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the soleil group, llc - octinoxate (unii: 4y5p7mud51) (octinoxate - unii:4y5p7mud51), octisalate (unii: 4x49y0596w) (octisalate - unii:4x49y0596w), zinc oxide (unii: soi2loh54z) (zinc cation - unii:13s1s8sf37), avobenzone (unii: g63qqf2nox) (avobenzone - unii:g63qqf2nox) - helps prevent sunburn. if used as directed with other sun protection measures (see directions: ), decreases the risk of skin cancer and early skin aging caused by the sun. sunscreen

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shanghai kejing cleaning products co., ltd. - octinoxate (unii: 4y5p7mud51) (octinoxate - unii:4y5p7mud51), octisalate (unii: 4x49y0596w) (octisalate - unii:4x49y0596w), oxybenzone (unii: 95oos7ve0y) (oxybenzone - unii:95oos7ve0y), titanium dioxide (unii: 15fix9v2jp) (titanium dioxide - unii:15fix9v2jp) - purpose sunscreen uses : helps prevent sunburn

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the procter & gamble manufacturing company - avobenzone (unii: g63qqf2nox) (avobenzone - unii:g63qqf2nox), homosalate (unii: v06sv4m95s) (homosalate - unii:v06sv4m95s), octisalate (unii: 4x49y0596w) (octisalate - unii:4x49y0596w), octocrylene (unii: 5a68wgf6wm) (octocrylene - unii:5a68wgf6wm), oxybenzone (unii: 95oos7ve0y) (oxybenzone - unii:95oos7ve0y) - - helps prevent sunburn - if used as directed with other sun protection measures (see directions ), decreases the risk of skin cancer and early skin aging caused by the sun

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elemis limited - avobenzone 1.0% } octinoxate 1.0%} octocrylene 0.5%} - sunscreen - helps prevent sunburn - higher spf gives more sunburn protection

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walgreen company - carboxymethylcellulose sodium (unii: k679obs311) (carboxymethylcellulose - unii:05jzi7b19x) - uses - for the temporary relief of buring, irritation, and discomofort due to dryness of the eye or exposure to wind or sun - may be used as a protectant against further irritation stop use and ask a doctor if - you experience eye pain - changes in vision occur - continued redness or irritation of the eye lasts - condition worsens or persists for more than 72 hours directions - to open, twis and pull tab to remove - instill 1 or 2 drops in the affected eye(s) as needed - children under 6 years of age: ask a doctor

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aruba aloe balm nv - titanium dioxide (unii: 15fix9v2jp) (titanium dioxide - unii:15fix9v2jp), zinc oxide (unii: soi2loh54z) (zinc cation - unii:13s1s8sf37) - - helps prevent sunburn. - if used as directed with other sun protection measures (see directions), decreases the risk of skin cancer and early skin aging caused by the sun.

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stream2sea, llc - titanium dioxide (unii: 15fix9v2jp) (titanium dioxide - unii:15fix9v2jp) - helps prevent sunburn. sunscreen.

