Diclofenac Sodium Extended-Release

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Overview

What is Diclofenac Sodium Extended-Release?

Diclofenac sodium, USP extended-release, is a benzeneacetic acid derivative. The chemical name is 2-[(2,6-dichlorophenyl)amino] benzeneacetic acid, monosodium salt. The molecular weight is 318.13. Its molecular formula is CHCNNaO, and it has the following structural formula:

Each extended-release tablet for oral administration contains 100 mg of diclofenac sodium, USP. In addition, each tablet contains the following inactive ingredients: carnauba wax, cetyl alcohol, colloidal silicon dioxide, hypromellose, lactose monohydrate, magnesium stearate, povidone, synthetic yellow iron oxide, talc, titanium dioxide, and triacetin.

What does Diclofenac Sodium Extended-Release look like?

What are the available doses of Diclofenac Sodium Extended-Release?

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What should I talk to my health care provider before I take Diclofenac Sodium Extended-Release?

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How should I use Diclofenac Sodium Extended-Release?

Carefully consider the potential benefits and risks of diclofenac sodium extended-release and other treatment options before deciding to use diclofenac sodium extended-release. Use the lowest effective dose for the shortest duration consistent with individual patient treatment goals (see ).

Diclofenac sodium extended-release tablets are indicated:

• For relief of signs and symptoms of osteoarthritis

• For relief of signs and symptoms of rheumatoid arthritis

Carefully consider the potential benefits and risks of diclofenac sodium extended-release and other treatment options before deciding to use diclofenac sodium extended-release. Use the lowest effective dose for the shortest duration consistent with individual patient treatment goals (see ).

After observing the response to initial therapy with diclofenac sodium extended-release, the dose and frequency should be adjusted to suit an individual patient’s needs.

For the relief of osteoarthritis, the recommended dosage is 100 mg q.d.

For the relief of rheumatoid arthritis, the recommended dosage is 100 mg q.d. In the rare patient where diclofenac sodium extended-release 100 mg/day is unsatisfactory, the dose may be increased to 100 mg b.i.d. if the benefits outweigh the clinical risks of increased side effects.

Different formulations of diclofenac (diclofenac sodium delayed-release tablets; diclofenac sodium extended-release tablets; diclofenac potassium immediate-release tablets) are not necessarily bioequivalent even if the milligram strength is the same.

What interacts with Diclofenac Sodium Extended-Release?

Diclofenac sodium extended-release tablets are contraindicated in patients with known hypersensitivity to diclofenac.

Diclofenac sodium extended-release should not be given to patients who have experienced asthma, urticaria, or other allergic-type reactions after taking aspirin or other NSAIDs. Severe, rarely fatal, anaphylactic-like reactions to NSAIDs have been reported in such patients (see , and ).

Diclofenac sodium extended-release is contraindicated for the treatment of peri-operative pain in the setting of coronary artery bypass graft (CABG) surgery (see ).

What are the warnings of Diclofenac Sodium Extended-Release?

Cardiovascular Effects

Clinical trials of several COX-2 selective and nonselective NSAIDs of up to three years duration have shown an increased risk of serious cardiovascular (CV) thrombotic events, myocardial infarction, and stroke, which can be fatal. All NSAIDs, both COX-2 selective and nonselective, may have a similar risk. Patients with known CV disease or risk factors for CV disease may be at greater risk. To minimize the potential risk for an adverse CV event in patients treated with an NSAID, the lowest effective dose should be used for the shortest duration possible. Physicians and patients should remain alert for the development of such events, even in the absence of previous CV symptoms. Patients should be informed about the signs and/or symptoms of serious CV events and the steps to take if they occur.

There is no consistent evidence that concurrent use of aspirin mitigates the increased risk of serious CV thrombotic events associated with NSAID use. The concurrent use of aspirin and an NSAID does increase the risk of serious GI events (see ).

Two large, controlled, clinical trials of a COX-2 selective NSAID for the treatment of pain in the first 10-14 days following CABG surgery found an increased incidence of myocardial infarction and stroke (see ).

