Den europeiske union - latvisk - EMA (European Medicines Agency)

kyowa kirin holdings b.v. - burosumabs - hypophosphatemia, familial; hypophosphatemic rickets, x-linked dominant; osteomalacia - zāles kaulu slimību ārstēšanai - crysvita is indicated for the treatment of x-linked hypophosphataemia, in children and adolescents aged 1 to 17 years with radiographic evidence of bone disease, and in adults. crysvita is indicated for the treatment of fgf23-related hypophosphataemia in tumour-induced osteomalacia associated with phosphaturic mesenchymal tumours that cannot be curatively resected or localised in children and adolescents aged 1 to 17 years and in adults.

Den europeiske union - islandsk - EMA (European Medicines Agency)

kyowa kirin holdings b.v. - burosumab - hypophosphatemia, familial; hypophosphatemic rickets, x-linked dominant; osteomalacia - lyf til að meðhöndla beinsjúkdóma - crysvita is indicated for the treatment of x-linked hypophosphataemia, in children and adolescents aged 1 to 17 years with radiographic evidence of bone disease, and in adults. crysvita is indicated for the treatment of fgf23-related hypophosphataemia in tumour-induced osteomalacia associated with phosphaturic mesenchymal tumours that cannot be curatively resected or localised in children and adolescents aged 1 to 17 years and in adults.

Den europeiske union - dansk - EMA (European Medicines Agency)

kyowa kirin holdings b.v. - burosumab - hypophosphatemia, familial; hypophosphatemic rickets, x-linked dominant; osteomalacia - narkotika til behandling af knoglesygdomme - crysvita is indicated for the treatment of x-linked hypophosphataemia, in children and adolescents aged 1 to 17 years with radiographic evidence of bone disease, and in adults. crysvita is indicated for the treatment of fgf23-related hypophosphataemia in tumour-induced osteomalacia associated with phosphaturic mesenchymal tumours that cannot be curatively resected or localised in children and adolescents aged 1 to 17 years and in adults.

Den europeiske union - norsk - EMA (European Medicines Agency)

kyowa kirin holdings b.v. - burosumab - hypophosphatemia, familial; hypophosphatemic rickets, x-linked dominant; osteomalacia - legemidler til behandling av bein sykdommer - crysvita is indicated for the treatment of x-linked hypophosphataemia, in children and adolescents aged 1 to 17 years with radiographic evidence of bone disease, and in adults. crysvita is indicated for the treatment of fgf23-related hypophosphataemia in tumour-induced osteomalacia associated with phosphaturic mesenchymal tumours that cannot be curatively resected or localised in children and adolescents aged 1 to 17 years and in adults.

USA - engelsk - NLM (National Library of Medicine)

