MOBIC Meloxicam 15mg Tablet 1's
RXDRUG-DR-XY41947-1pc
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Features
Brand
Mobic
Full Details
Dosage Strength
15 mg
Drug Ingredients
- Meloxicam
Drug Packaging
Tablet 1's
Generic Name
Meloxicam
Dosage Form
Tablet
Registration Number
DR-XY41947
Drug Classification
Prescription Drug (RX)
Description
Indications/Uses
Symptomatic treatment of painful osteoarthritis (arthrosis, degenerative joint disease), rheumatoid arthritis, ankylosing spondylitis and similar conditions requiring anti-inflammatory treatment.
Dosage/Direction for Use
RA Initially 15 mg/day, may be reduced to 7.5 mg/day. OA 7.5 mg/day, may be increased to 15 mg/day. Max: 15 mg/day.
Click to view Mobic detailed prescribing information
Overdosage
In case of overdose, the standard measures of gastric evacuation and general supportive measures should be used as there is no known antidote. It has been shown in a clinical trial that cholestyramine accelerates the elimination of meloxicam.
Administration
May be taken with or without food: May be taken w/ meals if GI discomfort occurs.
Contraindications
Patients with known hypersensitivity to meloxicam or any excipient of Mobic. There is a potential for cross-sensitivity to acetylsalicylic acid and other NSAIDs.
Mobic should not be given to patients who have developed signs of asthma, nasal polyps, angioedema or urticaria following the administration of acetylsalicylic acid or other NSAIDs.
Active peptic ulceration, severe hepatic insufficiency, nondialysed severe renal insufficiency, overt gastrointestinal bleeding, recent cerebrovascular bleeding or other bleeding disorders, severe uncontrolled heart failure; children and adolescents <12 years, pregnancy or breastfeeding.
Mobic should not be given to patients who have developed signs of asthma, nasal polyps, angioedema or urticaria following the administration of acetylsalicylic acid or other NSAIDs.
Active peptic ulceration, severe hepatic insufficiency, nondialysed severe renal insufficiency, overt gastrointestinal bleeding, recent cerebrovascular bleeding or other bleeding disorders, severe uncontrolled heart failure; children and adolescents <12 years, pregnancy or breastfeeding.
Special Precautions
As with other NSAIDs, caution should be exercised when treating patients with a history of gastrointestinal disease and in patients receiving treatment with anticoagulants. Patients with gastrointestinal symptoms should be monitored.
Mobic should be withdrawn if peptic ulceration or gastrointestinal bleeding occurs. Gastrointestinal bleeding, ulceration or perforation can occur at any time during treatment, with or without warning symptoms or a previous history of serious gastrointestinal events. The consequences of such events are generally more serious in the elderly.
Special attention should be paid in patients reporting mucocutaneous adverse events and consideration given to discontinuing Mobic. NSAIDs inhibit the synthesis of renal prostaglandins which play a supportive role in the maintenance of renal perfusion. In patients whose renal blood flow and blood volume are decreased, administration of an NSAID may precipitate overt renal decompensation which is typically followed by recovery to pre-treatment state upon discontinuation of nonsteroidal anti-inflammatory therapy. Patients at greatest risk of such a reaction are dehydrated patients, those with congestive heart failure, liver cirrhosis, nephrotic syndrome and overt renal disease, those receiving a diuretic, ACE inhibitor or angiotensin II receptor antagonist, or those having undergone major surgical procedures which led to hypovolemia. In such patients, the volume of diuresis and the renal function should be carefully monitored at the beginning of therapy.
In rare instances, NSAIDs may be the cause of interstitial nephritis, glomerulonephritis, renal medullary necrosis or nephrotic syndrome.
The dose of Mobic in patients with end-stage renal failure on hemodialysis should not be higher than 7.5 mg. No dose reduction is required in patients with mild or moderate renal impairment (ie, in patients with a creatinine clearance >25 mL/min).
As with other NSAIDs, occasional elevations of serum transaminases or other parameters of liver function have been reported. In most cases, these have been small and transient increases above the normal range. If the abnormality is significant or persistent, Mobic should be stopped and follow up tests carried out.
No dose reduction is required in patients with clinically stable liver cirrhosis.
Frail or debilitated patients may tolerate side effects less well and such patients should be carefully supervised. As with other NSAIDs, caution should be used in the treatment of elderly patients who are more likely to be suffering from impaired renal, hepatic or cardiac functions.