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actavis pharma, inc. - ramelteon (unii: 901as54i69) (ramelteon - unii:901as54i69) - ramelteon tablets are indicated for the treatment of insomnia characterized by difficulty with sleep onset. the clinical trials performed in support of efficacy were up to six months in duration. the final formal assessments of sleep latency were performed after two days of treatment during the crossover study (elderly only), at five weeks in the six week studies (adults and elderly), and at the end of the six month study (adults and elderly) [see clinical studies (14)] . patients who develop angioedema after treatment with ramelteon tablets should not be rechallenged with the drug. patients should not take ramelteon tablets in conjunction with fluvoxamine [see drug interactions (7)] . risk summary available data from postmarketing reports with ramelteon tablets use in pregnant women have not identified a drug-associated risk of major birth defects, miscarriage, or adverse maternal or fetal outcomes. in animal studies, ramelteon produced evidence of developmental toxicity, including teratogenic effects, in rats at doses greater than 36 times the recommended human dose (rhd) of 8 mg/day based on body surface area (mg/m2 ) (see data ). the estimated background risk of major birth defects and miscarriage for the indicated population is unknown. all pregnancies have a background risk of birth defect, loss, or other adverse outcomes. 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. data animal data oral administration of ramelteon (10, 40, 150 or 600 mg/kg/day) to pregnant rats during the period of organogenesis was associated with increased incidences of fetal structural abnormalities (malformations and variations) at doses greater than 40 mg/kg/day. the no-effect dose is approximately 50 times the rhd based on mg/m2 . treatment of pregnant rabbits during the period of organogenesis produced no evidence of embryo-fetal toxicity at oral doses of up to 300 mg/kg/day (or up to 720 times the rhd based on mg/m2 ). when rats were orally administered ramelteon (30, 100, or 300 mg/kg/day) throughout gestation and lactation, growth retardation, developmental delay, and behavioral changes were observed in the offspring at doses greater than 30 mg/kg/day. the no-effect dose is 36 times the rhd based on mg/m2 . increased incidences of malformation and death among offspring were seen at the highest dose. risk summary there are no data regarding the presence of ramelteon or its metabolites in human milk, the effects on the breastfed infant, or the effects on milk production. ramelteon and/or its metabolites are present in rat milk. when a drug is present in animal milk, it is likely that the drug will be present in human milk. because of the mechanism of action of ramelteon, there is a potential risk for somnolence in a breastfed infant (see clinical considerations) . the developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for ramelteon tablets and any potential adverse effects on the breastfed infant from ramelteon tablets or from the underlying maternal condition. clinical considerations infants exposed to ramelteon tablets through breastmilk should be monitored for somnolence and feeding problems. a lactating woman may consider interrupting breastfeeding and pumping and discarding breast milk during treatment and for 25 hours (approximately 5 elimination half-lives) after ramelteon tablets administration in order to minimize drug exposure to a breastfed infant. safety and effectiveness of ramelteon tablets in pediatric patients have not been established. further study is needed prior to determining that this product may be used safely in prepubescent and pubescent patients. a total of 654 subjects in double-blind, placebo-controlled, efficacy trials who received ramelteon tablets were at least 65 years of age; of these, 199 were 75 years of age or older. no overall differences in safety or efficacy were observed between elderly and younger adult subjects. a double-blind, randomized, placebo-controlled study in elderly subjects with insomnia (n=33) evaluated the effect of a single dose of ramelteon tablets on balance, mobility, and memory functions after middle of the night awakening. there is no information on the effect of multiple dosing. night time dosing of ramelteon tablets 8 mg did not impair middle of the night balance, mobility, or memory functions relative to placebo. the effects on night balance in the elderly cannot be definitively known from this study. the respiratory depressant effect of ramelteon tablets was evaluated in a crossover design study of subjects (n=26) with mild to moderate copd after administering a single 16 mg dose or placebo, and in a separate study (n=25), the effects of ramelteon tablets on respiratory parameters were evaluated after administering an 8 mg dose or placebo in a crossover design to patients with moderate to severe copd, defined as patients who had forced expiratory volume at one second (fev1 )/forced vital capacity ratio of <70%, and a fev1 <80% of predicted with <12% reversibility to albuterol. treatment with a single dose of ramelteon tablets has no demonstrable respiratory depressant effects in subjects with mild to severe copd, as measured by arterial o2 saturation (sao2). there is no available information on the respiratory effects of multiple doses of ramelteon tablets in patients with copd. the respiratory depressant effects in patients with copd cannot be definitively known from this study. the effects of ramelteon tablets were evaluated after administering a 16 mg dose or placebo in a crossover design to subjects (n=26) with mild to moderate obstructive sleep apnea. treatment with ramelteon tablets 16 mg for one night showed no difference compared with placebo on the apnea/hypopnea index (the primary outcome variable), apnea index, hypopnea index, central apnea index, mixed apnea index, and obstructive apnea index. treatment with a single dose of ramelteon tablets does not exacerbate mild to moderate obstructive sleep apnea. there is no available information on the respiratory effects of multiple doses of ramelteon tablets in patients with sleep apnea. the effects on exacerbation in patients with mild to moderate sleep apnea cannot be definitively known from this study. ramelteon has not been studied in subjects with severe obstructive sleep apnea; use of ramelteon tablets is not recommended in such patients. exposure to ramelteon tablets was increased by four-fold in subjects with mild hepatic impairment and by more than ten-fold in subjects with moderate hepatic impairment. ramelteon tablets should be used with caution in patients with moderate hepatic impairment [see clinical pharmacology (12.4)] . ramelteon tablets are not recommended in patients with severe hepatic impairment. no effects on cmax and auc0-t of parent drug or m-ii were seen. no adjustment of ramelteon tablets dosage is required in patients with renal impairment [see clinical pharmacology (12.4)] . ramelteon tablets are not a controlled substance. discontinuation of ramelteon in animals or in humans after chronic administration did not produce withdrawal signs. ramelteon does not appear to produce physical dependence. human data a laboratory abuse potential study was performed with ramelteon tablets [see clinical studies (14.2)] . animal data ramelteon did not produce any signals from animal behavioral studies indicating that the drug produces rewarding effects. monkeys did not self-administer ramelteon and the drug did not induce a conditioned place preference in rats. there was no generalization between ramelteon and midazolam. ramelteon did not affect rotorod performance, an indicator of disruption of motor function, and it did not potentiate the ability of diazepam to interfere with rotorod performance.

