美国 - 英文 - NLM (National Library of Medicine)

heritage pharmaceuticals inc. d/b/a avet pharmaceuticals inc. - desipramine hydrochloride (unii: 1y58do4my1) (desipramine - unii:tg537d343b) - desipramine hydrochloride 10 mg - desipramine hydrochloride tablets, usp is indicated for the treatment of depression. the use of maois intended to treat psychiatric disorders with desipramine hydrochloride or within 14 days of stopping treatment with desipramine hydrochloride is contraindicated because of an increased risk of serotonin syndrome. the use of desipramine hydrochloride within 14 days of stopping an maoi intended to treat psychiatric disorders is also contraindicated (see warnings and dosage and administration). starting desipramine hydrochloride 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 warnings and dosage and administration). desipramine hydrochloride is contraindicated in the acute recovery period following myocardial infarction. it should not be used in those who have shown prior hypersensitivity to the drug. cross-sensitivity between this and other dibenzazepines is a possibility.

美国 - 英文 - NLM (National Library of Medicine)

keltman pharmaceuticals inc. - sertraline hydrochloride (unii: uti8907y6x) (sertraline - unii:quc7nx6wmb) - sertraline hydrochloride 50 mg - major depressive disorder – sertraline hydrochloride is indicated for the treatment of major depressive disorder in adults. the efficacy of sertraline hydrochloride in the treatment of a major depressive episode was established in six to eight week controlled trials of adult outpatients whose diagnoses corresponded most closely to the dsm-iii category of major depressive disorder (see clinical trials under clinical pharmacology). a major depressive episode implies a prominent and relatively persistent depressed or dysphoric mood that usually interferes with daily functioning (nearly every day for at least 2 weeks); it should include at least 4 of the following 8 symptoms: change in appetite, change in sleep, psychomotor agitation or retardation, loss of interest in usual activities or decrease in sexual drive, increased fatigue, feelings of guilt or worthlessness, slowed thinking or impaired concentration, and a suicide attempt or suicidal ideation. the antidepressant action of sertraline hydrochloride in hos

美国 - 英文 - NLM (National Library of Medicine)

keltman pharmaceuticals inc. - ketorolac tromethamine (unii: 4eve5946bq) (ketorolac tromethamine - unii:4eve5946bq) - ketorolac tromethamine 10 mg - carefully consider the potential benefits and risks of ketorolac tromethamine and other treatment options before deciding to use ketorolac tromethamine. use the lowest effective dose for the shortest duration consistent with individual patient treatment goals. ketorolac tromethamine tablets are indicated for the short-term (≤ 5 days) management of moderately severe acute pain that requires analgesia at the opioid level, usually in a postoperative setting. therapy should always be initiated with iv or im dosing of ketorolac tromethamine, and ketorolac tromethamine tablets are to be used only as continuation treatment, if necessary. the total combined duration of use of ketorolac tromethamine tablets and ketorolac tromethamine is not to exceed 5 days of use because of the potential of increasing the frequency and severity of adverse reactions associated with the recommended doses (see warnings , precautions , dosage and administration , and adverse reactions ). patients should be switched to alternative analges

美国 - 英文 - NLM (National Library of Medicine)

keltman pharmaceuticals inc. - indomethacin (unii: xxe1cet956) (indomethacin - unii:xxe1cet956) - indomethacin 75 mg - carefully consider the potential benefits and risks of indomethacin extended-release capsules and other treatment options before deciding to use indomethacin extended-release capsules. use the lowest effective dose for the shortest duration consistent with individual patient treatment goals (see warnings ). indomethacin extended-release capsules have been found effective in active stages of the following: 1. moderate to severe rheumatoid arthritis including acute flares of chronic disease. 2. moderate to severe ankylosing spondylitis. 3. moderate to severe osteoarthritis. 4. acute painful shoulder (bursitis and/or tendinitis). indomethacin extended-release capsules is not recommended for the treatment of acute gouty arthritis. indomethacin may enable the reduction of steroid dosage in patients receiving steroids for the more severe forms of rheumatoid arthritis. in such instances the steroid dosage should be reduced slowly and the patients followed very closely for any possible adverse effects. the use of ind