Induction of sodium, potassium and water retention and interference with the natriuretic effects of diuretics may occur with NSAIDs. Cardiac failure or hypertension may be precipitated or exacerbated in susceptible patients as a result.
Effects on the Ability to Drive or Operate Machinery: There are no specific studies about effects on the ability to drive vehicles and to use machinery. Patients who experience visual disturbances, drowsiness or other central nervous system disturbances should refrain from these activities.
Use in pregnancy & lactation: Although no teratogenic effects were seen in preclinical testing, Mobic should not be used during pregnancy and breastfeeding.
Use in children: As a dosage for use in children has yet to be established, usage should be restricted to adults. (See Contraindications.)
Mobic should be withdrawn if peptic ulceration or gastrointestinal bleeding occurs. Gastrointestinal bleeding, ulceration or perforation can occur at any time during treatment, with or without warning symptoms or a previous history of serious gastrointestinal events. The consequences of such events are generally more serious in the elderly.
Special attention should be paid in patients reporting mucocutaneous adverse events and consideration given to discontinuing Mobic. NSAIDs inhibit the synthesis of renal prostaglandins which play a supportive role in the maintenance of renal perfusion. In patients whose renal blood flow and blood volume are decreased, administration of an NSAID may precipitate overt renal decompensation which is typically followed by recovery to pre-treatment state upon discontinuation of nonsteroidal anti-inflammatory therapy. Patients at greatest risk of such a reaction are dehydrated patients, those with congestive heart failure, liver cirrhosis, nephrotic syndrome and overt renal disease, those receiving a diuretic, ACE inhibitor or angiotensin II receptor antagonist, or those having undergone major surgical procedures which led to hypovolemia. In such patients, the volume of diuresis and the renal function should be carefully monitored at the beginning of therapy.
In rare instances, NSAIDs may be the cause of interstitial nephritis, glomerulonephritis, renal medullary necrosis or nephrotic syndrome.
The dose of Mobic in patients with end-stage renal failure on hemodialysis should not be higher than 7.5 mg. No dose reduction is required in patients with mild or moderate renal impairment (ie, in patients with a creatinine clearance >25 mL/min).
As with other NSAIDs, occasional elevations of serum transaminases or other parameters of liver function have been reported. In most cases, these have been small and transient increases above the normal range. If the abnormality is significant or persistent, Mobic should be stopped and follow up tests carried out.
No dose reduction is required in patients with clinically stable liver cirrhosis.
Frail or debilitated patients may tolerate side effects less well and such patients should be carefully supervised. As with other NSAIDs, caution should be used in the treatment of elderly patients who are more likely to be suffering from impaired renal, hepatic or cardiac functions.
Induction of sodium, potassium and water retention and interference with the natriuretic effects of diuretics may occur with NSAIDs. Cardiac failure or hypertension may be precipitated or exacerbated in susceptible patients as a result.
Effects on the Ability to Drive or Operate Machinery: There are no specific studies about effects on the ability to drive vehicles and to use machinery. Patients who experience visual disturbances, drowsiness or other central nervous system disturbances should refrain from these activities.
Use in pregnancy & lactation: Although no teratogenic effects were seen in preclinical testing, Mobic should not be used during pregnancy and breastfeeding.
Use in children: As a dosage for use in children has yet to be established, usage should be restricted to adults. (See Contraindications.)
Adverse Reactions
Dyspepsia, nausea, vomiting, abdominal pain, constipation, flatulence, diarrhea; leukopenia, thrombocytopenia, anemia, anaphylactic & anaphylactoid reaction, confusional state, disorientation, altered mood, pruritus, rash; dizziness, somnolence, headache, visual disturbance, conjunctivitis, vertigo, tinnitus, increased BP, flushing, asthma, GI perforation, GI hemorrhage, gastroduodenal ulcer, colitis, gastritis, esophagitis, stomatitis, edema, hepatitis, toxic epidermal necrolysis, SJS, angioedema, dermatitis bullous, erythema multiforme, photosensitivity reaction, acute renal failure, palpitations, female infertility, delayed ovulation.
Drug Interactions
Other NSAIDs Including Salicylates in High Doses: Concomitant administration of >1 NSAID may increase the risk of gastrointestinal ulceration and bleeding through synergistic action.
Oral Anticoagulants, Ticlopidine, Systemically Administered Heparin, Thrombolytics: Increased risk of bleeding. If such co-prescribing cannot be avoided, close monitoring of the effects of anticoagulants is required.
