Australia - English - Department of Health (Therapeutic Goods Administration)

arrotex pharmaceuticals pty ltd - risedronate sodium hemipentahydrate, quantity: 5.74 mg (equivalent: risedronate sodium, qty 5 mg) - tablet, film coated - excipient ingredients: lactose monohydrate; microcrystalline cellulose; magnesium stearate; crospovidone; hyprolose; titanium dioxide; hypromellose; macrogol 8000; colloidal anhydrous silica; iron oxide yellow; macrogol 400 - ? treatment of osteoporosis,? treatment of glucocorticoid-induced osteoporosis,? preservation of bone mineral density in patients on long term corticosteroid therapy

United States - English - NLM (National Library of Medicine)

greenstone llc - risedronate sodium hemi-pentahydrate (unii: hu2yaq274o) (risedronic acid - unii:km2z91756z), risedronate sodium monohydrate (unii: f67l43ut5c) (risedronic acid - unii:km2z91756z) - risedronate sodium is indicated for the treatment and prevention of osteoporosis in postmenopausal women. in postmenopausal women with osteoporosis, risedronate sodium reduces the incidence of vertebral fractures and a composite endpoint of nonvertebral osteoporosis-related fractures [see clinical studies ( 14.1 , 14.2 ) ]. risedronate sodium is indicated for treatment to increase bone mass in men with osteoporosis. risedronate sodium is indicated for the treatment and prevention of glucocorticoid-induced osteoporosis in men and women who are either initiating or continuing systemic glucocorticoid treatment (daily dosage of greater than or equal to 7.5 mg of prednisone or equivalent) for chronic diseases. patients treated with glucocorticoids should receive adequate amounts of calcium and vitamin d. risedronate sodium is indicated for treatment of paget’s disease of bone in men and women. the optimal duration of use has not been determined. the safety and effectiveness of risedronate sodium for the treatment of osteoporosis are based on clinical data of three years duration. all patients on bisphosphonate therapy should have the need for continued therapy re-evaluated on a periodic basis. patients at low-risk for fracture should be considered for drug discontinuation after 3 to 5 years of use. patients who discontinue therapy should have their risk for fracture re-evaluated periodically. risedronate sodium is contraindicated in patients with the following conditions: - abnormalities of the esophagus which delay esophageal emptying such as stricture or achalasia [see warnings and precautions ( 5.1 ) ] - inability to stand or sit upright for at least 30 minutes [see dosage and administration ( 2 ), warnings and precautions ( 5.1 ) ] - hypocalcemia [see warnings and precautions ( 5.2 ) ] - known hypersensitivity to risedronate sodium or any of its excipients. angioedema, generalized rash, bullous skin reactions, stevens-johnson syndrome and toxic epidermal necrolysis have been reported [see adverse reactions ( 6.2 ) ] risk summary available data on the use of risedronate sodium in pregnant women are insufficient to inform a drug-associated risk of adverse maternal or fetal outcomes. discontinue risedronate sodium when pregnancy is recognized. in animal reproduction studies, daily oral administration of risedronate to pregnant rats during organogenesis decreased neonatal survival and body weight at doses approximately 5 and 26 times, respectively, the highest recommended human daily dose of 30 mg (based on body surface area, mg/m2 ). a low incidence of cleft palate was observed in fetuses of dams treated at doses approximately equal to the 30 mg human daily dose. delayed skeletal ossification was observed in fetuses of dams treated at approximately 2.5 to 5 times the 30 mg human daily dose. periparturient mortality due to maternal hypocalcemia occurred in dams and neonates upon daily oral administration of risedronate to pregnant rats during mating and/or gestation starting at doses equivalent to the 30 mg daily human dose. bisphosphonates are incorporated into the bone matrix, from which they are gradually released over a period of years. the amount of bisphosphonate incorporated into adult bone and available for release into the systemic circulation is directly related to the dose and duration of bisphosphonate use. consequently, based on the mechanism of action of bisphosphonates, there is a potential risk of fetal harm, predominantly skeletal, if a woman becomes pregnant after completing a course of bisphosphonate therapy. the impact of variables such as time between cessation of bisphosphonate therapy to conception, the particular bisphosphonate used, and the route of administration (intravenous versus oral) on this risk has not been studied. the estimated background risk of major birth defects and miscarriage for the indicated populations is unknown. all pregnancies have a background risk of birth defects, loss, or other adverse outcomes. in the u.s. general population, the estimated background risks of major birth defects and miscarriage in clinically recognized pregnancies is 2-4% and 15-20%, respectively. data animal data in animal studies, pregnant rats received risedronate sodium during organogenesis at doses equivalent to 1 to 26 times the 30 mg human daily dose (based on body surface