans 5.71 mg/kg.
[L7610]
It is not advisable to administer celecoxib in patients with renal impairment or advanced hepatic impairment, as this may lead to increased serum concentrations, causing toxicity.
[L7646]
Symptoms of overdose may include breathing difficulties, coma, drowsiness, gastrointestinal bleeding, high blood pressure, kidney failure, nausea, sluggishness, stomach pain, and vomiting.
[L3293]
Because serious gastrointestinal tract ulceration and bleeding can occur without preceding symptoms, patients should be monitored for signs/symptoms of gastrointestinal bleeding. Symptomatic and supportive measures should be taken in a celecoxib overdose. The induction of emesis or administration of active charcoal should take place if the patient is seen within 4 hours of celecoxib ingestion.
Diuresis, urinary alkalinization, hemodialysis, or hemoperfusion may not be useful in a celecoxib overdose due to its high level of protein binding.
[L7646]
[L7610]
It is not advisable to administer celecoxib in patients with renal impairment or advanced hepatic impairment, as this may lead to increased serum concentrations, causing toxicity.
[L7646]
Symptoms of overdose may include breathing difficulties, coma, drowsiness, gastrointestinal bleeding, high blood pressure, kidney failure, nausea, sluggishness, stomach pain, and vomiting.
[L3293]
Because serious gastrointestinal tract ulceration and bleeding can occur without preceding symptoms, patients should be monitored for signs/symptoms of gastrointestinal bleeding. Symptomatic and supportive measures should be taken in a celecoxib overdose. The induction of emesis or administration of active charcoal should take place if the patient is seen within 4 hours of celecoxib ingestion.
Diuresis, urinary alkalinization, hemodialysis, or hemoperfusion may not be useful in a celecoxib overdose due to its high level of protein binding.
[L7646]
How it works
Mechanism of action
Unlike most NSAIDs, which inhibit both types of cyclooxygenases (COX-1 and COX-2), celecoxib is a selective noncompetitive inhibitor of cyclooxygenase-2 (COX-2) enzyme. COX-2 is expressed heavily in inflamed tissues where it is induced by inflammatory mediators.[L7646] The inhibition of this enzyme reduces the synthesis of metabolites that include prostaglandin E2 (PGE2), prostacyclin (PGI2), thromboxane (TXA2), prostaglandin D2 (PGD2), and prostaglandin F2 (PGF2). Resultant inhibition of these mediators leads to the alleviation of pain and inflammation.[A34124][L7646]
By inhibiting prostaglandin synthesis, non-steroidal anti-inflammatory drugs (NSAIDs) cause mucosal damage, ulceration and ulcer complication throughout the gastrointestinal tract.[L7646] Celecoxib poses less of an ulceration risk than other NSAIDS, owing to its decreased effect on gastric mucosal prostaglandin synthesis when compared to placebo.[A34152]
Celecoxib exerts anticancer effects by binding to the cadherin-11 (CDH11)protein, which is thought to be involved in the progression of tumors, and inhibiting the 3-phosphoinositide-dependent kinase-1 (PDK-1) signaling mechanism.[T647,A11861] In addition, celecoxib has been found to inhibit carbonic anhydrase enzymes 2 and 3, further enhancing its anticancer effects.[A28426][A20066]
As mentioned in the pharmacodynamics section of this drug entry, celecoxib may cause an increased risk of thrombotic events. The risk of thrombosis resulting from COX-2 inhibition is caused by the vasoconstricting actions of thromboxane A2, leading to enhanced platelet aggregation, which is uncontrolled when the actions of prostacyclin, a platelet aggregation inhibitor, are suppressed through the inhibition of COX-2.[L7622]
By inhibiting prostaglandin synthesis, non-steroidal anti-inflammatory drugs (NSAIDs) cause mucosal damage, ulceration and ulcer complication throughout the gastrointestinal tract.[L7646] Celecoxib poses less of an ulceration risk than other NSAIDS, owing to its decreased effect on gastric mucosal prostaglandin synthesis when compared to placebo.[A34152]
Celecoxib exerts anticancer effects by binding to the cadherin-11 (CDH11)protein, which is thought to be involved in the progression of tumors, and inhibiting the 3-phosphoinositide-dependent kinase-1 (PDK-1) signaling mechanism.[T647,A11861] In addition, celecoxib has been found to inhibit carbonic anhydrase enzymes 2 and 3, further enhancing its anticancer effects.[A28426][A20066]
As mentioned in the pharmacodynamics section of this drug entry, celecoxib may cause an increased risk of thrombotic events. The risk of thrombosis resulting from COX-2 inhibition is caused by the vasoconstricting actions of thromboxane A2, leading to enhanced platelet aggregation, which is uncontrolled when the actions of prostacyclin, a platelet aggregation inhibitor, are suppressed through the inhibition of COX-2.[L7622]
Pharmacodynamics
Celecoxib inhibits cyclooxygenase 2 (COX-2) enzyme, reducing pain and inflammation. It is important to note that though the risk of bleeding with celecoxib is lower than with certain other NSAIDS, it exists nonetheless and caution must be observed when it is administered to those with a high risk of gastrointestinal bleeding.[L7607]
A note on the risk of cardiovascular events
