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risedronate sodium 35 mg tab generic actonel

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Uses

Osteoporosis

Risedronate sodium is used for the prevention and treatment of postmenopausal osteoporosis; the drug also is used in men with osteoporosis to increase bone mass.

In addition to adequate intake of calcium/vitamin D and other lifestyle modifications (e.g., exercise, avoidance of excessive alcohol and tobacco use), experts recommend that pharmacologic therapy for osteoporosis be considered in postmenopausal women and in men 50 years of age or older who are at high risk of fractures (generally those who have experienced a previous hip or vertebral fracture or who have low bone mineral density [BMD]); pharmacologic therapy also may be considered in postmenopausal women and in men 50 years of age or older who have low bone mass, although there is less evidence supporting overall fracture risk reduction in such patients. When selecting an appropriate pharmacologic agent, use of a drug with proven antifracture efficacy is recommended. Available options include bisphosphonates (e.g., alendronate, risedronate, zoledronic acid, ibandronate), denosumab, raloxifene, calcitonin, or teriparatide with varying levels of recommendation given in expert guidelines based on the available evidence supporting fracture risk reduction for each drug. Choice of therapy should be individualized based on the potential benefits and adverse effects of therapy as well as patient preferences, comorbidities, and risk factors. For additional information on the prevention and treatment of osteoporosis,

Prevention in Postmenopausal Women

Risedronate is used for the prevention of osteoporosis in postmenopausal women. Risk factors for postmenopausal osteoporosis and related fractures include early menopause, advanced age, low BMD, low body mass index (BMI), previous fracture or family history of fracture/osteoporosis, excessive alcohol intake, smoking, inadequate physical activity, low calcium and vitamin D intake, certain drugs (e.g., glucocorticoids), and medical conditions or diseases (e.g., rheumatoid arthritis, diabetes mellitus, Cushing syndrome, hyperparathyroidism).

In a double-blind, placebo-controlled study in early postmenopausal women (42-63 years of age), risedronate sodium administration (5 mg daily for 2 years) was associated with an increase in BMD in the lumbar spine, femoral neck, and trochanter bone compared with placebo. In another study, increases in BMD in the femoral neck and midshaft radius were observed in postmenopausal women (37-82 years of age) with osteopenia who received risedronate sodium (5 mg daily for 1 year) and conjugated estrogens (0.625 mg daily) compared with those who received conjugated estrogens without risedronate. Bone histology studies in postmenopausal women treated with risedronate sodium 5 mg daily plus estrogen indicate that the bone formed had normal lamellar structure and mineralization.

Efficacy of risedronate 35 mg once weekly for the prevention of osteoporosis was evaluated in a randomized, double-blind, placebo-controlled study in 278 postmenopausal women. All women received daily supplementation with vitamin D (400 units) and calcium (1 g). After 1 year of treatment, risedronate substantially increased BMD at the lumbar spine, total proximal femur, femoral neck, and trochanter compared with placebo (least-square mean increase in BMD of 2.9, 1.5, 1.2, and 1.8%, respectively).

Treatment in Postmenopausal Women

Risedronate is used in the treatment of osteoporosis in postmenopausal women.

In placebo-controlled studies in postmenopausal women with osteoporosis, therapy with risedronate sodium 5 mg daily for 2-3 years substantially increased BMD in the lumbar spine, femoral neck, and femoral trochanter and maintained BMD at the midshaft radius while patients treated with placebo lost BMD at all sites. Bone histology studies in postmenopausal women with osteoporosis treated with risedronate sodium 5 mg daily indicate that bone formed during treatment with the drug is of normal quality. Risedronate therapy reduced the incidence of vertebral and nonvertebral (e.g., wrist, humerus, hip, pelvis, leg) fractures among postmenopausal women with osteoporosis who had previously sustained vertebral fractures.

In a 1-year controlled study in postmenopausal women with osteoporosis, risedronate sodium 35 or 50 mg once weekly (as immediate-release tablets) produced increases in lumbar spine and hip BMD similar to those observed with a dosage of 5 mg daily.

In a 1-year double-blind, active-controlled study, risedronate sodium 35 mg once weekly (as delayed-release tablets) was found to be noninferior to a dosage of 5 mg daily (as immediate-release tablets) with respect to mean change in BMD from baseline.