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st. mary's medical park pharmacy - duloxetine hydrochloride (unii: 9044sc542w) (duloxetine - unii:o5tnm5n07u) - duloxetine delayed-release capsules are indicated for the treatment of: - major depressive disorder [see clinical studies ( 14.1 )] . - generalized anxiety disorder [see clinical studies ( 14.2 )] . - diabetic peripheral neuropathy [see clinical studies ( 14.3 )] . - chronic musculoskeletal pain [see clinical studies ( 14.5 )] .          monoamine oxidase inhibitors (maois)   - the use of maois intended to treat psychiatric disorders with duloxetine or within 5 days of stopping treatment with duloxetine is contraindicated because of an increased risk of serotonin syndrome. the use of duloxetine within 14 days of stopping an maoi intended to treat psychiatric disorders is also contraindicated [see dosage and administration ( 2.8) and warnings and precautions ( 5.4)].          starting duloxetine in a patient who is being treated with maois such as linezolid or intravenous methylene blue is also contraindicated because of an increased risk of serotonin syndrome [see dosage and administration ( 2.9) and warnings and precautions ( 5.4)].          pregnancy category c          risk summary — there are no adequate and well-controlled studies of duloxetine administration in pregnant women. in animal studies with duloxetine, fetal weights were decreased but there was no evidence of teratogenicity in pregnant rats and rabbits at oral doses administered during the period of organogenesis up to 4 and 7 times the maximum recommended human dose (mrhd) of 120 mg/day, respectively. when duloxetine was administered orally to pregnant rats throughout gestation and lactation, pup weights at birth and pup survival to 1 day postpartum were decreased at a dose 2 times the mrhd. at this dose, pup behaviors consistent with increased reactivity, such as increased startle response to noise and decreased habituation of locomotor activity were observed. post-weaning growth was not adversely affected. duloxetine should be used in pregnancy only if the potential benefit justifies the potential risk to the fetus.          clinical considerations          fetal/neonatal adverse reaction — neonates exposed during pregnancy to serotonin - norepinephrine reuptake inhibitors (snris) or selective serotonin reuptake inhibitors (ssris) have developed complications requiring prolonged hospitalization, respiratory support, and tube feeding which can arise immediately upon delivery. reported clinical findings have included respiratory distress, cyanosis, apnea, seizures, temperature instability, feeding difficulty, vomiting, hypoglycemia, hypotonia, hypertonia, hyperreflexia, tremor, jitteriness, irritability, and constant crying. these features are consistent with either a direct toxic effect of the snris or ssris, or possibly, a drug discontinuation syndrome. it should be noted that, in some cases, the clinical picture is consistent with serotonin syndrome [see warnings and precautions ( 5.4)] .          data          animal data — in animal reproduction studies, duloxetine has been shown to have adverse effects on embryo/fetal and postnatal development.          when duloxetine was administered orally to pregnant rats and rabbits during the period of organogenesis, there was no evidence of teratogenicity at doses up to 45 mg/kg/day (4 times the maximum recommended human dose (mrhd) of 120 mg/day on a mg/m 2 basis, in rat; 7 times the mrhd in rabbit). however, fetal weights were decreased at this dose, with a no-effect dose of 10 mg/kg/day approximately equal to the mrhd in rats; 2 times the mrhd in rabbits).          when duloxetine was administered orally to pregnant rats throughout gestation and lactation, the survival of pups to 1 day postpartum and pup body weights at birth and during the lactation period were decreased at a dose of 30 mg/kg/day (2 times the mrhd); the no-effect dose was 10 mg/kg/day. furthermore, behaviors consistent with increased reactivity, such as increased startle response to noise and decreased habituation of locomotor activity, were observed in pups following maternal exposure to 30 mg/kg/day. post-weaning growth and reproductive performance of the progeny were not affected adversely by maternal duloxetine treatment.          