Significant concerns regarding the safety of COX-2 selective NSAIDs emerged in the early 2000s. [Rofecoxib], another member of the COX-2 inhibitor drug class, also known as Vioxx, was withdrawn from the market due to prothrombotic cardiovascular risks.[L7622] Following an FDA Advisory Committee meeting in 2005, in which data from large clinical outcome trials were evaluated, the FDA concluded that the risk for cardiovascular thrombotic events for both COX-2 selective NSAIDs and nonselective NSAIDs was evident.[L3293] It was determined that the benefits of celecoxib treatment, however, outweighed the risks.[L7622] Postmarketing cardiovascular outcomes trial (PRECISION) revealed that the lowest possible dose of celecoxib was similar in cardiovascular safety to moderate strength doses of both naproxen and ibuprofen. Patients who had previous cardiovascular events including acute MI, coronary revascularization, or coronary stent insertion were not evaluated in the trial. It is not advisable to administer NSAIDS to these groups of patients.[L3293]
A note on the risk of cardiovascular events
Significant concerns regarding the safety of COX-2 selective NSAIDs emerged in the early 2000s. [Rofecoxib], another member of the COX-2 inhibitor drug class, also known as Vioxx, was withdrawn from the market due to prothrombotic cardiovascular risks.[L7622] Following an FDA Advisory Committee meeting in 2005, in which data from large clinical outcome trials were evaluated, the FDA concluded that the risk for cardiovascular thrombotic events for both COX-2 selective NSAIDs and nonselective NSAIDs was evident.[L3293] It was determined that the benefits of celecoxib treatment, however, outweighed the risks.[L7622] Postmarketing cardiovascular outcomes trial (PRECISION) revealed that the lowest possible dose of celecoxib was similar in cardiovascular safety to moderate strength doses of both naproxen and ibuprofen. Patients who had previous cardiovascular events including acute MI, coronary revascularization, or coronary stent insertion were not evaluated in the trial. It is not advisable to administer NSAIDS to these groups of patients.[L3293]
Pharmacokinetics
How the body processes this drug — absorption, distribution, metabolism, and elimination
Absorption
Celecoxib is absorbed rapidly in the gastrointestinal tract.
[A34124]
When a single oral dose of 200 mg was given to healthy research subjects, the peak plasma levels of celecoxib occurred within 3 hours.
[A34124][L7646]
The Cmax is 705 ng/mL.
[L3296]
When multiple doses are given, steady-state concentrations are reached on or before day 5. When taken with a high-fat meal, peak plasma levels are delayed for about 1 to 2 hours with an increase in total absorption (AUC) of 10% to 20%.
[L7646]
The AUC of celecoxib has been shown to be significantly lower in patients with chronic renal impairment.
[A4983][L7646]
A meta-analysis of pharmacokinetic studies has suggested an approximately 40% higher AUC (area under the curve) of celecoxib in black patients compared to Caucasians for unknown reasons.
[L3296]
[A34124]
When a single oral dose of 200 mg was given to healthy research subjects, the peak plasma levels of celecoxib occurred within 3 hours.
[A34124][L7646]
The Cmax is 705 ng/mL.
[L3296]
When multiple doses are given, steady-state concentrations are reached on or before day 5. When taken with a high-fat meal, peak plasma levels are delayed for about 1 to 2 hours with an increase in total absorption (AUC) of 10% to 20%.
[L7646]
The AUC of celecoxib has been shown to be significantly lower in patients with chronic renal impairment.
[A4983][L7646]
A meta-analysis of pharmacokinetic studies has suggested an approximately 40% higher AUC (area under the curve) of celecoxib in black patients compared to Caucasians for unknown reasons.
[L3296]
Half-life
The effective half-life of celecoxib is approximately 11 hours when a single 200 mg dose is given to healthy subjects.
[L3296][L7646]
The terminal half-life of celecoxib varies because of its low solubility, which prolongs absorption.
[L7646]
[L3296][L7646]
The terminal half-life of celecoxib varies because of its low solubility, which prolongs absorption.
[L7646]
Protein binding
The protein binding of celecoxib is 97%, and it is primarily bound to albumin.
[A4983][L7646]
[A4983][L7646]
Volume of distribution
The apparent volume of distribution of celecoxib at steady state (Vss/F) is about 429 L[L3296], which suggests wide distribution into various tissues. Celecoxib is not preferentially bound to red blood cells.
[L7646]
Another resource reports a volume of distribution of 455 ± 166L.
[A4983]
[L7646]
Another resource reports a volume of distribution of 455 ± 166L.
[A4983]
Metabolism
A large part of celecoxib metabolism is mediated by cytochrome P450 2C9 in the liver with some contribution from CYP3A4 and CYP2C8 and possible contributions from CYP2D6.[A34124,A181379,A38563,T647] It is metabolized by biotransformation to carboxylic acid and glucuronide metabolites.
[A4983]
Three metabolites, a primary alcohol, a carboxylic acid, and a glucuronide conjugate, have been found in human plasma after celecoxib administration.
[A34124]
These are considered inactive metabolites in regards to COX enzyme inhibition. Patients who are known or suspected to have decreased cytochrome P450 2C9 activity or function, based on their previous history, should be administered celecoxib with caution as they may have abnormally high serum concentrations resulting from decreased metabolism celecoxib.
[L7646]
[A4983]
Three metabolites, a primary alcohol, a carboxylic acid, and a glucuronide conjugate, have been found in human plasma after celecoxib administration.