Lithium: NSAIDs have been reported to increase lithium plasma levels. It is recommended that plasma lithium levels be monitored when initiating, adjusting and discontinuing Mobic.
Methotrexate: As with other NSAIDs, Mobic may increase the hematologic toxicity of methotrexate. In this situation, strict monitoring of blood cell count is recommended.
Contraception: NSAIDs have been reported to decrease the efficacy of intrauterine devices.
Diuretics: Treatment with NSAIDs is associated with the potential for acute renal insufficiency in patients who are dehydrated. Patients receiving Mobic and diuretics should be adequately hydrated and be monitored for renal function prior to initiating treatment.
Antihypertensives (eg, β-blockers, ACE inhibitors, Vasodilators, Diuretics): A reduced effect of the antihypertensive drug by inhibition of vasodilating prostaglandins has been reported during treatment with NSAIDs.
Cholestyramine binds to meloxicam in the gastrointestinal tract leading to a faster elimination of meloxicam.
Nephrotoxicity of cyclosporin may be enhanced by NSAIDs via renal prostaglandin-mediated effects. During combined treatment, renal function is to be measured. No relevant pharmacokinetic drug-drug interactions were detected with respect to the concomitant administration of antacids, cimetidine, digoxin and furosemide. Interactions with oral antidiabetics cannot be excluded.
Oral Anticoagulants, Ticlopidine, Systemically Administered Heparin, Thrombolytics: Increased risk of bleeding. If such co-prescribing cannot be avoided, close monitoring of the effects of anticoagulants is required.
Lithium: NSAIDs have been reported to increase lithium plasma levels. It is recommended that plasma lithium levels be monitored when initiating, adjusting and discontinuing Mobic.
Methotrexate: As with other NSAIDs, Mobic may increase the hematologic toxicity of methotrexate. In this situation, strict monitoring of blood cell count is recommended.
Contraception: NSAIDs have been reported to decrease the efficacy of intrauterine devices.
Diuretics: Treatment with NSAIDs is associated with the potential for acute renal insufficiency in patients who are dehydrated. Patients receiving Mobic and diuretics should be adequately hydrated and be monitored for renal function prior to initiating treatment.
Antihypertensives (eg, β-blockers, ACE inhibitors, Vasodilators, Diuretics): A reduced effect of the antihypertensive drug by inhibition of vasodilating prostaglandins has been reported during treatment with NSAIDs.
Cholestyramine binds to meloxicam in the gastrointestinal tract leading to a faster elimination of meloxicam.
Nephrotoxicity of cyclosporin may be enhanced by NSAIDs via renal prostaglandin-mediated effects. During combined treatment, renal function is to be measured. No relevant pharmacokinetic drug-drug interactions were detected with respect to the concomitant administration of antacids, cimetidine, digoxin and furosemide. Interactions with oral antidiabetics cannot be excluded.
Storage
Store below 30°C.
Action
Pharmacology: Mobic is a nonsteroidal anti-inflammatory drug (NSAID) of the enolic acid class which has shown anti-inflammatory, analgesic and antipyretic properties in animals. Meloxicam showed potent anti-inflammatory activity in all standard models of inflammation. A common mechanism for these effects may exist in the ability of meloxicam to inhibit the biosynthesis of prostaglandins, which are known mediators of inflammation.
Comparison of the ulcerogenic dose and the anti-inflammatory effective dose in the rat adjuvant arthritis confirmed a superior therapeutic margin in animals over standard NSAIDs. In vivo, meloxicam inhibited prostaglandin biosynthesis more potently at the site of inflammation than in the gastric mucosa or the kidney. These differences are thought to be related to a selective inhibition of COX-2 relative to COX-1. The selective inhibition of COX-2 relative to COX-1 by meloxicam has been demonstrated in vitro on various cell systems: Guinea pig macrophages, bovine aortic endothelial cells (for testing of COX-1 activity), mouse macrophages (for testing of COX-2 activity), and human recombinant enzymes expressed in cos-cells. Evidence is now accumulating that COX-2 inhibition provides the therapeutic effects of NSAIDs whereas inhibition of constitutive COX-1 is responsible for gastric and renal side effects. Clinical studies demonstrated a lower incidence of gastrointestinal adverse events including perforations, ulcers or bleeds with the recommended doses of meloxicam than standard doses of other NSAIDs.