美国 - 英文 - NLM (National Library of Medicine)

mylan pharmaceuticals inc. - buprenorphine hydrochloride (unii: 56w8mw3en1) (buprenorphine - unii:40d3scr4gz), naloxone hydrochloride dihydrate (unii: 5q187997ee) (naloxone - unii:36b82amq7n) - buprenorphine and naloxone sublingual film is indicated for treatment of opioid dependence. buprenorphine and naloxone sublingual film should be used as part of a complete treatment plan that includes counseling and psychosocial support. buprenorphine and naloxone sublingual film is contraindicated in patients with a history of hypersensitivity to buprenorphine or naloxone as serious adverse reactions, including anaphylactic shock, have been reported [see warnings and precautions (5.9)] . the data on use of buprenorphine, one of the active ingredients in buprenorphine and naloxone sublingual film, in pregnancy, are limited; however, these data do not indicate an increased risk of major malformations specifically due to buprenorphine exposure. there are limited data from randomized clinical trials in women maintained on buprenorphine that were not designed appropriately to assess the risk of major malformations [see data] . observational studies have reported on congenital malformations among buprenorphine-exposed pregnancies, but were also not designed appropriately to assess the risk of congenital malformations specifically due to buprenorphine exposure [see data] . the extremely limited data on sublingual naloxone exposure in pregnancy are not sufficient to evaluate a drug-associated risk. reproductive and developmental studies in rats and rabbits identified adverse events at clinically relevant and higher doses. embryofetal death was observed in both rats and rabbits administered buprenorphine during the period of organogenesis at doses approximately 6 and 0.3 times, respectively, the human sublingual dose of 16 mg/day of buprenorphine. pre- and postnatal development studies in rats demonstrated increased neonatal deaths at 0.3 times and above and dystocia at approximately 3 times the human sublingual dose of 16 mg/day of buprenorphine. no clear teratogenic effects were seen when buprenorphine was administered during organogenesis with a range of doses equivalent to or greater than the human sublingual dose of 16 mg/day of buprenorphine. however, increases in skeletal abnormalities were noted in rats and rabbits administered buprenorphine daily during organogenesis at doses approximately 0.6 and approximately equal to the human sublingual dose of 16 mg/day of buprenorphine, respectively. in a few studies, some events such as acephalus and omphalocele were also observed but these findings were not clearly treatment-related [see data] . based on animal data, advise pregnant women of the potential risk to a fetus. the estimated background risk of major birth defects and miscarriage for the indicated population are 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 2-4% and 15-20%, respectively. untreated opioid addiction in pregnancy is associated with adverse obstetrical outcomes such as low birth weight, preterm birth, and fetal death. in addition, untreated opioid addiction often results in continued or relapsing illicit opioid use. dosage adjustments of buprenorphine may be required during pregnancy, even if the patient was maintained on a stable dose prior to pregnancy. withdrawal signs and symptoms should be monitored closely and the dose adjusted as necessary. neonatal opioid withdrawal syndrome may occur in newborn infants of mothers who are receiving treatment with buprenorphine and naloxone sublingual film. neonatal opioid withdrawal syndrome presents as irritability, hyperactivity and abnormal sleep pattern, high pitched cry, tremor, vomiting, diarrhea, and/or failure to gain weight. signs of neonatal withdrawal usually occur in the first days after birth. the duration and severity of neonatal opioid withdrawal syndrome may vary. observe newborns for signs of neonatal opioid withdrawal syndrome and manage accordingly [see warnings and precautions (5.5)] . opioid-dependent women on buprenorphine maintenance therapy may require additional analgesia during labor. studies have been conducted to evaluate neonatal outcomes in women exposed to buprenorphine during pregnancy. limited data on malformations from trials, observational studies, case series, and case reports on buprenorphine use in pregnancy do not indicate an increased risk of major malformations specifically due to buprenorphine. several factors may complicate the interpretation of investigations of the children of women who take buprenorphine during pregnancy, including maternal use of illicit drugs, late presentation for prenatal care, infection, poor compliance, poor nutrition, and psychosocial circumstances. interpretation of data is complicated further by the lack of information on untreated opioid-dependent pregnant