Meloxicam Tablets

Meloxicam is a nonsteroidal anti-inflammatory analgesic (NSAID) of the enolic acid class that exhibits anti-inflammatory, analgesic and antipyretic properties in animal studies. Meloxicam has anti-inflammatory activity in all standard inflammatory models. The common mechanism of action is that meloxicam inhibits the biosynthesis of known inflammatory mediators, prostaglandins. Compared with its ulcerogenic dose in rats and its effective anti-inflammatory dose for adjuvant arthritis, meloxicam has a significantly wider safety margin than other typical NSAIDs. In vivo, meloxicam has a stronger inhibitory effect on prostaglandin biosynthesis at inflammatory sites than on prostaglandin biosynthesis in the gastric mucosa or kidneys. This improvement in safety is due to the fact that meloxicam selectively inhibits COX-2 more than COX-1. Meloxicam's highly selective inhibition of COX-2 has been demonstrated in a variety of in vitro cell lines, such as guinea pig macrophages, calf aortic endothelial cells (to test COX-1 activity), mouse macrophages (to test COX-2 activity) and human cos cells. There is increasing evidence that NSAIDs achieve their therapeutic effects by inhibiting COX-2, while the inhibition of tissue enzyme COX-1 causes gastrointestinal and renal side effects. Clinical studies have shown that the incidence of gastrointestinal adverse reactions including perforation, ulceration or bleeding is lower when using the recommended dose of meloxicam than when using other standard doses of NSAIDs. A large number of toxicological experiments have confirmed the safety of meloxicam. The oral median lethal dose (LD50) ranges from 98 mg/kg for female mice to 800 mg/kg for miniature pigs. Intravenous administration ranges from about 52 mg/kg for rats to 100-200 mg/kg for miniature pigs. The main symptoms of toxicity include decreased motility, anemia and cyanosis. Most deaths are caused by gastric ulcers and subsequent perforation peritonitis. Multiple dose toxicity studies conducted in mice and miniature pigs have shown that, like the use of other NSAIDs, the use of meloxicam can lead to some characteristic changes, such as gastrointestinal ulcers and erosions and renal papillary necrosis in long-term studies. Gastrointestinal side effects were observed at oral doses of 1 mg/kg and above in rats and at doses of 3 mg/kg and above in miniature pigs. Intravenous doses of 0.4 mg/kg in rats and 9 mg/kg and above in miniature pigs caused gastrointestinal damage. Renal papillary necrosis occurred only in rats with lifetime exposure to meloxicam at doses of 0.6 mg/kg or above. Reproductive toxicity studies in rats and rabbits showed no teratogenic effects at oral doses of 4 mg/kg in mice and 80 mg/kg in rabbits. Embryotoxicity was observed at doses of 2.5 mg/kg in mice and 20 mg/kg or above in rabbits. Prolonged gestation and labor and increased mortality were observed in perinatal and postnatal studies at doses of 0.125 mg/kg and above. This is a typical phenomenon of prostaglandin inhibition. Meloxicam showed no mutagenic or clastogenic activity in aberration tests using cultured Chinese giant voles ovarian cells Ames, intermediate hosts, nucleoli, HGPRT, and chromosomes. In carcinogenicity studies with mice and rats, no tumorigenic or carcinogenic effects were found at doses of 0.8 mg/kg for rats and 8 mg/kg for mice. In lifelong studies with mice and rats, meloxicam did not damage articular cartilage, and it is considered to have no effect on cartilage in these species. Meloxicam did not induce an immune response in experiments with mice and guinea pigs. Some experiments have shown that the phototoxicity of meloxicam is lower than that of previous NSAIDs, and in this respect it is similar to piroxicam and tenoxicam. In local tolerance studies, meloxicam was well tolerated by different routes of administration, including intravenous, intramuscular, anal, skin and eye.

The main ingredient of this product is meloxicam, and its chemical name is 4-hydroxy-2-methyl-N-(5-methyl-2-thiazolyl)-2H-1,2-benzothiazine-3-carboxamide-1,1-dioxide.

This product is light yellow tablet.