area, mg/m2 ). survival of neonates was decreased in dams treated during gestation with oral doses approximately 5 times the human dose, and body weight was decreased in neonates of dams treated with approximately 26 times the human dose. a low incidence of cleft palate was observed in fetuses of dams treated with oral doses approximately equal to the human dose. the number of fetuses exhibiting incomplete ossification of sternebrae or skull of dams treated with approximately 2.5 times the human dose was significantly increased compared to controls. both incomplete ossification and unossified sternebrae were increased in fetuses of dams treated with oral doses approximately 5 times the human dose. no significant ossification effects were seen in fetuses of rabbits treated with oral doses approximately 7 times the human dose (the highest dose tested). however, 1 of 14 litters were aborted and 1 of 14 litters were delivered prematurely. periparturient mortality due to maternal hypocalcemia occurred in dams and neonates when pregnant rats were treated daily during mating and/or gestation with oral doses equivalent to the human dose or higher. risk summary there are no data on the presence of risedronate in human milk, the effects on the breastfed infant, or the effects on milk production. a small degree of lacteal transfer occurred in nursing rats. the concentration of the drug in animal milk does not necessarily predict the concentration of drug in human milk. however, when a drug is present in animal milk, it is likely that the drug will be present in human milk. the developmental and health benefits of breast-feeding should be considered along with the mother’s clinical need for risedronate sodium and any potential adverse effects on the breast-fed child from risedronate sodium or from the underlying maternal condition. data animal data risedronate was detected in neonates of lactating rats given a single oral dose of risedronate at 24-hours post-dosing, indicating a small degree of lacteal transfer. risedronate sodium is not indicated for use in pediatric patients. the safety and effectiveness of risedronate was assessed in a one-year, randomized, double-blind, placebo-controlled study of 143 pediatric patients (94 received risedronate) with osteogenesis imperfecta (oi). the enrolled population was predominantly patients with mild osteogenesis imperfecta (85% type-i), aged 4 to less than 16 years, 50% male and 82% caucasian, with a mean lumbar spine bmd z-score of -2.08 (2.08 standard deviations below the mean for age-matched controls). patients received either a 2.5 mg (less than or equal to 30 kg body weight) or 5 mg (greater than 30 kg body weight) daily oral dose. after one year, an increase in lumbar spine bmd in the risedronate group compared to the placebo group was observed. however, treatment with risedronate did not result in a reduction in the risk of fracture in pediatric patients with osteogenesis imperfecta. in risedronate sodium-treated subjects, no mineralization defects were noted in paired bone biopsy specimens obtained at baseline and month 12. the overall safety profile of risedronate in oi patients treated for up to 12 months was generally similar to that of adults with osteoporosis. however, there was an increased incidence of vomiting compared to placebo. in this study, vomiting was observed in 15% of children treated with risedronate and 6% of patients treated with placebo. other adverse events reported in greater than or equal to 10% of patients treated with risedronate and with a higher frequency than placebo were: pain in the extremity (21% with risedronate versus 16% with placebo), headache (20% versus 8%), back pain (17% versus 10%), pain (15% versus 10%), upper abdominal pain (11% versus 8%), and bone pain (10% versus 4%). of the patients receiving risedronate sodium in postmenopausal osteoporosis studies [see clinical studies ( 14 ) ], 47% were between 65 and 75 years of age, and 17% were over 75. the corresponding proportions were 26% and 11% in glucocorticoid-induced osteoporosis trials, and 40% and 26% in paget’s disease trials. no overall differences in efficacy between geriatric and younger patients were observed in these studies. in the male osteoporosis trial, 28% of patients receiving risedronate sodium were between 65 and 75 years of age and 9% were over 75. the lumbar spine bmd response for risedronate sodium compared to placebo was 5.6% for subjects less than 65 years and 2.9% for subjects greater than or equal to 65 years. no overall differences in safety between geriatric and younger patients were observed in the risedronate sodium trials, but greater sensitivity of some older individuals cannot be ruled out. risedronate sodium is not recommended for use in patients with severe renal impairment (creatinine clearance less than 30 ml/min) because of lack of clinical experience. no dosage adjustment is necessary in patients with a creatinine clearance greater than or equal to 30 ml/min. no studies have been performed to assess risedronate’s safety or efficacy in patients with hepatic impairment. risedronate is not metabolized in human liver preparations. dosage adjustment is unlikely to be needed in patients with hepatic impairment.

