美国 - 英文 - NLM (National Library of Medicine)

golden state medical supply, inc. - clonazepam (unii: 5pe9fde8gb) (clonazepam - unii:5pe9fde8gb) - clonazepam 0.5 mg - seizure disorders: clonazepam tablets, usp are useful alone or as an adjunct in the treatment of the lennox-gastaut syndrome (petit mal variant), akinetic, and myoclonic seizures. in patients with absence seizures (petit mal) who have failed to respond to succinimides, clonazepam may be useful. some loss of effect may occur during the course of clonazepam treatment (see precautions:  loss of effect ). panic disorder: clonazepam tablets, usp are indicated for the treatment of panic disorder, with or without agoraphobia, as defined in dsm-v. panic disorder is characterized by the occurrence of unexpected panic attacks and associated concern about having additional attacks, worry about the implications or consequences of the attacks, and/or a significant change in behavior related to the attacks. the efficacy of clonazepam was established in two 6- to 9-week trials in panic disorder patients whose diagnoses corresponded to the dsm-iiir category of panic disorder (see

美国 - 英文 - NLM (National Library of Medicine)

golden state medical supply, inc. - bupropion hydrochloride (unii: zg7e5poy8o) (bupropion - unii:01zg3tpx31) - bupropion hydrochloride 100 mg - bupropion hydrochloride extended-release tablets (sr) are indicated for the treatment of major depressive disorder (mdd), as defined by the diagnostic and statistical manual (dsm ) . the efficacy of bupropion in the treatment of a major depressive episode was established in two 4-week controlled inpatient trials and one 6-week controlled outpatient trial of adult subjects with mdd [see clinical studies ( 14)] . the efficacy of bupropion in maintaining an antidepressant response for up to 44 weeks following 8 weeks of acute treatment was demonstrated in a placebo-controlled trial [see clinical studies ( 14)] . - bupropion hydrochloride extended-release tablets (sr) are contraindicated in patients with a seizure disorder. - bupropion hydrochloride extended-release tablets (sr) are contraindicated in patients with a current or prior diagnosis of bulimia or anorexia nervosa as a higher incidence of seizures was observed

美国 - 英文 - NLM (National Library of Medicine)

golden state medical supply, inc. - alendronate sodium (unii: 2uy4m2u3ra) (alendronic acid - unii:x1j18r4w8p) - alendronic acid 35 mg - alendronate sodium tablets, usp are indicated for the treatment of osteoporosis in postmenopausal women. in postmenopausal women, alendronate sodium tablets, usp increase bone mass and reduces the incidence of fractures, including those of the hip and spine (vertebral compression fractures). [see clinical studies (14.1).] alendronate sodium tablets, usp are indicated for the prevention of postmenopausal osteoporosis [see clinical studies (14.2)] . alendronate sodium tablets, usp are indicated for treatment to increase bone mass in men with osteoporosis [see clinical studies (14.3)] . alendronate sodium tablets, usp are indicated for the treatment of glucocorticoid-induced osteoporosis in men and women receiving glucocorticoids in a daily dosage equivale

美国 - 英文 - NLM (National Library of Medicine)

golden state medical supply, inc. - diclofenac potassium (unii: l4d5ua6cb4) (diclofenac - unii:144o8ql0l1) - carefully consider the potential benefits and risks of diclofenac potassium tablets and other treatment options before deciding to use diclofenac potassium tablets. use the lowest effective dose for the shortest duration consistent with individual patient treatment goals (see warnings: gastrointestinal bleeding, ulceration, and perforation). diclofenac potassium tablets are indicated: - for treatment of primary dysmenorrhea - for relief of mild to moderate pain - for relief of the signs and symptoms of osteoarthritis - for relief of the signs and symptoms of rheumatoid arthritis diclofenac potassium tablets are contraindicated in the following patients: - known hypersensitivity (e.g., anaphylactic reactions and serious skin reactions) to diclofenac or any components of the drug product (see warnings: anaphylactic reactions, serious skin reactions). - history of asthma, urticaria, or allergic-type reactions after taking aspirin or other nsaids. severe, sometimes fat

美国 - 英文 - NLM (National Library of Medicine)