Indicated for the symptomatic treatment of rheumatoid arthritis and symptomatic treatment of painful osteoarthritis (arthrosis, degenerative osteoarthritis).

Oral administration, swallow with water or liquid. Rheumatoid arthritis: 15 mg (2 tablets) per day, depending on the response after treatment, the dose can be reduced to 7.5 mg (1 tablet)/day. Osteoarthritis: 7.5 mg (1 tablet)/day, if necessary, the dose can be increased to 15 mg (2 tablets)/day. For patients with increased adverse reactions: the initial dose of treatment is 7.5 mg (1 tablet)/day. Patients with severe renal failure on dialysis: the dose should not exceed 7.5 mg (1 tablet)/day. The maximum recommended daily dose of meloxicam tablets is 15 mg (2 tablets). The dosage for children has not yet been determined and is currently limited to adult use.

The adverse events listed below occurred after the administration of meloxicam, however their frequency is based on the results recorded in clinical trials, regardless of whether there is a causal relationship with the use of meloxicam. This information is based on clinical trials conducted on 3,750 patients for more than 18 months, with patients taking oral meloxicam tablets at a dose of 7.5 mg or 15 mg per day. (The average course of treatment was 127 days). 1 Gastrointestinal: Frequency greater than 1%: dyspepsia, nausea, vomiting, abdominal pain, constipation, flatulence, diarrhea. Frequency between 0.1% and 1%: transient abnormal liver function indicators (such as increased transaminases or bilirubin), belching, esophagitis, gastroduodenal ulcer, latent or visible gastrointestinal bleeding. Frequency less than 0.1%: gastrointestinal perforation, colitis

1. People who are known to be allergic to the active ingredient meloxicam or its excipients. 2. Patients who have experienced asthma, rhinitis, angioedema or urticaria after using acetylsalicylic acid or other NSAIDs (non-steroidal anti-inflammatory drugs) should not use meloxicam tablets. 3. Active peptic ulcer. 4. Severe liver dysfunction. 5. Non-dialysis severe renal dysfunction. 6. Children and adolescents under 15 years old. 7. Pregnant or breastfeeding women.

Large doses of other NSAIDs, including salicylates, and the simultaneous use of more than one NSAID may increase the likelihood of gastrointestinal ulcers and bleeding through synergistic effects. Oral anticoagulants, ampicillin, systemic heparin, and thrombolytics may increase the likelihood of bleeding. If the above combination medications are unavoidable, the effects of anticoagulants must be closely monitored. Lithium: NSAIDs have been reported to increase plasma lithium concentrations, so it is recommended to monitor plasma lithium levels when starting, adjusting, and stopping meloxicam. Methotrexate: Similar to other NSAIDs, meloxicam can increase the hematotoxicity of methotrexate. In this case, strict monitoring of blood cell counts is recommended. Contraception: NSAIDs have been reported to reduce the effectiveness of intrauterine contraceptive devices. Diuretics: When using NSAIDs, patients with diuretic dehydration may develop acute renal insufficiency, so patients using meloxicam and diuretics should ensure adequate blood volume and monitor renal function before starting treatment. Antihypertensive drugs (e.g., beta-receptor blockers, ACE inhibitors, vasodilators, diuretics) have been reported to reduce the effect of antihypertensive drugs during NSAID treatment by inhibiting prostaglandins that cause vasodilation. Cholestyramine combined with meloxicam in the gastrointestinal tract can accelerate the elimination of meloxicam. NSAIDs may increase the renal toxicity of cyclosporine, which is mediated by renal prostaglandins. Renal function should be measured during combined treatment. No pharmacokinetic drug interactions were observed when antacids, cimetidine, digoxin, and furosemide were used simultaneously. Interactions with oral hypoglycemic drugs cannot be ruled out.

Sealed and light-proof.

7.5 mg

60 months.

China Pharmaceutical University Pharmaceutical Co., Ltd.

• Founded in:

  1994-12-05

• Address:

  No. 50, Majia Street, Gulou District, Nanjing

• Tax NO.:

  91320000134755425F

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  98 million yuan

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