women, who would be the most appropriate group for comparison. rather, women on another form of opioid medication-assisted treatment, or women in the general population are generally used as the comparison group. however, women in these comparison groups may be different from women prescribed buprenorphine-containing products with respect to maternal factors that may lead to poor pregnancy outcomes. in a multicenter, double-blind, randomized, controlled trial [maternal opioid treatment: human experimental research (mother)] designed primarily to assess neonatal opioid withdrawal effects, opioid-dependent pregnant women were randomized to buprenorphine (n = 86) or methadone (n = 89) treatment, with enrollment at an average gestational age of 18.7 weeks in both groups. a total of 28 of the 86 women in the buprenorphine group (33%) and 16 of the 89 women in the methadone group (18%) discontinued treatment before the end of pregnancy. among women who remained in treatment until delivery, there was no difference between buprenorphine-treated and methadone-treated groups in the number of neonates requiring nows treatment or in the peak severity of nows. buprenorphine-exposed neonates required less morphine (mean total dose, 1.1 mg vs. 10.4 mg), had shorter hospital stays (10.0 days vs. 17.5 days), and shorter duration of treatment for nows (4.1 days vs. 9.9 days) compared to the methadone-exposed group. there were no differences between groups in other primary outcomes (neonatal head circumference,) or secondary outcomes (weight and length at birth, preterm birth, gestational age at delivery, and 1-minute and 5-minute apgar scores), or in the rates of maternal or neonatal adverse events. the outcomes among mothers who discontinued treatment before delivery and may have relapsed to illicit opioid use are not known. because of the imbalance in discontinuation rates between the buprenorphine and methadone groups, the study findings are difficult to interpret. the exposure margins listed below are based on body surface area comparisons (mg/m2 ) to the human sublingual dose of 16 mg buprenorphine via buprenorphine and naloxone sublingual tablets. effects on embryo-fetal development were studied in sprague-dawley rats and russian white rabbits following oral (1:1) and intramuscular (im) (3:2) administration of mixtures of buprenorphine and naloxone during the period of organogenesis. following oral administration to rats no teratogenic effects were observed at buprenorphine doses up to 250 mg/kg/day (estimated exposure approximately 150 times the human sublingual dose of 16 mg) in the presence of maternal toxicity (mortality). following oral administration to rabbits, no teratogenic effects were observed at buprenorphine doses up to 40 mg/kg/day (estimated exposure approximately 50 times, the human sublingual dose of 16 mg) in the absence of clear maternal toxicity. no definitive drug-related teratogenic effects were observed in rats and rabbits at im doses up to 30 mg/kg/day (estimated exposure approximately 20 times and 35 times, respectively, the human sublingual dose of 16 mg). maternal toxicity resulting in mortality was noted in these studies in both rats and rabbits. acephalus was observed in one rabbit fetus from the low-dose group and omphalocele was observed in two rabbit fetuses from the same litter in the mid-dose group; no findings were observed in fetuses from the high-dose group. maternal toxicity was seen in the high-dose group but not at the lower doses where the findings were observed. following oral administration of buprenorphine to rats, dose-related post-implantation losses, evidenced by increases in the numbers of early resorptions with consequent reductions in the numbers of fetuses, were observed at doses of 10 mg/kg/day or greater (estimated exposure approximately 6 times the human sublingual dose of 16 mg). in the rabbit, increased post-implantation losses occurred at an oral dose of 40 mg/kg/day. following im administration in the rat and the rabbit, post-implantation losses, as evidenced by decreases in live fetuses and increases in resorptions, occurred at 30 mg/kg/day. buprenorphine was not teratogenic in rats or rabbits after im or subcutaneous (sc) doses up to 5 mg/kg/day (estimated exposure was approximately 3 and 6 times, respectively, the human sublingual dose of 16 mg), after iv doses up to 0.8 mg/kg/day (estimated exposure was approximately 0.5 times and equal to, respectively, the human sublingual dose of 16 mg), or after oral doses up to 160 mg/kg/day in rats (estimated exposure was approximately 95 times the human sublingual dose of 16 mg) and 25 mg/kg/day in rabbits (estimated exposure was approximately 30 times the human daily sublingual dose of 16 mg). significant increases in skeletal abnormalities (e.g., extra thoracic vertebra or thoraco-lumbar ribs) were noted in rats after sc administration