amgen inc - denosumab (unii: 4eqz6yo2hi) (denosumab - unii:4eqz6yo2hi) - denosumab 60 mg in 1 ml - prolia is indicated for the treatment of postmenopausal women with osteoporosis at high risk for fracture, defined as a history of osteoporotic fracture, or multiple risk factors for fracture; or patients who have failed or are intolerant to other available osteoporosis therapy. in postmenopausal women with osteoporosis, prolia reduces the incidence of vertebral, nonvertebral, and hip fractures [see clinical studies (14.1)] . prolia is indicated for treatment to increase bone mass in men with osteoporosis at high risk for fracture, defined as a history of osteoporotic fracture, or multiple risk factors for fracture; or patients who have failed or are intolerant to other available osteoporosis therapy [see clinical studies (14.2)] . prolia is indicated for the treatment of glucocorticoid-induced osteoporosis in men and women at high risk of fracture who are either initiating or continuing systemic glucocorticoids in a daily dosage equivalent to 7.5 mg or greater of prednisone and expected to remain on glucocorticoids for at least 6 months. high risk of fracture is defined as a history of osteoporotic fracture, multiple risk factors for fracture, or patients who have failed or are intolerant to other available osteoporosis therapy [see clinical studies (14.3)] . prolia is indicated as a treatment to increase bone mass in men at high risk for fracture receiving androgen deprivation therapy (adt) for nonmetastatic prostate cancer. in these patients prolia also reduced the incidence of vertebral fractures [see clinical studies (14.4)] . prolia is indicated as a treatment to increase bone mass in women at high risk for fracture receiving adjuvant aromatase inhibitor therapy for breast cancer [see clinical studies (14.5)] . prolia is contraindicated in: - patients with hypocalcemia: pre-existing hypocalcemia must be corrected prior to initiating therapy with prolia [see warnings and precautions (5.1)] . - pregnant women: prolia may cause fetal harm when administered to a pregnant woman. in women of reproductive potential, pregnancy testing should be performed prior to initiating treatment with prolia [see use in specific populations (8.1)] . - patients with hypersensitivity to prolia: prolia is contraindicated in patients with a history of systemic hypersensitivity to any component of the product. reactions have included anaphylaxis, facial swelling, and urticaria [see warnings and precautions (5.3), adverse reactions (6.2)] . risk summary prolia is contraindicated for use in pregnant women because it may cause harm to a fetus. there are insufficient data with denosumab use in pregnant women to inform any drug-associated risks for adverse developmental outcomes. in utero denosumab exposure from cynomolgus monkeys dosed monthly with denosumab throughout pregnancy at a dose 50-fold higher than the recommended human dose based on body weight resulted in increased fetal loss, stillbirths, and postnatal mortality, and absent lymph nodes, abnormal bone growth, and decreased neonatal growth [see data] . data animal data the effects of denosumab on prenatal development have been studied in both cynomolgus monkeys and genetically engineered mice in which rank ligand (rankl) expression was turned off by gene removal (a "knockout mouse"). in cynomolgus monkeys dosed subcutaneously with denosumab throughout pregnancy starting at gestational day 20 and at a pharmacologically active dose 50-fold higher than the recommended human dose based on body weight, there was increased fetal loss during gestation, stillbirths, and postnatal mortality. other findings in offspring included absence of axillary, inguinal, mandibular, and mesenteric lymph nodes; abnormal bone growth, reduced bone strength, reduced hematopoiesis, dental dysplasia, and tooth malalignment; and decreased neonatal growth. at birth out to 1 month of age, infants had measurable blood levels of denosumab (22-621% of maternal levels). following a recovery period from birth out to 6 months of age, the effects on bone quality and strength returned to normal; there were no adverse effects on tooth eruption, though dental dysplasia was still apparent; axillary and inguinal lymph nodes remained absent, while mandibular and mesenteric lymph nodes were present, though small; and minimal to moderate mineralization in multiple tissues was seen in one recovery animal. there was no evidence of maternal harm prior to labor; adverse maternal effects occurred infrequently during labor. maternal mammary gland development was normal. there was no fetal noael (no observable adverse effect level) established for this study because only one dose of 50 mg/kg was evaluated. mammary gland histopathology at 6 months of age was normal in female offspring exposed to denosumab in utero ; however, development and lactation have not been fully evaluated. in rankl knockout mice, absence of rankl (the target of denosumab) also caused fetal lymph node agenesis and led to postnatal impairment of dentition and bone growth. pregnant rankl knockout mice showed altered maturation of the maternal mammary gland, leading to impaired lactation [see use in specific populations (8.2), nonclinical toxicology (13.2)] . the no effect dose for denosumab-induced teratogenicity is unknown. however, a cmax of 22.9 ng/ml was identified in cynomolgus monkeys as a level in which no biologic effects (noel) of denosumab were observed (no inhibition of rankl) [see clinical pharmacology (12.3)] . risk summary there is no information regarding the presence of denosumab in human milk, the effects on the breastfed infant, or the effects on milk production. denosumab was detected in the maternal milk of cynomolgus monkeys up to 1 month after the last dose of denosumab (≤ 0.5% milk:serum ratio) and maternal mammary gland development was normal, with no impaired lactation. however, pregnant rankl knockout mice showed altered maturation of the maternal mammary gland, leading to impaired lactation [see use in specific populations (8.1), nonclinical toxicology (13.2)] . based on findings in animals, prolia can cause fetal harm when administered to a pregnant woman [see use in specific populations (8.1)] . pregnancy testing verify the pregnancy status of females of reproductive potential prior to initiating prolia treatment. contraception females advise females of reproductive potential to use effective contraception during therapy, and for at least 5 months after the last dose of prolia. males denosumab was present at low concentrations (approximately 2% of serum exposure) in the seminal fluid of male subjects given prolia. following vaginal intercourse, the maximum amount of denosumab delivered to a female partner would result in exposures approximately 11000 times lower than the prescribed 60 mg subcutaneous dose, and at least 38 times lower than the noel in monkeys. therefore, male condom use would not be necessary as it is unlikely that a female partner or fetus would be exposed to pharmacologically relevant concentrations of denosumab via seminal fluid [see clinical pharmacology (12.3)] . the safety and effectiveness of prolia have not been established in pediatric patients. in one multicenter, open-label study conducted in 153 pediatric patients with osteogenesis imperfecta, aged 2 to 17 years, evaluating fracture risk reduction, efficacy was not established. hypercalcemia has been reported in pediatric patients with osteogenesis imperfecta treated with denosumab products, including prolia. some cases required hospitalization and were complicated by acute renal injury [see warnings and precautions (5.11)]. clinical studies in pediatric patients with osteogenesis imperfecta were terminated early due to the occurrence of life-threatening events and hospitalizations due to hypercalcemia. based on results from animal studies, prolia may negatively affect long-bone growth and dentition in pediatric patients below the age of 4 years. juvenile animal toxicity data treatment with prolia may impair long-bone growth in children with open growth plates and may inhibit eruption of dentition. in neonatal rats, inhibition of rankl (the target of prolia therapy) with a construct of osteoprotegerin bound to fc (opg-fc) at doses ≤ 10 mg/kg was associated with inhibition of bone growth and tooth eruption. adolescent primates treated with denosumab at doses 10 and 50 times (10 and 50 mg/kg dose) higher than the recommended human dose of 60 mg administered every 6 months, based on body weight (mg/kg), had abnormal growth plates, considered to be consistent with the pharmacological activity of denosumab [see nonclinical toxicology (13.2)]. cynomolgus monkeys exposed in utero to denosumab exhibited bone abnormalities, an absence of axillary, inguinal, mandibular, and mesenteric lymph nodes, reduced hematopoiesis, tooth malalignment, and decreased neonatal growth. some bone abnormalities recovered once exposure was ceased following birth; however, axillary, and inguinal lymph nodes remained absent 6 months post-birth [see use in specific populations (8.1)] . of the total number of patients in clinical studies of prolia, 9943 patients (76%) were ≥ 65 years old, while 3576 (27%) were ≥ 75 years old. of the patients in the osteoporosis study in men, 133 patients (55%) were ≥ 65 years old, while 39 patients (16%) were ≥ 75 years old. of the patients in the glucocorticoid-induced osteoporosis study, 355 patients (47%) were ≥ 65 years old, while 132 patients (17%) were ≥ 75 years old. no overall differences in safety or efficacy were observed between these patients and younger patients, and other reported clinical experience has not identified differences in responses between the elderly and younger patients, but greater sensitivity of some older individuals cannot be ruled out. no dose adjustment is necessary in patients with renal impairment. severe hypocalcemia resulting in hospitalization, life-threatening events and fatal cases have been reported postmarketing. in clinical studies, patients with advanced chronic kidney disease (i.e., egfr < 30 ml/min/1.73 m2 ), including dialysis-dependent patients, were at greater risk of developing hypocalcemia. the presence of underlying chronic kidney disease-mineral bone disorder (ckd-mbd, renal osteodystrophy) markedly increases the risk of hypocalcemia. concomitant use of calcimimetic drugs may also worsen hypocalcemia risk. consider the benefits and risks to the patient when administering prolia to patients with advanced chronic kidney disease. monitor calcium and mineral levels (phosphorus and magnesium). adequate intake of calcium and vitamin d is important in patients with advanced chronic kidney disease including dialysis-dependent patients [see dosage and administration (2.2),warnings and precautions (5.1), adverse reactions (6.1) and clinical pharmacology (12.3)] .