NSAIDs can lead to onset of new hypertension or worsening of pre-existing hypertension, either of which may contribute to the increased incidence of CV events. Patients taking thiazides or loop diuretics may have impaired response to these therapies when taking NSAIDs. NSAIDs, including diclofenac sodium extended-release, should be used with caution in patients with hypertension. Blood pressure (BP) should be monitored closely during the initiation of NSAID treatment and throughout the course of therapy.

Fluid retention and edema have been observed in some patients taking NSAIDs. Diclofenac sodium extended-release should be used with caution in patients with fluid retention or heart failure.

Gastrointestinal (GI) Effects - Risk of GI Ulceration, Bleeding, and Perforation

NSAIDs, including diclofenac sodium extended-release, can cause serious gastrointestinal (GI) adverse events including inflammation, bleeding, ulceration, and perforation of the stomach, small intestine, or large intestine, which can be fatal. These serious adverse events can occur at any time, with or without warning symptoms, in patients treated with NSAIDs. Only one in five patients, who develop a serious upper GI adverse event on NSAID therapy, is symptomatic. Upper GI ulcers, gross bleeding, or perforation caused by NSAIDs occur in approximately 1% of patients treated for 3-6 months, and in about 2-4% of patients treated for one year. These trends continue with longer duration of use, increasing the likelihood of developing a serious GI event at some time during the course of therapy. However, even short-term therapy is not without risk.

NSAIDs should be prescribed with extreme caution in those with a prior history of ulcer disease or gastrointestinal bleeding. Patients with a who use NSAIDs have a greater than 10-fold increased risk for developing a GI bleed compared to patients with neither of these risk factors. Other factors that increase the risk for GI bleeding in patients treated with NSAIDs include concomitant use of oral corticosteroids or anticoagulants, longer duration of NSAID therapy, smoking, use of alcohol, older age, and poor general health status. Most spontaneous reports of fatal GI events are in elderly or debilitated patients and therefore, special care should be taken in treating this population.

To minimize the potential risk for an adverse GI event in patients treated with an NSAID, the lowest effective dose should be used for the shortest possible duration. Patients and physicians should remain alert for signs and symptoms of GI ulceration and bleeding during NSAID therapy and promptly initiate additional evaluation and treatment if a serious GI adverse event is suspected. This should include discontinuation of the NSAID until a serious GI adverse event is ruled out. For high risk patients, alternate therapies that do not involve NSAIDs should be considered.

Renal Effects

Caution should be used when initiating treatment with diclofenac sodium extended-release in patients with considerable dehydration.

Long-term administration of NSAIDs has resulted in renal papillary necrosis and other renal injury. Renal toxicity has also been seen in patients in whom renal prostaglandins have a compensatory role in the maintenance of renal perfusion. In these patients, administration of a nonsteroidal anti-inflammatory drug may cause a dose-dependent reduction in prostaglandin formation and, secondarily, in renal blood flow, which may precipitate overt renal decompensation. Patients at greatest risk of this reaction are those with impaired renal function, heart failure, liver dysfunction, those taking diuretics and ACE inhibitors, and the elderly. Discontinuation of non-steroidal anti-inflammatory drug therapy is usually followed by recovery to the pretreatment state.

No information is available from controlled clinical studies regarding the use of diclofenac sodium extended-release in patients with advanced renal disease. Therefore, treatment with diclofenac sodium extended-release is not recommended in these patients with advanced renal disease. If diclofenac sodium extended-release therapy must be initiated, close monitoring of the patient's renal function is advisable.

Hepatic Effects

Elevations of one or more liver tests may occur during therapy with diclofenac sodium extended-release. These laboratory abnormalities may progress, may remain unchanged, or may be transient with continued therapy. Borderline elevations (i.e., less than 3 times the ULN [ULN = the upper limit of the normal range]) or greater elevations of transaminases occurred in about 15% of diclofenac-treated patients. Of the markers of hepatic function, ALT (SGPT) is recommended for the monitoring of liver injury.