of 1 mg/kg/day and up (estimated exposure was approximately 0.6 times the human sublingual dose of 16 mg), but were not observed at oral doses up to 160 mg/kg/day. increases in skeletal abnormalities in rabbits after im administration of 5 mg/kg/day (estimated exposure was approximately 6 times the human daily sublingual dose of 16 mg) in the absence of maternal toxicity or oral administration of 1 mg/kg/day or greater (estimated exposure was approximately equal to the human sublingual dose of 16 mg) were not statistically significant. in rabbits, buprenorphine produced statistically significant pre-implantation losses at oral doses of 1 mg/kg/day or greater and post-implantation losses that were statistically significant at iv doses of 0.2 mg/kg/day or greater (estimated exposure approximately 0.3 times the human daily sublingual dose of 16 mg). no maternal toxicity was noted at doses causing post-implantation loss in this study. dystocia was noted in pregnant rats treated intramuscularly with buprenorphine from gestation day 14 through lactation day 21 at 5 mg/kg/day (approximately 3 times the human sublingual dose of 16 mg). fertility, pre- and post-natal development studies with buprenorphine in rats indicated increases in neonatal mortality after oral doses of 0.8 mg/kg/day and up (approximately 0.5 times the human daily sublingual dose of 16 mg), after im doses of 0.5 mg/kg/day and up (approximately 0.3 times the human sublingual dose of 16 mg), and after sc doses of 0.1 mg/kg/day and up (approximately 0.06 times the human sublingual dose of 16 mg). an apparent lack of milk production during these studies likely contributed to the decreased pup viability and lactation indices. delays in the occurrence of righting reflex and startle response were noted in rat pups at an oral dose of 80 mg/kg/day (approximately 50 times the human sublingual dose of 16 mg). based on two studies in 13 lactating women maintained on buprenorphine treatment, buprenorphine and its metabolite norbuprenorphine were present in low levels in human milk and infant urine. available data have not shown adverse reactions in breastfed infants. there are no data on the combination product buprenorphine and naloxone in breastfeeding, however oral absorption of naloxone is limited. the developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for buprenorphine and naloxone sublingual film and any potential adverse effects on the breastfed child from the drug or from the underlying maternal condition. advise breastfeeding women taking buprenorphine products to monitor the infant for increased drowsiness and breathing difficulties. data were consistent from two studies (n = 13) of breastfeeding infants whose mothers were maintained on sublingual doses of buprenorphine ranging from 2.4 to 24 mg/day, showing that the infants were exposed to less than 1% of the maternal daily dose. in a study of six lactating women who were taking a median sublingual buprenorphine dose of 0.29 mg/kg/day 5 to 8 days after delivery, breast milk provided a median infant dose of 0.42 mcg/kg/day of buprenorphine and 0.33 mcg/kg/day of norbuprenorphine, equal to 0.2% and 0.12%, respectively, of the maternal weight-adjusted dose (relative dose/kg (%) of norbuprenorphine was calculated from the assumption that buprenorphine and norbuprenorphine are equipotent). data from a study of seven lactating women who were taking a median sublingual buprenorphine dose of 7 mg/day an average of 1.12 months after delivery indicated that the mean milk concentrations (cavg ) of buprenorphine and norbuprenorphine were 3.65 mcg/l and 1.94 mcg/l respectively. based on the study data, and assuming milk consumption of 150 ml/kg/day, an exclusively breastfed infant would receive an estimated mean absolute infant dose (aid) of 0.55 mcg/kg/day of buprenorphine and 0.29 mcg/kg/day of norbuprenorphine, or a mean relative infant dose (rid) of 0.38% and 0.18%, respectively, of the maternal weight-adjusted dose. chronic use of opioids may cause reduced fertility in females and males of reproductive potential. it is not known whether these effects on fertility are reversible [see adverse reactions (6.2), clinical pharmacology (12.2), nonclinical toxicology (13.1)] . the safety and effectiveness of buprenorphine and naloxone sublingual film have not been established in pediatric patients. this product is not appropriate for the treatment of neonatal abstinence syndrome in neonates, because it contains naloxone, an opioid antagonist. clinical studies of buprenorphine and naloxone sublingual film, buprenorphine and naloxone sublingual tablets, or buprenorphine sublingual tablets did not include sufficient numbers of subjects aged 65 and over to determine whether they responded differently than younger subjects. other reported clinical experience has not identified differences in responses between the elderly and