Israel - English - Ministry of Health

novo nordisk ltd., israel - semaglutide - solution for injection - semaglutide 1.34 mg / 1 ml - semaglutide - wegovy is indicated as an adjunct to a reduced-calorie diet and increased physical activity for weight management, including weight loss and weight maintenance, in adults with an initial body mass index (bmi) of • ≥30 kg/m2 (obesity), or • ≥27 kg/m2 to <30 kg/m2 (overweight) in the presence of at least one weight-related comorbidity e.g. dysglycaemia (prediabetes or type 2 diabetes mellitus), hypertension, dyslipidaemia, obstructive sleep apnoea or cardiovascular disease.

Israel - English - Ministry of Health

novo nordisk ltd., israel - semaglutide - solution for injection - semaglutide 1.34 mg / 1 ml - semaglutide - wegovy is indicated as an adjunct to a reduced-calorie diet and increased physical activity for weight management, including weight loss and weight maintenance, in adults with an initial body mass index (bmi) of • ≥30 kg/m2 (obesity), or • ≥27 kg/m2 to <30 kg/m2 (overweight) in the presence of at least one weight-related comorbidity e.g. dysglycaemia (prediabetes or type 2 diabetes mellitus), hypertension, dyslipidaemia, obstructive sleep apnoea or cardiovascular disease.

Israel - English - Ministry of Health

novo nordisk ltd., israel - semaglutide - solution for injection - semaglutide 2.27 mg / 1 ml - semaglutide - wegovy is indicated as an adjunct to a reduced-calorie diet and increased physical activity for weight management, including weight loss and weight maintenance, in adults with an initial body mass index (bmi) of • ≥30 kg/m2 (obesity), or • ≥27 kg/m2 to <30 kg/m2 (overweight) in the presence of at least one weight-related comorbidity e.g. dysglycaemia (prediabetes or type 2 diabetes mellitus), hypertension, dyslipidaemia, obstructive sleep apnoea or cardiovascular disease.

Israel - English - Ministry of Health

novo nordisk ltd., israel - semaglutide - solution for injection - semaglutide 3.2 mg / 1 ml - semaglutide - wegovy is indicated as an adjunct to a reduced-calorie diet and increased physical activity for weight management, including weight loss and weight maintenance, in adults with an initial body mass index (bmi) of • ≥30 kg/m2 (obesity), or • ≥27 kg/m2 to <30 kg/m2 (overweight) in the presence of at least one weight-related comorbidity e.g. dysglycaemia (prediabetes or type 2 diabetes mellitus), hypertension, dyslipidaemia, obstructive sleep apnoea or cardiovascular disease.

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

remedyrepack inc. - semaglutide (unii: 53axn4nnhx) (semaglutide - unii:53axn4nnhx) - ozempic is indicated: - as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus [see clinical studies ( 14.1)] . - to reduce the risk of major adverse cardiovascular events (cardiovascular death, non-fatal myocardial infarction or non-fatal stroke) in adults with type 2 diabetes mellitus and established cardiovascular disease [see clinical studies ( 14.4 ) ]. limitations of use - ozempic has not been studied in patients with a history of pancreatitis. consider other antidiabetic therapies in patients with a history of pancreatitis [see warnings and precautions ( 5.2)] . - ozempic is not indicated for use in patients with type 1 diabetes mellitus. ozempic is contraindicated in patients with: - a personal or family history of medullary thyroid carcinoma (mtc) or in patients with multiple endocrine neoplasia syndrome type 2 (men 2)