In clinical trials, meaningful elevations (i.e., more than 3 times the ULN) of AST (GOT) (ALT was not measured in all studies) occurred in about 2% of approximately 5,700 patients at some time during diclofenac treatment. In a large, open-label, controlled trial of 3,700 patients treated for 2-6 months, patients were monitored first at 8 weeks and 1,200 patients were monitored again at 24 weeks. Meaningful elevations of ALT and/or AST occurred in about 4% of patients and included marked elevations (i.e., more than 8 times the ULN) in about 1% of the 3,700 patients. In that open-label study, a higher incidence of borderline (less than 3 times the ULN), moderate (3-8 times the ULN), and marked (>8 times the ULN) elevations of ALT or AST was observed in patients receiving diclofenac when compared to other NSAIDs. Elevations in transaminases were seen more frequently in patients with osteoarthritis than in those with rheumatoid arthritis.

Almost all meaningful elevations in transaminases were detected before patients became symptomatic. Abnormal tests occurred during the first 2 months of therapy with diclofenac in 42 of the 51 patients in all trials who developed marked transaminase elevations.

In postmarketing reports, cases of drug-induced hepatotoxicity have been reported in the first month, and in some cases, the first 2 months of therapy, but can occur at any time during treatment with diclofenac. Postmarketing surveillance has reported cases of severe hepatic reactions, including liver necrosis, jaundice, fulminant hepatitis with and without jaundice, and liver failure. Some of these reported cases resulted in fatalities or liver transplantation.

Physicians should measure transaminases periodically in patients receiving long-term therapy with diclofenac, because severe hepatotoxicity may develop without a prodrome of distinguishing symptoms. The optimum times for making the first and subsequent transaminase measurements are not known. Based on clinical trial data and postmarketing experiences, transaminases should be monitored within 4 to 8 weeks after initiating treatment with diclofenac. However, severe hepatic reactions can occur at any time during treatment with diclofenac.

If abnormal liver tests persist or worsen, if clinical signs and/or symptoms consistent with liver disease develop, or if systemic manifestations occur (e.g., eosinophilia, rash, abdominal pain, diarrhea, dark urine, etc.), diclofenac sodium extended-release should be discontinued immediately.

To minimize the possibility that hepatic injury will become severe between transaminase measurements, physicians should inform patients of the warning signs and symptoms of hepatotoxicity (e.g., nausea, fatigue, lethargy, diarrhea, pruritus, jaundice, right upper quadrant tenderness, and "flu-like" symptoms), and the appropriate action patients should take if these signs and symptoms appear.

To minimize the potential risk for an adverse liver related event in patients treated with diclofenac sodium extended-release, the lowest effective dose should be used for the shortest duration possible. Caution should be exercised in prescribing diclofenac sodium extended-release with concomitant drugs that are known to be potentially hepatotoxic (e.g., antibiotics, anti-epileptics).

Anaphylactoid Reactions

As with other NSAIDs, anaphylactoid reactions may occur in patients without known prior exposure to diclofenac sodium extended-release tablets. Diclofenac sodium extended-release should not be given to patients with the aspirin triad. This symptom complex typically occurs in asthmatic patients who experience rhinitis with or without nasal polyps, or who exhibit severe, potentially fatal bronchospasm after taking aspirin or other NSAIDs. (See and .) Emergency help should be sought in cases where an anaphylactoid reaction occurs.

Skin Reactions

NSAIDs, including diclofenac sodium extended-release, can cause serious skin adverse events such as exfoliative dermatitis, Stevens-Johnson Syndrome (SJS), and toxic epidermal necrolysis (TEN), which can be fatal. These serious events may occur without warning. Patients should be informed about the signs and symptoms of serious skin manifestations and use of the drug should be discontinued at the first appearance of skin rash or any other sign of hypersensitivity.

Pregnancy

In late pregnancy, as with other NSAIDs, diclofenac sodium extended-release should be avoided because it may cause premature closure of the ductus arteriosus.

What are the precautions of Diclofenac Sodium Extended-Release?

General

Diclofenac sodium extended-release tablets cannot be expected to substitute for corticosteroids or to treat corticosteroid insufficiency. Abrupt discontinuation of corticosteroids may lead to disease exacerbation. Patients on prolonged corticosteroid therapy should have their therapy tapered slowly if a decision is made to discontinue corticosteroids.