In 2 double-blind trials, risedronate sodium in a monthly dosage of 150 mg was found to be noninferior to a regimen of 5 mg daily in increasing BMD. Risedronate was administered as a single 150-mg tablet once a month in one of the studies and as a 75-mg tablet on 2 consecutive days each month in the other study. In both studies, the mean change in BMD for the lumbar spine and other skeletal sites was similar between the monthly and daily dosing regimens.

Treatment in Men

Risedronate is used for the treatment of osteoporosis in men to increase bone mass.

Efficacy and safety of the drug for this use is based principally on results of a double-blind, placebo-controlled study in men 36-84 years of age (mean age: 60.6 years) with osteoporosis (defined as a femoral neck BMD of at least 2 standard deviations below the normal adult mean and a lumbar spine BMD of at least 1 standard deviation below the normal adult mean, or a femoral neck BMD of at least 1 standard deviation below the normal adult mean and a lumbar spine BMD of at least 2.5 standard deviations below the normal adult mean). All patients received supplemental calcium (1 g daily) and vitamin D (400-500 units daily). Treatment with risedronate sodium 35 mg once weekly substantially increased BMD in the lumbar spine, femoral neck, trochanter, and total hip compared with placebo (mean treatment differences of 4.5, 1.1, 2.2, and 1.5%, respectively). Increases in BMD were apparent as early as 6 months (the earliest time point tested) after initiation of risedronate therapy. Few vertebral and nonvertebral fractures were reported in this study, and no difference in fracture rates was observed between the treatment groups.

Glucocorticoid-induced Osteoporosis

Risedronate is used for the prevention and treatment of glucocorticoid-induced osteoporosis. The manufacturer recommends use of risedronate in men and women who are either initiating or continuing systemic glucocorticoid therapy for chronic disease in a daily dosage equivalent to at least 7.5 mg of prednisone.

The American College of Rheumatology (ACR) recommends optimizing calcium and vitamin D intake and lifestyle modifications (e.g., diet, smoking cessation, weight-bearing or resistance-training exercise) in all patients receiving long-term glucocorticoid therapy; in addition, pharmacologic therapy with an oral bisphosphonate is recommended in patients who are considered to be at moderate-to-high risk of fracture. Oral bisphosphonates generally are preferred because of their demonstrated antifracture benefits as well as their safety and low cost; other options include IV bisphosphonates, teriparatide, denosumab, and raloxifene (for postmenopausal women if no other therapy is appropriate). For additional information on the use of bisphosphonates for prevention and treatment of glucocorticoid-induced osteoporosis,

Prevention

In a placebo-controlled, double-blind, randomized study, risedronate sodium 5 mg daily for 1 year prevented bone loss in men and women with a variety of underlying diseases (e.g., rheumatoid arthritis, temporal arteritis, polymyalgia rheumatica, systemic lupus erythematosus, asthma) who had initiated glucocorticoid therapy within 3 months of study entry and had normal mean lumbar spine BMD. BMD was maintained or increased in patients receiving risedronate while patients receiving placebo experienced decreases in BMD at the lumbar spine, femoral neck, and trochanter. In patients who underwent bone biopsies at the end of the study, bone histology was normal in patients receiving risedronate and corticosteroids.

Treatment

In patients with glucocorticoid-induced osteopenia or osteoporosis who had been receiving glucocorticoids for at least 6 months before study entry, therapy with risedronate sodium (5 mg daily for 1 year) was associated with a 2.7 or 1.9% increase in BMD at the lumbar spine or femoral neck, respectively, compared with placebo. A dosage of 2.5 daily of risedronate sodium was not substantially more effective than placebo in this study. When both risedronate dosage groups were combined, risedronate therapy also was associated with a decreased incidence of vertebral fractures relative to placebo.

Paget Disease of Bone

Risedronate is used in the treatment of Paget disease of bone (osteitis deformans).