United States - English - NLM (National Library of Medicine)

zydus pharmaceuticals usa inc. - risedronate sodium anhydrous (unii: ofg5exg60l) (risedronic acid - unii:km2z91756z) - risedronate sodium delayed-release tablets are indicated for the treatment of osteoporosis in postmenopausal women. in postmenopausal women, risedronate sodium has been shown to reduce the incidence of vertebral fractures and a composite endpoint of nonvertebral osteoporosis-related fractures [see clinical studies (14.1) ]. the optimal duration of use has not been determined. the safety and effectiveness of risedronate sodium delayed-release tablets for the treatment of osteoporosis are based on clinical data of one year duration. all patients on bisphosphonate therapy should have the need for continued therapy re-evaluated on a periodic basis. patients at low-risk for fracture should be considered for drug discontinuation after 3 to 5 years of use. patients who discontinue therapy should have their risk for fracture re-evaluated periodically. risedronate sodium delayed-release tablets are contraindicated in patients with the following conditions: -   abnormalities of the esophagus which delay esophageal empt

Australia - English - Department of Health (Therapeutic Goods Administration)

arrotex pharmaceuticals pty ltd - risedronate sodium hemipentahydrate, quantity: 173.4 mg - tablet, film coated - excipient ingredients: hypromellose; magnesium stearate; crospovidone; titanium dioxide; hyprolose; colloidal anhydrous silica; macrogol 8000; lactose; monobasic sodium phosphate dihydrate; dibasic sodium phosphate; indigo carmine aluminium lake; monobasic sodium phosphate monohydrate - the treatment of osteoporosis,the treatment of glucocorticoid-induced osteoporosis,the preservation of bone-mineral density in patients on long term corticosteroid therapy

United States - English - NLM (National Library of Medicine)

zydus lifesciences limited - risedronate sodium anhydrous (unii: ofg5exg60l) (risedronic acid - unii:km2z91756z) - risedronate sodium delayed-release tablets are indicated for the treatment of osteoporosis in postmenopausal women. in postmenopausal women, risedronate sodium has been shown to reduce the incidence of vertebral fractures and a composite endpoint of nonvertebral osteoporosis-related fractures [see clinical studies (14.1) ]. the optimal duration of use has not been determined. the safety and effectiveness of risedronate sodium delayed-release tablets for the treatment of osteoporosis are based on clinical data of one year duration. all patients on bisphosphonate therapy should have the need for continued therapy re-evaluated on a periodic basis. patients at low-risk for fracture should be considered for drug discontinuation after 3 to 5 years of use. patients who discontinue therapy should have their risk for fracture re-evaluated periodically. risedronate sodium delayed-release tablets are contraindicated in patients with the following conditions: - abnormalities of the esophagus which delay esophageal e