The pharmacological activity of diclofenac sodium extended-release in reducing fever and inflammation may diminish the utility of these diagnostic signs in detecting complications of presumed noninfectious, painful conditions.

Hematological Effects

Anemia is sometimes seen in patients receiving NSAIDs, including diclofenac sodium extended-release. This may be due to fluid retention, occult or gross GI blood loss, or an incompletely described effect upon erythropoiesis. Patients on long-term treatment with NSAIDs, including diclofenac sodium extended-release, should have their hemoglobin or hematocrit checked if they exhibit any signs or symptoms of anemia.

NSAIDs inhibit platelet aggregation and have been shown to prolong bleeding time in some patients. Unlike aspirin, their effect on platelet function is quantitatively less, of shorter duration, and reversible. Patients receiving diclofenac sodium extended-release who may be adversely affected by alterations in platelet function, such as those with coagulation disorders or patients receiving anticoagulants, should be carefully monitored.

Preexisting Asthma

Patients with asthma may have aspirin-sensitive asthma. The use of aspirin in patients with aspirin-sensitive asthma has been associated with severe bronchospasm which can be fatal. Since cross-reactivity, including bronchospasm, between aspirin and other nonsteroidal anti-inflammatory drugs has been reported in such aspirin-sensitive patients, diclofenac sodium extended-release should not be administered to patients with this form of aspirin sensitivity and should be used with caution in patients with preexisting asthma.

Information for Patients

Patients should be informed of the following information before initiating therapy with an NSAID and periodically during the course of ongoing therapy. Patients should also be encouraged to read the NSAID Medication Guide that accompanies each prescription dispensed.

Laboratory Tests

Because serious GI tract ulcerations and bleeding can occur without warning symptoms, physicians should monitor for signs or symptoms of GI bleeding. In patients on long-term treatment with NSAIDs, including diclofenac sodium extended-release, the CBC and a chemistry profile (including transaminase levels) should be checked periodically. If clinical signs and symptoms consistent with liver or renal disease develop, systemic manifestations occur (e.g., eosinophilia, rash, etc.) or if abnormal liver tests persist or worsen, diclofenac sodium extended-release should be discontinued.

Drug Interactions

Aspirin:When diclofenac sodium extended-release is administered with aspirin, its protein binding is reduced. The clinical significance of this interaction is not known; however, as with other NSAIDs, concomitant administration of diclofenac and aspirin is not generally recommended because of the potential of increased adverse effects.

MethotrexateNSAIDs have been reported to competitively inhibit methotrexate accumulation in rabbit kidney slices. This may indicate that they could enhance the toxicity of methotrexate. Caution should be used when NSAIDs are administered concomitantly with methotrexate.

CyclosporineDiclofenac sodium extended-release, like other NSAIDs, may affect renal prostaglandins and increase the toxicity of certain drugs. Therefore, concomitant therapy with diclofenac sodium extended-release may increase cyclosporine’s nephrotoxicity. Caution should be used when diclofenac sodium extended-release is administered concomitantly with cyclosporine.

ACE-inhibitors:Reports suggest that NSAIDs may diminish the antihypertensive effect of ACE inhibitors. This interaction should be given consideration in patients taking NSAIDs concomitantly with ACE inhibitors.

Furosemide:Clinical studies, as well as post-marketing observations, have shown that diclofenac sodium extended-release can reduce the natriuretic effect of furosemide and thiazides in some patients. This response has been attributed to inhibition of renal prostaglandin synthesis. During concomitant therapy with NSAIDs, the patient should be observed closely for signs of renal failure (see ), as well as to assure diuretic efficacy.

Lithium:NSAIDs have produced an elevation of plasma lithium levels and a reduction in renal lithium clearance. The mean minimum lithium concentration increased 15% and the renal clearance was decreased by approximately 20%. These effects have been attributed to inhibition of renal prostaglandin synthesis by the NSAID. Thus, when NSAIDs and lithium are administered concurrently, subjects should be observed carefully for signs of lithium toxicity.