risk summary          duloxetine is present in human milk. in a published study, lactating women who were weaning their infants were given duloxetine. at steady state, the concentration of duloxetine in breast milk was approximately 25% that of maternal plasma. the estimated daily infant dose was approximately 0.14% of the maternal dose. the developmental and health benefits of human milk feeding should be considered along with the mother’s clinical need for duloxetine and any potential adverse effects on the milk-fed child from the drug or from the underlying maternal condition. exercise caution when duloxetine is administered to a nursing woman.          data          the disposition of duloxetine was studied in 6 lactating women who were at least 12 weeks postpartum and had elected to wean their infants. the women were given 40 mg of duloxetine twice daily for 3.5 days. the peak concentration measured in breast milk occurred at a median of 3 hours after the dose. the amount of duloxetine in breast milk was approximately 7 mcg/day while on that dose; the estimated daily infant dose was approximately 2 mcg/kg/day. the presence of duloxetine metabolites in breast milk was not examined. generalized anxiety disorder — in pediatric patients aged 7 to 17 years, efficacy was demonstrated in one 10 week, placebo-controlled trial. the study included 272 pediatric patients with gad of which 47% were 7 to 11 years of age. duloxetine demonstrated superiority over placebo as measured by greater improvement in the pediatric anxiety rating scale (pars) for gad severity score [see clinical studies ( 14.2)]. the safety and effectiveness in pediatric patients less than 7 years of age have not been established. major depressive disorder — efficacy was not demonstrated in two 10-week, placebo-controlled trials with 800 pediatric patients with mdd, age 7-17. neither duloxetine nor an active control (indicated for treatment of pediatric depression) was superior to placebo. the safety and effectiveness in pediatric patients less than 7 years of age have not been established. the most frequently observed adverse reactions in the clinical trials included nausea, headache, decreased weight, and abdominal pain. decreased appetite and weight loss have been observed in association with the use of ssris and snris. perform regular monitoring of weight and growth in children and adolescents treated with an snri such as duloxetine [see adverse reactions ( 6.11)]. use of duloxetine in a child or adolescent must balance the potential risks with the clinical need [see boxed warning and warnings and precautions ( 5.1)]. animal data — duloxetine administration to young rats from post-natal day 21 (weaning) through post-natal day 90 (adult) resulted in decreased body weights that persisted into adulthood, but recovered when drug treatment was discontinued; slightly delayed (~1.5 days) sexual maturation in females, without any effect on fertility; and a delay in learning a complex task in adulthood, which was not observed after drug treatment was discontinued. these effects were observed at the high dose of 45 mg/kg/day (2 times the mrhd, for a child); the no-effect-level was 20 mg/kg/day (≈1 times the mrhd, for a child). of the 2,418 patients in premarketing clinical studies of duloxetine for mdd, 5.9% (143) were 65 years of age or over. of the 1041 patients in clbp premarketing studies, 21.2% (221) were 65 years of age or over. of the 487 patients in oa premarketing studies, 40.5% (197) were 65 years of age or over. of the 1,074 patients in the dpnp premarketing studies, 33% (357) were 65 years of age or over. in the mdd, gad, dpnp, oa, clbp, and other studies, no overall differences in safety or effectiveness were generally observed between these subjects and younger subjects, 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. ssris and snris, including duloxetine have been associated with cases of clinically significant hyponatremia in elderly patients, who may be at greater