Adult: 200 mg daily as a single dose or in 2 divided doses, may increase up to 200 mg bid as needed. Max: 400 mg daily. Use the lowest effective dose for the shortest possible duration. Elderly: <50 kg: Initiate at the lowest recommended dose.
Oral Acute pain, Primary dysmenorrhoea
Adult: Initially, 400 mg, followed by an additional dose of 200 mg if needed on day 1. Maintenance: 200 mg bid if needed. Use the lowest effective dose for the shortest possible duration. Treatment recommendations may vary among individual products and between countries (refer to specific product guidelines). Elderly: <50 kg: Initiate at the lowest recommended dose.
Oral Rheumatoid arthritis
Adult: 100 mg or 200 mg bid. Max: 400 mg daily. Use the lowest effective dose for the shortest possible duration. Elderly: <50 kg: Initiate at the lowest recommended dose.
Oral Ankylosing spondylitis
Adult: 200 mg as a single dose or in 2 divided doses, may increase to 400 mg as a single dose or in 2 divided doses if needed. Max: 400 mg daily. Use the lowest effective dose for the shortest possible duration. Elderly: <50 kg: Initiate at the lowest recommended dose.
Oral Acute migraine attacks
Adult: With or without aura: 120 mg as a single dose. Max: 120 mg/24 hours. Use the lowest effective dose for the shortest possible duration. Treatment recommendations may vary among individual products and between countries (refer to specific product guidelines). Elderly: <50 kg: Initiate at the lowest recommended dose.
Oral Juvenile idiopathic arthritis
Child: ≥2 years ≥10 kg to ≤25 kg: 50 mg bid; >25 kg: 100 mg bid. Use the lowest effective dose for the shortest possible duration. Treatment recommendations may vary among individual products and between countries (refer to specific product guidelines).
Special Patient Group
Pharmacogenomics:
Celecoxib is mainly metabolised by CYP2C9 enzyme into hydroxycelecoxib. CYP2C9 is a highly polymorphic gene which may influence metabolism and clearance of celecoxib, thus affecting drug exposure and potential safety. Genetic testing may be considered.
CYP2C9
According to CPIC, CYP2C9*1 is a normal function allele. Individuals carrying CYP2C9*1 allele in combination with another normal function allele may have an increased metabolism of celecoxib as compared to those carrying at least 1 copy of a decreased or no function allele. However, other genetic and clinical factors may also influence the metabolism of celecoxib.
According to CPIC, CYP2C9*2 is a decreased function allele. Individuals carrying CYP2C9*2 allele in combination with a normal, decreased allele, or no function allele may have decreased metabolism of celecoxib as compared to those with 2 normal function alleles. However, other genetic and clinical factors may also influence the metabolism of celecoxib.
According to CPIC, CYP2C9*3 is a no function allele. Individuals carrying the CYP2C9*3 allele in combination with a normal, decreased, or no function allele may have decreased metabolism of celecoxib as compared to those with 2 normal function alleles. However, other genetic and clinical factors may also influence the metabolism of celecoxib.
According to CPIC, CYP2C9*13 is a no function allele. Individuals carrying the CYP2C9*13 allele in combination with a normal, decreased, or no function allele may have decreased metabolism of celecoxib as compared to those with 2 normal function alleles. However, other genetic and clinical factors may also influence the metabolism of celecoxib.
Clinical Pharmacogenetics Implementation Consortium (CPIC) Guideline as of March 2020:
Phenotype/Genotype
Implications
Recommendations
CYP2C9 normal metaboliser
Individuals carrying 2 normal function alleles (e.g. *1/*1) with an activity score of 2
Normal metabolism
Initiate treatment with recommended starting dose.
CYP2C9 intermediate metaboliser
Individuals carrying 1 normal function allele plus 1 decreased function allele, or 1 normal function allele plus one no function allele, or 2 decreased function alleles (e.g. *1/*2) with an activity score of 1.5
Mildly reduced metabolism
Initiate treatment with recommended starting dose. Use the lowest effective dosage for the shortest duration (in accordance with prescribing information and consistent with individual patient treatment goals).
