Ireland - English - HPRA (Health Products Regulatory Authority)

pco manufacturing ltd. - budesonide - gastro-resistant capsule, hard - 3 milligram(s) - corticosteroids acting locally; budesonide

Ireland - English - HPRA (Health Products Regulatory Authority)

merit pharmaceuticals limited - budesonide; formoterol fumarate dihydrate - inhalation powder - 200 µg/6 µg/inhalation - formoterol and budesonide

Ireland - English - HPRA (Health Products Regulatory Authority)

merit pharmaceuticals limited - budesonide dihydrate; formoterol fumarate dihydrate - inhalation powder - 400/12 µg/µg - formoterol and budesonide

Ireland - English - HPRA (Health Products Regulatory Authority)

imed healthcare ltd. - budesonide - gastro-resistant capsule, hard - 3 milligram(s) - budesonide

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

a-s medication solutions - budesonide (unii: q3oks62q6x) (budesonide - unii:q3oks62q6x), formoterol fumarate (unii: w34shf8j2k) (formoterol - unii:5zz84gcw8b) - symbicort is indicated for the treatment of asthma in patients 6 years of age and older. symbicort should be used for patients not adequately controlled on a long-term asthma-control medication such as an inhaled corticosteroid (ics) or whose disease warrants initiation of treatment with both an inhaled corticosteroid and long-acting beta2-adrenergic agonist (laba). important limitations of use: symbicort 160/4.5 is indicated for the maintenance treatment of airflow obstruction in patients with chronic obstructive pulmonary disease (copd) including chronic bronchitis and/or emphysema. symbicort 160/4.5 is also indicated to reduce exacerbations of copd. symbicort 160/4.5 is the only strength indicated for the treatment of copd. important limitations of use: the use of symbicort is contraindicated in the following conditions: risk summary there are no adequate and well-controlled studies of symbicort or one of its individual components, formoterol fumarate, in pregnant women; however studies are available for the other component budesonide. in animal reproduction studies, symbicort, administered by the inhalation route, was teratogenic, embryocidal, and reduced fetal weights in rats at less than the maximum recommended human daily inhalation dose (mrhdid) on a mcg/m2 basis. budesonide alone, administered by the subcutaneous route, was teratogenic, embryocidal, and reduced fetal weights in rats and rabbits at less than the mrhdid, but these effects were not seen in rats that received inhaled doses up to 4 times the mrhdid. studies of pregnant women have not shown that inhaled budesonide alone increases the risk of abnormalities when administered during pregnancy. experience with oral corticosteroids suggests that rodents are more prone to teratogenic effects from corticosteroid exposure than humans. formoterol fumarate alone, administered by the oral route, was teratogenic in rats and rabbits at 1600 and 65,000 times the mrhdid, respectively. formoterol fumarate was also embryocidal, increased pup loss at birth and during lactation, and decreased pup weight in rats at 110 times the mrhdid. these adverse effects generally occurred at large multiples of the mrhdid when formoterol fumarate was administered by the oral route to achieve high systemic exposures. no teratogenic, embryocidal, or developmental effects were seen in rats that received inhalation doses up to 375 times the mrhdid. the estimated background risk of major birth defects and miscarriage of the indicated populations is unknown. in the u.s. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively. clinical considerations disease-associated maternal and/or embryo/fetal risk in women with poorly or moderately controlled asthma, there is an increased risk of several perinatal adverse outcomes such as preeclampsia in the mother and prematurity, low birth weight, and small for gestational age in the neonate. pregnant women with asthma should be closely monitored and medication adjusted as necessary to maintain optimal asthma control. labor or delivery there are no well-controlled human studies that have investigated the effects of symbicort during labor and delivery. because of the potential for beta-agonist interference with uterine contractility, use of symbicort during labor should be restricted to those patients in whom the benefits clearly outweigh the risk. data human data studies of pregnant women have not shown that inhaled budesonide increases the risk of abnormalities when administered during pregnancy. the results from a large population-based prospective cohort epidemiological study reviewing data from three swedish registries covering approximately 99% of the pregnancies from 1995-1997 (i.e., swedish medical birth registry; registry of congenital malformations; child cardiology registry) indicate no increased risk for congenital malformations from the use of inhaled budesonide during early pregnancy. congenital malformations were studied in 2014 infants born to mothers reporting the use of inhaled budesonide for asthma in early pregnancy (usually 10-12 weeks after the last menstrual period), the period when most major organ malformations occur. the rate of recorded congenital malformations was similar compared to the general population rate (3.8% vs. 3.5%, respectively). in addition, after exposure to inhaled budesonide, the number of infants born with orofacial clefts was similar to the expected number in