Six months after initiation of therapy in a clinical study in men and women with moderate to severe Paget disease of bone (serum alkaline phosphatase concentrations at least twice the upper limit of normal), normalization of serum alkaline phosphatase concentrations occurred in 77% of patients receiving risedronate sodium (30 mg daily for 2 months) and in 11% of those receiving etidronate disodium (400 mg daily for 6 months). At month 18 (16 and 12 months after discontinuance of risedronate and etidronate, respectively), 53% of those who had received risedronate remained in biochemical remission, compared with 14% of those treated with etidronate. Risedronate has been effective in a limited number of patients with refractory Paget disease who had not responded to prior therapy with etidronate or calcitonin. Bone biopsies of non-Pagetic bone in patients with Paget disease of bone treated with risedronate did not reveal evidence of osteomalacia, impairment of bone remodeling, or an appreciable decline in bone turnover.

Dosage and Administration

General

Hypocalcemia and other disturbances of bone and mineral metabolism must be corrected before risedronate therapy is initiated. Patients should receive supplemental calcium and vitamin D if their dietary intake is inadequate, particularly in patients with Paget disease of bone.

Administration

Risedronate sodium is administered orally.

Immediate-release Tablets

To facilitate absorption, risedronate immediate-release tablets should be taken with a full glass (180-240 mL) of plain water at least 30 minutes before the first food, beverage, or other orally administered drug or supplement (including calcium, antacids, or vitamins) of the day. Because of the potential for oropharyngeal irritation, patients should be instructed not to suck or chew the tablets. Patients should be instructed to avoid lying down for at least 30 minutes following administration of risedronate to facilitate delivery of the drug to the stomach and minimize potential esophageal irritation.

Delayed-release Tablets

Risedronate 35 mg delayed-release tablets should be taken in the morning immediately following breakfast; delayed-release tablets should not be administered under fasting conditions to minimize the risk of abdominal pain when using this formulation. The tablets should be swallowed whole with at least 120 mL of plain water (and not chewed, cut, or crushed). Patients should be instructed to avoid lying down for at least 30 minutes following administration of risedronate to facilitate delivery of the drug to the stomach and minimize potential esophageal irritation.

Dosage

Osteoporosis

For treatment of osteoporosis in postmenopausal women, the usual dosage of risedronate sodium is 5 mg once daily, 35 mg (given as immediate-release or delayed-release tablets) once weekly, or 150 mg monthly (given as a 150-mg tablet once monthly or a 75-mg tablet on 2 consecutive days per month).

For the prevention of osteoporosis in postmenopausal women, the usual dosage of risedronate sodium is 5 mg once daily or 35 mg once weekly as immediate release tablets. Alternatively, a dosage of 150 mg once monthly (given as a 150-mg tablet or as a 75-mg tablet on 2 consecutive days) may be considered.

For the treatment of osteoporosis in men, the recommended dosage of risedronate sodium is 35 mg once weekly.

If a weekly 35-mg dose of risedronate sodium is missed, the missed dose should be taken the next morning after the day it is remembered, followed by resumption of the regular weekly schedule on the originally chosen day. Patients should not take 2 risedronate sodium 35-mg tablets on the same day.

If a monthly 150-mg dose of risedronate sodium is missed and the next scheduled dose is more than 7 days away, patients should take the missed dose the next morning after it is remembered and resume the regular schedule. If the next scheduled dose is within 7 days, patients should wait until the next month's scheduled dose and resume their regular dosing schedule at that time; more than one 150-mg tablet should not be taken within the same week.

If one or both doses are missed in patients receiving the consecutive-day dosing schedule (i.e., risedronate sodium 75 mg on 2 consecutive days per month) and the next month's scheduled dose is more than 7 days away, patients should be instructed as follows: if both 75-mg doses are missed, one dose should be taken the next morning after it is remembered followed by the second dose the next consecutive morning; if only one 75-mg dose is missed, the missed dose should be taken the next morning after it is remembered. The regular dosing schedule should then be resumed; more than two 75-mg tablets should not be taken within the same week. If one or both doses are missed in patients receiving the consecutive-day dosing schedule and the next month's scheduled doses are within 7 days, patients should wait until the time of the next month's scheduled dose and resume their regular dosing schedule at that time.

The optimal duration of bisphosphonate treatment for osteoporosis has not been established. Safety and efficacy of risedronate for the treatment of osteoporosis are based on clinical data over 3 years (for the immediate-release tablets) or 1 year (for the 35-mg delayed-release tablets). Some evidence suggests that increased durations of bisphosphonate use may be associated with an increased risk of some adverse effects (e.g., atypical fractures, jaw osteonecrosis). All patients receiving a bisphosphonate should have periodic evaluations to determine the need for continued therapy. Discontinuance of bisphosphonate therapy may be considered after 3-5 years of use for patients who are assessed to be at low risk of fracture. Risk of fracture should be evaluated periodically in patients who discontinue therapy.