golden state medical supply, inc. - tamoxifen citrate (unii: 7frv7310n6) (tamoxifen - unii:094zi81y45) - tamoxifen citrate tablets are effective in the treatment of metastatic breast cancer in women and men. in premenopausal women with metastatic breast cancer, tamoxifen is an alternative to oophorectomy or ovarian irradiation. available evidence indicates that patients whose tumors are estrogen receptor positive are more likely to benefit from tamoxifen therapy. tamoxifen citrate tablets are indicated for the treatment of node-positive breast cancer in women following total mastectomy or segmental mastectomy, axillary dissection, and breast irradiation. in some tamoxifen adjuvant studies, most of the benefit to date has been in the subgroup with four or more positive axillary nodes. tamoxifen citrate tablets are indicated for the treatment of axillary node-negative breast cancer in women following total mastectomy or segmental mastectomy, axillary dissection, and breast irradiation. the estrogen and progesterone receptor values may help to predict whether adjuvant tamoxifen therapy is likely to be beneficial. tamoxifen reduces the occurrence of contralateral breast cancer in patients receiving adjuvant tamoxifen therapy for breast cancer. in women with dcis, following breast surgery and radiation, tamoxifen citrate tablets are indicated to reduce the risk of invasive breast cancer (see boxed warning at the beginning of the label). the decision regarding therapy with tamoxifen for the reduction in breast cancer incidence should be based upon an individual assessment of the benefits and risks of tamoxifen therapy. current data from clinical trials support 5 years of adjuvant tamoxifen therapy for patients with breast cancer. tamoxifen citrate tablets are indicated to reduce the incidence of breast cancer in women at high risk for breast cancer. this effect was shown in a study of 5 years planned duration with a median follow-up of 4.2 years. twenty-five percent of the participants received drug for 5 years. the longer-term effects are not known. in this study, there was no impact of tamoxifen on overall or breast cancer-related mortality (see boxed warning at the beginning of the label). tamoxifen citrate tablets are indicated only for high-risk women. "high risk" is defined as women at least 35 years of age with a 5 year predicted risk of breast cancer ≥ 1.67%, as calculated by the gail model. examples of combinations of factors predicting a 5 year risk ≥ 1.67% are: age 35 or older and any of the following combination of factors: - one first degree relative with a history of breast cancer, 2 or more benign biopsies, and a history of a breast biopsy showing atypical hyperplasia; or - at least 2 first degree relatives with a history of breast cancer, and a personal history of at least 1 breast biopsy; or - lcis age 40 or older and any of the following combination of factors: - one first degree relative with a history of breast cancer, 2 or more benign biopsies, age at first live birth 25 or older, and age at menarche 11 or younger; or - at least 2 first degree relatives with a history of breast cancer, and age at first live birth 19 or younger; or - one first degree relative with a history of breast cancer, and a personal history of a breast biopsy showing atypical hyperplasia. age 45 or older and any of the following combination of factors: - at least 2 first degree relatives with a history of breast cancer and age at first live birth 24 or younger; or - one first degree relative with a history of breast cancer with a personal history of a benign breast biopsy, age at menarche 11 or less and age at first live birth 20 or more. age 50 or older and any of the following combination of factors: - at least 2 first degree relatives with a history of breast cancer; or - history of 1 breast biopsy showing atypical hyperplasia, and age at first live birth 30 or older and age at menarche 11 or less; or - history of at least 2 breast biopsies with a history of atypical hyperplasia, and age at first live birth 30 or more. age 55 or older and any of the following combination of factors: - one first degree relative with a history of breast cancer with a personal history of a benign breast biopsy, and age at menarche 11 or less; or - history of at least 2 breast biopsies with a history of atypical hyperplasia, and age at first live birth 20 or older. age 60 or older and: - five-year predicted risk of breast cancer ≥ 1.67%, as calculated by the gail model. for women whose risk factors are not described in the above examples, the gail model is necessary to estimate absolute breast cancer risk. health care professionals can obtain a gail model risk assessment tool by dialing 1-844-825-8500. there are insufficient data available regarding the effect of tamoxifen on breast cancer incidence in women with inherited mutations (brca1, brca2) to be able to make specific recommendations on the effectiveness of tamoxifen in these patients. after an assessment of the risk of developing breast cancer, the decision regarding therapy with tamoxifen for the reduction in breast cancer incidence should be based upon an individual assessment of the benefits and risks of tamoxifen therapy. in the nsabp p-1 trial, tamoxifen treatment lowered the risk of developing breast cancer during the follow-up period of the trial, but did not eliminate breast cancer risk (see table 3 in clinical pharmacology ). tamoxifen citrate tablets are contraindicated in patients with known hypersensitivity to the drug or any of its ingredients. tamoxifen citrate tablets are contraindicated in women who require concomitant coumarin-type anticoagulant therapy or in women with a history of deep-vein thrombosis or pulmonary embolus.

美国 - 英文 - NLM (National Library of Medicine)