the normal population (4 children vs. 3.3, respectively). these same data were utilized in a second study bringing the total to 2534 infants whose mothers were exposed to inhaled budesonide. in this study, the rate of congenital malformations among infants whose mothers were exposed to inhaled budesonide during early pregnancy was not different from the rate for all newborn babies during the same period (3.6%). animal data symbicort in an embryo-fetal development study in pregnant rats dosed during the period of organogenesis from gestation days 6-16, symbicort produced umbilical hernia in fetuses at doses less than the mrhdid (on a mcg/m2 basis at maternal inhaled doses of 12/0.66 mcg/kg/day and above). fetal weights were reduced at approximately 5 and 3 times the mrhdid, respectively (on an auc basis at a maternal inhaled dose of 80/4.4 mcg/kg (budesonide/formoterol)). no teratogenic or embryocidal effects were detected at doses less than the mrhdid (on a mcg/m2 basis at a maternal inhaled dose of 2.5/0.14 mcg/kg/day). budesonide in a fertility and reproduction study, male rats were subcutaneously dosed for 9 weeks and females for 2 weeks prior to pairing and throughout the mating period. females were dosed up until weaning of their offspring. budesonide caused a decrease in prenatal viability and viability in the pups at birth and during lactation, along with a decrease in maternal body-weight gain, at doses less than the mrhdid (on a mcg/m2 basis at maternal subcutaneous doses of 20 mcg/kg/day and above). no such effects were noted at a dose less than the mrhdid (on a mcg/m2 basis at a maternal subcutaneous dose of 5 mcg/kg/day). in an embryo-fetal development study in pregnant rabbits dosed during the period of organogenesis from gestation days 6-18, budesonide produced fetal loss, decreased fetal weight, and skeletal abnormalities at doses less than the mrhdid (on a mcg/m2 basis at a maternal subcutaneous dose of 25 mcg/kg/day). in an embryo-fetal development study in pregnant rats dosed during the period of organogenesis from gestation days 6-15, budesonide produced similar adverse fetal effects at doses approximately 8 times the mrhdid (on a mcg/m2 basis at a maternal subcutaneous dose of 500 mcg/kg/day). in another embryo-fetal development study in pregnant rats, no teratogenic or embryocidal effects were seen at doses up to 4 times the mrhdid (on a mcg/m2 basis at maternal inhalation doses up to 250 mcg/kg/day). in a peri-and post-natal development study, rats dosed from gestation day 15 to postpartum day 21, budesonide had no effects on delivery, but did have an effect on growth and development of offspring. offspring survival was reduced and surviving offspring had decreased mean body weights at birth and during lactation at doses less than the mrhdid and higher (on a mcg/m2 basis at maternal subcutaneous doses of 20 mcg/kg/day and higher). these findings occurred in the presence of maternal toxicity. formoterol in a fertility and reproduction study, male rats were orally dosed for 9 weeks and females for 2 weeks prior to pairing and throughout the mating period. females were either dosed up to gestation day 19 or up until weaning of their offspring. males were dosed up to 25 weeks. umbilical hernia was observed in rat fetuses at oral doses 1600 times and greater than the mrhdid (on a mcg/m2 basis at maternal oral doses of 3000 mcg/kg/day and higher). brachygnathia was observed in rat fetuses at a dose 8000 times the mrhdid (on a mcg/m2 basis at a maternal oral dose of 15,000 mcg/kg/day). pregnancy was prolonged at a dose 8000 times the mrhdid (on a mcg/m2 basis at a maternal oral dose of 15,000 mcg/kg/day). fetal and pup deaths occurred at doses approximately 1600 times the mrhdid and higher (on a mcg/m2 basis at oral doses of 3000 mcg/kg/day and higher) during gestation. in an embryo-fetal development study in pregnant rats dosed during the period of organogenesis from gestation days 6-15, no teratogenic, embryocidal or developmental effects were seen at doses up to 375 times the mrhdid (on a mcg/m2 basis with maternal inhalation doses up to 690 mcg/kg/day). in an embryo-fetal development study in pregnant rabbits dosed during the period of organogenesis from gestation days 6-18, subcapsular cysts on the liver were observed in the fetuses at a dose 65,000 times the mrhdid (on a mcg/m2 basis with a maternal oral dose of 60,000 mcg/kg/day). no teratogenic effects were observed at doses up to 3800 times the mrhdid (on a mcg/m2 basis at maternal oral doses up to 3500 mcg/kg/day). in a pre- and post-natal development study, pregnant female rats received formoterol at oral doses of 0, 210, 840, and 3400 mcg/kg/day from gestation day 6 through the lactation period. pup survival was decreased from birth to postpartum day 26 at doses 110 times the mrhdid and higher (on a mcg/m2 basis at maternal oral doses of 210 mcg/kg/day and higher), although there was no evidence of a dose- response relationship. there were no treatment-related effects on the physical, functional, and behavioral development of rat pups. risk summary there are no available data on the effects of symbicort, budesonide or formoterol fumarate on the breastfed child or on milk production. budesonide, like other inhaled corticosteroids, is present in human milk [see data]. there are no available data on the presence of formoterol fumarate in human milk. formoterol fumarate is present in