risk for this adverse event [see warnings and precautions ( 5.13)] . in an analysis of data from all placebo-controlled-trials, patients treated with duloxetine reported a higher rate of falls compared to patients treated with placebo. the increased risk appears to be proportional to a patient’s underlying risk for falls. underlying risk appears to increase steadily with age. as elderly patients tend to have a higher prevalence of risk factors for falls such as medications, medical comorbidities and gait disturbances, the impact of increasing age by itself on falls during treatment with duloxetine is unclear. falls with serious consequences including bone fractures and hospitalizations have been reported [see warnings and precautions ( 5.3) and adverse reactions ( 6.10)] . the pharmacokinetics of duloxetine after a single dose of 40 mg were compared in healthy elderly females (65 to 77 years) and healthy middle-age females (32 to 50 years). there was no difference in the cmax, but the auc of duloxetine was somewhat (about 25%) higher and the half-life about 4 hours longer in the elderly females. population pharmacokinetic analyses suggest that the typical values for clearance decrease by approximately 1% for each year of age between 25 to 75 years of age; but age as a predictive factor only accounts for a small percentage of between-patient variability. dosage adjustment based on the age of the patient is not necessary.       duloxetine's half-life is similar in men and women. dosage adjustment based on gender is not necessary.          duloxetine bioavailability (auc) appears to be reduced by about one-third in smokers. dosage modifications are not recommended for smokers.          no specific pharmacokinetic study was conducted to investigate the effects of race.          patients with clinically evident hepatic impairment have decreased duloxetine metabolism and elimination. after a single 20 mg dose of duloxetine, 6 cirrhotic patients with moderate liver impairment (child-pugh class b) had a mean plasma duloxetine clearance about 15% that of age- and gender-matched healthy subjects, with a 5-fold increase in mean exposure (auc). although c max was similar to normals in the cirrhotic patients, the half-life was about 3 times longer [see dosage and administration ( 2.6) and warnings and precautions ( 5.14)] .          limited data are available on the effects of duloxetine in patients with end-stage renal disease (esrd). after a single 60 mg dose of duloxetine, c max and auc values were approximately 100% greater in patients with end-stage renal disease receiving chronic intermittent hemodialysis than in subjects with normal renal function. the elimination half-life, however, was similar in both groups. the aucs of the major circulating metabolites, 4-hydroxy duloxetine glucuronide and 5-hydroxy, 6-methoxy duloxetine sulfate, largely excreted in urine, were approximately 7- to 9-fold higher and would be expected to increase further with multiple dosing. population pk analyses suggest that mild to moderate degrees of renal impairment (estimated crcl 30 to 80 ml/min) have no significant effect on duloxetine apparent clearance [see dosage and administration ( 2.6) and warnings and precautions ( 5.14)] .          in animal studies, duloxetine did not demonstrate barbiturate-like (depressant) abuse potential.          while duloxetine has not been systematically studied in humans for its potential for abuse, there was no indication of drug-seeking behavior in the clinical trials. however, it is not possible to predict on the basis of premarketing experience the extent to which a cns active drug will be misused, diverted, and/or abused once marketed. consequently, physicians should carefully evaluate patients for a history of drug abuse and follow such patients closely, observing them for signs of misuse or abuse of duloxetine (e.g., development of tolerance, incrementation of dose, drug-seeking behavior).          in drug dependence studies, duloxetine did not demonstrate dependence-producing potential in rats.

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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.