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

novo nordisk - semaglutide (unii: 53axn4nnhx) (semaglutide - unii:53axn4nnhx) - rybelsus is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. limitations of use rybelsus is contraindicated in patients with: risk summary available data with rybelsus use in pregnant women are insufficient to evaluate for a drug-associated risk of major birth defects, miscarriage or other adverse maternal or fetal outcomes. there are clinical considerations regarding the risks of poorly controlled diabetes in pregnancy (see clinical considerations) . based on animal reproduction studies, there may be potential risks to the fetus from exposure to rybelsus during pregnancy. rybelsus should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. in pregnant rats administered semaglutide during organogenesis, embryofetal mortality, structural abnormalities and alterations to growth occurred at maternal exposures below the maximum recommended human dose (mrhd) based on auc. in rabbits and cynomolgus monkeys administered semaglutide during organogenesis, early pregnancy losses and structural abnormalities were observed at exposure below the mrhd (rabbit) and ≥10-fold the mrhd (monkey). these findings coincided with a marked maternal body weight loss in both animal species (see data) . the estimated background risk of major birth defects is 6 to 10% in women with pre-gestational diabetes with an hba1c >7 and has been reported to be as high as 20 to 25% in women with a hba1c >10. 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 fetal risk poorly controlled diabetes during pregnancy increases the maternal risk for diabetic ketoacidosis, pre- eclampsia, spontaneous abortions, preterm delivery, and delivery complications. poorly controlled diabetes increases the fetal risk for major birth defects, stillbirth, and macrosomia related morbidity. data animal data in a combined fertility and embryofetal development study in rats, subcutaneous doses of 0.01, 0.03 and 0.09 mg/kg/day (0.2-, 0.7-, and 2.1-fold the mrhd) were administered to males for 4 weeks prior to and throughout mating and to females for 2 weeks prior to mating, and throughout organogenesis to gestation day 17. in parental animals, pharmacologically mediated reductions in body weight gain and food consumption were observed at all dose levels. in the offspring, reduced growth and fetuses with visceral (heart blood vessels) and skeletal (cranial bones, vertebra, ribs) abnormalities were observed at the human exposure. in an embryofetal development study in pregnant rabbits, subcutaneous doses of 0.0010, 0.0025 or 0.0075 mg/kg/day (0.06-, 0.6-, and 4.4-fold the mrhd) were administered throughout organogenesis from gestation day 6 to 19. pharmacologically mediated reductions in maternal body weight gain and food consumption were observed at all dose levels. early pregnancy losses and increased incidences of minor visceral (kidney, liver) and skeletal (sternebra) fetal abnormalities were observed at ≥0.0025 mg/kg/day, at clinically relevant exposures. in an embryofetal development study in pregnant cynomolgus monkeys, subcutaneous doses of 0.015, 0.075, and 0.15 mg/kg twice weekly (1.9-, 9.9-, and 29-fold the mrhd) were administered throughout organogenesis, from gestation day 16 to 50. pharmacologically mediated, marked initial maternal body weight loss and reductions in body weight gain and food consumption coincided with the occurrence of sporadic abnormalities (vertebra, sternebra, ribs) at ≥0.075 mg/kg twice weekly (> 9x human exposure). in a pre- and postnatal development study in pregnant cynomolgus monkeys, subcutaneous doses of 0.015, 0.075, and 0.15 mg/kg twice weekly (1.3-, 6.4-, and 14-fold the mrhd) were administered from gestation day 16 to 140. pharmacologically mediated marked initial maternal body weight loss and reductions in body weight gain and food consumption coincided with an increase in early pregnancy losses and led to delivery of slightly smaller offspring at ≥0.075 mg/kg twice weekly (> 6x human exposure). salcaprozate sodium (snac), an absorption enhancer in rybelsus, crosses the placenta and reaches fetal tissues in rats. in a pre- and postnatal development study in pregnant sprague dawley rats, snac was administered orally at 1,000 mg/kg/day (exposure levels were not measured) on gestation day 7 through lactation day 20. an increase in gestation length, an increase in the number of stillbirths and a decrease in pup viability were observed. risk summary there are no data on the presence of semaglutide in human milk, the effects on the breastfed infant, or the effects on milk production. semaglutide was present in the milk of lactating rats. snac and/or its metabolites concentrated in the milk of lactating rats. when a substance is present in animal milk, it is likely that the substance will be present in human milk (see data) . there are no data on the presence of snac in human milk. since the activity of ugt2b7, an enzyme involved in snac clearance, is lower in infants compared to adults, higher snac plasma levels may occur in neonates and infants. because of the unknown potential for serious adverse reactions in the breastfed infant due to the possible accumulation of snac from breastfeeding and because there are alternative formulations of semaglutide that can be used during lactation, advise patients that breastfeeding is not recommended during treatment with rybelsus. data in lactating rats, semaglutide was detected in milk at levels 3- to 12-fold lower than in maternal plasma. snac and/or its metabolites were detected in milk of lactating rats following a single maternal administration on lactation day 10. mean levels of snac and/or its metabolites in milk were approximately 2- to 12-fold higher than in maternal plasma. discontinue rybelsus in women at least 2 months before a planned pregnancy due to the long washout period for semaglutide [see use in specific populations (8.1)] . the safety and effectiveness of rybelsus have not been established in pediatric patients. in the pool of glycemic control trials, 1229 (30%) rybelsus-treated patients were 65 years of age and over and 199 (5%) rybelsus-treated patients were 75 years of age and over [see clinical studies (14)] . in pioneer 6, the cardiovascular outcomes trial, 891 (56%) rybelsus-treated patients were 65 years of age and over and 200 (13%) rybelsus-treated patients were 75 years of age and over. no overall differences in safety or effectiveness for rybelsus have been observed between patients 65 years of age and older and younger adult patients. the safety and effectiveness of rybelsus was evaluated in a 26-week clinical study that included 324 patients with moderate renal impairment (egfr 30 to 59 ml/min/1.73m2 ) [see clinical studies (14.1)]. in patients with renal impairment including end-stage renal disease (esrd), no clinically relevant change in semaglutide pharmacokinetics (pk) was observed [see clinical pharmacology (12.3)] . no dose adjustment of rybelsus is recommended for patients with renal impairment. in a study in subjects with different degrees of hepatic impairment, no clinically relevant change in semaglutide pharmacokinetics (pk) was observed [see clinical pharmacology (12.3)] . no dose adjustment of rybelsus is recommended for patients with hepatic impairment.