rat milk [see data ]. the developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for symbicort and any potential adverse effects on the breastfed infant from symbicort or from the underlying maternal condition. data human data with budesonide delivered via dry powder inhaler indicates that the total daily oral dose of budesonide available in breast milk to the infant is approximately 0.3% to 1% of the dose inhaled by the mother [see clinical pharmacology (12.3)] . for symbicort, the dose of budesonide available to the infant in breast milk, as a percentage of the maternal dose, would be expected to be similar. in the fertility and reproduction study in rats, plasma levels of formoterol were measured in pups on post-natal day 15 [see use in specific populations (8.1)] . it was estimated that the maximum plasma concentration that the pups received from the maternal animal, at the highest dose of 15 mg/kg, after nursing was 4.4% (0.24 nmol/l for a litter vs. 5.5 nmol/l for the mother). safety and effectiveness of symbicort in asthma patients 12 years of age and older have been established in studies up to 12 months. in the two 12-week, double-blind, placebo-controlled us pivotal studies 25 patients 12 to 17 years of age were treated with symbicort twice daily [see clinical studies (14.1)] . efficacy results in this age group were similar to those observed in patients 18 years and older. there were no obvious differences in the type or frequency of adverse events reported in this age group compared with patients 18 years of age and older. the safety and effectiveness of symbicort 80/4.5 in asthma patients 6 to less than 12 years of age have been established in studies of up to 12-week duration [see clinical studies (14.1) ]. the safety profile in these patients was consistent to that observed in patients 12 years of age and older who also received symbicort [see adverse reactions (6.1) ]. the safety and effectiveness of symbicort in asthma patients less than 6 years of age have not been established. controlled clinical studies have shown that orally inhaled corticosteroids including budesonide, a component of symbicort, may cause a reduction in growth velocity in pediatric patients. this effect has been observed in the absence of laboratory evidence of hpa-axis suppression, suggesting that growth velocity is a more sensitive indicator of systemic corticosteroid exposure in pediatric patients than some commonly used tests of hpa-axis function. the long-term effect of this reduction in growth velocity associated with orally inhaled corticosteroids, including the impact on final height are unknown. the potential for “catch-up” growth following discontinuation of treatment with orally inhaled corticosteroids has not been adequately studied. in a study of asthmatic children 5 to 12 years of age, those treated with budesonide dpi 200 mcg twice daily (n=311) had a 1.1 centimeter reduction in growth compared with those receiving placebo (n=418) at the end of one year; the difference between these two treatment groups did not increase further over three years of additional treatment. by the end of 4 years, children treated with budesonide dpi and children treated with placebo had similar growth velocities. conclusions drawn from this study may be confounded by the unequal use of corticosteroids in the treatment groups and inclusion of data from patients attaining puberty during the course of the study. the growth of pediatric patients receiving orally inhaled corticosteroids, including symbicort, should be monitored. if a child or adolescent on any corticosteroid appears to have growth suppression, the possibility that he/she is particularly sensitive to this effect should be considered. the potential growth effects of prolonged treatment should be weighed against the clinical benefits obtained. to minimize the systemic effects of orally inhaled corticosteroids, including symbicort, each patient should be titrated to the lowest strength that effectively controls his/her asthma [see dosage and administration (2)] . of the total number of asthma patients treated with symbicort twice daily in two 12-week studies and a 26-week postmarketing study, 791 were 65 years of age or older, of whom 141 were 75 years of age or older. in the copd studies of 6 to 12 months duration, 810 patients treated with symbicort 160/4.5, two inhalations twice daily were 65 years old and above and of those, 177 patients were 75 years of age and older. no overall differences in safety or effectiveness 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. as with other products containing beta2 -agonists, special caution should be observed when using symbicort in geriatric patients who have concomitant cardiovascular disease that could be adversely affected by beta2 -agonists. based on available data for symbicort or its active components, no adjustment of dosage of symbicort in geriatric patients is warranted. formal pharmacokinetic studies using symbicort have not been conducted in patients with hepatic impairment. however, since both budesonide and formoterol fumarate are predominantly cleared by hepatic metabolism, impairment of liver function may lead to accumulation of budesonide and formoterol fumarate in plasma. therefore, patients with hepatic disease should be closely monitored. formal pharmacokinetic studies using symbicort have not been conducted in patients with renal impairment.