Warfarin:The effects of warfarin and NSAIDs on GI bleeding are synergistic, such that users of both drugs together have a risk of serious GI bleeding higher than users of either drug alone.

Pregnancy

Teratogenic Effects:

Reproductive studies conducted in rats and rabbits have not demonstrated evidence of developmental abnormalities. However, animal reproduction studies are not always predictive of human response. There are no adequate and well-controlled studies in pregnant women.

Nonteratogenic Effects:Because of the known effects of nonsteroidal anti-inflammatory drugs on the fetal cardiovascular system (closure of ductus arteriosus), use during pregnancy (particularly late pregnancy) should be avoided.

Labor and Delivery

In rat studies with NSAIDs, as with other drugs known to inhibit prostaglandin synthesis, an increased incidence of dystocia, delayed parturition, and decreased pup survival occurred. The effects of diclofenac sodium extended-release on labor and delivery in pregnant women are unknown.

Nursing Mothers

It is not known whether this drug is excreted in human milk. Because many drugs are excreted in human milk and because of the potential for serious adverse reactions in nursing infants from diclofenac sodium extended-release, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother.

Pediatric Use

Safety and effectiveness in pediatric patients have not been established.

Geriatric Use

As with any NSAIDs, caution should be exercised in treating the elderly (65 years and older).

What are the side effects of Diclofenac Sodium Extended-Release?

In patients taking diclofenac sodium extended-release tablets, or other NSAIDs, the most frequently reported adverse experiences occurring in approximately 1%-10% of patients are:

Gastrointestinal experiences including: abdominal pain, constipation, diarrhea, dyspepsia, flatulence, gross bleeding/perforation, heartburn, nausea, GI ulcers (gastric/duodenal) and vomiting.

Abnormal renal function, anemia, dizziness, edema, elevated liver enzymes, headaches, increased bleeding time, pruritus, rashes and tinnitus.

Additional adverse experiences reported occasionally include:

Body As A Whole:

Cardiovascular System:

Digestive System:

Hemic And Lymphatic System:

Metabolic And Nutritional:

Nervous System:

Respiratory System:

Skin And Appendages:

Special Senses:

Urogenital System:

Other adverse reactions, which occur rarely are:

Body As A Whole:

Cardiovascular System:

Digestive System

Hemic And Lymphatic System:

Metabolic And Nutritional:

Nervous System:

Respiratory System:

Skin And Appendages:

Special Senses:

What should I look out for while using Diclofenac Sodium Extended-Release?

Diclofenac sodium extended-release tablets are contraindicated in patients with known hypersensitivity to diclofenac.

Diclofenac sodium extended-release should not be given to patients who have experienced asthma, urticaria, or other allergic-type reactions after taking aspirin or other NSAIDs. Severe, rarely fatal, anaphylactic-like reactions to NSAIDs have been reported in such patients (see , and ).

Diclofenac sodium extended-release is contraindicated for the treatment of peri-operative pain in the setting of coronary artery bypass graft (CABG) surgery (see ).

What might happen if I take too much Diclofenac Sodium Extended-Release?

Symptoms following acute NSAID overdoses are usually limited to lethargy, drowsiness, nausea, vomiting, and epigastric pain, which are generally reversible with supportive care. Gastrointestinal bleeding can occur. Hypertension, acute renal failure, respiratory depression and coma may occur, but are rare. Anaphylactoid reactions have been reported with therapeutic ingestion of NSAIDs, and may occur following an overdose.

Patients should be managed by symptomatic and supportive care following a NSAID overdose. There are no specific antidotes. Emesis and/or activated charcoal (60 to 100 g in adults, 1 to 2 g/kg in children) and/or osmotic cathartic may be indicated in patients seen within 4 hours of ingestion with symptoms or following a large overdose (5 to 10 times the usual dose). Forced diuresis, alkalinization of urine, hemodialysis, or hemoperfusion may not be useful due to high protein binding.

How should I store and handle Diclofenac Sodium Extended-Release?

