roval for this indication may be contingent upon verification and description of clinical benefit in a confirmatory clinical trial. ( 1 )

with a systemic corticosteroid is recommended. when discontinuing therapy [see dosing and administration ( 2 )] or switching between corticosteroids, monitor for signs of adrenal axis suppression. patients with moderate to severe hepatic impairment (child-pugh class b and c respectively) could be at an increased risk of hypercorticism and adrenal axis suppression due to an increased systemic exposure of oral budesonide. avoid use in patients with severe hepatic impairment (child-pugh class c). monitor for increased signs and/or symptoms of hypercorticism in patients with moderate hepatic impairment (child-pugh class b) [see use in specific populations ( 8.6 ), clinical pharmacology ( 12.3 )] . 5.2 risks of immunosupression patients who are on drugs that suppress the immune system are more susceptible to infection than healthy individuals. chickenpox and measles, for example, can have a more serious or even fatal course in susceptible patients or patients on immunosuppressant doses of corticosteroids. avoid corticosteroid therapy in patients with active or quiescent tuberculosis infection, untreated fungal, bacterial, systemic viral or parasitic infections, or ocular herpes simplex. avoid exposure to active, easily-transmitted infections (e.g., chicken pox, measles). corticosteroid therapy may decrease the immune response to some vaccines. how the dose, route, and duration of corticosteroid administration affect the risk of developing a disseminated infection is not known. the contribution of the underlying disease and/or prior corticosteroid treatment to the risk is also not known. if exposed to chickenpox, consider therapy with varicella zoster immune globulin (vzig) or pooled intravenous immunoglobulin (ivig). if exposed to measles, consider prophylaxis with pooled intramuscular immunoglobulin (ig). if chickenpox develops, consider treatment with antiviral agents. 5.3 other corticosteroid effects tarpeyo is a systemically available corticosteroid and is expected to cause related adverse reactions. monitor patients with hypertension, prediabetes, diabetes mellitus, osteoporosis, peptic ulcer, glaucoma or cataracts, or with a family history of diabetes or glaucoma, or with any other condition where corticosteroids may have unwanted effects.

domized controlled study in 197 patients. the most common adverse reactions reported in greater than or equal to 5% of tarpeyo-treated patients are listed in table 1 . the majority of adverse reactions were mild or moderate in severity. table 1: reported adverse reactions occurring in greater than or equal to 5% of tarpeyo treated patients, and greater than or equal to 2% higher than placebo adverse reaction tarpeyo 16 mg (n=97) placebo (n=100) n (%) n (%) patients with any adverse reaction 84 (87) 73 (73) hypertension 15 (16) 2 (2) peripheral edema 14 (14) 4 (4) muscle spasms 13 (13) 4 (4) acne 11 (11) 2 (2) dermatitis 7 (7) 1 (1) weight increased 7 (7) 3 (3) dyspnea 6 (6) 0 (0) face edema 6 (6) 1 (1) dyspepsia 5 (5) 2 (2) fatigue 5 (5) 2 (2) hirsutism 5 (5) 0 (0) most adverse reactions that occurred at a greater incidence for tarpeyo compared to placebo were consistent with hypercortisolism.