CYP2C9 intermediate metaboliser
Individuals carrying 1 normal function allele plus 1 decreased function allele, or 1 normal function allele plus one no function allele, or 2 decreased function alleles (e.g. *1/*3, *2/*2) with an activity score of 1
Moderately reduced metabolism; higher plasma concentrations may increase the risk of toxicities
Initiate treatment with lowest recommended starting dose. Cautiously titrate dose upward to clinical effect or maximum recommended dose. Use the lowest effective dosage for the shortest duration (in accordance with prescribing information and consistent with individual patient treatment goals). Monitor for adverse events (e.g. blood pressure, kidney function) during therapy.
CYP2C9 poor metaboliser
Individuals carrying 1 no function allele plus 1 decreased function allele, or 2 no function alleles
Significantly reduced metabolism and prolonged half-life; higher plasma concentrations may increase the risk and severity of toxicities
Initiate therapy with 25-50% of the lowest recommended starting dose. Cautiously titrate dose upward to clinical effect or 25-50% of the maximum recommended dose. Use the lowest effective dosage for the shortest duration (in accordance with prescribing information and consistent with individual patient treatment goals). Upward dose titration should not occur until after steady-state is reached (at least 5 days following 1st dose). Monitor for adverse events (e.g. blood pressure, kidney function) during therapy. Alternatively, may consider other therapy not metabolised by CYP2C9.
In contrast, the US Food and Drug Administration drug label for celecoxib recommends to reduce the starting dose to half of the lowest recommended dose in patients who are known (based on genotyping) or suspected (based on the previous history with other CYP2C9 substrates) poor metabolisers of CYP2C9 (e.g. CYP2C9*3/*3). In patients with juvenile rheumatoid arthritis who are known or suspected to be poor metabolisers of CYP2C9, consider using alternative treatments.
Renal Impairment
Severe: Contraindicated.
Hepatic Impairment
Moderate (Child-Pugh class B): Reduce dose by 50%. Severe (Child-Pugh class C or ≥10 score): Contraindicated.
Administration
May be taken with or without food.
Contraindications
Hypersensitivity to celecoxib, aspirin, sulfonamides or other NSAIDs. History of asthma, urticaria, acute rhinitis, nasal polyps, angioneurotic oedema or other allergic-type reactions after taking aspirin or other NSAIDs. Active peptic ulceration or gastrointestinal bleeding, inflammatory bowel disease, CHF (NYHA II-IV), established ischaemic heart disease, cerebrovascular disease or peripheral arterial disease. Use in the setting of CABG surgery. Severe renal (CrCl <30 mL/min) and hepatic (Child-Pugh class C or ≥10 score) impairment. Pregnancy and lactation.
Special Precautions
Patient with history of gastrointestinal complications (e.g. ulceration and bleeding), hypertension, diabetes mellitus, hyperlipidaemia, recent MI, and other CV disease risk factors (e.g. smoking, alcoholism); pre-existing asthma (without known aspirin sensitivity), pre-existing oedema, hypovolaemia. Dehydrated patient. May mask underlying fever and other signs of inflammation. Not indicated for the preventive treatment of migraine. CYP2C9 poor metabolisers. Mild to moderate renal and moderate hepatic impairment. Children and elderly.