[A34124]
These are considered inactive metabolites in regards to COX enzyme inhibition. Patients who are known or suspected to have decreased cytochrome P450 2C9 activity or function, based on their previous history, should be administered celecoxib with caution as they may have abnormally high serum concentrations resulting from decreased metabolism celecoxib.
[L7646]
Route of elimination
Celecoxib is primarily eliminated by hepatic metabolism with small amounts (<3%) of the unchanged drug found in both the urine and feces.
[A4983]
About 57% of an oral dose of celecoxib is excreted in the feces and 27% is found to be excreted into the urine in the form of metabolites. The main metabolite in urine and feces is identified as the carboxylic acid metabolite (73%). The amount of glucuronide in the urine is reported to be low.
[L7646]
[A4983]
About 57% of an oral dose of celecoxib is excreted in the feces and 27% is found to be excreted into the urine in the form of metabolites. The main metabolite in urine and feces is identified as the carboxylic acid metabolite (73%). The amount of glucuronide in the urine is reported to be low.
[L7646]
Clearance
Apparent clearance (CL/F), single oral 200 mg dose, healthy subjects = 27.7 L/hr.
[L7646]
Clearance may be decreased by about 47% in patients with chronic renal insufficiency, according to a pharmacokinetic study. Studies have not been performed in patients with severe renal impairment.
[L7646]
[L7646]
Clearance may be decreased by about 47% in patients with chronic renal insufficiency, according to a pharmacokinetic study. Studies have not been performed in patients with severe renal impairment.
[L7646]
Drug targets(7)
Proteins and enzymes this drug interacts with in the body
Prostaglandin G/H synthase 2
PTGS2
inhibitor
Specific functionenzyme binding
Cellular location
Microsome membrane
General function & pharmacology
Dual cyclooxygenase and peroxidase in the biosynthesis pathway of prostanoids, a class of C20 oxylipins mainly derived from arachidonate ((5Z,8Z,11Z,14Z)-eicosatetraenoate, AA, C20:4(n-6)), with a particular role in the inflammatory response .
PMID:11939906 PMID:16373578 PMID:19540099 PMID:22942274 PMID:26859324 PMID:27226593 PMID:7592599 PMID:7947975 PMID:9261177
The cyclooxygenase activity oxygenates AA to the hydroperoxy endoperoxide prostaglandin G2 (PGG2), and the peroxidase activity reduces PGG2 to the hydroxy endoperoxide prostaglandin H2 (PGH2), the precursor of all 2-series prostaglandins and thromboxanes .
PMID:16373578 PMID:22942274 PMID:26859324 PMID:27226593 PMID:7592599 PMID:7947975 PMID:9261177
This complex transformation is initiated by abstraction of hydrogen at carbon 13 (with S-stereochemistry), followed by insertion of molecular O2 to form the endoperoxide bridge between carbon 9 and 11 that defines prostaglandins. The insertion of a second molecule of O2 (bis-oxygenase activity) yields a hydroperoxy group in PGG2 that is then reduced to PGH2 by two electrons .
PMID:16373578 PMID:22942274 PMID:26859324 PMID:27226593 PMID:7592599 PMID:7947975 PMID:9261177
Similarly catalyzes successive cyclooxygenation and peroxidation of dihomo-gamma-linoleate (DGLA, C20:3(n-6)) and eicosapentaenoate (EPA, C20:5(n-3)) to corresponding PGH1 and PGH3, the precursors of 1- and 3-series prostaglandins .
PMID:11939906 PMID:19540099
In an alternative pathway of prostanoid biosynthesis, converts 2-arachidonoyl lysophopholipids to prostanoid lysophopholipids, which are then hydrolyzed by intracellular phospholipases to release free prostanoids .
PMID:27642067
Metabolizes 2-arachidonoyl glycerol yielding the glyceryl ester of PGH2, a process that can contribute to pain response .
PMID:22942274
Generates lipid mediators from n-3 and n-6 polyunsaturated fatty acids (PUFAs) via a lipoxygenase-type mechanism. Oxygenates PUFAs to hydroperoxy compounds and then reduces them to corresponding alcohols .
PMID:11034610 PMID:11192938 PMID:9048568 PMID:9261177
Plays a role in the generation of resolution phase interaction products (resolvins) during both sterile and infectious inflammation .
PMID:12391014
Metabolizes docosahexaenoate (DHA, C22:6(n-3)) to 17R-HDHA, a precursor of the D-series resolvins (RvDs) .
PMID:12391014
As a component of the biosynthetic pathway of E-series resolvins (RvEs), converts eicosapentaenoate (EPA, C20:5(n-3)) primarily to 18S-HEPE that is further metabolized by ALOX5 and LTA4H to generate 18S-RvE1 and 18S-RvE2 .
PMID:21206090
In vascular endothelial cells, converts docosapentaenoate (DPA, C22:5(n-3)) to 13R-HDPA, a precursor for 13-series resolvins (RvTs) shown to activate macrophage phagocytosis during bacterial infection .
PMID:26236990
In activated leukocytes, contributes to oxygenation of hydroxyeicosatetraenoates (HETE) to diHETES (5,15-diHETE and 5,11-diHETE) .