Pharmacokinetics: Meloxicam is well-absorbed following peroral (89%) and rectal administration. Tablets and suppositories are bioequivalent to capsules. The absorption is not altered by concomitant food intake. Drug concentrations are dose-proportional for peroral 7.5- and 15-mg doses, respectively. Steady-state conditions are achieved in 3-5 days. Continuous treatment for periods of >1 year results in similar drug concentrations to those seen once steady state is first achieved. In plasma, >99% is bound to plasma proteins. Once-daily dosing leads to drug plasma concentrations with a relatively small peak-trough fluctuation in the range of 0.4-1 mcg/mL for 7.5-mg doses or 0.8-2 mcg/mL for 15-mg doses, although values outside this range have been encountered (Cmin and Cmax at steady state, respectively). Meloxicam penetrates well into synovial fluid to give concentrations approximately half of those in plasma.
Meloxicam is extensively metabolized and <5% of the daily dose is excreted unchanged in the feces, while only traces of the unchanged compound are excreted in the urine. The major metabolic pathway is the oxidation of the methyl group of the thiazolyl-moiety of the substance, followed by urinary or fecal excretion of the metabolites. About ½ of the substance is excreted in the urine, the remainder in the stool. Meloxicam is eliminated from the body with a mean elimination half-life of 20 hrs. Neither hepatic, mild nor moderate renal insufficiency do substantially affect meloxicam pharmacokinetics.
Plasma clearance is on average 8 mL/min. Clearance is decreased in the elderly. Volume of distribution is low, on average, 11 L. Interindividual variation is in the order of 30-40%.
Toxicology: An extensive toxicological program confirmed that meloxicam has an acceptable safety profile.
Oral LD50 values ranged from about 98 mg/kg in female rats up to >800 mg/kg in minipigs. Intravenous values ranged from about 52 mg/kg in rats to 100-200 mg/kg in minipigs. Main signs of toxicity included reduced motor activity , anemia and cyanosis. Most deaths occurred as a consequence of gastric ulcers and subsequent perforative peritonitis.
Repeated dose toxicity studies in rats and minipigs showed characteristic changes reported with other NSAIDs eg, gastrointestinal ulcerations and erosions and in the long-term studies, renal papillary necrosis. Gastrointestinal side effects were observed at oral doses of ≥1 mg/kg in rats and of ≥3 mg/kg in minipigs. After IV administration, doses of 0.4 mg/kg in rats and 9 mg/kg in minipigs caused gastrointestinal lesions. Renal papillary necrosis occurred only in rats at doses of ≥0.6 mg/kg after lifetime exposure to meloxicam.
Toxicity studies on reproduction in rats and rabbits did not reveal teratogenicity up to oral doses of 4 mg/kg in rats and 80 mg/kg in rabbits. Doses of 2.5 mg/kg in rats and ≥20 mg/kg in rabbits were embryotoxic. Prolongation of gestation and labour and an increased incidence of stillbirths, which is a well-known phenomenon of prostaglandin inhibition, occurred in the peri- and postnatal study at doses of ≥0.125 mg/kg.
Meloxicam showed no mutagenic or clastogenic activity in the Ames, the host-mediated, the micronucleus, the HGPRT (V79), and the chromosomal aberration tests in cultured Chinese hamster ovary cells.
Carcinogenicity studies in rats and mice did not show a tumorigenic or carcinogenic potential up to dose levels of 0.8 mg/kg in rats and 8 mg/kg in mice.
In lifetime studies in rats and mice, meloxicam did not damage articular cartilage . It was considered to be chondroneutral in these species.
Meloxicam did not induce immunogenic reactions in tests on mice and guinea pigs.
In several tests, meloxicam proved to be less phototoxic than older NSAIDs but similar in this respect to both piroxicam and tenoxicam.
In local tolerance studies, meloxicam was well-tolerated by all tested routes of administration: IV, IM, rectal, dermal and ocular administration.
Comparison of the ulcerogenic dose and the anti-inflammatory effective dose in the rat adjuvant arthritis confirmed a superior therapeutic margin in animals over standard NSAIDs. In vivo, meloxicam inhibited prostaglandin biosynthesis more potently at the site of inflammation than in the gastric mucosa or the kidney. These differences are thought to be related to a selective inhibition of COX-2 relative to COX-1. The selective inhibition of COX-2 relative to COX-1 by meloxicam has been demonstrated in vitro on various cell systems: Guinea pig macrophages, bovine aortic endothelial cells (for testing of COX-1 activity), mouse macrophages (for testing of COX-2 activity), and human recombinant enzymes expressed in cos-cells. Evidence is now accumulating that COX-2 inhibition provides the therapeutic effects of NSAIDs whereas inhibition of constitutive COX-1 is responsible for gastric and renal side effects. Clinical studies demonstrated a lower incidence of gastrointestinal adverse events including perforations, ulcers or bleeds with the recommended doses of meloxicam than standard doses of other NSAIDs.