h rats and rabbits at these dose levels (see data ) . the estimated background risk of major birth defects and miscarriage of 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. clinical considerations disease-associated maternal and/or embryo/fetal risk iga nephropathy in pregnancy is associated with adverse maternal outcomes, including increased rates of cesarean section, pregnancy-induced hypertension, pre-eclampsia and preterm delivery, and adverse fetal/neonatal outcomes, including stillbirth and low birth weight. fetal/neonatal adverse reactions hypoadrenalism may occur in infants born to mothers receiving corticosteroids during pregnancy. infants should be carefully observed for signs of hypoadrenalism, such as poor feeding, irritability, weakness, and vomiting, and managed accordingly [see warnings and precautions ( 5.1 )]. data animal data budesonide was teratogenic and embryo-lethal in rabbits and rats. in an embryo-fetal development study in pregnant rats dosed subcutaneously with budesonide during the period of organogenesis on gestation days 6 to 15 there were effects on fetal development and survival at subcutaneous doses up to approximately 500 mcg/kg in rats (approximately 0.3 times the maximum recommended human dose (mrhd) on a body surface area basis). in an embryo-fetal development study in pregnant rabbits dosed during the period of organogenesis on gestation days 6 to 18, there was an increase in maternal abortion, and effects on fetal development and reduction in litter weights at subcutaneous doses from approximately 25 mcg/kg (approximately 0.03 times the mrhd on a body surface area basis). maternal toxicity, including reduction in body weight gain, was observed at subcutaneous doses of 5 mcg/kg in rabbits (approximately 0.006 times the maximum recommended human dose on a body surface area basis) and 500 mcg/kg in rats (approximately 0.3 times the maximum recommended human dose on a body surface area basis). in a peri- and post-natal development study, subcutaneous treatment of pregnant rats with budesonide during the period from day 15 post coitum to day 21 post partum, budesonide had no effects on delivery, but did have an effect on growth and development of offspring. in addition, offspring survival was reduced and surviving offspring had decreased mean body weights at birth and during lactation at exposures ≥ 0.012 times the mrhd (on a mg/m 2 basis at maternal subcutaneous doses of 20 mcg/kg/day and higher). these findings occurred in the presence of maternal toxicity. 8.2 lactation risk summary breastfeeding is not expected to result in significant exposure of the infant to tarpeyo. lactation studies have not been conducted with oral budesonide, including tarpeyo, and no information is available on the effects of the drug on the breastfed infant or the effects on the drug on milk production. one published study reports that budesonide is present in human milk following maternal inhalation of budesonide (see data ). routine monitoring of linear growth in infants is recommended with chronic use of budesonide in the nursing mother. the developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for tarpeyo and any potential adverse effects on the breastfed infant from tarpeyo, or from the underlying maternal condition. data one published study reports that budesonide is present in human milk following maternal inhalation of budesonide, which resulted in infant doses approximately 0.3% to 1% of the maternal weight-adjusted dosage and a milk to plasma ratio was approximately 0.5. budesonide was not detected in plasma, and no adverse events were noted in the breastfed infants following maternal use of inhaled budesonide. assuming a daily average milk intake of about 150 ml/kg/day and a milk to plasma ratio of 0.5, the estimated oral dose of budesonide for a 5 kg infant is expected to be less than 2 mcg/day for a maternal dose of 16 mg tarpeyo. assuming 100% bio-availability in the infant this is about 0.1% of the maternal dose and about 3% of the highest inhaled dose used clinically for asthma in infants. 8.4 pediatric use the safety and efficacy of tarpeyo in pediatric patients have not been established. 8.5 geriatric use clinical studies of tarpeyo did not include sufficient numbers of subjects aged 65 and over to determine whether they respond differently from younger subjects. other reported clinical experience has not identified differences in responses between the elderly and younger patients. in general, dose selection for an elderly patient should be cautious, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy. 8.6 hepatic impairment patients with moderate to severe hepatic impairment (child-pugh class b and c, respectively) could be at an increased risk of hypercorticism and adrenal axis suppression due to an increased systemic exposure to budesonide [see warnings and precautions ( 5.1 ) and clinical pharmacology ( 12.3 )] . avoid use in patients with severe hepatic impairments (child-pugh class c). monitor for increased signs and/or symptoms of hypercorticism in patients with moderate hepatic impairment (child-pugh class b).