PMID:22068350 PMID:26282205
Can also use linoleate (LA, (9Z,12Z)-octadecadienoate, C18:2(n-6)) as substrate and produce hydroxyoctadecadienoates (HODEs) in a regio- and stereospecific manner, being (9R)-HODE ((9R)-hydroxy-(10E,12Z)-octadecadienoate) and (13S)-HODE ((13S)-hydroxy-(9Z,11E)-octadecadienoate) its major products (By similarity).
During neuroinflammation, plays a role in neuronal secretion of specialized preresolving mediators (SPMs) 15R-lipoxin A4 that regulates phagocytic microglia (By similarity)
PMID:11939906 PMID:16373578 PMID:19540099 PMID:22942274 PMID:26859324 PMID:27226593 PMID:7592599 PMID:7947975 PMID:9261177
The cyclooxygenase activity oxygenates AA to the hydroperoxy endoperoxide prostaglandin G2 (PGG2), and the peroxidase activity reduces PGG2 to the hydroxy endoperoxide prostaglandin H2 (PGH2), the precursor of all 2-series prostaglandins and thromboxanes .
PMID:16373578 PMID:22942274 PMID:26859324 PMID:27226593 PMID:7592599 PMID:7947975 PMID:9261177
This complex transformation is initiated by abstraction of hydrogen at carbon 13 (with S-stereochemistry), followed by insertion of molecular O2 to form the endoperoxide bridge between carbon 9 and 11 that defines prostaglandins. The insertion of a second molecule of O2 (bis-oxygenase activity) yields a hydroperoxy group in PGG2 that is then reduced to PGH2 by two electrons .
PMID:16373578 PMID:22942274 PMID:26859324 PMID:27226593 PMID:7592599 PMID:7947975 PMID:9261177
Similarly catalyzes successive cyclooxygenation and peroxidation of dihomo-gamma-linoleate (DGLA, C20:3(n-6)) and eicosapentaenoate (EPA, C20:5(n-3)) to corresponding PGH1 and PGH3, the precursors of 1- and 3-series prostaglandins .
PMID:11939906 PMID:19540099
In an alternative pathway of prostanoid biosynthesis, converts 2-arachidonoyl lysophopholipids to prostanoid lysophopholipids, which are then hydrolyzed by intracellular phospholipases to release free prostanoids .
PMID:27642067
Metabolizes 2-arachidonoyl glycerol yielding the glyceryl ester of PGH2, a process that can contribute to pain response .
PMID:22942274
Generates lipid mediators from n-3 and n-6 polyunsaturated fatty acids (PUFAs) via a lipoxygenase-type mechanism. Oxygenates PUFAs to hydroperoxy compounds and then reduces them to corresponding alcohols .
PMID:11034610 PMID:11192938 PMID:9048568 PMID:9261177
Plays a role in the generation of resolution phase interaction products (resolvins) during both sterile and infectious inflammation .
PMID:12391014
Metabolizes docosahexaenoate (DHA, C22:6(n-3)) to 17R-HDHA, a precursor of the D-series resolvins (RvDs) .
PMID:12391014
As a component of the biosynthetic pathway of E-series resolvins (RvEs), converts eicosapentaenoate (EPA, C20:5(n-3)) primarily to 18S-HEPE that is further metabolized by ALOX5 and LTA4H to generate 18S-RvE1 and 18S-RvE2 .
PMID:21206090
In vascular endothelial cells, converts docosapentaenoate (DPA, C22:5(n-3)) to 13R-HDPA, a precursor for 13-series resolvins (RvTs) shown to activate macrophage phagocytosis during bacterial infection .
PMID:26236990
In activated leukocytes, contributes to oxygenation of hydroxyeicosatetraenoates (HETE) to diHETES (5,15-diHETE and 5,11-diHETE) .
PMID:22068350 PMID:26282205
Can also use linoleate (LA, (9Z,12Z)-octadecadienoate, C18:2(n-6)) as substrate and produce hydroxyoctadecadienoates (HODEs) in a regio- and stereospecific manner, being (9R)-HODE ((9R)-hydroxy-(10E,12Z)-octadecadienoate) and (13S)-HODE ((13S)-hydroxy-(9Z,11E)-octadecadienoate) its major products (By similarity).
During neuroinflammation, plays a role in neuronal secretion of specialized preresolving mediators (SPMs) 15R-lipoxin A4 that regulates phagocytic microglia (By similarity)
Sialidase-1
NEU1
inhibitor
Specific functionalpha-sialidase activity
Cellular location
Lysosome membrane
General function & pharmacology
Catalyzes the removal of sialic acid (N-acetylneuraminic acid) moieties from glycoproteins and glycolipids. To be active, it is strictly dependent on its presence in the multienzyme complex. Appears to have a preference for alpha 2-3 and alpha 2-6 sialyl linkage
Signal transducer and activator of transcription 3
STAT3
inhibitor
Specific functionCCR5 chemokine receptor binding
Cellular location
Cytoplasm
General function & pharmacology
Signal transducer and transcription activator that mediates cellular responses to interleukins, KITLG/SCF, LEP and other growth factors .
PMID:10688651 PMID:12359225 PMID:12873986 PMID:15194700 PMID:15653507 PMID:16285960 PMID:17344214 PMID:18242580 PMID:18782771 PMID:22306293 PMID:23084476 PMID:28262505 PMID:32929201 PMID:38404237
Once activated, recruits coactivators, such as NCOA1 or MED1, to the promoter region of the target gene .