golden state medical supply, inc. - dexlansoprazole (unii: uye4t5i70x) (dexlansoprazole - unii:uye4t5i70x) - dexlansoprazole delayed-release capsules are indicated in patients 12 years of age and older for healing of all grades of erosive esophagitis (ee) for up to eight weeks. dexlansoprazole delayed-release capsules are indicated in patients 12 years of age and older to maintain healing of ee and relief of heartburn for up to six months in adults and 16 weeks in patients 12 to 17 years of age. dexlansoprazole delayed-release capsules are indicated in patients 12 years of age and older for the treatment of heartburn associated with symptomatic non-erosive gastroesophageal reflux disease (gerd) for four weeks. - dexlansoprazole delayed-release capsules are contraindicated in patients with known hypersensitivity to any component of the formulation [see description (11)] . hypersensitivity reactions may include anaphylaxis, anaphylactic shock, angioedema, bronchospasm, acute tubulointerstitial nephritis and urticaria [see warnings and precautions (5.2), adverse reactions (6)] . - ppis, including dexlansoprazole delayed-release capsules, are contraindicated with rilpivirine-containing products [see drug interactions (7)] . risk summary there are no studies with dexlansoprazole use in pregnant women to inform a drug-associated risk. dexlansoprazole is the r-enantiomer of lansoprazole, and published observational studies of lansoprazole use during pregnancy did not demonstrate an association of adverse pregnancy-related outcomes with lansoprazole (see data) . in animal reproduction studies, oral administration of lansoprazole to rats during organogenesis through lactation at 1.8 times the maximum recommended human dexlansoprazole dose produced reductions in the offspring in femur weight, femur length, crown-rump length and growth plate thickness (males only) on postnatal day 21 (see data) . these effects were associated with reduction in body weight gain. advise pregnant women of the potential risk to the fetus. 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 us 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 human data dexlansoprazole is the r-enantiomer of lansoprazole. available data from published observational studies failed to demonstrate an association of adverse pregnancy-related outcomes and lansoprazole use. methodological limitations of these observational studies cannot definitely establish or exclude any drug- associated risk during pregnancy. in a prospective study by the european network of teratology information services, outcomes from a group of 62 pregnant women administered median daily doses of 30 mg of lansoprazole were compared to a control group of 868 pregnant women who did not take any ppis. there was no difference in the rate of major malformations between women exposed to ppis and the control group, corresponding to a relative risk (rr)=1.04, [95% confidence interval (ci) 0.25-4.21]. in a population-based retrospective cohort study covering all live births in denmark from 1996 to 2008, there was no significant increase in major birth defects during analysis of first trimester exposure to lansoprazole in 794 live births. a meta-analysis that compared 1,530 pregnant women exposed to ppis in at least the first trimester with 133,410 unexposed pregnant women showed no significant increases in risk for congenital malformations or spontaneous abortion with exposure to ppis (for major malformations odds ratio (or)=1.12, [95% ci 0.86- 1.45] and for spontaneous abortions or=1.29, [95% ci 0.84-1.97]). animal data an embryo-fetal development study conducted in rabbits at oral dexlansoprazole doses up to 30 mg/kg/day (approximately nine times the maximum recommended human dexlansoprazole dose [60 mg/day] based on body surface area) during organogenesis showed no effects on fetuses due to dexlansoprazole. in addition, embryo-fetal development studies performed in rats with oral lansoprazole at doses up to 150 mg/kg/day (40 times the recommended human lansoprazole dose based on body surface area) during organogenesis and in rabbits with oral lansoprazole at doses up to 30 mg/kg/day (16 times the recommended human lansoprazole dose based on body surface area) during organogenesis revealed no effects on fetuses due to lansoprazole. a pre- and postnatal developmental toxicity study in rats with additional endpoints to evaluate bone development was performed with lansoprazole at oral doses of 10 to 100 mg/kg/day (0.2 to 1.8 times the maximum recommended human dexlansoprazole dose of 60 mg based on dexlansoprazole auc [area under the plasma concentration-time curve]) administered during organogenesis through lactation. maternal effects observed at 100 mg/kg/day (1.8 times the maximum recommended human dexlansoprazole dose of 60 mg based on dexlansoprazole auc) included increased gestation period, decreased body weight gain during gestation, and decreased food consumption. the number of stillbirths was increased at this dose, which may have been secondary to maternal toxicity. body weight of pups was reduced at 100 mg/kg/day starting on postnatal day 11. femur weight, femur length, and crown-rump length were reduced at 100 mg/kg/day on postnatal day 21. femur weight was still decreased in the 100 mg/kg/day group at age 17 to 18 weeks. growth plate thickness was decreased in the 100 mg/kg/day males on postnatal day 21, and was increased in the 30 and 100 mg/kg/day males at age 17 to 18 weeks. the effects on bone parameters were associated with reduction in body weight gain. risk summary there is no information regarding the presence of dexlansoprazole in human milk, the effects on the breastfed infant, or the effects on milk production. however, lansoprazole and its metabolites are present in rat milk . the developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for dexlansoprazole delayed-release capsules and any potential adverse effects on the breastfed child from dexlansoprazole delayed-release capsules or from the underlying maternal condition. the safety and effectiveness of dexlansoprazole delayed-release capsules have been established in pediatric patients 12 years to 17 years of age for the healing of all grades of ee, the maintenance of healed ee and relief of heartburn, and treatment of heartburn associated with symptomatic non-erosive gerd. use of dexlansoprazole delayed-release capsules in this age group is supported by evidence from adequate and well-controlled studies of dexlansoprazole delayed-release capsules in adults with additional safety, efficacy and pharmacokinetic data in pediatric patients 12 to 17 years of age. the adverse reaction profile in patients 12 to 17 years of age was similar to adults [see dosage and administration (2.1), adverse reactions (6.1), clinical pharmacology (12.3), clinical studies (14)] . the safety and effectiveness of dexlansoprazole