younger patients. due to possible decreased hepatic, renal, or cardiac function and of concomitant disease or other drug therapy in geriatric patients, the decision to prescribe buprenorphine and naloxone sublingual film should be made cautiously in individuals 65 years of age or older and these patients should be monitored for signs and symptoms of toxicity or overdose. the effect of hepatic impairment on the pharmacokinetics of buprenorphine and naloxone has been evaluated in a pharmacokinetic study. both drugs are extensively metabolized in the liver. while no clinically significant changes have been observed in subjects with mild hepatic impairment; the plasma levels have been shown to be higher and half-life values have been shown to be longer for both buprenorphine and naloxone in subjects with moderate and severe hepatic impairment. the magnitude of the effects on naloxone are greater than that on buprenorphine in both moderately and severely impaired subjects. the difference in magnitude of the effects on naloxone and buprenorphine are greater in subjects with severe hepatic impairment than in subjects with moderate hepatic impairment, and therefore the clinical impact of these effects is likely to be greater in patients with severe hepatic impairment than in patients with moderate hepatic impairment. buprenorphine and naloxone products should be avoided in patients with severe hepatic impairment and may not be appropriate for patients with moderate hepatic impairment [see warnings and precautions (5.12), clinical pharmacology (12.3)] . no differences in buprenorphine pharmacokinetics were observed between 9 dialysis-dependent and 6 normal patients following iv administration of 0.3 mg buprenorphine. the effects of renal failure on naloxone pharmacokinetics are unknown. buprenorphine and naloxone sublingual film contains buprenorphine, a schedule iii controlled substance under the controlled substances act. buprenorphine, like morphine and other opioids, has the potential for being abused and is subject to criminal diversion. this should be considered when prescribing or dispensing buprenorphine in situations when the clinician is concerned about an increased risk of misuse, abuse, or diversion. healthcare professionals should contact their state professional licensing board or state controlled substances authority for information on how to prevent and detect abuse or diversion of this product. patients who continue to misuse, abuse, or divert buprenorphine products or other opioids should be provided with or referred for more intensive and structured treatment. abuse of buprenorphine poses a risk of overdose and death. this risk is increased with the abuse of buprenorphine and alcohol and other substances, especially benzodiazepines. the healthcare provider may be able to more easily detect misuse or diversion by maintaining records of medication prescribed including date, dose, quantity, frequency of refills, and renewal requests of medication prescribed. proper assessment of the patient, proper prescribing practices, periodic re-evaluation of therapy, and proper handling and storage of the medication are appropriate measures that help to limit abuse of opioid drugs. buprenorphine is a partial agonist at the mu-opioid receptor and chronic administration produces physical dependence of the opioid type, characterized by moderate withdrawal signs and symptoms upon abrupt discontinuation or rapid taper. the withdrawal syndrome is typically milder than seen with full agonists and may be delayed in onset [see warnings and precautions (5.7)] . neonatal opioid withdrawal syndrome (nows) is an expected and treatable outcome of prolonged use of opioids during pregnancy [see warnings and precautions (5.5)] . buprenorphine and naloxone sublingual film (bue″ pre nor′ feen nal ox′ one) this “instructions for use” contains information on how to correctly take buprenorphine and naloxone sublingual film. important information you need to know before taking buprenorphine and naloxone sublingual film: preparing to take buprenorphine and naloxone sublingual film: figure 1 to take buprenorphine and naloxone sublingual film under your tongue (sublingual administration): figure 2 to take buprenorphine and naloxone sublingual film on the inside of your cheek (buccal administration): figure 3   if you take too many buprenorphine and naloxone sublingual films or overdose, call poison control or get emergency medical help right away. storing buprenorphine and naloxone sublingual film: disposing of buprenorphine and naloxone sublingual film: if you need help with disposal of buprenorphine and naloxone sublingual film, call mylan at 1-877-446-3679 (1-877-4-info-rx). this “instructions for use” has been approved by the u.s. food and drug administration. manufactured for: mylan pharmaceuticals inc. morgantown, wv 26505 u.s.a. revised: 4/2024 bnsf:r9