PMID:15653507 PMID:16285960 PMID:17344214 PMID:18782771 PMID:28262505 PMID:32929201
May mediate cellular responses to activated FGFR1, FGFR2, FGFR3 and FGFR4 .
PMID:12873986
Upon activation of IL6ST/gp130 signaling by interleukin-6 (IL6), binds to the IL6-responsive elements identified in the promoters of various acute-phase protein genes .
PMID:12359225
Activated by IL31 through IL31RA .
PMID:15194700
Acts as a regulator of inflammatory response by regulating differentiation of naive CD4(+) T-cells into T-helper Th17 or regulatory T-cells (Treg): acetylation promotes its transcription activity and cell differentiation while deacetylation and oxidation of lysine residues by LOXL3 inhibits differentiation .
PMID:28065600 PMID:28262505
Involved in cell cycle regulation by inducing the expression of key genes for the progression from G1 to S phase, such as CCND1 .
PMID:17344214
Mediates the effects of LEP on melanocortin production, body energy homeostasis and lactation (By similarity). May play an apoptotic role by transctivating BIRC5 expression under LEP activation .
PMID:18242580
Cytoplasmic STAT3 represses macroautophagy by inhibiting EIF2AK2/PKR activity .
PMID:23084476
Plays a crucial role in basal beta cell functions, such as regulation of insulin secretion (By similarity). Following JAK/STAT signaling activation and as part of a complex with NFATC3 and NFATC4, binds to the alpha-beta E4 promoter region of CRYAB and activates transcription in cardiomyocytes (By similarity)
PMID:10688651 PMID:12359225 PMID:12873986 PMID:15194700 PMID:15653507 PMID:16285960 PMID:17344214 PMID:18242580 PMID:18782771 PMID:22306293 PMID:23084476 PMID:28262505 PMID:32929201 PMID:38404237
Once activated, recruits coactivators, such as NCOA1 or MED1, to the promoter region of the target gene .
PMID:15653507 PMID:16285960 PMID:17344214 PMID:18782771 PMID:28262505 PMID:32929201
May mediate cellular responses to activated FGFR1, FGFR2, FGFR3 and FGFR4 .
PMID:12873986
Upon activation of IL6ST/gp130 signaling by interleukin-6 (IL6), binds to the IL6-responsive elements identified in the promoters of various acute-phase protein genes .
PMID:12359225
Activated by IL31 through IL31RA .
PMID:15194700
Acts as a regulator of inflammatory response by regulating differentiation of naive CD4(+) T-cells into T-helper Th17 or regulatory T-cells (Treg): acetylation promotes its transcription activity and cell differentiation while deacetylation and oxidation of lysine residues by LOXL3 inhibits differentiation .
PMID:28065600 PMID:28262505
Involved in cell cycle regulation by inducing the expression of key genes for the progression from G1 to S phase, such as CCND1 .
PMID:17344214
Mediates the effects of LEP on melanocortin production, body energy homeostasis and lactation (By similarity). May play an apoptotic role by transctivating BIRC5 expression under LEP activation .
PMID:18242580
Cytoplasmic STAT3 represses macroautophagy by inhibiting EIF2AK2/PKR activity .
PMID:23084476
Plays a crucial role in basal beta cell functions, such as regulation of insulin secretion (By similarity). Following JAK/STAT signaling activation and as part of a complex with NFATC3 and NFATC4, binds to the alpha-beta E4 promoter region of CRYAB and activates transcription in cardiomyocytes (By similarity)
Carbonic anhydrase 2
CA2
inhibitor
Specific functionarylesterase activity
Cellular location
Cytoplasm
General function & pharmacology
Catalyzes the reversible hydration of carbon dioxide .
PMID:11327835 PMID:11802772 PMID:11831900 PMID:12056894 PMID:12171926 PMID:1336460 PMID:14736236 PMID:15300855 PMID:15453828 PMID:15667203 PMID:15865431 PMID:16106378 PMID:16214338 PMID:16290146 PMID:16686544 PMID:16759856 PMID:16807956 PMID:17127057 PMID:17251017 PMID:17314045 PMID:17330962 PMID:17346964 PMID:17540563 PMID:17588751 PMID:17705204 PMID:18024029 PMID:18162396 PMID:18266323 PMID:18374572 PMID:18481843 PMID:18618712 PMID:18640037 PMID:18942852 PMID:1909891 PMID:1910042 PMID:19170619 PMID:19186056 PMID:19206230 PMID:19520834 PMID:19778001 PMID:7761440 PMID:7901850 PMID:8218160 PMID:8262987 PMID:8399159 PMID:8451242 PMID:8485129 PMID:8639494 PMID:9265618 PMID:9398308
Can also hydrate cyanamide to urea .
PMID:10550681 PMID:11015219
Stimulates the chloride-bicarbonate exchange activity of SLC26A6 .
PMID:15990874
Essential for bone resorption and osteoclast differentiation .