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. clinical considerations disease-associated maternal and/or embryo/fetal risk iga nephropathy in pregnancy is associated with adverse maternal outcomes, including increased rates of cesarean section, pregnancy-induced hypertension, pre-eclampsia and preterm delivery, and adverse fetal/neonatal outcomes, including stillbirth and low birth weight. fetal/neonatal adverse reactions hypoadrenalism may occur in infants born to mothers receiving corticosteroids during pregnancy. infants should be carefully observed for signs of hypoadrenalism, such as poor feeding, irritability, weakness, and vomiting, and managed accordingly [see warnings and precautions ( 5.1 )]. data animal data budesonide was teratogenic and embryo-lethal in rabbits and rats. in an embryo-fetal development study in pregnant rats dosed subcutaneously with budesonide during the period of organogenesis on gestation days 6 to 15 there were effects on fetal development and survival at subcutaneous doses up to approximately 500 mcg/kg in rats (approximately 0.3 times the maximum recommended human dose (mrhd) on a body surface area basis). in an embryo-fetal development study in pregnant rabbits dosed during the period of organogenesis on gestation days 6 to 18, there was an increase in maternal abortion, and effects on fetal development and reduction in litter weights at subcutaneous doses from approximately 25 mcg/kg (approximately 0.03 times the mrhd on a body surface area basis). maternal toxicity, including reduction in body weight gain, was observed at subcutaneous doses of 5 mcg/kg in rabbits (approximately 0.006 times the maximum recommended human dose on a body surface area basis) and 500 mcg/kg in rats (approximately 0.3 times the maximum recommended human dose on a body surface area basis). in a peri- and post-natal development study, subcutaneous treatment of pregnant rats with budesonide during the period from day 15 post coitum to day 21 post partum, budesonide had no effects on delivery, but did have an effect on growth and development of offspring. in addition, offspring survival was reduced and surviving offspring had decreased mean body weights at birth and during lactation at exposures ≥ 0.012 times the mrhd (on a mg/m 2 basis at maternal subcutaneous doses of 20 mcg/kg/day and higher). these findings occurred in the presence of maternal toxicity.

mg to healthy subjects, the average geometric mean c max (cv%) was 4.4 ng/ml (58.3), and auc 0-24 was 24.1 h*ng/ml (49.7). median t lag (min, max) was 3.1 h (0, 6) while median t max (min, max) was 5.1 h (4.5, 10). food effect there was no clinically relevant food effect observed on the overall systemic exposure of budesonide when either a moderate or high fat meal was consumed 1 hour after administration of tarpeyo. distribution approximately 85 to 90% of budesonide binds to plasma proteins in blood over the concentration range of 0.43 to 99 ng/ml. the volume of distribution at steady state reported in the literature is 3 to 4 l/kg. metabolism budesonide is metabolized by the liver (and to lesser extent the gut), primarily by oxidative pathways via cyp3a4 to two main metabolites, 16α-hydroxyprednisolone and 6β-hydroxybudesonide, which have less than 1% of the corticosteroid activity of budesonide. elimination budesonide had a high plasma clearance, 0.9 to 1.8 l/min in healthy adults, which is close to the estimated liver blood flow, and, accordingly, suggests that budesonide is a high hepatic clearance drug. following single oral administration of tarpeyo 16 mg to healthy subjects, the elimination half-life (t½) for tarpeyo ranged from 5.0 to 6.8 hours. excretion budesonide was excreted in urine and feces in the form of metabolites. after oral as well as intravenous administration of micronized [ 3 h]-budesonide, approximately 60% of the recovered radioactivity was found in urine. the major metabolites, including 16α-hydroxyprednisolone and 6β-hydroxybudesonide, are mainly renally excreted, intact or in conjugated forms. no unchanged budesonide was detected in urine. specific populations age, race, and body weight the effect of age, race, and body weight on the pharmacokinetics of tarpeyo has not been established. sex of the 143 healthy volunteers included in the phase 1 studies, 29% were female. pharmacokinetics of budesonide was similar between males and females. hepatic impairment subjects with moderate hepatic