美国 - 英文 - NLM (National Library of Medicine)

mylan pharmaceuticals inc. - methylphenidate (unii: 207zz9qz49) (methylphenidate - unii:207zz9qz49) - methylphenidate transdermal system is indicated for the treatment of attention deficit hyperactivity disorder (adhd) in pediatric patients 6 to 17 years of age. methylphenidate transdermal system is contraindicated in patients known to be hypersensitive to methylphenidate or other components of the product (fluoropolymer-coated polyester, hydrophobic colloidal silica, mineral oil, polyester/ethylene vinyl acetate laminate film backing, polyisobutylene adhesive and white ink). the white ink contains acrylic polymers, polyethylene wax, polytetrafluoroethylene, polyvinylpyrrolidone, sodium dioctyl sulfosuccinate and titanium dioxide [see description (11) ] . methylphenidate transdermal system is contraindicated during treatment with monoamine oxidase inhibitors, and within a minimum of 14 days following discontinuation of treatment with a monoamine oxidase inhibitor (hypertensive crises may result). there is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to adhd medications, including methylphenidate transdermal system, during pregnancy. healthcare providers are encouraged to register patients by calling the national pregnancy registry for adhd medications at 1-866-961-2388 or visit https://womensmentalhealth.org/adhd-medications/. published studies and post-marketing reports on methylphenidate use during pregnancy are insufficient to identify a drug-associated risk of major birth defects, miscarriage or adverse maternal or fetal outcomes. there are risks to the fetus associated with the use of cns stimulants during pregnancy (see clinical considerations) . no effects on morphological development were observed in embryo-fetal development studies with oral administration of methylphenidate to pregnant rats and rabbits during organogenesis. however, spina bifida was observed in rabbits when given oral doses of 200 mg/kg/day. when methylphenidate was administered orally to rats throughout pregnancy and lactation, offspring growth and survival were decreased at maternally toxic doses (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 clinical recognized pregnancies is 2-4% and 15-20%, respectively. cns stimulants, such as methylphenidate transdermal system, can cause vasoconstriction and thereby decrease placental perfusion. no fetal and/or neonatal adverse reactions have been reported with the use of therapeutic doses of methylphenidate during pregnancy; however, premature delivery and low birth weight infants have been reported in amphetamine-dependent mothers. animal reproduction toxicity studies with transdermal methylphenidate have not been performed. in embryo-fetal development studies conducted in rats and rabbits, methylphenidate was administered orally to pregnant animals during the period of organogenesis, at doses up to 100 and 200 mg/kg/day, respectively. no evidence of morphological development effects was found either of the species; however, increased incidences of fetal skeletal variations were observed in rats at 60 mg/kg or greater and an increase in fetal visceral variations was seen in rabbits at the highest dose. in a previous study, methylphenidate was shown to have malformations (increased incidence of fetal spina bifida) in rabbits when given oral doses of 200 mg/kg/day. when methylphenidate was administered orally to rats throughout pregnancy and lactation at doses of up to 60 mg/kg/day, offspring growth and survival were decreased at maternally toxic doses. in a study in which oral methylphenidate was given to rats throughout pregnancy and lactation at doses up to 60 mg/kg/day, offspring weights and survival were decreased at 40 mg/kg/day and above; these doses caused some maternal toxicity. limited published literature, based on breast milk sampling from five mothers, reports that methylphenidate is present in human milk, which resulted in infant doses of 0.16% to 0.7% of the maternal weight-adjusted dosage and a milk/plasma ratio ranging between 1.1 and 2.7. there are no reports of adverse effects on the breastfed infant and no effects on milk production. long-term neurodevelopmental effects on infants from stimulant exposure are unknown. the developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for methylphenidate transdermal system and any potential adverse effects on the breastfed infant from methylphenidate or from the underlying maternal condition. monitor breastfeeding infants for adverse reactions, such as agitation, insomnia, anorexia, and reduced weight gain. the safety and effectiveness of methylphenidate transdermal system in pediatric patients less than 6 years have not been established. long-term effects of methylphenidate in children have not been well established. the safety and effectiveness of methylphenidate transdermal system for the treatment of adhd have been established in pediatric patients 6 to 17 years. growth should be monitored during treatment with stimulants, including methylphenidate transdermal system. children who are not growing or gaining weight as expected may need to have their treatment interrupted [see warnings and precautions (5.8)] . rats treated with methylphenidate early in the postnatal period through sexual maturation demonstrated a decrease in spontaneous locomotor activity in adulthood. a deficit in acquisition of a specific learning task was observed in