Store at controlled room temperature 20° to 25°C (68° to 77°F) [see USP] .Diclofenac Sodium Extended-Release Tablets, USP are available as follows:100 mg - Each unscored, yellow, round, beveled edge, film-coated tablet imprinted with on one side and 717 on the other side contains 100 mg of Diclofenac Sodium, USP. Tablets are supplied in bottles of 100 with a child-resistant closure (NDC 0228-2717-11).Store at 25°C (77°F); excursions permitted to 15° to 30°C (59° to 86°F). Protect from moisture.Dispense in a tight, light-resistant container as defined in the USP.Manufactured by: Actavis Elizabeth LLC200 Elmora Avenue Elizabeth, NJ 0720740-8831Revised — March 2009Repackaged by: Rebel Distributors Corp.3607 Old Conejo Rd.Thousand Oaks, CA 91320Revised - June 2009 Diclofenac Sodium Extended-Release Tablets, USP are available as follows:100 mg - Each unscored, yellow, round, beveled edge, film-coated tablet imprinted with on one side and 717 on the other side contains 100 mg of Diclofenac Sodium, USP. Tablets are supplied in bottles of 100 with a child-resistant closure (NDC 0228-2717-11).Store at 25°C (77°F); excursions permitted to 15° to 30°C (59° to 86°F). Protect from moisture.Dispense in a tight, light-resistant container as defined in the USP.Manufactured by: Actavis Elizabeth LLC200 Elmora Avenue Elizabeth, NJ 0720740-8831Revised — March 2009Repackaged by: Rebel Distributors Corp.3607 Old Conejo Rd.Thousand Oaks, CA 91320Revised - June 2009 Diclofenac Sodium Extended-Release Tablets, USP are available as follows:100 mg - Each unscored, yellow, round, beveled edge, film-coated tablet imprinted with on one side and 717 on the other side contains 100 mg of Diclofenac Sodium, USP. Tablets are supplied in bottles of 100 with a child-resistant closure (NDC 0228-2717-11).Store at 25°C (77°F); excursions permitted to 15° to 30°C (59° to 86°F). Protect from moisture.Dispense in a tight, light-resistant container as defined in the USP.Manufactured by: Actavis Elizabeth LLC200 Elmora Avenue Elizabeth, NJ 0720740-8831Revised — March 2009Repackaged by: Rebel Distributors Corp.3607 Old Conejo Rd.Thousand Oaks, CA 91320Revised - June 2009 Diclofenac Sodium Extended-Release Tablets, USP are available as follows:100 mg - Each unscored, yellow, round, beveled edge, film-coated tablet imprinted with on one side and 717 on the other side contains 100 mg of Diclofenac Sodium, USP. Tablets are supplied in bottles of 100 with a child-resistant closure (NDC 0228-2717-11).Store at 25°C (77°F); excursions permitted to 15° to 30°C (59° to 86°F). Protect from moisture.Dispense in a tight, light-resistant container as defined in the USP.Manufactured by: Actavis Elizabeth LLC200 Elmora Avenue Elizabeth, NJ 0720740-8831Revised — March 2009Repackaged by: Rebel Distributors Corp.3607 Old Conejo Rd.Thousand Oaks, CA 91320Revised - June 2009 Diclofenac Sodium Extended-Release Tablets, USP are available as follows:100 mg - Each unscored, yellow, round, beveled edge, film-coated tablet imprinted with on one side and 717 on the other side contains 100 mg of Diclofenac Sodium, USP. Tablets are supplied in bottles of 100 with a child-resistant closure (NDC 0228-2717-11).Store at 25°C (77°F); excursions permitted to 15° to 30°C (59° to 86°F). Protect from moisture.Dispense in a tight, light-resistant container as defined in the USP.Manufactured by: Actavis Elizabeth LLC200 Elmora Avenue Elizabeth, NJ 0720740-8831Revised — March 2009Repackaged by: Rebel Distributors Corp.3607 Old Conejo Rd.Thousand Oaks, CA 91320Revised - June 2009 Diclofenac Sodium Extended-Release Tablets, USP are available as follows:100 mg - Each unscored, yellow, round, beveled edge, film-coated tablet imprinted with on one side and 717 on the other side contains 100 mg of Diclofenac Sodium, USP. Tablets are supplied in bottles of 100 with a child-resistant closure (NDC 0228-2717-11).Store at 25°C (77°F); excursions permitted to 15° to 30°C (59° to 86°F). Protect from moisture.Dispense in a tight, light-resistant container as defined in the USP.Manufactured by: Actavis Elizabeth LLC200 Elmora Avenue Elizabeth, NJ 0720740-8831Revised — March 2009Repackaged by: Rebel Distributors Corp.3607 Old Conejo Rd.Thousand Oaks, CA 91320Revised - June 2009 Diclofenac Sodium Extended-Release Tablets, USP are available as follows:100 mg - Each unscored, yellow, round, beveled edge, film-coated tablet imprinted with on one side and 717 on the other side contains 100 mg of Diclofenac Sodium, USP. Tablets are supplied in bottles of 100 with a child-resistant closure (NDC 0228-2717-11).Store at 25°C (77°F); excursions permitted to 15° to 30°C (59° to 86°F). Protect from moisture.Dispense in a tight, light-resistant container as defined in the USP.Manufactured by: Actavis Elizabeth LLC200 Elmora Avenue Elizabeth, NJ 0720740-8831Revised — March 2009Repackaged by: Rebel Distributors Corp.3607 Old Conejo Rd.Thousand Oaks, CA 91320Revised - June 2009 Diclofenac Sodium Extended-Release Tablets, USP are available as follows:100 mg - Each unscored, yellow, round, beveled edge, film-coated tablet imprinted with on one side and 717 on the other side contains 100 mg of Diclofenac Sodium, USP. Tablets are supplied in bottles of 100 with a child-resistant closure (NDC 0228-2717-11).Store at 25°C (77°F); excursions permitted to 15° to 30°C (59° to 86°F). Protect from moisture.Dispense in a tight, light-resistant container as defined in the USP.Manufactured by: Actavis Elizabeth LLC200 Elmora Avenue Elizabeth, NJ 0720740-8831Revised — March 2009Repackaged by: Rebel Distributors Corp.3607 Old Conejo Rd.Thousand Oaks, CA 91320Revised - June 2009