impairment (child-pugh class b) had 3.5 times the budesonide auc compared with healthy volunteers while subjects with mild hepatic impairment (child-pugh class a) had approximately 40% higher budesonide auc compared with healthy volunteers. patients with severe hepatic impairment (child-pugh class c) have not been studied. renal impairment intact budesonide is not excreted renally. the main metabolites of budesonide, which have negligible corticosteroid activity, are largely (60%) excreted in urine. drug interaction studies budesonide is metabolized via cyp3a4. potent inhibitors of cyp3a4 can increase plasma levels of budesonide. thus, clinically relevant drug interactions with potent cyp3a inhibitors, such as ketoconazole, itraconazole, ritonavir, indinavir, saquinavir, erythromycin, cyclosporine, and grapefruit juice, are to be expected. conversely, induction of cyp3a4 potentially could result in the lowering of budesonide plasma concentrations. effects of other drugs on budesonide ketoconazole in an open, non-randomized, cross-over study, 6 healthy subjects were given budesonide 10 mg as a single dose, either alone or concomitantly with the last ketoconazole dose of 3 days treatment with ketoconazole 100 mg twice daily. co-administration of ketoconazole resulted in 8-fold the auc of budesonide, compared to budesonide alone. in an open, randomized, cross-over study 8 healthy subjects were given entocort ec 3 mg as a single dose, either alone or concomitantly with the last ketoconazole dose of 4 days treatment with ketoconazole 200 mg once daily. co-administration of ketoconazole resulted in 6.5-fold the auc of budesonide, compared to budesonide alone. grapefruit juice in an open, randomized, cross-over study, 8 healthy subjects were given entocort ec 3 mg, either alone, or concomitantly with 600 ml concentrated grapefruit juice (which inhibits cyp3a4 activity predominantly in the intestinal mucosa), on the last of 4 daily administrations. concomitant administration of grapefruit juice resulted in doubling the bioavailability of budesonide compared to budesonide alone. proton pump inhibitors the pharmacokinetics of tarpeyo have not been evaluated in combination with proton pump inhibitors (ppis). since the disintegration of tarpeyo is ph dependent, the release properties and uptake of budesonide may be altered when tarpeyo is taken after treatment with ppis. in a study assessing intragastric and intraduodenal ph in healthy volunteers after repeated dosing with the ppi omeprazole 40 mg once daily, intragastric and intraduodenal ph did not exceed that required for disintegration of tarpeyo. beyond the duodenum, ppis such as omeprazole are unlikely to affect ph. oral contraceptives (cyp3a4 substrates) in a parallel study, the pharmacokinetics of budesonide were not significantly different between healthy female subjects who received oral contraceptives containing desogestrel 0.15 mg and ethinyl estradiol 30 μg and healthy female subjects who did not receive oral contraceptives. budesonide 4.5 mg once daily for one week did not affect the plasma concentrations of ethinyl estradiol, a cyp3a4 substrate. the effect of budesonide 16 mg once daily on the plasma concentrations of desogestrel and ethinyl estradiol was not studied.

. elimination budesonide had a high plasma clearance, 0.9 to 1.8 l/min in healthy adults, which is close to the estimated liver blood flow, and, accordingly, suggests that budesonide is a high hepatic clearance drug. following single oral administration of tarpeyo 16 mg to healthy subjects, the elimination half-life (t½) for tarpeyo ranged from 5.0 to 6.8 hours. excretion budesonide was excreted in urine and feces in the form of metabolites. after oral as well as intravenous administration of micronized [ 3 h]-budesonide, approximately 60% of the recovered radioactivity was found in urine. the major metabolites, including 16α-hydroxyprednisolone and 6β-hydroxybudesonide, are mainly renally excreted, intact or in conjugated forms. no unchanged budesonide was detected in urine. specific populations age, race, and body weight the effect of age, race, and body weight on the pharmacokinetics of tarpeyo has not been established. sex of the 143 healthy volunteers included in the phase 1 studies, 29% were female. pharmacokinetics of budesonide was similar between males and females. hepatic impairment subjects with moderate hepatic impairment (child-pugh class b) had 3.5 times the