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

a-s medication solutions - semaglutide (unii: 53axn4nnhx) (semaglutide - unii:53axn4nnhx) - ozempic is indicated: limitations of use ozempic is contraindicated in patients with: risk summary there are limited data with semaglutide use in pregnant women to inform a drug-associated risk for adverse developmental outcomes. there are clinical considerations regarding the risks of poorly controlled diabetes in pregnancy (see clinical considerations) . based on animal reproduction studies, there may be potential risks to the fetus from exposure to semaglutide during pregnancy. ozempic should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. in pregnant rats administered semaglutide during organogenesis, embryofetal mortality, structural abnormalities and alterations to growth occurred at maternal clinical exposure based on auc. in rabbits and cynomolgus monkeys administered semaglutide during organogenesis, early pregnancy losses or structural abnormalities were observed at clinical exposure (rabbit) and ≥2-fold the mrhd (monkey). these findings coincided wi

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

a-s medication solutions - semaglutide (unii: 53axn4nnhx) (semaglutide - unii:53axn4nnhx) - ozempic is indicated: limitations of use ozempic is contraindicated in patients with: risk summary there are limited data with semaglutide use in pregnant women to inform a drug-associated risk for adverse developmental outcomes. there are clinical considerations regarding the risks of poorly controlled diabetes in pregnancy (see clinical considerations) . based on animal reproduction studies, there may be potential risks to the fetus from exposure to semaglutide during pregnancy. ozempic should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. in pregnant rats administered semaglutide during organogenesis, embryofetal mortality, structural abnormalities and alterations to growth occurred at maternal clinical exposure based on auc. in rabbits and cynomolgus monkeys administered semaglutide during organogenesis, early pregnancy losses or structural abnormalities were observed at clinical exposure (rabbit) and ≥2-fold the mrhd (monkey). these findings coincided wi