United States - English - NLM (National Library of Medicine)

sun pharmaceutical industires inc. - risedronate sodium (unii: ofg5exg60l) (risedronic acid - unii:km2z91756z) - risedronate sodium delayed-release tablets are indicated for the treatment of osteoporosis in postmenopausal women. in postmenopausal women, risedronate sodium has been shown to reduce the incidence of vertebral fractures and a composite endpoint of nonvertebral osteoporosis-related fractures [see clinical studies (14.1) ]. the optimal duration of use has not been determined. the safety and effectiveness of risedronate sodium delayed-release tablets for the treatment of osteoporosis are based on clinical data of one year duration. all patients on bisphosphonate therapy should have the need for continued therapy re-evaluated on a periodic basis. patients at low-risk for fracture should be considered for drug discontinuation after 3 to 5 years of use. patients who discontinue therapy should have their risk for fracture re-evaluated periodically. risk summary available data on use of risedronate sodium in pregnant women are insufficient to inform drug-associated risk of adverse maternal or fetal outcomes. discon

United States - English - NLM (National Library of Medicine)

northstar rxllc - risedronate sodium (unii: ofg5exg60l) (risedronic acid - unii:km2z91756z) - risedronate sodium delayed-release tablets are indicated for the treatment of osteoporosis in postmenopausal women. in postmenopausal women, risedronate sodium has been shown to reduce the incidence of vertebral fractures and a composite endpoint of nonvertebral osteoporosis-related fractures [see clinical studies (14.1) ]. the optimal duration of use has not been determined. the safety and effectiveness of risedronate sodium delayed-release tablets for the treatment of osteoporosis are based on clinical data of one year duration. all patients on bisphosphonate therapy should have the need for continued therapy re-evaluated on a periodic basis. patients at low-risk for fracture should be considered for drug discontinuation after 3 to 5 years of use. patients who discontinue therapy should have their risk for fracture re-evaluated periodically. risk summary available data on use of risedronate sodium in pregnant women are insufficient to inform drug-associated risk of adverse maternal or fetal outcomes. discon

United States - English - NLM (National Library of Medicine)

allergan, inc. - risedronate sodium hemi-pentahydrate (unii: hu2yaq274o) (risedronic acid - unii:km2z91756z), risedronate sodium monohydrate (unii: f67l43ut5c) (risedronic acid - unii:km2z91756z) - risedronate sodium anhydrous 30.1 mg - atelvia is indicated for the treatment of osteoporosis in postmenopausal women. in postmenopausal women, risedronate sodium has been shown to reduce the incidence of vertebral fractures and a composite endpoint of nonvertebral osteoporosis-related fractures [see clinical studies (14.1) ]. the optimal duration of use has not been determined. the safety and effectiveness of atelvia for the treatment of osteoporosis are based on clinical data of one year duration. all patients on bisphosphonate therapy should have the need for continued therapy re-evaluated on a periodic basis. patients at low-risk for fracture should be considered for drug discontinuation after 3 to 5 years of use. patients who discontinue therapy should have their risk for fracture re-evaluated periodically. atelvia is contraindicated in patients with the following conditions: • abnormalities of the esophagus which delay esophageal emptying such as stricture or achalasia [see warnings and precautions (5.2) ]  • inability to stand or sit upri

Australia - English - Department of Health (Therapeutic Goods Administration)

arrotex pharmaceuticals pty ltd - risedronate sodium hemipentahydrate, quantity: 40.5 mg (equivalent: risedronate sodium, qty 35 mg) - tablet, film coated - excipient ingredients: colloidal anhydrous silica; iron oxide red; macrogol 8000; magnesium stearate; hyprolose; lactose; titanium dioxide; hypromellose; crospovidone; iron oxide yellow - - treatment of osteoporosis. - treatment of glucocorticoid-induced osteoporosis. - preservation of bone mineral density in patients on long term corticosteroid therapy.

Australia - English - Department of Health (Therapeutic Goods Administration)

gm pharma international pty ltd - risedronate sodium hemipentahydrate, quantity: 173.4 mg - tablet, film coated - excipient ingredients: lactose; hyprolose; hypromellose; crospovidone; titanium dioxide; magnesium stearate; colloidal anhydrous silica; macrogol 8000; monobasic sodium phosphate dihydrate; dibasic sodium phosphate; indigo carmine aluminium lake; monobasic sodium phosphate monohydrate - the treatment of osteoporosis,the treatment of glucocorticoid-induced osteoporosis,the preservation of bone-mineral density in patients on long term corticosteroid therapy