PMID:15300855
Involved in the regulation of fluid secretion into the anterior chamber of the eye. Contributes to intracellular pH regulation in the duodenal upper villous epithelium during proton-coupled peptide absorption
PMID:11327835 PMID:11802772 PMID:11831900 PMID:12056894 PMID:12171926 PMID:1336460 PMID:14736236 PMID:15300855 PMID:15453828 PMID:15667203 PMID:15865431 PMID:16106378 PMID:16214338 PMID:16290146 PMID:16686544 PMID:16759856 PMID:16807956 PMID:17127057 PMID:17251017 PMID:17314045 PMID:17330962 PMID:17346964 PMID:17540563 PMID:17588751 PMID:17705204 PMID:18024029 PMID:18162396 PMID:18266323 PMID:18374572 PMID:18481843 PMID:18618712 PMID:18640037 PMID:18942852 PMID:1909891 PMID:1910042 PMID:19170619 PMID:19186056 PMID:19206230 PMID:19520834 PMID:19778001 PMID:7761440 PMID:7901850 PMID:8218160 PMID:8262987 PMID:8399159 PMID:8451242 PMID:8485129 PMID:8639494 PMID:9265618 PMID:9398308
Can also hydrate cyanamide to urea .
PMID:10550681 PMID:11015219
Stimulates the chloride-bicarbonate exchange activity of SLC26A6 .
PMID:15990874
Essential for bone resorption and osteoclast differentiation .
PMID:15300855
Involved in the regulation of fluid secretion into the anterior chamber of the eye. Contributes to intracellular pH regulation in the duodenal upper villous epithelium during proton-coupled peptide absorption
Carbonic anhydrase 3
CA3
inhibitor
Specific functioncarbonate dehydratase activity
Cellular location
Cytoplasm
General function & pharmacology
Reversible hydration of carbon dioxide
Metabolizing enzymes(5)
Enzymes involved in drug metabolism — important for understanding drug interactions
Enzyme activity key
substrate
inhibitor
inducer
CYP3A4Cytochrome P450 3A4
substrate
CYP2C9Cytochrome P450 2C9
substrate
CYP2D6Cytochrome P450 2D6
substrate
inhibitor
CYP2C8Cytochrome P450 2C8
substrate
PTGS2Prostaglandin G/H synthase 2
inhibitor
Transporters(4)
Proteins that transport this drug across cell membranes
ATP-binding cassette sub-family C member 4
ABCC4
inhibitor
Specific function15-hydroxyprostaglandin dehydrogenase (NAD+) activity
Cellular location
Basolateral cell membrane
General function & pharmacology
ATP-dependent transporter of the ATP-binding cassette (ABC) family that actively extrudes physiological compounds and xenobiotics from cells. Transports a range of endogenous molecules that have a key role in cellular communication and signaling, including cyclic nucleotides such as cyclic AMP (cAMP) and cyclic GMP (cGMP), bile acids, steroid conjugates, urate, and prostaglandins .
PMID:11856762 PMID:12523936 PMID:12835412 PMID:12883481 PMID:15364914 PMID:15454390 PMID:16282361 PMID:17959747 PMID:18300232 PMID:26721430
Mediates the ATP-dependent efflux of glutathione conjugates such as leukotriene C4 (LTC4) and leukotriene B4 (LTB4) too. The presence of GSH is necessary for the ATP-dependent transport of LTB4, whereas GSH is not required for the transport of LTC4 .
PMID:17959747
Mediates the cotransport of bile acids with reduced glutathione (GSH) .
PMID:12523936 PMID:12883481 PMID:16282361
Transports a wide range of drugs and their metabolites, including anticancer, antiviral and antibiotics molecules .
PMID:11856762 PMID:12105214 PMID:15454390 PMID:17344354 PMID:18300232
Confers resistance to anticancer agents such as methotrexate PMID:11106685
PMID:11856762 PMID:12523936 PMID:12835412 PMID:12883481 PMID:15364914 PMID:15454390 PMID:16282361 PMID:17959747 PMID:18300232 PMID:26721430
Mediates the ATP-dependent efflux of glutathione conjugates such as leukotriene C4 (LTC4) and leukotriene B4 (LTB4) too. The presence of GSH is necessary for the ATP-dependent transport of LTB4, whereas GSH is not required for the transport of LTC4 .
PMID:17959747
Mediates the cotransport of bile acids with reduced glutathione (GSH) .
PMID:12523936 PMID:12883481 PMID:16282361
Transports a wide range of drugs and their metabolites, including anticancer, antiviral and antibiotics molecules .
PMID:11856762 PMID:12105214 PMID:15454390 PMID:17344354 PMID:18300232
Confers resistance to anticancer agents such as methotrexate PMID:11106685
Bile salt export pump
ABCB11
inhibitor
Specific functionABC-type bile acid transporter activity
Cellular location
Apical cell membrane
General function & pharmacology
Catalyzes the transport of the major hydrophobic bile salts, such as taurine and glycine-conjugated cholic acid across the canalicular membrane of hepatocytes in an ATP-dependent manner, therefore participates in hepatic bile acid homeostasis and consequently to lipid homeostasis through regulation of biliary lipid secretion in a bile salts dependent manner .
PMID:15791618 PMID:16332456 PMID:18985798 PMID:19228692 PMID:20010382 PMID:20398791 PMID:22262466 PMID:24711118 PMID:29507376 PMID:32203132
Transports taurine-conjugated bile salts more rapidly than glycine-conjugated bile salts .
PMID:16332456
Also transports non-bile acid compounds, such as pravastatin and fexofenadine in an ATP-dependent manner and may be involved in their biliary excretion PMID:15901796 PMID:18245269
PMID:15791618 PMID:16332456 PMID:18985798 PMID:19228692 PMID:20010382 PMID:20398791 PMID:22262466 PMID:24711118 PMID:29507376 PMID:32203132
Transports taurine-conjugated bile salts more rapidly than glycine-conjugated bile salts .