delayed-release capsules has not been established in pediatric patients less than 12 years of age. dexlansoprazole delayed-release capsules are not recommended in pediatric patients less than two years of age [see warnings and precautions (5.12)] . nonclinical studies in juvenile rats treated with lansoprazole (the racemic mixture) have demonstrated adverse effects of heart valve thickening and bone changes at dexlansoprazole exposures which are expected to be similar to or higher than the dexlansoprazole exposure in pediatric patients one year to two years of age, as described below in juvenile animal toxicity data . the use of dexlansoprazole delayed-release capsules is not recommended for the treatment of symptomatic gerd in pediatric patients one month to less than one year of age because lansoprazole was not shown to be effective in a multicenter, double-blind controlled trial. juvenile animal toxicity data heart valve thickening in two oral toxicity studies, thickening of the mitral heart valve occurred in juvenile rats treated with lansoprazole. heart valve thickening was observed primarily with oral dosing initiated on postnatal day 7 (age equivalent to neonatal humans) and postnatal day 14 (human age equivalent of approximately one year) at doses of 250 mg/kg/day and higher (at postnatal day 7 and postnatal day 14 respectively, 2.5 and 1.8 times the expected dexlansoprazole exposure based on auc in pediatric patients one year to two years of age). the treatment durations associated with heart valve thickening ranged from 5 days to 8 weeks. the findings reversed or trended towards reversibility after a 4-week drug-free recovery period. the incidence of heart valve thickening after initiation of dosing on postnatal day 21 (human age equivalent of approximately two years) was limited to a single rat (1/24) in groups given 500 mg/kg/day for 4 or 8 weeks (2.1 times the expected dexlansoprazole exposure based on auc in pediatric patients one year to two years of age). based on the low incidence of heart valve thickening in 21-day old rats and the equivalent human age, the risk of heart valve injury does not appear to be relevant to patients two years of age and older. bone changes in an eight-week oral toxicity study of lansoprazole in juvenile rats with dosing initiated on postnatal day 7, doses equal to or greater than 100 mg/kg/day (dexlansoprazole exposure based on auc approximately equal to that in pediatric patients one year to two years of age) produced delayed growth, with impairment of weight gain observed as early as postnatal day 10 (age equivalent to neonatal humans). at the end of treatment, the signs of impaired growth at 100 mg/kg/day and higher included reductions in body weight (14 to 44% compared to controls), absolute weight of multiple organs, femur weight, femur length and crown-rump length. femoral growth plate thickness was reduced only in males and only at the 500 mg/kg/day dose. the effects related to delayed growth persisted through the end of the four-week recovery period. longer term data were not collected. of the total number of patients (n=4548) in clinical studies of dexlansoprazole delayed-release capsules, 11% of patients were aged 65 years and over, while 2% were 75 years and over. no overall differences in safety or effectiveness were observed between these patients and younger patients and other reported clinical experience has not identified significant differences in responses between geriatric and younger patients, but greater sensitivity of some older individuals cannot be ruled out [see clinical pharmacology (12.3)] . no dosage adjustment for dexlansoprazole delayed-release capsules is necessary for patients with mild hepatic impairment (child-pugh class a). in a study of adult patients with moderate hepatic impairment (child-pugh class b) who received a single dose of 60 mg dexlansoprazole delayed-release capsules, there was a significant increase in systemic exposure of dexlansoprazole compared to healthy subjects with normal hepatic function [see clinical pharmacology (12.3)] . therefore, for patients with moderate hepatic impairment (child-pugh class b), dosage reduction is recommended for the healing of ee [see dosage and administration (2.2)]. no studies have been conducted in patients with severe hepatic impairment (child-pugh class c); the use of dexlansoprazole delayed-release capsules is not recommended for these patients [see dosage and administration (2.2)] . taking dexlansoprazole delayed-release capsules with applesauce: - place 1 tablespoon of applesauce into a clean container. - carefully open the capsule and sprinkle the granules onto the applesauce. - swallow the applesauce and granules right away. do not chew the granules. do not save the applesauce and granules for later use. giving dexlansoprazole delayed-release capsules with water using an oral syringe: - place 20 ml of water into a clean container. - carefully open the capsule and empty the granules into the container of water. - use an oral syringe to draw up the water and granule mixture. - gently swirl the oral syringe to keep the granules from settling. - place the tip of the oral syringe in your mouth. give the medicine right away. do not save the water and granule mixture for later use. - refill the syringe with 10 ml of water and swirl gently. place the tip of the oral syringe in your mouth and give the medicine that is left in the syringe. - repeat step 6. giving dexlansoprazole delayed-release capsules with water through a nasogastric tube (ng tube): for people who have an ng tube that is size 16 french or larger , dexlansoprazole delayed-release capsules may be given as follows: - place 20 ml of water into a clean container. - carefully open the capsule and empty the granules into the container of water. - use a 60 ml catheter-tip syringe to draw up the water and granule mixture. - gently swirl the catheter-tip syringe to keep the granules from settling. - connect the catheter-tip syringe to the ng tube. - give the mixture right away through the ng tube that goes into the stomach. do not save the water and granule mixture for later use. - refill the catheter-tip syringe with 10 ml of water and swirl gently. flush the ng tube with the water. - repeat step 7. how should i store dexlansoprazole delayed-release capsules? - store dexlansoprazole delayed-release capsules at room temperature between 68°f to 77°f (20°c to 25°c). keep dexlansoprazole delayed-release capsules and all medicines out of the reach of children. manufactured for: twi pharmaceuticals usa, inc. paramus, nj 07652 this instructions for use have been approved by the u.s. food and drug administration. manufactured by: twi pharmaceuticals, inc. taoyuan city, 320023, taiwan revised: 07/2023 all trademark names are the property of their respective owners. marketed by: gsms, inc. camarillo, ca 93012 usa