Israel - engelsk - Ministry of Health

amgen europe b.v. - denosumab - solution for injection - denosumab 60 mg / 1 ml - denosumab - denosumab - treatment of osteoporosis in postmenopausal women and in men at increased risk of fractures. in postmenopausal women prolia significantly reduces the risk of vertebral, non vertebral and hip fractures. treatment of bone loss associated with hormone ablation in men with prostate cancer at increased risk of fractures. in men with prostate cancer receiving hormone ablation, prolia significantly reduces the risk of vertebral fractures.treatment of bone loss associated with long-term systemic glucocorticoid therapy of a daily dosage equivalent to 7.5 mg or greater of prednisone and expected to remain on glucocorticoids for at least 3 months, in adult patients at high risk of fracture.

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

amgen australia pty ltd - denosumab, quantity: 60 mg/ml - injection, solution - excipient ingredients: acetate; water for injections; polysorbate 20; sodium hydroxide; sorbitol - the treatment of osteoporosis in postmenopausal women. prolia significantly reduces the risk of vertebral, non-vertebral and hip fractures.,treatment to increase bone mass in men with osteopaenia receiving androgen deprivation therapy for non-metastatic prostate cancer (see clinical trials).,treatment to increase bone mass in men with osteoporosis at increased risk of fracture.,treatment to increase bone mass in women and men at increased risk of fracture due to long-term systemic glucocorticoid therapy.

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

amgen australia pty ltd - denosumab, quantity: 120 mg - injection, solution - excipient ingredients: sorbitol; sodium hydroxide; glacial acetic acid; water for injections; polysorbate 20 - prevention of skeletal related events in patients with multiple myeloma and in patients with bone metastases from solid tumours. treatment of giant cell tumour of bone in adults or skeletally mature adolescents that is recurrent, or unresectable, or resectable but associated with severe morbidity. treatment of hypercalcaemia of malignancy that is refractory to intravenous bisphosphonate.

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

kyowa kirin australia pty ltd - burosumab, quantity: 30 mg - injection, solution - excipient ingredients: sorbitol; histidine; methionine; polysorbate 80; water for injections; hydrochloric acid - crysvita (burosumab) is indicated for the treatment of x-linked hypophosphataemia (xlh) in adults, adolescents and children 1 year of age or older.

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

kyowa kirin australia pty ltd - burosumab, quantity: 20 mg - injection, solution - excipient ingredients: sorbitol; histidine; methionine; polysorbate 80; water for injections; hydrochloric acid - crysvita (burosumab) is indicated for the treatment of x-linked hypophosphataemia (xlh) in adults, adolescents and children 1 year of age or older.