Glucocorticoid-induced Osteoporosis

For the prevention or treatment of glucocorticoid-induced osteoporosis, the usual adult dosage of risedronate sodium is 5 mg once daily. The manufacturer states that safety and efficacy of risedronate when given for periods exceeding 1 year in the prevention or treatment of glucocorticoid-induced osteoporosis have not been established.

Paget Disease

For the treatment of Paget disease of bone, the usual dosage of risedronate sodium in adults is 30 mg administered once daily for 2 months. After a post-treatment observation period of at least 2 months, a second course of risedronate sodium at the same dosage should be considered if there is evidence of recurrence of the disease process or if the initial treatment fails to normalize serum alkaline phosphatase concentrations. No data are available on the safety and efficacy of more than one course of retreatment with risedronate sodium for Paget disease.

Special Populations

Risedronate should not be used in patients with severe renal impairment (creatinine clearance less than 30 mL/minute). Adjustments in risedronate sodium dosage are not necessary in patients with mild-to-moderate renal impairment (creatinine clearance 30 mL/minute or greater), geriatric patients, or in patients with hepatic impairment.

Cautions

Contraindications

Hypocalcemia, known hypersensitivity to risedronate or any ingredient in the formulation, inability to stand or sit upright for at least 30 minutes, or abnormalities of the esophagus that delay esophageal emptying (e.g., stricture, achalasia).

Warnings/Precautions

Formulation Considerations

Risedronate immediate-release tablets (e.g., Actonel) and risedronate delayed-release tablets (Atelvia) contain the same active ingredient; patients should not receive both formulations concomitantly.

Upper GI Effects

Because severe adverse esophageal effects including esophagitis, esophageal ulcers, and/or erosions (occasionally with bleeding and rarely followed by esophageal stricture or perforation) have been reported in patients receiving oral bisphosphonates, clinicians should be alert to any sign or symptom associated with such adverse effects. Patients should be instructed to discontinue risedronate and contact a clinician if dysphagia, odynophagia, retrosternal pain, or new or worsening heartburn occurs. The incidence of severe adverse esophageal effects is greater in patients who do not drink the recommended amount of water when taking oral bisphosphonates and in those who do not avoid lying down for at least 30 minutes following administration or who continue to take the drugs after experiencing symptoms suggestive of esophageal irritation; therefore, patients should be instructed carefully about proper administration of risedronate.(See Dosage and Administration: Administration.) Risedronate should be used with caution in patients with active upper GI disease (e.g., Barrett's esophagus, dysphagia, other esophageal diseases, gastritis, duodenitis, ulcers).

Gastric or duodenal ulcers, including some that were severe and with complications, have been reported in patients receiving oral bisphosphonates during postmarketing experience, although no increased risk was observed in controlled clinical trials.

Although data are conflicting, there is some evidence suggesting a possible association between use of oral bisphosphonates and an increased risk of esophageal cancer. During the period of postmarketing surveillance from October 1995 (initial marketing of alendronate) through mid-May 2008, FDA received reports of esophageal cancer in 23 patients in the US receiving alendronate (as the suspect drug in 21 cases and the concomitant drug in 2 cases); 8 deaths were reported. An additional 31 cases of esophageal cancer were reported at the time in patients in Europe and Japan who had received an oral bisphosphonate, including alendronate, risedronate, ibandronate, and etidronate. In a large case-control study in a cohort of patients from the UK General Practice Research Database, risk of esophageal cancer was increased by 30% in patients who had at least one prescription issued for an oral bisphosphonate (alendronate, etidronate, or risedronate) compared with those not receiving such prescriptions; the risk was approximately doubled among patients who had 10 or more prescriptions issued for an oral bisphosphonate or who had an estimated duration of bisphosphonate use (calculated as the time between the first and last prescription issued during the observation period) of more than 3 years. However, another retrospective cohort study that used the same database found no evidence of an increased risk of esophageal cancer in patients receiving oral bisphosphonates. Other observational studies, including a study in patients receiving long-term alendronate therapy and a cohort study of Danish patients with fractures, have shown either no risk or a reduced risk of esophageal cancer following use of oral bisphosphonates. Because of conflicting findings and limitations of currently available data, additional study is needed to determine the association, if any, between oral bisphosphonate use and esophageal cancer. FDA states that benefits of oral bisphosphonates in reducing the risk of serious fractures continue to outweigh their potential risks in patients with osteoporosis and that it is important to consider that esophageal cancer is rare, especially in women. FDA also states that there is insufficient information at this time to recommend routine endoscopic screening in asymptomatic patients receiving oral bisphosphonates. Avoidance of oral bisphosphonates in patients with Barrett's esophagus, a known precursor to esophageal adenocarcinoma, has been recommended.