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Clinical Information

Chemical Structure

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Clinical Pharmacology

Diclofenac sodium extended-release is a nonsteroidal anti-inflammatory drug (NSAID) that exhibits anti-inflammatory, analgesic, and antipyretic activities in animal models. The mechanism of action of diclofenac sodium extended-release, like that of other NSAIDs, is not completely understood but may be related to prostaglandin synthetase inhibition.

Non-Clinical Toxicology

Diclofenac sodium extended-release tablets are contraindicated in patients with known hypersensitivity to diclofenac.

Diclofenac sodium extended-release should not be given to patients who have experienced asthma, urticaria, or other allergic-type reactions after taking aspirin or other NSAIDs. Severe, rarely fatal, anaphylactic-like reactions to NSAIDs have been reported in such patients (see , and ).

Diclofenac sodium extended-release is contraindicated for the treatment of peri-operative pain in the setting of coronary artery bypass graft (CABG) surgery (see ).

Aspirin:When diclofenac sodium extended-release is administered with aspirin, its protein binding is reduced. The clinical significance of this interaction is not known; however, as with other NSAIDs, concomitant administration of diclofenac and aspirin is not generally recommended because of the potential of increased adverse effects.

MethotrexateNSAIDs have been reported to competitively inhibit methotrexate accumulation in rabbit kidney slices. This may indicate that they could enhance the toxicity of methotrexate. Caution should be used when NSAIDs are administered concomitantly with methotrexate.

CyclosporineDiclofenac sodium extended-release, like other NSAIDs, may affect renal prostaglandins and increase the toxicity of certain drugs. Therefore, concomitant therapy with diclofenac sodium extended-release may increase cyclosporine’s nephrotoxicity. Caution should be used when diclofenac sodium extended-release is administered concomitantly with cyclosporine.