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

a-s medication solutions - liraglutide (unii: 839i73s42a) (liraglutide - unii:839i73s42a) - saxenda is indicated as an adjunct to a reduced-calorie diet and increased physical activity for chronic weight management in: limitations of use saxenda is contraindicated in: risk summary saxenda is contraindicated during pregnancy because weight loss offers no potential benefit to a pregnant woman and may result in fetal harm [see clinical considerations] . there are no available data with liraglutide in pregnant women to inform a drug associated risk for major birth defects and miscarriage. saxenda should not be used during pregnancy. if a patient wishes to become pregnant, or pregnancy occurs, treatment with saxenda should be discontinued. animal reproduction studies identified increased adverse embryofetal developmental outcomes from exposure during pregnancy. liraglutide exposure was associated with early embryonic deaths and an imbalance in some fetal abnormalities in pregnant rats administered liraglutide during organogenesis at doses that approximate clinical exposures at the maximum recommended human dose (mrhd) of 3 mg/day. in pregnant rabbits administered liraglutide during organogenesis, decreased fetal weight and an increased incidence of major fetal abnormalities were seen at exposures below the human exposures at the mrhd [see animal data] . the estimated background risk of major birth defects and miscarriage for the indicated populations is unknown. in the u.s. general population, the estimated background risk of major birth defects and miscarriage of clinically recognized pregnancies is 2-4% and 15-20%, respectively. clinical considerations disease-associated maternal and/or embryofetal risk a minimum weight gain, and no weight loss, is recommended for all pregnant women, including those who are already overweight or obese, due to the necessary weight gain that occurs in maternal tissues during pregnancy. animal data liraglutide has been shown to be teratogenic in rats at or above 0.8-times systemic exposures in obese humans resulting from the maximum recommended human dose (mrhd) of 3 mg/day based on plasma area under the time-concentration curve (auc) comparison. liraglutide has been shown to cause reduced growth and increased total major abnormalities in rabbits at systemic exposures below exposure in obese humans at the mrhd based on plasma auc comparison. female rats given subcutaneous doses of 0.1, 0.25 and 1 mg/kg/day liraglutide beginning 2 weeks before mating through gestation day 17 had estimated systemic exposures 0.8-, 3-, and 11-times the exposure in obese humans at the mrhd based on plasma auc comparison. the number of early embryonic deaths in the 1 mg/kg/day group increased slightly. fetal abnormalities and variations in kidneys and blood vessels, irregular ossification of the skull, and a more complete state of ossification occurred at all doses. mottled liver and minimally kinked ribs occurred at the highest dose. the incidence of fetal malformations in liraglutide-treated groups exceeding concurrent and historical controls were misshapen oropharynx and/or narrowed opening into larynx at 0.1 mg/kg/day and umbilical hernia at 0.1 and 0.25 mg/kg/day. pregnant rabbits given subcutaneous doses of 0.01, 0.025 and 0.05 mg/kg/day liraglutide from gestation day 6 through day 18 inclusive, had estimated systemic exposures less than the exposure in obese humans at the mrhd of 3 mg/day at all doses, based on plasma auc comparison. liraglutide decreased fetal weight and dose-dependently increased the incidence of total major fetal abnormalities at all doses. the incidence of malformations exceeded concurrent and historical controls at 0.01 mg/kg/day (kidneys, scapula), greater than or equal to 0.01 mg/kg/day (eyes, forelimb), 0.025 mg/kg/day (brain, tail and sacral vertebrae, major blood vessels and heart, umbilicus), greater than or equal to 0.025 mg/kg/day (sternum) and at 0.05 mg/kg/day (parietal bones, major blood vessels). irregular ossification and/or skeletal abnormalities occurred in the skull and jaw, vertebrae and ribs, sternum, pelvis, tail, and scapula; and dose-dependent minor skeletal variations were observed. visceral abnormalities occurred in blood vessels, lung, liver, and esophagus. bilobed or bifurcated gallbladder was seen in all treatment groups, but not in the control group. in pregnant female rats given subcutaneous doses of 0.1, 0.25 and 1 mg/kg/day liraglutide from gestation day 6 through weaning or termination of nursing on lactation day 24, estimated systemic exposures were 0.8-, 3-, and 11-times exposure in obese humans at the mrhd of 3 mg/day, based on plasma auc comparison. a slight delay in parturition was observed in the majority of treated rats. group mean body weight of neonatal rats from liraglutide-treated dams was lower than neonatal rats from control group dams. bloody scabs and agitated behavior occurred in male rats descended from dams treated with 1 mg/kg/day liraglutide. group mean body weight from birth to postpartum day 14 trended lower in f2 generation rats descended from liraglutide-treated rats compared to f2 generation rats descended from controls, but differences did not reach statistical significance for any group. risk summary there are no data on the presence of liraglutide in human milk, the effects on the breastfed infant, or effects on milk production. liraglutide was present in the milk of lactating rats (see data ). the developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for saxenda and any potential adverse effects on the breastfed infant from saxenda or from the underlying maternal condition. data in lactating rats, liraglutide was present unchanged in milk at concentrations approximately 50% of maternal plasma concentrations. the safety and effectiveness of saxenda as an adjunct to a reduced-calorie diet and increased physical activity for chronic weight management have been established in pediatric patients aged 12 years and older with body weight above 60 kg and an initial bmi corresponding to 30 kg/m2 or greater for adults (obese) by international cut-offs (see table 2). use of saxenda for this indication is supported by a 56-week double-blind, placebo-controlled clinical trial in 