美国 - 英文 - NLM (National Library of Medicine)

golden state medical supply, inc. - citalopram hydrobromide (unii: i1e9d14f36) (citalopram - unii:0dhu5b8d6v) - citalopram 10 mg - citalopram tablets are indicated for the treatment of major depressive disorder (mdd) in adults [see clinical studies (14)]. citalopram tablets are contraindicated in patients: - taking, or within 14 days of stopping, maois (including maois such as linezolid or intravenous methylene blue) because of an increased risk of serotonin syndrome [see warnings and precautions (5.3), drug interactions (7)]. - taking pimozide because of risk of qt prolongation [see drug interactions (7)]. - with known hypersensitivity to citalopram or any of the inactive ingredients in citalopram tablets. reactions have included angioedema and anaphylaxis [see adverse reactions (6.2)]. there is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to antidepressants during pregnancy. healthcare providers are encouraged to register patients by calling the national pregnancy registry for antidepressants at 1-844-405-6185 or visiting online at https://womensmentalhealth.org/research/pregnancyregistry/antidepressants. available data from published epidemiologic studies and postmarketing reports with citalopram use in pregnancy have not established an increased risk of major birth defects or miscarriage. published studies demonstrated that citalopram levels in both cord blood and amniotic fluid are similar to those observed in maternal serum. there are risks of persistent pulmonary hypertension of the newborn (pphn) (see data) and/or poor neonatal adaptation with exposure to selective serotonin reuptake inhibitors (ssris), including citalopram, during pregnancy. there also are risks associated with untreated depression in pregnancy (see clinical considerations). in animal reproduction studies, citalopram caused adverse embryo/fetal effects at doses that caused maternal toxicity (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 the clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively. disease-associated maternal and/or embryo/fetal risk women who discontinue antidepressants during pregnancy are more likely to experience a relapse of major depression than women who continue antidepressants. this finding is from a prospective longitudinal study of 201 pregnant women with a history of major depressive disorder who were euthymic and taking antidepressants at the beginning of pregnancy. consider the risk of untreated depression when discontinuing or changing treatment with antidepressant medication during pregnancy and postpartum. fetal/neonatal adverse reactions neonates exposed to citalopram and other ssris late in third trimester have developed complications requiring prolonged hospitalization, respiratory support, and tube feeding. such complications 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 findings are consistent with either a direct toxic effect of 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 (5.3)]. human data exposure during late pregnancy to ssris may have an increased risk for persistent pulmonary hypertension of the newborn (pphn). pphn occurs in 1-2 per 1,000 live births in the general population and is associated with substantial neonatal morbidity and mortality. animal data citalopram was administered orally to pregnant rats during the period of organogenesis at doses of 32, 56, and 112 mg/kg/day, which are approximately 8, 14, and 27 times the maximum recommended human dose (mrhd) of 40 mg, based on mg/m 2 body surface area. citalopram caused maternal toxicity of cns clinical signs and decreased weight gain at 112 mg/kg/day, which is 27 times the mrhd. at this maternally toxic dose, citalopram decreased embryo/fetal growth and survival and increased fetal abnormalities (including cardiovascular and skeletal defects). the no observed adverse effect level (noael) for maternal and embryo fetal toxicity is 56 mg/kg/day, which is approximately 14 times the mrhd. citalopram was administered orally to pregnant rabbits during the period of organogenesis at doses up to 16 mg/kg/day, which is approximately 8 times the mrhd of 40 mg, based on mg/m 2 body surface area. no maternal or embryo fetal toxicity was observed. the noael for maternal and embryo fetal toxicity is 16 mg/kg/day, which is approximately 8 times the mrhd. citalopram was administered orally to pregnant rats during late gestation and lactation periods at doses of 4.8, 12.8, and 32 mg/kg/day, which are approximately 1, 3, and 8 times the mrhd of 40 mg, based on mg/m 2 body surface area. citalopram increased offspring mortality during the first 4 days of birth and decreased offspring growth at 32 mg/kg/day, which is approximately 8 times the mrhd. the noael for developmental toxicity is 12.8 mg/kg/day, which is approximately 3 times the mrhd. in a separate study, similar effects on offspring mortality and growth were seen when dams were treated throughout gestation and early lactation at doses ≥ 24 mg/kg/day, which is approximately 6 times the mrhd. a noael was not determined in that study. data from the published literature report the presence of citalopram in human milk at relative infant doses ranging between 0.7 to 9.4% of the maternal weight-adjusted dosage and a milk/plasma ratio ranging between 0.78 to 4.3. there are reports of breastfed infants exposed to citalopram experiencing irritability, restlessness, excessive somnolence, decreased feeding, and weight loss (see clinical considerations). there is no information about effects of citalopram on milk production. the developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for citalopram tablets and any potential adverse effects on the breastfed child from citalopram tablets or from the underlying maternal condition. monitor breastfeeding infants for adverse reactions, such as irritability, restlessness, excessive somnolence, decreased feeding, and weight loss. the safety and effectiveness of citalopram tablets have not been established in pediatric patients. two placebo-controlled trials in 407 pediatric patients with mdd have been conducted with citalopram tablets, and the data were not sufficient to support use in pediatric patients. antidepressants increase the risk of suicidal thoughts and behaviors in pediatric patients [see boxed warning, warnings and precautions (5.1)]. decreased appetite and weight loss have been observed in association with the use of ssris in pediatric patients. of 4422 patients in clinical studies of citalopram tablets, 1357 were 60 and over, 1034 were 65 and over, and 457 were 75 and over. in two pharmacokinetic studies, citalopram auc was increased by 23% and 30%, respectively, in subjects ≥ 60 years of age as compared to younger subjects, and its half-life was increased by 30% and 50%, respectively [see clinical pharmacology (12.3)]. therefore, the maximum recommended dosage in patients 60 years of age and older is lower than younger patients [see dosage and administration (2.3), warnings and precautions (5.2)]. ssris, including citalopram, have been associated with cases of clinically significant hyponatremia in elderly patients, who may be at greater risk for this adverse reaction [see warnings and precautions (5.9)]. increased citalopram exposure occurs in patients with hepatic impairment. the maximum recommended dosage of citalopram tablets is lower in patients with hepatic impairment [see dosage and administration (2.3), clinical pharmacology (12.3)]. citalopram hydrobromide is not a controlled substance. animal studies suggest that the abuse liability of citalopram tablets is low. citalopram tablets have not been systematically studied in humans for its potential for abuse, tolerance, or physical dependence. the premarketing clinical experience with citalopram tablets did not reveal any drug-seeking behavior. however, these observations were not systematic and it is not possible to predict, on the basis of this limited experience, the extent to which a cns-active drug will be misused, diverted, and/or abused once marketed. consequently, health care providers should carefully evaluate citalopram tablets patients for history of drug abuse and follow such patients closely, observing them for signs of misuse or abuse (e.g., development of tolerance, incrementations of dose, drug-seeking behavior).