PMID:16332456
Also transports non-bile acid compounds, such as pravastatin and fexofenadine in an ATP-dependent manner and may be involved in their biliary excretion PMID:15901796 PMID:18245269
ATP-dependent translocase ABCB1
ABCB1
substrate
Specific functionABC-type xenobiotic transporter activity
Cellular location
Cell membrane
General function & pharmacology
Translocates drugs and phospholipids across the membrane .
PMID:2897240 PMID:35970996 PMID:8898203 PMID:9038218 PMID:35507548
Catalyzes the flop of phospholipids from the cytoplasmic to the exoplasmic leaflet of the apical membrane. Participates mainly to the flop of phosphatidylcholine, phosphatidylethanolamine, beta-D-glucosylceramides and sphingomyelins .
PMID:8898203
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells PMID:2897240 PMID:35970996 PMID:9038218
PMID:2897240 PMID:35970996 PMID:8898203 PMID:9038218 PMID:35507548
Catalyzes the flop of phospholipids from the cytoplasmic to the exoplasmic leaflet of the apical membrane. Participates mainly to the flop of phosphatidylcholine, phosphatidylethanolamine, beta-D-glucosylceramides and sphingomyelins .
PMID:8898203
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells PMID:2897240 PMID:35970996 PMID:9038218
Broad substrate specificity ATP-binding cassette transporter ABCG2
ABCG2
substrate
Specific functionABC-type xenobiotic transporter activity
Cellular location
Cell membrane
General function & pharmacology
Broad substrate specificity ATP-dependent transporter of the ATP-binding cassette (ABC) family that actively extrudes a wide variety of physiological compounds, dietary toxins and xenobiotics from cells .
PMID:11306452 PMID:12958161 PMID:19506252 PMID:20705604 PMID:28554189 PMID:30405239 PMID:31003562
Involved in porphyrin homeostasis, mediating the export of protoporphyrin IX (PPIX) from both mitochondria to cytosol and cytosol to extracellular space, it also functions in the cellular export of heme .
PMID:20705604 PMID:23189181
Also mediates the efflux of sphingosine-1-P from cells .
PMID:20110355
Acts as a urate exporter functioning in both renal and extrarenal urate excretion .
PMID:19506252 PMID:20368174 PMID:22132962 PMID:31003562 PMID:36749388
In kidney, it also functions as a physiological exporter of the uremic toxin indoxyl sulfate (By similarity). Also involved in the excretion of steroids like estrone 3-sulfate/E1S, 3beta-sulfooxy-androst-5-en-17-one/DHEAS, and other sulfate conjugates .
PMID:12682043 PMID:28554189 PMID:30405239
Mediates the secretion of the riboflavin and biotin vitamins into milk (By similarity). Extrudes pheophorbide a, a phototoxic porphyrin catabolite of chlorophyll, reducing its bioavailability (By similarity).
Plays an important role in the exclusion of xenobiotics from the brain (Probable). It confers to cells a resistance to multiple drugs and other xenobiotics including mitoxantrone, pheophorbide, camptothecin, methotrexate, azidothymidine, and the anthracyclines daunorubicin and doxorubicin, through the control of their efflux .
PMID:11306452 PMID:12477054 PMID:15670731 PMID:18056989 PMID:31254042
In placenta, it limits the penetration of drugs from the maternal plasma into the fetus (By similarity). May play a role in early stem cell self-renewal by blocking differentiation (By similarity).
In inflammatory macrophages, exports itaconate from the cytosol to the extracellular compartment and limits the activation of TFEB-dependent lysosome biogenesis involved in antibacterial innate immune response
PMID:11306452 PMID:12958161 PMID:19506252 PMID:20705604 PMID:28554189 PMID:30405239 PMID:31003562
Involved in porphyrin homeostasis, mediating the export of protoporphyrin IX (PPIX) from both mitochondria to cytosol and cytosol to extracellular space, it also functions in the cellular export of heme .
PMID:20705604 PMID:23189181
Also mediates the efflux of sphingosine-1-P from cells .
PMID:20110355
Acts as a urate exporter functioning in both renal and extrarenal urate excretion .
PMID:19506252 PMID:20368174 PMID:22132962 PMID:31003562 PMID:36749388
In kidney, it also functions as a physiological exporter of the uremic toxin indoxyl sulfate (By similarity). Also involved in the excretion of steroids like estrone 3-sulfate/E1S, 3beta-sulfooxy-androst-5-en-17-one/DHEAS, and other sulfate conjugates .
PMID:12682043 PMID:28554189 PMID:30405239
Mediates the secretion of the riboflavin and biotin vitamins into milk (By similarity). Extrudes pheophorbide a, a phototoxic porphyrin catabolite of chlorophyll, reducing its bioavailability (By similarity).
Plays an important role in the exclusion of xenobiotics from the brain (Probable). It confers to cells a resistance to multiple drugs and other xenobiotics including mitoxantrone, pheophorbide, camptothecin, methotrexate, azidothymidine, and the anthracyclines daunorubicin and doxorubicin, through the control of their efflux .