Osteonecrosis of the Jaw

Osteonecrosis and osteomyelitis of the jaw have been reported in patients, principally in those with cancer, who have received bisphosphonates. Most instances of jaw osteonecrosis have occurred in association with tooth extraction and/or local infection with delayed healing. Known risk factors for osteonecrosis of the jaw include invasive dental procedures (e.g., tooth extraction, dental implants, boney surgery), cancer, concomitant therapies (e.g., chemotherapy, corticosteroids, angiogenesis inhibitors), poor oral hygiene, and comorbid disorders (e.g., periodontal and/or other preexisting dental disease, anemia, coagulopathy, infection, ill-fitting dentures). Risk also may be increased with increased duration of bisphosphonate use. Discontinuance of bisphosphonate treatment may reduce the risk for osteonecrosis of the jaw in patients requiring invasive dental procedures. Clinical judgment of the treating clinician and/or oral surgeon should guide the management of each patient based on individual benefit/risk assessment. Patients who develop osteonecrosis of the jaw while receiving bisphosphonate therapy should receive care by an oral surgeon. In these patients, extensive dental surgery to treat osteonecrosis of the jaw may exacerbate the condition. Discontinuance of bisphosphonate therapy should be considered based on assessment of benefits and risks in individual patients.

Atypical Fracture of the Femur

Atypical, low-energy, or low-trauma femoral fractures have been reported in bisphosphonate-treated patients. These fractures can occur anywhere in the femoral shaft from the subtrochanteric region of the hip (i.e., below the lesser trochanter) to above the supracondylar flare and are transverse or short oblique in orientation without evidence of comminution. Such fractures generally have occurred with use of bisphosphonate therapy for more than 3 years (median 7 years in one analysis of available data). The magnitude of this risk is unclear, although such fractures appear to be rare; in addition, causality has not been established since atypical fractures also have occurred in patients not receiving bisphosphonates. Most cases of atypical femoral fractures with bisphosphonate therapy have been reported in individuals receiving treatment for osteoporosis. Such fractures most commonly occur in individuals with minimal or no trauma. Most individuals have reported prodromal symptoms presenting as dull, aching thigh pain for weeks to months prior to the occurrence of an atypical fracture. Bilateral involvement (i.e., a fracture in the contralateral limb) and evidence of delayed healing of the fracture also may be present. Concomitant use of glucocorticoid, estrogen, and proton-pump inhibitor therapy may increase the risk of an atypical fracture.

Individuals with a history of bisphosphonate exposure presenting with new thigh or groin pain should be evaluated for possible atypical femoral fracture; an assessment of the contralateral limb also should be performed to rule out possible bilateral involvement (i.e., presence of radiographic change or fracture). Interruption of bisphosphonate therapy should be considered in individuals presenting with symptoms suggestive of a possible femoral fracture following completion of a comprehensive risk-benefit assessment performed on an individualized basis. Bisphosphonate therapy should be discontinued if a femoral shaft fracture is confirmed.