budesonide auc compared with healthy volunteers while subjects with mild hepatic impairment (child-pugh class a) had approximately 40% higher budesonide auc compared with healthy volunteers. patients with severe hepatic impairment (child-pugh class c) have not been studied. renal impairment intact budesonide is not excreted renally. the main metabolites of budesonide, which have negligible corticosteroid activity, are largely (60%) excreted in urine. drug interaction studies budesonide is metabolized via cyp3a4. potent inhibitors of cyp3a4 can increase plasma levels of budesonide. thus, clinically relevant drug interactions with potent cyp3a inhibitors, such as ketoconazole, itraconazole, ritonavir, indinavir, saquinavir, erythromycin, cyclosporine, and grapefruit juice, are to be expected. conversely, induction of cyp3a4 potentially could result in the lowering of budesonide plasma concentrations. effects of other drugs on budesonide ketoconazole in an open, non-randomized, cross-over study, 6 healthy subjects were given budesonide 10 mg as a single dose, either alone or concomitantly with the last ketoconazole dose of 3 days treatment with ketoconazole 100 mg twice daily. co-administration of ketoconazole resulted in 8-fold the auc of budesonide, compared to budesonide alone. in an open, randomized, cross-over study 8 healthy subjects were given entocort ec 3 mg as a single dose, either alone or concomitantly with the last ketoconazole dose of 4 days treatment with ketoconazole 200 mg once daily. co-administration of ketoconazole resulted in 6.5-fold the auc of budesonide, compared to budesonide alone. grapefruit juice in an open, randomized, cross-over study, 8 healthy subjects were given entocort ec 3 mg, either alone, or concomitantly with 600 ml concentrated grapefruit juice (which inhibits cyp3a4 activity predominantly in the intestinal mucosa), on the last of 4 daily administrations. concomitant administration of grapefruit juice resulted in doubling the bioavailability of budesonide compared to budesonide alone. proton pump inhibitors the pharmacokinetics of tarpeyo have not been evaluated in combination with proton pump inhibitors (ppis). since the disintegration of tarpeyo is ph dependent, the release properties and uptake of budesonide may be altered when tarpeyo is taken after treatment with ppis. in a study assessing intragastric and intraduodenal ph in healthy volunteers after repeated dosing with the ppi omeprazole 40 mg once daily, intragastric and intraduodenal ph did not exceed that required for disintegration of tarpeyo. beyond the duodenum, ppis such as omeprazole are unlikely to affect ph. oral contraceptives (cyp3a4 substrates) in a parallel study, the pharmacokinetics of budesonide were not significantly different between healthy female subjects who received oral contraceptives containing desogestrel 0.15 mg and ethinyl estradiol 30 μg and healthy female subjects who did not receive oral contraceptives. budesonide 4.5 mg once daily for one week did not affect the plasma concentrations of ethinyl estradiol, a cyp3a4 substrate. the effect of budesonide 16 mg once daily on the plasma concentrations of desogestrel and ethinyl estradiol was not studied.

e of hepatocellular tumors at an oral dose of 50 mcg/kg (approximately 0.03 times the mrhd of a body surface area basis). the concurrent reference corticosteroids (prednisolone and triamcinolone acetonide) showed similar findings. in a 91-week study in mice, budesonide caused no treatment-related carcinogenicity at oral doses up to 200 mcg/kg (approximately 0.06 times the mrhd on a body surface area basis). budesonide was not genotoxic in the ames text, the mouse lymphoma cell forward gene mutation (tk +/- ) test, the human lymphocyte chromosome aberration test, the drosophila melanogaster sex-linked recessive lethal test, the rat hepatocyte uds test and the mouse micronucleus test. in rats, budesonide had no effect on fertility at subcutaneous doses up to 80 mcg/kg (approximately 0.05 times the mrhd on a body surface area basis). however, it caused a decrease in prenatal viability and viability in pups at birth and during lactation, along with a decrease in maternal food consumption and body weight gain, at subcutaneous doses of 20 mcg/kg (approximately 0.012 times the mrhd on a body surface area basis) and above. no such effects were noted at 5 mcg/kg (approximately 0.003 times the mrhd on a body surface area basis).

