Ketoprofen is a potent non-steroidal anti-inflammatory drug (NSAID) of the propionic acid class, with analgesic, anti-inflammatory, and antipyretic properties. It is a non-selective inhibitor of cyclooxygenase (COX-1 and COX-2) enzymes, thereby inhibiting prostaglandin synthesis. The 20mg strength is commonly used for mild to moderate pain and inflammatory conditions in the Indian market, often as a lower-dose option for long-term management or for patients requiring a lower therapeutic dose.
Adult: For mild to moderate pain and inflammatory conditions: 20mg to 50mg, two to three times daily. The 20mg strength is typically used as 1 tablet 2-3 times a day, not exceeding 150mg/day. For chronic conditions like osteoarthritis, a lower dose of 20mg 2-3 times daily may be initiated.
Note: Should be taken with or immediately after food or a glass of milk to minimize gastrointestinal irritation. Tablet should be swallowed whole with a full glass of water. Do not crush or chew. Do not lie down for at least 10 minutes after taking the dose.
Ketoprofen exerts its therapeutic effects primarily through the non-selective, reversible inhibition of the enzyme cyclooxygenase (COX), both COX-1 and COX-2 isoforms. This inhibition blocks the conversion of arachidonic acid to prostaglandin G2 and subsequently to prostaglandin H2, the precursors of various prostaglandins (PGs), thromboxane A2, and prostacyclin. The reduction in prostaglandin synthesis, particularly PGE2 and PGI2, at sites of inflammation and injury mediates its anti-inflammatory, analgesic, and antipyretic actions.
Pregnancy: Category C (first and second trimester): Use only if potential benefit justifies potential risk to the fetus. Avoid in third trimester (Category D) due to risk of premature closure of ductus arteriosus, oligohydramnios, and inhibition of labor. Not recommended for use during pregnancy, especially near term.
Driving: May cause dizziness, drowsiness, vertigo, or blurred vision in some patients. Patients should be cautioned about operating machinery or driving until they know how the drug affects them.
| Aspirin (low-dose or high-dose) | Increased risk of GI ulceration and bleeding; pharmacodynamic antagonism for cardioprotection. | Major |
| Other NSAIDs (e.g., Ibuprofen, Diclofenac, Naproxen) | Additive toxicity, significantly increased risk of GI and renal adverse effects. | Major |
| Anticoagulants (Warfarin, Acenocoumarol) | Increased antiplatelet effect and potential for GI bleeding; increased INR risk. | Major |
| Antiplatelets (Clopidogrel, Ticagrelor) | Increased risk of bleeding. | Major |
| Corticosteroids (e.g., Prednisolone) | Synergistic increase in risk of GI ulceration and bleeding. | Major |
| Selective Serotonin Reuptake Inhibitors (SSRIs) e.g., Sertraline, Escitalopram | Increased risk of upper GI bleeding. | Moderate |
| ACE Inhibitors (e.g., Ramipril, Enalapril) / ARBs (e.g., Telmisartan) | Reduced antihypertensive effect; increased risk of renal impairment. | Moderate |
| Diuretics (e.g., Furosemide, Hydrochlorothiazide) | Reduced diuretic and antihypertensive efficacy; risk of renal failure. | Moderate |
| Lithium | Decreased renal clearance of lithium, leading to increased serum levels and toxicity. | Major |
| Methotrexate | Decreased renal clearance of methotrexate, increasing risk of bone marrow suppression and toxicity. | Major |
| Cyclosporine, Tacrolimus | Increased risk of nephrotoxicity. | Major |
| Quinolone Antibiotics (e.g., Ciprofloxacin) | Increased risk of CNS stimulation and seizures. | Moderate |