Musculoskeletal Pain

Severe, occasionally incapacitating bone, joint, and/or muscle pain have been reported infrequently during postmarketing experience in patients receiving bisphosphonates, including risedronate. The time to onset of symptoms varied from 1 day to years (mean onset about 3 months) after treatment initiation. Musculoskeletal pain has improved following discontinuance of the drug in most patients; however, some patients have reported slow or incomplete resolution of severe musculoskeletal pain. In some patients, musculoskeletal pain recurred upon subsequent rechallenge with the same drug or another bisphosphonate. The risk factors for and incidence of severe musculoskeletal pain associated with bisphosphonates are unknown. The association between bisphosphonates and severe musculoskeletal pain may be overlooked by clinicians, which may delay diagnosis, prolong pain and/or impairment, and necessitate the use of analgesics. Clinicians should evaluate whether bisphosphonate use might be responsible for severe musculoskeletal pain in patients who present with these symptoms; temporary or permanent discontinuance of therapy should be considered in such cases.

Metabolic Effects

Hypocalcemia and other disturbances of bone and mineral metabolism must be corrected before risedronate therapy is initiated, and patients with osteoporosis or Paget disease of bone should receive supplemental calcium and vitamin D if their daily dietary intake is inadequate.

Endocrine Effects

Before initiating risedronate therapy in patients receiving long-term glucocorticoid therapy, sex hormones should be measured and replacement therapy considered, if appropriate.

Atrial Fibrillation

While data are conflicting, a possible increased risk of atrial fibrillation has been identified with use of bisphosphonates.

Specific Populations

Pregnancy

Category C.

Lactation

Risedronate is distributed into milk in rats; it is not known whether the drug is distributed into human milk. Because of the potential for serious adverse effects from risedronate in nursing infants, a decision should be made whether to discontinue nursing or the drug.

Pediatric Use

Risedronate is not indicated for use in pediatric patients. Efficacy and safety of the drug in pediatric patients were evaluated in a 1-year, randomized, double-blind, placebo-controlled study in 143 pediatric patients 4 to less than 16 years of age with osteogenesis imperfecta. Although risedronate was effective in increasing lumbar spine bone mineral density (BMD) compared with placebo, therapy with the drug was not associated with a reduction in fracture risk. Adverse effects reported in the pediatric patients evaluated in this study generally were similar to those reported in adults with osteoporosis; however, an increased risk of vomiting relative to placebo was observed with risedronate.

Geriatric Use

No substantial differences in safety and efficacy have been observed in geriatric patients relative to younger adults.

Hepatic Impairment

Efficacy and safety of risedronate have not been evaluated in patients with hepatic impairment. Because the drug is not metabolized in the liver, the manufacturer states that dosage adjustments are not likely to be necessary in patients with hepatic impairment.

Renal Impairment

Risedronate is not recommended in patients with severe renal impairment (creatinine clearance less than 30 mL/minute). No dosage adjustments are necessary in patients with mild to moderate renal impairment (creatinine clearance of at least 30 mL/minute).

Common Adverse Effects

Adverse effects occurring in more than 5% of patients receiving daily risedronate therapy include back, chest or abdominal pain, pain (unspecified), hypertension, flu-like syndrome, peripheral edema, nausea, diarrhea, constipation, arthralgia, joint disorder,depression, headache, dizziness, myalgia, rash, cataract, pharyngitis, rhinitis, urinary tract infection, and infection (unspecified). Adverse effects occurring in more than 5% of patients receiving once-weekly risedronate include back or abdominal pain, pain (unspecified), hypertension, flu syndrome, infection (unspecified), accidental injury, overdose, nausea, constipation, dyspepsia, arthralgia, traumatic bone fracture, myalgia, headache, asthenia, and urinary tract infection.

Drug Interactions

Antacids or Mineral Supplements Containing Divalent Cations

Pharmacokinetic interaction (decreased risedronate absorption) is possible when risedronate is used concomitantly with antacids or mineral supplements containing divalent cations (e.g., calcium, magnesium, iron). Patients should not administer these supplements and antacids at the same time as risedronate.

Drugs Affecting Hepatic Microsomal Enzymes

Risedronate does not induce or inhibit cytochrome P-450 (CYP) isoenzymes and is not metabolized. Pharmacokinetic interaction unlikely.

Nonsteroidal Anti-inflammatory Agents

There is no evidence of increased adverse upper GI effects when risedronate is administered concomitantly with nonsteroidal anti-inflammatory agents (NSAIAs).

Histamine H2-receptor Antagonists, Proton Pump Inhibitors

There is no evidence of increased adverse upper GI effects when risedronate is administered concomitantly with histamine H2-receptor antagonists or proton pump inhibitors.

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