at an oral dose of 50 mcg/kg (approximately 0.03 times the mrhd of a body surface area basis). the concurrent reference corticosteroids (prednisolone and triamcinolone acetonide) showed similar findings. in a 91-week study in mice, budesonide caused no treatment-related carcinogenicity at oral doses up to 200 mcg/kg (approximately 0.06 times the mrhd on a body surface area basis). budesonide was not genotoxic in the ames text, the mouse lymphoma cell forward gene mutation (tk +/- ) test, the human lymphocyte chromosome aberration test, the drosophila melanogaster sex-linked recessive lethal test, the rat hepatocyte uds test and the mouse micronucleus test. in rats, budesonide had no effect on fertility at subcutaneous doses up to 80 mcg/kg (approximately 0.05 times the mrhd on a body surface area basis). however, it caused a decrease in prenatal viability and viability in pups at birth and during lactation, along with a decrease in maternal food consumption and body weight gain, at subcutaneous doses of 20 mcg/kg (approximately 0.012 times the mrhd on a body surface area basis) and above. no such effects were noted at 5 mcg/kg (approximately 0.003 times the mrhd on a body surface area basis).

73 m 2 . the mean baseline upcr was 1.6 g/g and 25% of patients had proteinuria >3.5 g/24 hours. approximately 73% of patients had a history of hypertension and 5% had a history of type 2 diabetes mellitus. at baseline, 98% were treated with an ace inhibitor or arb and <1% of patients were on an sglt2 inhibitor. the primary endpoint was the percentage reduction in upcr at 9 months compared to baseline. the results are shown in table 2 . table 2: analysis of the primary efficacy endpoint at 9 months in phase 3 study nef-301 a all patients with a upcr reading regardless of use of prohibited medication at 9 months. b adjusted geometric least squares mean ratio of upcr relative to baseline were based on a longitudinal repeated measures model. c the estimate of the ratio of geometric mean ratio of upcr relative to baseline comparing tarpeyo 16 mg with placebo was reported as percentage reduction along with the respective 95% confidence interval from the longitudinal repeated measures model and p-values. ci: confidence interval; upcr: urine protein creatinine ratio. primary endpoint: upcr g/g a tarpeyo 16 mg (n=97) placebo (n=102) percentage reduction from baseline (adjusted for baseline) b 34% 5% tarpeyo 16 mg versus placebo : percentage reduction (95% ci) c ; 2-sided p-value 31% (16% to 42%); p=0.0001 the treatment effect for the upcr endpoint at 9 months were consistent across key subgroups, including key demographic (such as age, sex, race) and baseline disease (such as baseline proteinuria) characteristics.

d, crushed or broken and to take tarpeyo in the morning, at least 1 hour before a meal [see dosage and administration ( 2 )]. advise patients to avoid the consumption of grapefruit juice for the duration of their tarpeyo therapy [see drug interactions ( 7.1 )]. tarpeyo is a trademark of calliditas therapeutics ab, or its affiliates. © 2021 calliditas therapeutics ab (publ) manufactured for and distributed by: calliditas therapeutics ab stockholm, sweden patent: http://www.calliditas.com/patents

family history of diabetes or glaucoma. have or have had tuberculosis. have high blood pressure (hypertension). have decreased bone mineral density (osteoporosis). have stomach ulcers. are pregnant or plan to become pregnant. tarpeyo may harm your unborn baby. talk to your healthcare provider about the possible risk to your unborn baby if you take tarpeyo when you are pregnant. are breastfeeding or plan to breastfeed. it is not known if tarpeyo passes into your breast milk or if it will affect your baby. talk to your healthcare provider about the best way to feed your baby during treatment with tarpeyo. tell your healthcare provider about all the medicines you take, including prescription and over-the-counter medicines, vitamins, and herbal supplements. tarpeyo and other medicines may affect each other causing side effects. how should i take tarpeyo? take tarpeyo exactly as your healthcare provider tells you. your healthcare provider will decide how long you should take tarpeyo. do not stop taking tarpeyo without first talking with your healthcare provider. take your prescribed dose of