Canada - English - Health Canada

tillotts pharma gmbh - budesonide - enema - 2.3mg - budesonide 2.3mg - anti-inflammatory agents

Canada - English - Health Canada

tillotts pharma gmbh - budesonide - capsule (sustained-release) - 3mg - budesonide 3mg - adrenals

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

prometheus laboratories inc - budesonide (unii: q3oks62q6x) (budesonide - unii:q3oks62q6x) - budesonide 3 mg - entocort ec is indicated for - the treatment of mild to moderate active crohn's disease involving the iluem and/or the ascending colon and - the maintenance of clinical remission of mild to moderate crohn's disease involving the ileum and/or the ascending colon for up to 3 months. the maintenance of clinical remission of mild to moderate crohn's disease involving the ileum and/or the ascending colon for up to 3 months. entocort ec is contraindicated in patients with known hypersensitivity to budesonide.

New Zealand - English - Medsafe (Medicines Safety Authority)

astrazeneca limited - budesonide 80ug equivalent to 100 µg per actuation;  ; formoterol fumarate 2.25ug equivalent to 3 µg per actuation, as dihydrate - aerosol inhaler, metered dose - active: budesonide 80ug equivalent to 100 µg per actuation   formoterol fumarate 2.25ug equivalent to 3 µg per actuation, as dihydrate excipient: apaflurane macrogol 1000 povidone - symbicort rapihaler 100/3 is indicated in the treatment of asthma to achieve overall asthma control, including the prevention and relief of symptoms as well as the reduction of the risk of exacerbations. symbicort rapihaler 100/3 is suitable for any asthma severity, where the use of inhaled corticosteroids is appropriate. approved treatment approaches differ for patients aged 6 to 11 years from those approved for patients aged 12 years of age and over. see section 4.2 for clarification prior to prescribing.