美国 - 英文 - NLM (National Library of Medicine)

golden state medical supply, inc. - desvenlafaxine succinate (unii: zb22enf0xr) (desvenlafaxine - unii:ng99554anw) - desvenlafaxine 25 mg - desvenlafaxine extended-release tablets are indicated for the treatment of adults with major depressive disorder (mdd) [see clinical studies ( 14)] . - hypersensitivity to desvenlafaxine succinate, venlafaxine hydrochloride or to any excipients in the desvenlafaxine extended-release tablets formulation. angioedema has been reported in patients treated with desvenlafaxine extended-release tablets [see adverse reactions ( 6.1 )] . - the use of maois intended to treat psychiatric disorders with desvenlafaxine extended-release tablets or within 7 days of stopping treatment with desvenlafaxine extended-release tablets is contraindicated because of an increased risk of serotonin syndrome. the use of desvenlafaxine extended-release tablets within 14 days of stopping an maoi intended to treat psychiatric disorders is also contraindicated [see dosage and administration ( 2.7 ) and warnings and precautions ( 5.2 )] . - starting

美国 - 英文 - NLM (National Library of Medicine)

golden state medical supply, inc. - rabeprazole sodium (unii: 3l36p16u4r) (rabeprazole - unii:32828355ll) - rabeprazole sodium delayed-release tablets are indicated for short-term (4 to 8 weeks) treatment in the healing and symptomatic relief of erosive or ulcerative gastroesophageal reflux disease (gerd). for those patients who have not healed after 8 weeks of treatment, an additional 8-week course of rabeprazole sodium delayed-release tablets may be considered. rabeprazole sodium delayed-release tablets are indicated for maintaining healing and reduction in relapse rates of heartburn symptoms in patients with erosive or ulcerative gastroesophageal reflux disease (gerd maintenance). controlled studies do not extend beyond 12 months. rabeprazole sodium delayed-release tablets are indicated for the treatment of daytime and nighttime heartburn and other symptoms associated with gerd in adults for up to 4 weeks. rabeprazole sodium delayed-release tablets are indicated for short-term (up to four weeks) treatment in the healing and symptomatic relief of duodenal ulcers. most patients heal within four weeks. rabeprazole sodium delayed-release tablets, in combination with amoxicillin and clarithromycin as a three drug regimen, are indicated for the treatment of patients with h. pylori infection and duodenal ulcer disease (active or history within the past 5 years) to eradicate h. pylori . eradication of h. pylori has been shown to reduce the risk of duodenal ulcer recurrence. in patients who fail therapy, susceptibility testing should be done. if resistance to clarithromycin is demonstrated or susceptibility testing is not possible, alternative antimicrobial therapy should be instituted [see clinical pharmacology ( 12.2) and the full prescribing information for clarithromycin ] . rabeprazole sodium delayed-release tablets are indicated for the long-term treatment of pathological hypersecretory conditions, including zollinger-ellison syndrome. rabeprazole sodium delayed-release tablets are indicated for the treatment of symptomatic gerd in adolescents 12 years of age and above for up to 8 weeks. - rabeprazole sodium delayed-release tablets are contraindicated in patients with known hypersensitivity to rabeprazole, substituted benzimidazoles, or to any component of the formulation. hypersensitivity reactions may include anaphylaxis, anaphylactic shock, angioedema, bronchospasm, acute tubulointerstitial nephritis, and urticaria [see warnings and precautions ( 5.3), adverse reactions ( 6)] . rabeprazole sodium delayed-release tablets are contraindicated in patients with known hypersensitivity to rabeprazole, substituted benzimidazoles, or to any component of the formulation. hypersensitivity reactions may include anaphylaxis, anaphylactic shock, angioedema, bronchospasm, acute tubulointerstitial nephritis, and urticaria [see warnings and precautions ( 5.3), adverse reactions ( 6)] . - ppis, including rabeprazole sodium delayed-release tablets, are contraindicated with rilpivirine-containing products [see drug interactions ( 7)] . ppis, including rabeprazole sodium delayed-release tablets, are contraindicated with rilpivirine-containing products [see drug interactions ( 7)] . - for information about contraindications of antibacterial agents (clarithromycin and amoxicillin) indicated in combination with rabeprazole sodium delayed-release tablets, refer to the contraindications section of their package inserts. for information about contraindications of antibacterial agents (clarithromycin and amoxicillin) indicated in combination with