PMID:11306452 PMID:12477054 PMID:15670731 PMID:18056989 PMID:31254042
In placenta, it limits the penetration of drugs from the maternal plasma into the fetus (By similarity). May play a role in early stem cell self-renewal by blocking differentiation (By similarity).
In inflammatory macrophages, exports itaconate from the cytosol to the extracellular compartment and limits the activation of TFEB-dependent lysosome biogenesis involved in antibacterial innate immune response
Biological pathways(2)
Scientific references(21)
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Celecoxib compared with sustained-release paracetamol for osteoarthritis: a series of n-of-1 trials.
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Celecoxib for the Prevention of Sporadic Colorectal Adenomas.
New England Journal of Medicine
2006355(9):873-884. doi: 10.1056/nejmoa061355
Sandberg M., Yasar U., Stromberg P., Hoog J.O., Eliasson E.
Oxidation of celecoxib by polymorphic cytochrome P450 2C9 and alcohol dehydrogenase.
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ATC classification(5 codes)
ATC N02AJ16
ATC M01AH01
ATC G01AE10
ATC L01XX33
ATC C08CA51
Affected organisms(1)
Humans and other mammals
Experimental properties(6)
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Celecoxib
Additional database identifiers
Drugs Product Database (DPD)
11865
ChemSpider
2562
BindingDB
11639
PDB
CEL
ZINC
ZINC000002570895
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9605
GenAtlas
PTGS2
GeneCards
PTGS2
GenBank Gene Database
L15326
GenBank Protein Database
291988
Guide to Pharmacology
1376
UniProt Accession
PGH2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:7758
GenAtlas
NEU1
GeneCards
NEU1
GenBank Gene Database
AF040958
GenBank Protein Database
2773339
Guide to Pharmacology
3214
UniProt Accession
NEUR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11364
GenAtlas
STAT3
GeneCards
STAT3
GenBank Gene Database
AF029311
Guide to Pharmacology
2994
UniProt Accession
STAT3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1373
GenAtlas
CA2
GeneCards
CA2
GenBank Gene Database
M77181
GenBank Protein Database
179780
Guide to Pharmacology
3092
UniProt Accession
CAH2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1374
GeneCards
CA3
GenBank Gene Database
AK313254
GenBank Protein Database
189053812
UniProt Accession
CAH3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1750
GeneCards
CDH11
UniProt Accession
CAD11_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8816
GenAtlas
PDPK1
GeneCards
PDPK1
GenBank Gene Database
AF017995
GenBank Protein Database
2407613
Guide to Pharmacology
1519
UniProt Accession
PDPK1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2623
GenAtlas
CYP2C9
GeneCards
CYP2C9
GenBank Gene Database
AY341248
Guide to Pharmacology
1326
UniProt Accession
CP2C9_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2625
GenAtlas
CYP2D6
GeneCards
CYP2D6
GenBank Gene Database
M20403
GenBank Protein Database
181350
Guide to Pharmacology
1329
UniProt Accession
CP2D6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2622
GenAtlas
CYP2C8
GeneCards
CYP2C8
GenBank Gene Database
M17397
Guide to Pharmacology
1325
UniProt Accession
CP2C8_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9605
GenAtlas
PTGS2
GeneCards
PTGS2
GenBank Gene Database
L15326
GenBank Protein Database
291988
Guide to Pharmacology
1376
UniProt Accession
PGH2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:55
GenAtlas
ABCC4
GeneCards
ABCC4
GenBank Gene Database
AF071202
GenBank Protein Database
3335173
Guide to Pharmacology
782
UniProt Accession
MRP4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:42
GenAtlas
ABCB11
GeneCards
ABCB11
GenBank Gene Database
AF091582
GenBank Protein Database
3873243
Guide to Pharmacology
778
UniProt Accession
ABCBB_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:40
GenAtlas
ABCB1
GeneCards
ABCB1
GenBank Gene Database
M14758
GenBank Protein Database
307180
Guide to Pharmacology
768
UniProt Accession
MDR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:74
GenAtlas
ABCG2
GeneCards
ABCG2
GenBank Gene Database
AF103796
GenBank Protein Database
4185796
Guide to Pharmacology
792
UniProt Accession
ABCG2_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
Knox C., Wilson M., Klinger C.M., et al
DrugBank 6.
0: the DrugBank Knowledgebase for 2024
Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
Wishart D.S., Feunang Y.D., Guo A.C., et al
DrugBank 5.
0: a major update to the DrugBank database for 2018
Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
Show earlier publications
Law V., Knox C., Djoumbou Y., et al
DrugBank 4.
0: shedding new light on drug metabolism
Nucleic Acids Res. 2014 Jan 142(1):D1091-7
Knox C., Law V., Jewison T., et al
DrugBank 3.
0: a comprehensive resource for 'omics' research on drugs
Nucleic Acids Res. 2011 Jan39(Database issue):D1035-41
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a knowledgebase for drugs, drug actions and drug targets.
Nucleic Acids Research
2008 Jan36(Database issue):D901-6
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a comprehensive resource for in silico drug discovery and exploration.
Nucleic Acids Research
2006 Jan 134(Database issue):D668-72
Source: go.drugbank.comCC BY-NC 4.0
Updated 4 months ago(8 Mar 2026)Structured knowledge from the free knowledge base
WHO INN:celecoxib
International Nonproprietary Name
Linked open data from Wikidata (Q408801), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication. WHO INN from the World Health Organization.