Pharmacokinetics: Meloxicam is well-absorbed following peroral (89%) and rectal administration. Tablets and suppositories are bioequivalent to capsules. The absorption is not altered by concomitant food intake. Drug concentrations are dose-proportional for peroral 7.5- and 15-mg doses, respectively. Steady-state conditions are achieved in 3-5 days. Continuous treatment for periods of >1 year results in similar drug concentrations to those seen once steady state is first achieved. In plasma, >99% is bound to plasma proteins. Once-daily dosing leads to drug plasma concentrations with a relatively small peak-trough fluctuation in the range of 0.4-1 mcg/mL for 7.5-mg doses or 0.8-2 mcg/mL for 15-mg doses, although values outside this range have been encountered (Cmin and Cmax at steady state, respectively). Meloxicam penetrates well into synovial fluid to give concentrations approximately half of those in plasma.
Meloxicam is extensively metabolized and <5% of the daily dose is excreted unchanged in the feces, while only traces of the unchanged compound are excreted in the urine. The major metabolic pathway is the oxidation of the methyl group of the thiazolyl-moiety of the substance, followed by urinary or fecal excretion of the metabolites. About ½ of the substance is excreted in the urine, the remainder in the stool. Meloxicam is eliminated from the body with a mean elimination half-life of 20 hrs. Neither hepatic, mild nor moderate renal insufficiency do substantially affect meloxicam pharmacokinetics.
Plasma clearance is on average 8 mL/min. Clearance is decreased in the elderly. Volume of distribution is low, on average, 11 L. Interindividual variation is in the order of 30-40%.
Toxicology: An extensive toxicological program confirmed that meloxicam has an acceptable safety profile.
Oral LD50 values ranged from about 98 mg/kg in female rats up to >800 mg/kg in minipigs. Intravenous values ranged from about 52 mg/kg in rats to 100-200 mg/kg in minipigs. Main signs of toxicity included reduced motor activity , anemia and cyanosis. Most deaths occurred as a consequence of gastric ulcers and subsequent perforative peritonitis.
Repeated dose toxicity studies in rats and minipigs showed characteristic changes reported with other NSAIDs eg, gastrointestinal ulcerations and erosions and in the long-term studies, renal papillary necrosis. Gastrointestinal side effects were observed at oral doses of ≥1 mg/kg in rats and of ≥3 mg/kg in minipigs. After IV administration, doses of 0.4 mg/kg in rats and 9 mg/kg in minipigs caused gastrointestinal lesions. Renal papillary necrosis occurred only in rats at doses of ≥0.6 mg/kg after lifetime exposure to meloxicam.
Toxicity studies on reproduction in rats and rabbits did not reveal teratogenicity up to oral doses of 4 mg/kg in rats and 80 mg/kg in rabbits. Doses of 2.5 mg/kg in rats and ≥20 mg/kg in rabbits were embryotoxic. Prolongation of gestation and labour and an increased incidence of stillbirths, which is a well-known phenomenon of prostaglandin inhibition, occurred in the peri- and postnatal study at doses of ≥0.125 mg/kg.
Meloxicam showed no mutagenic or clastogenic activity in the Ames, the host-mediated, the micronucleus, the HGPRT (V79), and the chromosomal aberration tests in cultured Chinese hamster ovary cells.
Carcinogenicity studies in rats and mice did not show a tumorigenic or carcinogenic potential up to dose levels of 0.8 mg/kg in rats and 8 mg/kg in mice.
In lifetime studies in rats and mice, meloxicam did not damage articular cartilage . It was considered to be chondroneutral in these species.
Meloxicam did not induce immunogenic reactions in tests on mice and guinea pigs.
In several tests, meloxicam proved to be less phototoxic than older NSAIDs but similar in this respect to both piroxicam and tenoxicam.
In local tolerance studies, meloxicam was well-tolerated by all tested routes of administration: IV, IM, rectal, dermal and ocular administration.
MedsGo Class
Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)
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