rabeprazole sodium delayed-release tablets, refer to the contraindications section of their package inserts. risk summary there are no available human data on rabeprazole sodium delayed-release tablets use in pregnant women to inform the drug associated risk. the background risk of major birth defects and miscarriage for the indicated populations are unknown. however, the background risk in the u.s. general population of major birth defects is 2 to 4% and of miscarriage is 15 to 20% of clinically recognized pregnancies. no evidence of adverse developmental effects were seen in animal reproduction studies with rabeprazole administered during organogenesis at 13 and 8 times the human area under the plasma concentration-time curve (auc) at the recommended dose for gerd, in rats and rabbits, respectively [see data] . changes in bone morphology were observed in offspring of rats treated with oral doses of a different ppi through most of pregnancy and lactation. when maternal administration was confined to gestation only, there were no effects on bone physeal morphology in the offspring at any age  [see  data] . data animal data embryo-fetal developmental studies have been performed in rats during organogenesis at intravenous doses of rabeprazole up to 50 mg/kg/day (plasma auc of 11.8 μg•hr/ml, about 13 times the human exposure at the recommended oral dose for gerd) and rabbits at intravenous doses up to 30 mg/kg/day (plasma auc of 7.3 μg•hr/ml, about 8 times the human exposure at the recommended oral dose for gerd) and have revealed no evidence of harm to the fetus due to rabeprazole. administration of rabeprazole to rats in late gestation and during lactation at an oral dose of 400 mg/kg/day (about 195-times the human oral dose based on mg/m 2 ) resulted in decreases in body weight gain of the pups. a pre- and postnatal developmental toxicity study in rats with additional endpoints to evaluate bone development was performed with a different ppi at about 3.4 to 57 times an oral human dose on a body surface area basis. decreased femur length, width and thickness of cortical bone, decreased thickness of the tibial growth plate, and minimal to mild bone marrow hypocellularity were noted at doses of this ppi equal to or greater than 3.4 times an oral human dose on a body surface area basis. physeal dysplasia in the femur was also observed in offspring after in utero and lactational exposure to the ppi at doses equal to or greater than 33.6 times an oral human dose on a body surface area basis. effects on maternal bone were observed in pregnant and lactating rats in a pre- and postnatal toxicity study when the ppi was administered at oral doses of 3.4 to 57 times an oral human dose on a body surface area basis. when rats were dosed from gestational day 7 through weaning on postnatal day 21, a statistically significant decrease in maternal femur weight of up to 14% (as compared to placebo treatment) was observed at doses equal to or greater than 33.6 times an oral human dose on a body surface area basis. a follow-up developmental toxicity study in rats with further time points to evaluate pup bone development from postnatal day 2 to adulthood was performed with a different ppi at oral doses of 280 mg/kg/day (about 68 times an oral human dose on a body surface area basis) where drug administration was from either gestational day 7 or gestational day 16 until parturition. when maternal administration was confined to gestation only, there were no effects on bone physeal morphology in the offspring at any age. risk summary lactation studies have not been conducted to assess the presence of rabeprazole in human milk, the effects of rabeprazole on the breastfed infant, or the effects of rabeprazole on milk production. rabeprazole is present in rat milk. the development and health benefits of breastfeeding should be considered along with the mother’s clinical need for rabeprazole sodium delayed-release tablets and any potential adverse effects on the breastfed infant from rabeprazole sodium delayed-release tablets or from the underlying maternal condition. the safety and effectiveness of rabeprazole sodium delayed-release tablets have been established in pediatric patients for adolescent patients 12 years of age and older for the treatment of symptomatic gerd. use of rabeprazole sodium delayed-release tablets in this age group is supported by adequate and well controlled studies in adults and a multicenter, randomized, open-label, parallel-group study in 111 adolescent patients 12 to 16 years of age. patients had a clinical diagnosis of symptomatic gerd, or suspected or endoscopically proven gerd and were randomized to either 10 mg or 20 mg once daily for up to 8 weeks for the evaluation of safety and efficacy. the adverse reaction profile in adolescent patients was similar to that of adults. the related reported adverse reactions that occurred in ≥2% of patients were headache (5%) and nausea (2%). there were no adverse reactions reported in these studies that were not previously observed in adults.  