251 pediatric patients aged 12 to 17 years, a pharmacokinetic study in pediatric patients, and studies in adults with obesity [see clinical pharmacology (12.3), clinical studies (14.1,14.2)]. in the pediatric clinical trial, there was one death due to suicide in a saxenda-treated patient [see warnings and precautions (5.8)] ; one saxenda-treated patient had an event of pancreatitis [see warnings and precautions (5.2)] ; more episodes of hypoglycemia confirmed by self blood glucose monitoring occurred in saxenda-treated patients compared to placebo [see warnings and precautions (5.4), adverse reactions (6.1)] ; and mean increases in resting heart rate of 3 to 7 bpm from baseline were observed with saxenda-treated patients [see warnings and precautions (5.5)] . the safety and effectiveness of saxenda have not been established in patients less than 12 years of age. in the saxenda clinical trials, 232 (6.9%) of the saxenda-treated patients were 65 years of age and over, and 17 (0.5%) of the saxenda-treated patients were 75 years of age and over. no overall differences in safety or effectiveness were observed between these patients and younger patients, but greater sensitivity of some older individuals cannot be ruled out. there is limited experience with saxenda in patients with mild, moderate, and severe renal impairment, including end‑stage renal disease. however, there have been postmarketing reports of acute renal failure and worsening of chronic renal failure with liraglutide, which may sometimes require hemodialysis [see warnings and precautions (5.6), adverse reactions (6.2)] . saxenda should be used with caution in this patient population [see clinical pharmacology (12.3)] . there is limited experience in patients with mild, moderate, or severe hepatic impairment. therefore, saxenda should be used with caution in this patient population [see clinical pharmacology (12.3)] . saxenda slows gastric emptying. saxenda has not been studied in patients with pre-existing gastroparesis. step 1. prepare your pen with a new needle always use a new needle for each injection. this will prevent contamination, infection, leakage of saxenda, and blocked needles leading to the wrong dose. never use a bent or damaged needle. do not attach a new needle to your pen until you are ready to take your injection. step 2. check the saxenda flow with each new pen. always make sure that a drop appears at the needle tip before you use a new pen for the first time. this makes sure that saxenda flows. if no drop appears, you will not inject any saxenda, even though the dose counter may move. this may mean that there is a blocked or damaged needle. a small drop may remain at the needle tip, but it will not be injected. only check the saxenda flow before your first injection with each new pen. step 3. select your dose always use the dose counter and the dose pointer to see how many mg you select. you will hear a “click” every time you turn the dose selector. do not set the dose by counting the number of clicks you hear. do not use the pen scale to set the dose. it does not show exactly how much saxenda is left in your pen. only doses of 0.6 mg, 1.2 mg, 1.8 mg, 2.4 mg or 3 mg can be selected with the dose selector. the selected dose must line up exactly with the dose pointer to make sure that you get a correct dose. the dose selector changes the dose. only the dose counter and dose pointer will show how many mg you select for each dose. you can select up to 3 mg each dose. when your pen contains less than 3 mg the dose counter stops before 3 mg is shown. the dose selector clicks differently when turned forward, backwards or past the number of mg left. do not count the pen clicks. how much saxenda is left? if you need more saxenda than what is left in your pen only if trained or told by your healthcare provider, you may split your dose between your current pen and a new pen. use a calculator to plan the doses as instructed by your healthcare provider. be very careful to calculate correctly. if you are not sure how to split your dose using 2 pens, then select and inject the dose you need with a new pen. step 4. inject your dose always watch the dose counter to know how many mg you inject. hold the dose button down until the dose counter shows 0. you may see a drop of saxenda at the needle tip after injecting. this is normal and does not affect your dose. step 5. after your injection if you do not have a sharps container, follow a 1-handed needle recapping method. carefully slip the needle into the outer needle cap. dispose of the needle in a sharps container as soon as possible. never try to put the inner needle cap back on the needle. you may stick yourself with the needle. always remove the needle from your pen. this prevents contamination, infection, leakage of saxenda, and blocked needles leading to the wrong dose. if the needle is blocked, you will not inject any saxenda. always dispose of the needle after each injection . important caring for your pen how should i store my saxenda pen? this medication guide and instructions for use have been approved by the u.s. food and drug administration. december 2020

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

novo nordisk - insulin degludec (unii: 54q18076qb) (insulin degludec - unii:54q18076qb), liraglutide (unii: 839i73s42a) (liraglutide - unii:839i73s42a) - insulin degludec 100 [iu] in 1 ml - xultophy 100/3.6 is a combination of insulin degludec and liraglutide and is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. limitations of use: xultophy 100/3.6 is contraindicated: risk summary based on animal reproduction studies, there may be risks to the fetus from exposure to liraglutide during pregnancy. xultophy 100/3.6 should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. there are no available data with xultophy 100/3.6, insulin degludec or liraglutide in pregnant women to inform a drug associated risk for major birth defects and miscarriage. there are clinical considerations regarding the risks of poorly controlled diabetes in pregnancy [see clinical considerations]. for insulin degludec, rats and rabbits were exposed in animal reproduction studies at 5 times (rat) and 10 times (rabbit) the human exposure at a dose of 0.75 u/kg/day. no adverse outcomes were observed for pregnant ani