ACE-inhibitors:Reports suggest that NSAIDs may diminish the antihypertensive effect of ACE inhibitors. This interaction should be given consideration in patients taking NSAIDs concomitantly with ACE inhibitors.

Furosemide:Clinical studies, as well as post-marketing observations, have shown that diclofenac sodium extended-release can reduce the natriuretic effect of furosemide and thiazides in some patients. This response has been attributed to inhibition of renal prostaglandin synthesis. During concomitant therapy with NSAIDs, the patient should be observed closely for signs of renal failure (see ), as well as to assure diuretic efficacy.

Lithium:NSAIDs have produced an elevation of plasma lithium levels and a reduction in renal lithium clearance. The mean minimum lithium concentration increased 15% and the renal clearance was decreased by approximately 20%. These effects have been attributed to inhibition of renal prostaglandin synthesis by the NSAID. Thus, when NSAIDs and lithium are administered concurrently, subjects should be observed carefully for signs of lithium toxicity.

Warfarin:The effects of warfarin and NSAIDs on GI bleeding are synergistic, such that users of both drugs together have a risk of serious GI bleeding higher than users of either drug alone.

Diclofenac sodium extended-release tablets cannot be expected to substitute for corticosteroids or to treat corticosteroid insufficiency. Abrupt discontinuation of corticosteroids may lead to disease exacerbation. Patients on prolonged corticosteroid therapy should have their therapy tapered slowly if a decision is made to discontinue corticosteroids.

The pharmacological activity of diclofenac sodium extended-release in reducing fever and inflammation may diminish the utility of these diagnostic signs in detecting complications of presumed noninfectious, painful conditions.

In patients taking diclofenac sodium extended-release tablets, or other NSAIDs, the most frequently reported adverse experiences occurring in approximately 1%-10% of patients are:

Gastrointestinal experiences including: abdominal pain, constipation, diarrhea, dyspepsia, flatulence, gross bleeding/perforation, heartburn, nausea, GI ulcers (gastric/duodenal) and vomiting.

Abnormal renal function, anemia, dizziness, edema, elevated liver enzymes, headaches, increased bleeding time, pruritus, rashes and tinnitus.

Additional adverse experiences reported occasionally include:

Body As A Whole:

Cardiovascular System:

Digestive System:

Hemic And Lymphatic System:

Metabolic And Nutritional:

Nervous System:

Respiratory System:

Skin And Appendages:

Special Senses:

Urogenital System:

Other adverse reactions, which occur rarely are:

Body As A Whole:

Cardiovascular System:

Digestive System

Hemic And Lymphatic System:

Metabolic And Nutritional:

Nervous System:

Respiratory System:

Skin And Appendages:

Special Senses:

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Reference

This information is obtained from the National Institute of Health's Standard Packaging Label drug database.
"https://dailymed.nlm.nih.gov/dailymed/"

While we update our database periodically, we cannot guarantee it is always updated to the latest version.

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Professional

Clonazepam Description Each single-scored tablet, for oral administration, contains 0.5 mg, 1 mg, or 2 mg Clonazepam, USP, a benzodiazepine. Each tablet also contains corn starch, lactose monohydrate, magnesium stearate, microcrystalline cellulose, and povidone. Clonazepam tablets USP 0.5 mg contain Yellow D&C No. 10 Aluminum Lake. Clonazepam tablets USP 1 mg contain Yellow D&C No. 10 Aluminum Lake, as well as FD&C Blue No. 1 Aluminum Lake. Chemically, Clonazepam, USP is 5-(o-chlorophenyl)-1,3-dihydro-7-nitro-2H-1,4-benzodiazepin-2-one. It is a light yellow crystalline powder. It has the following structural formula: C15H10ClN3O3 M.W. 315.72

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Interactions

A total of 440 drugs (1549 brand and generic names) are known to interact with Imbruvica (ibrutinib). 228 major drug interactions (854 brand and generic names) 210 moderate drug interactions (691 brand and generic names) 2 minor drug interactions (4 brand and generic names) Show all medications in the database that may interact with Imbruvica (ibrutinib).

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