Adverse Reactions
Significant: Fluid retention, oedema, new-onset hypertension or worsening of pre-existing hypertension, new-onset or exacerbation of heart failure; medication-overuse headache, anaemia, mild and transient transaminase elevations, acute kidney injury, interstitial nephritis, renal papillary necrosis (prolonged use). Cardiac disorders: Angina pectoris. Gastrointestinal disorders: Nausea, abdominal pain, diarrhoea, dyspepsia, flatulence, vomiting, dysphagia, GERD, irritable bowel syndrome. General disorders and administration site conditions: Influenza-like symptoms. Injury, poisoning and procedural complications: Accidental injury. Investigations: Increased blood creatinine, weight increased. Musculoskeletal and connective tissue disorders: Arthralgia. Nervous system disorders: Headache, dizziness, hypertonia. Psychiatric disorders: Insomnia. Renal and urinary disorders: Nephrolithiasis, UTI. Reproductive system and breast disorders: Benign prostatic hyperplasia. Respiratory, thoracic and mediastinal disorders: Sinusitis, URTI, pharyngitis, dyspnoea, rhinitis, cough. Skin and subcutaneous tissue disorders: Rash, pruritus. Potentially Fatal: Gastrointestinal inflammation, perforation, ulceration, or bleeding; CV thrombotic events including MI and stroke, serious hypersensitivity reactions (e.g. anaphylaxis, angioedema, drug rash with eosinophilia and systemic symptoms), severe hepatic reactions (e.g. fulminant hepatitis, hepatic necrosis, hepatic failure). Very rarely, exfoliative dermatitis, Stevens-Johnson syndrome, toxic epidermal necrolysis.
PO: C (prior to 30 weeks gestation), D (starting at 30 weeks gestation), Z (NSAIDs caused foetal ductus arteriosus premature closure, foetal renal impairment and persistent pulmonary hypertension. Avoid near term, else use lowest dose for shortest time.)
Patient Counseling Information
This drug may cause dizziness, vertigo or somnolence, if affected, do not drive or operate machinery.
Monitoring Parameters
Monitor blood pressure during initial treatment and throughout therapy, CBC and chemistry profile periodically (prolonged use), liver and renal functions; signs and symptoms of gastrointestinal irritation.
Drug Interactions
Increased risk of gastrointestinal ulceration or bleeding with anticoagulants (e.g. apixaban), antiplatelet agents (e.g. aspirin), SSRIs, corticosteroids (e.g. glucocorticoids), and other NSAIDs. May reduce the antihypertensive effect of ACE inhibitors, ARBs, diuretics, β-blockers and other antihypertensive agents. May increase the nephrotoxic effect of ciclosporin and tacrolimus. Increases the serum concentration of lithium, digoxin and methotrexate. Increased plasma concentration with CYP2C9 inhibitors (e.g. fluconazole). Decreased plasma concentration with CYP2C9 inducers (e.g. rifampicin, carbamazepine, barbiturates), Al and Mg containing antacids. May increase serum concentration and toxicity of CYP2D6 substrates (e.g. aripiprazole, perhexiline, atomoxetine). Potentially Fatal: Increased risk of serious bleeding events with warfarin.
Food Interaction
High-fat meal may delay absorption time and increase bioavailability. Increased risk of gastrointestinal perforations, ulcers or bleedings with alcohol.
Action
Description: Mechanism of Action: Celecoxib, an NSAID, is a selective cyclooxygenase-2 (COX-2) inhibitor primarily responsible for the inhibition of prostaglandin synthesis. It exhibits anti-inflammatory, analgesic and antipyretic activities. Pharmacokinetics: Absorption: Well absorbed from the gastrointestinal tract. High-fat meal may delay absorption time and increase bioavailability. Time to peak plasma concentrations: Approx 2-3 hours. Distribution: Enters breast milk. Plasma protein binding: Approx 97%, mainly to albumin and to a lesser extent to α1-acid glycoprotein. Metabolism: Metabolised in the liver by CYP2C9 into inactive metabolites such as a primary alcohol, corresponding carboxylic acid and its glucuronide conjugate. Excretion: Via faeces (approx 57% as metabolites, <3% as unchanged drug); urine (27% as metabolites, <3% as unchanged drug). Elimination half-life: Approx 11 hours.
Chemical Structure
Celecoxib Source: National Center for Biotechnology Information. PubChem Compound Summary for CID 2662, Celecoxib. https://pubchem.ncbi.nlm.nih.gov/compound/Celecoxib. Accessed Mar. 28, 2023.
Sign Out
