This is a prescription medicine. A prescription is required from your veterinarian before we can supply this product. Please ensure that you have read the "How to Order" page before ordering this item.
All of our products are APVMA or TGA approved and identical to those used by your veterinarian. Please call or email us if you have any queries about any of the products on our site.
|Drug Name and Strength||Carprofen 100 mg|
|Indication||Relief of pain and inflammation in dogs.|
|Contraindications||Administration to cats, or to dogs suffering from cardiac, hepatic or renal disease, where there is a possibility of gastrointestinal ulceration or bleeding, or where there is evidence of a blood dyscrasia or previous hypersensitivity to carprofen.|
|Actions||Pharmacology Carprofen is a non-narcotic, nonsteroidal, anti-inflammatory drug with characteristic analgesic and antipyretic activity, approximately equipotent to indomethacin in animal models. As with other NSAIDs, the exact mode of action of carprofen has not been established; however, inhibition of prostaglandin synthesis accounts for at least part of its mechanism of action. Carprofen is a moderately potent inhibitor of phospholipase A2 and a reversible inhibitor of cyclooxygenase.Two unique cyclooxygenases have been described in mammals. The constitutive cyclooxygenase, COX-1, synthesises prostaglandins necessary for normal gastrointestinal and renal function. The inducible cyclooxygenase, COX-2, generates prostaglandins involved in inflammation. Inhibition of COX-1 is thought to be associated with gastrointestinal and renal toxicity while inhibition of COX-2 provides anti-inflammatory activity. The specificity of a particular NSAID for either COX-2 or COX-1 may vary from species to species. In an in vitro study using canine cell cultures, carprofen demonstrated a greater than 100-fold selective inhibition of COX-2 compared with COX-1.Carprofen has also been shown to inhibit the release of several prostaglandins in two inflammatory cell systems: rat polymorphonuclear leucocytes (PMN) and human rheumatoid synovial cells, indicating inhibition of acute (PMN system) and chronic (synovial cell system) inflammation reactions. In mice, carprofen has been shown to be a much weaker blocker of castor oil induced diarrhoea and arachidonic acid induced toxicity than indomethacin.This decreased effect of carprofen on prostaglandin synthesis in the gastrointestinal tract may explain its relatively low ulcerogenic activity compared to other drugs in its class.Several studies have demonstrated that carprofen has modulatory effects on both humoral and cellular immune responses.Data also indicates that carprofen inhibits the production of osteoclast activating factors (OAF), PGE1 and PGE2 by its inhibitory effects on prostaglandin biosynthesis.Whole blood clotting times were evaluated in dogs given carprofen at a dose rate of 9 mg/kg once daily for 14 days. At all observations both prior to and during treatment, the mean clotting times remained within the range of normal values.Pharmacokinetics Based on comparison with data obtained from intravenous administration, carprofen is rapidly and nearly completely absorbed (more than 90% bioavailable) when administered orally.The mean terminal half-life of carprofen is approximately eight hours (range 4.5 to 9.8 hours) after single oral doses varying from 1 to 25 mg/kg of bodyweight.After a 100 mg single intravenous bolus dose, the mean elimination half-life was approximately 11.7 hours in the dog.Carprofen is more than 99% bound to plasma protein and exhibits a very small volume of distribution.Carprofen is eliminated in the dog primarily by biotransformation in the liver, followed by rapid excretion of the resulting metabolites (the ester glucuronide of carprofen and the ether glucuronides of two phenolic metabolites, 7-hydroxy carprofen and 8-hydroxy carprofen) in the faeces (70 to 80%) and urine (10 to 20%).Some enterohepatic circulation of the drug has been observed. Studies have not revealed any evidence of chiral inversion of carprofen enantiomers.|
|Precautions||Do not exceed the stated dose.All dogs should undergo a thorough clinical examination and appropriate laboratory tests before introduction of NSAID therapy. During extended administration, appropriate re-evaluation and laboratory tests should be undertaken periodically.Use in dogs less than 6 weeks of age, or in aged animals, may involve additional risk. If such use cannot be avoided, such dogs may require a reduced dosage and careful clinical management.Avoid use in any dehydrated, hypovolaemic or hypotensive dogs, as there is a potential risk of increased renal toxicity.Avoid administration concurrently with other NSAIDs or corticosteroids. Appropriate ‘washout’ time should be allowed when changing therapy. If changing anti-inflammatory products, take into account the pharmacokinetic properties of the drugs used previously when considering the delay period between the individual drugs. Some NSAIDs may be highly bound to plasma proteins and compete with other highly bound drugs, which can lead to toxic effects.Concurrent administration of potential nephrotoxic drugs should be avoided. Specific studies to establish the safety of this product in breeding, pregnant or lactating bitches have not been undertaken, therefore use in these classes of dogs is not recommended or should be done with caution.NSAIDs can cause inhibition of phagocytosis and hence in the treatment of inflammatory conditions associated with bacterial infections, appropriate concurrent antimicrobial therapy should be instigated.As a class, cyclooxygenase inhibitory NSAIDs may be associated with gastrointestinal and renal toxicity. Effects may result from decreased prostaglandin production and inhibition of the enzyme cyclooxygenase, which is responsible for the formation of prostaglandins from arachidonic acid. When NSAIDs inhibit prostaglandins that cause inflammation they may also inhibit those prostaglandins which maintain homeostatic function. These antiprostaglandin effects may result in clinically significant disease in animals with pre-existing disease more often than in healthy animals. Sensitivity to drug associated adverse effects varies with the individual animal. NSAID therapy could unmask occult disease which has previously been undiagnosed due to the absence of clinical signs.Carprieve Tablets should be used with caution in dogs with bleeding disorders (e.g. von Willebrand's disease) as safety has not been established in dogs with these disorders. The safe use of Carprieve tablets in pregnant and lactating bitches and dogs used for breeding purposes has not been established.Studies to determine the activity of Carprieve tablets when administered concurrently with other protein bound drugs have not been conducted. Drug compatibility should be monitored closely in animals requiring additional therapy.First Aid If poisoning occurs, contact a doctor or Poisons Information Centre. Phone Australia 131 126.Disposal Dispose of empty containers or expired product by wrapping with paper and putting in garbage.|
|Dosage and Administration||2 to 4 mg/kg bodyweight/day. Dose, frequency and duration of treatment will depend on clinical response of the condition under treatment. Initial therapy at 4 mg/kg bodyweight/day given in two equally divided doses is generally recommended. Subject to clinical response, the dose may be reduced to 2 mg/kg bodyweight per day administered once daily.|
|Storage||Store below 25°C (air conditioning) in a dry place out of direct sunlight.|
|MSDS (external link)||Carprieve Tablets 100mg MSDS|
|Label (external link)||Carprieve Tablets 100mg Label|
|Manufacturer||Norbrook Laboratories Australia P/L|