tarpeyo 1 time each day in the morning, at least 1 hour before a meal. take tarpeyo capsules whole. do not open, chew, crush, or break tarpeyo capsules before swallowing. if you miss a dose of tarpeyo, take your prescribed dose at your next scheduled time. do not take two doses of tarpeyo at the same time. if you take too much tarpeyo, call your healthcare provider right away or go to the nearest hospital emergency room. what should i avoid while taking tarpeyo? do not eat grapefruit or drink grapefruit juice during your treatment with tarpeyo. eating grapefruit or drinking grapefruit juice can increase the level of tarpeyo in your blood. what are the possible side effects of tarpeyo? tarpeyo may cause serious side effects, including: effects of having too much corticosteroid medicine in your blood (hypercorticism). long-time use of tarpeyo can cause you to have signs and symptoms of too much cortisol, a stress hormone in your blood. tell your healthcare provider if you have any of the following signs and symptoms of hypercorticism: acne bruise easily rounding of your face (moon face) ankle swelling thicker or more hair on your body and face a fatty pad or hump between your shoulders (buffalo hump) pink or purple stretch marks on the skin of your abdomen, thighs, breasts, or arms adrenal suppression. when tarpeyo is taken for a long period of time (chronic use), adrenal suppression can happen. this is a condition in which the adrenal glands do not make enough steroid hormones. symptoms of adrenal suppression include: tiredness weakness nausea and vomiting low blood pressure tell your healthcare provider if you are under stress or have any symptoms of adrenal suppression during treatment with tarpeyo. risk of immunosuppression. tarpeyo weakens your immune system. taking medicines that weaken your immune system makes you more likely to get infections. avoid contact with people who have contagious diseases, such as chickenpox or measles, during treatment with tarpeyo. tell your healthcare provider right away if you come in contact with anyone who has chickenpox or measles. consult with your healthcare provider regarding appropriate vaccination scheduling. tell your healthcare provider if you develop any symptoms of infection during treatment with tarpeyo, including: fever feeling tired chills aches pain nausea and vomiting the most common side effects of tarpeyo include: high blood pressure swelling of the lower legs, ankles, and feet muscle cramp acne irritation or inflammation of the skin weight increase shortness of breath swelling of the face indigestion tiredness thicker or more hair on your body and face these are not all the possible side effects of tarpeyo. call your doctor for medical advice about side effects. you may report side effects to fda at 1-800-fda-1088. how should i store tarpeyo? store tarpeyo at room temperature between 68°f to 77°f (20°c to 25°c). keep tarpeyo in a tightly closed container. protect from moisture. keep tarpeyo and all medicines out of the reach of children. general information about the safe and effective use of tarpeyo. medicines are sometimes prescribed for purposes other than those listed in a patient information leaflet. do not use tarpeyo for a condition for which it was not prescribed. do not give tarpeyo to other people, even if they have the same symptoms you have. it may harm them. you can ask your pharmacist or healthcare provider for information about tarpeyo that is written for health professionals. what are the ingredients in tarpeyo? active ingredient: budesonide inactive ingredients: sugar spheres (sucrose and starch), hypromellose, polyethylene glycol, citric acid monohydrate, ethyl cellulose, medium chain triglycerides and oleic acid. the capsules contain: hypromellose and titanium oxide (e171). the printing ink on the capsules contain: shellac, propylene glycol and black iron oxide (e172). the enteric coating on the capsules contain: methacrylic acid and methacrylate copolymer, talc and dibutyl sebacate. manufactured for and distributed by: calliditas therapeutics ab, stockholm, sweden tarpeyo is a trademark of calliditas therapeutics ab, or its affiliates. © 2021 calliditas therapeutics ab (publ) patent: http://www.calliditas.com/patents for more information, go to www.tarpeyotouchpoints.com or call 1-933-444-8277.