females only. studies with transdermal methylphenidate have not been performed in juvenile animals. in a study conducted in young rats, methylphenidate was administered orally at doses of up to 100 mg/kg/day for 9 weeks, starting early in the postnatal period (postnatal day 7) and continuing through sexual maturity (postnatal week 10). when these animals were tested as adults (postnatal weeks 13-14), decreased spontaneous locomotor activity was observed in males and females previously treated with 50 mg/kg/day or greater, and a deficit in the acquisition of a specific learning task was seen in females exposed to the highest dose. the no effect level for juvenile neurobehavioral development in rats was 5 mg/kg/day. the clinical significance of the long-term behavioral effects observed in rats is unknown. methylphenidate transdermal system has not been studied in patients greater than 65 years of age. methylphenidate transdermal system contains methylphenidate, a schedule ii controlled substance. methylphenidate transdermal system has a high potential for abuse and misuse which can lead to the development of a substance use disorder, including addiction [see warnings and precautions (5.1)] . methylphenidate transdermal system can be diverted for non-medical use into illicit channels or distribution. abuse is the intentional non-therapeutic use of a drug, even once, to achieve a desired psychological or physiological effect. misuse is the intentional use, for therapeutic purposes, of a drug by an individual in a way other than prescribed by a health care provider or for whom it was not prescribed. drug addiction is a cluster of behavioral, cognitive, and physiological phenomena that may include a strong desire to take the drug, difficulties in controlling drug use (e.g., continuing drug use despite harmful consequences, giving a higher priority to drug use than other activities and obligations), and possible tolerance or physical dependence. misuse and abuse of methylphenidate may cause increased heart rate, respiratory rate, or blood pressure; sweating; dilated pupils; hyperactivity; restlessness; insomnia; decreased appetite; loss of coordination; tremors; flushed skin; vomiting; and/or abdominal pain. anxiety, psychosis, hostility, aggression, and suicidal or homicidal ideation have also been observed with cns stimulants abuse and/or misuse. misuse and abuse of cns stimulants, including methylphenidate transdermal system, can result in overdose and death [see overdosage (10)] , and this risk is increased with higher doses or unapproved methods of administration, such as snorting or injection. methylphenidate transdermal system may produce physical dependence. physical dependence is a state that develops as a result of physiological adaptation in response to repeated drug use, manifested by withdrawal signs and symptoms after abrupt discontinuation or a significant dose reduction of a drug. withdrawal signs and symptoms after abrupt discontinuation or dose reduction following prolonged use of cns stimulants including methylphenidate transdermal system include dysphoric mood; depression; fatigue; vivid, unpleasant dreams; insomnia or hypersomnia; increased appetite; and psychomotor retardation or agitation. methylphenidate transdermal system may produce tolerance. tolerance is a physiological state characterized by a reduced response to a drug after repeated administration (i.e., a higher dose of a drug is required to produce the same effect that was once obtained at a lower dose). methylphenidate transdermal system   cii (meth'' il fen' i date) 1. methylphenidate transdermal system dosing chart each carton of methylphenidate transdermal systems contains a methylphenidate transdermal system dosing chart to help you keep track of your methylphenidate transdermal system including: to use the methylphenidate transdermal system dosing chart, follow these instructions: methylphenidate transdermal system schedule for 9 hour dosing if you put the transdermal system on at: on the same day, remove the transdermal system at: 5:00 a.m. 2:00 p.m. 6:00 a.m. 3:00 p.m. 7:00 a.m. 4:00 p.m. 8:00 a.m. 5:00 p.m. 9:00 a.m. 6:00 p.m. 10:00 a.m. 7:00 p.m. 11:00 a.m. 8:00 p.m. 12:00 p.m. 9:00 p.m. 2. where to apply methylphenidate transdermal system figure a 3. before you apply methylphenidate transdermal system make sure your skin: 4. how to apply methylphenidate transdermal system figure b the methylphenidate transdermal system has 4 layers. the 4 layers are pictured below. the pictures show both sides of the transdermal system: figure c                                                                                  figure d layers: figure e figure f figure g figure h 5 . how to remove and throw away methylphenidate transdermal system this instructions for use has been approved by the u.s. food and drug administration. manufactured for: mylan pharmaceuticals inc. morgantown, wv 26505 u.s.a. revised: 1/2024 mpn:r5

菲律宾 - 英文 - FDA (Food And Drug Administration)

square pharmaceuticals, inc. - ambroxol hydrochloride - tablet - 30 mg

菲律宾 - 英文 - FDA (Food And Drug Administration)

square pharmaceuticals, inc. - ascorbic acid (as sodium ascorbate) - syrup - 100mg/5ml

菲律宾 - 英文 - FDA (Food And Drug Administration)

square pharmaceuticals, inc. - paracetamol - syrup - 250mg/ 5ml

菲律宾 - 英文 - FDA (Food And Drug Administration)

square pharmaceuticals, inc. - povidone-iodine - topical solution - 75 mg/ml (7.5 % w/v)