the safety and effectiveness of rabeprazole sodium delayed-release tablets have not been established in pediatric patients for: - healing of erosive or ulcerative gerd healing of erosive or ulcerative gerd - maintenance of healing of erosive or ulcerative gerd maintenance of healing of erosive or ulcerative gerd - treatment of symptomatic gerd treatment of symptomatic gerd - healing of duodenal ulcers healing of duodenal ulcers - helicobacter pylori eradication to reduce the risk of duodenal ulcer recurrence helicobacter pylori eradication to reduce the risk of duodenal ulcer recurrence - treatment of pathological hypersecretory conditions, including zollinger-ellison syndrome treatment of pathological hypersecretory conditions, including zollinger-ellison syndrome rabeprazole sodium delayed-release 20 mg tablets are not recommended for use in pediatric patients less than 12 years of age because the tablet strength exceeds the recommended dose for these patients [see dosage and administration ( 2)] . for pediatric patients 1 year to less than 12 years of age consider another rabeprazole formulation. the safety and effectiveness of a different dosage form and dosage strength of rabeprazole has been established in pediatric patients 1 to 11 years for the treatment of gerd. juvenile animal data studies in juvenile and young adult rats and dogs were performed. in juvenile animal studies rabeprazole sodium was administered orally to rats for up to 5 weeks and to dogs for up to 13 weeks, each commencing on day 7 post-partum and followed by a 13-week recovery period. rats were dosed at 5, 25, or 150 mg/kg/day and dogs were dosed at 3, 10, or 30 mg/kg/day. the data from these studies were comparable to those reported for young adult animals. pharmacologically mediated changes, including increased serum gastrin levels and stomach changes, were observed at all dose levels in both rats and dogs. these observations were reversible over the 13-week recovery periods. although body weights and/or crown-rump lengths were minimally decreased during dosing, no effects on the development parameters were noted in either juvenile rats or dogs. when juvenile animals were treated for 28 days with a different ppi at doses equal to or greater than 34 times the daily oral human dose on a body surface area basis, overall growth was affected and treatment-related decreases in body weight (approximately 14%) and body weight gain, and decreases in femur weight and femur length were observed. of the total number of subjects (n=2009) in clinical studies of rabeprazole sodium delayed-release tablets, 19% were 65 years and over, while 4% were 75 years and over. no overall differences in safety or effectiveness were 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. administration of rabeprazole sodium delayed-release tablets to patients with mild to moderate hepatic impairment (child-pugh class a and b, respectively) resulted in increased exposure and decreased elimination [see clinical pharmacology ( 12.3)] . no dosage adjustment is necessary in patients with mild to moderate hepatic impairment. there is no information in patients with severe hepatic impairment (child-pugh class c). avoid use of rabeprazole sodium delayed-release tablets in patients with severe hepatic impairment; however, if treatment is necessary, monitor patients for adverse reactions [see warnings and precautions ( 5), adverse reactions ( 6)] .

美国 - 英文 - NLM (National Library of Medicine)

golden state medical supply, inc. - mirtazapine (unii: a051q2099q) (mirtazapine - unii:a051q2099q) - mirtazapine tablets are indicated for the treatment of major depressive disorder (mdd) in adults [see clinical studies (14)] . mirtazapine tablets are contraindicated in patients: - taking, or within 14 days of stopping, maois (including the maois linezolid and intravenous methylene blue) because of an increased risk of serotonin syndrome [see warnings and precautions (5.3), drug interactions (7)] . - with a known hypersensitivity to mirtazapine or to any of the excipients in mirtazapine tablets . severe skin reactions, including drug reaction with eosinophilia and systemic symptoms (dress), stevens-johnson syndrome, bullous dermatitis, erythema multiforme and toxic epidermal necrolysis have been reported following the use of mirtazapine tablets [see warnings and precautions (5.6),  adverse reactions (6.2)]. there is a pregnancy ex