Australia - English - Department of Health (Therapeutic Goods Administration)

vitaco health australia pty ltd - colecalciferol,equisetum arvense,hydroxyapatite,menaquinone 7,magnesium oxide,manganese amino acid chelate,zinc gluconate -

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

golden state medical supply, inc. - etodolac (unii: 2m36281008) (etodolac - unii:2m36281008) - etodolac 200 mg - carefully consider the potential benefits and risks of etodolac capsules and tablets and other treatment options before deciding to use etodolac capsules and tablets. use the lowest effective dose for the shortest duration consistent with individual patient treatment goals (see warnings ). etodolac capsules and tablets are indicated: - for acute and long-term use in the management of signs and symptoms of the following: osteoarthritis rheumatoid arthritis - osteoarthritis - rheumatoid arthritis - for the management of acute pain etodolac capsules and tablets are contraindicated in patients with known hypersensitivity to etodolac or other ingredients in etodolac. etodolac capsules and tablets should not be given to patients who have experienced asthma, urticaria, or other allergic-type reactions after taking aspirin or other nsaids. severe, rarely fatal, anaphylactic-like reactions to nsaids have been reported in such patients (see warnings, anaphylactoid reactions an

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

golden state medical supply, inc. - mycophenolate mofetil (unii: 9242ecw6r0) (mycophenolic acid - unii:hu9dx48n0t) - mycophenolate mofetil 250 mg - mycophenolate mofetil (mmf) is indicated for the prophylaxis of organ rejection, in adult and pediatric recipients 3 months of age and older of allogeneic kidney [see clinical studies (14.1)] , heart [see clinical studies (14.2)] or liver transplants [see clinical studies (14.3)] , in combination with other immunosuppressants. allergic reactions to mycophenolate mofetil have been observed; therefore, mycophenolate mofetil is contraindicated in patients with a hypersensitivity to mycophenolate mofetil (mmf), mycophenolic acid (mpa) or any component of the drug product.   there is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to mycophenolate during pregnancy and those becoming pregnant within 6 weeks of discontinuing mycophenolate mofetil treatment. to report a pregnancy or obtain information about the registry, visit www.mycophenolaterems.com or call 1-800-617-8191. use of mycophenolate mofetil (mmf) during pregnancy is associated with an increased risk of first trimester pregnancy loss and an increased risk of multiple congenital malformations in multiple organ systems [see human data] . oral administration of mycophenolate to rats and rabbits during the period of organogenesis produced congenital malformations and pregnancy loss at doses less than the recommended clinical dose (0.01 to 0.05 times the recommended clinical doses in kidney and heart transplant patients) [see animal data] . consider alternative immunosuppressants with less potential for embryofetal toxicity. risks and benefits of mycophenolate mofetil should be discussed with the pregnant woman. the estimated background risk of pregnancy loss and congenital malformations in organ transplant populations is not clear. 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. a spectrum of congenital malformations (including multiple malformations in individual newborns) has been reported in 23 to 27% of live births in mmf exposed pregnancies, based on published data from pregnancy registries. malformations that have been documented include external ear, eye, and other facial abnormalities including cleft lip and palate, and anomalies of the distal limbs, heart, esophagus, kidney, and nervous system. based on published data from pregnancy registries, the risk of first trimester pregnancy loss has been reported at 45 to 49% following mmf exposure. in animal reproductive toxicology studies, there were increased rates of fetal resorptions and malformations in the absence of maternal toxicity. oral administration of mmf to pregnant rats from gestational day 7 to day 16 produced increased embryofetal lethality and fetal malformations including anophthalmia, agnathia, and hydrocephaly at doses equivalent to 0.015 and 0.01 times the recommended human doses for renal and cardiac transplant patients, respectively, when corrected for bsa. oral administration of mmf to pregnant rabbits from gestational day 7 to day 19 produced increased embryofetal lethality and fetal malformations included ectopia cordis, ectopic kidneys, diaphragmatic hernia, and umbilical hernia at dose equivalents as low as 0.05 and 0.03 times the recommended human doses for renal and cardiac transplant patients, respectively, when corrected for bsa. there are no data on the presence of mycophenolate in human milk, or the effects on milk production. there are limited data in the national transplantation pregnancy registry on the effects of mycophenolate on a breastfed child [see data] . studies in rats treated with mmf have shown mycophenolic acid (mpa) to be present in milk. because available data are limited, it is not possible to exclude potential risks to a breastfeeding infant. the developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for mycophenolate mofetil and any potential adverse effects on the breastfed infant from mycophenolate mofetil or from the underlying maternal condition. limited information is available from the national transplantation pregnancy registry. of seven infants reported by the national transplantation pregnancy registry to have been breastfed while the mother was taking mycophenolate, all were born at 34-40 weeks gestation, and breastfed for up to 14 months. no adverse events were reported. females of reproductive potential must be made aware of the increased risk of first trimester pregnancy loss and congenital malformations and must be counseled regarding pregnancy prevention and planning. for patients who are considering pregnancy, consider alternative immunosuppressants with less potential for embryofetal toxicity whenever possible. risks and benefits of mycophenolate mofetil should be discussed with the patient. to prevent unplanned exposure during pregnancy, all females of reproductive potential should have a serum or urine pregnancy test with a sensitivity of at least 25 miu/ml immediately before starting mycophenolate mofetil. another pregnancy test with the same sensitivity should be done 8 to 10 days later. repeat pregnancy tests should be performed during routine follow-up visits. results of all pregnancy tests should be discussed with the patient. in the event of a positive pregnancy test, consider alternative immunosuppressants with less potential for embryofetal toxicity whenever possible. females of reproductive potential taking mycophenolate mofetil must receive contraceptive counseling and use acceptable contraception (see table 9 for acceptable contraception methods). patients must use acceptable birth control during the entire mycophenolate mofetil therapy, and for 6 weeks after stopping mycophenolate mofetil, unless the patient chooses abstinence. patients should be aware that mycophenolate mofetil reduces blood levels of the hormones from the oral contraceptive pill and could theoretically reduce its effectiveness [see drug interactions (7.2)] . pick from the following birth control options: option 1 methods to use alone - intrauterine devices (iuds) - tubal sterilization - patient’s partner vasectomy or option 2 hormone methods choose 1 barrier methods choose 1 choose one hormone method and one barrier method estrogen and progesterone - oral contraceptive pill - transdermal patch - vaginal ring   progesterone-only - injection - implant and   - diaphragm with spermicide - cervical cap with spermicide - contraceptive sponge - male condom - female condom or option 3 barrier methods choose 1 barrier methods choose 1 choose one barrier method from each column (must choose two methods) - diaphragm with spermicide - cervical cap with spermicide - contraceptive sponge and - male condom - female condom genotoxic effects have been observed in animal studies at exposures exceeding the human therapeutic exposures by approximately 1.25 times. thus, the risk of genotoxic effects on sperm cells cannot be excluded. based on this potential risk, sexually active male patients and/or their female partners are recommended to use effective contraception during treatment of the male patient and for at least 90 days after cessation of treatment. also, based on the potential risk of genotoxic effects, male patients should not donate sperm during treatment with mycophenolate mofetil and for at least 90 days after cessation of treatment [see use in special populations (8.1), nonclinical toxicology (13.1), patient counseling information (17.10) ] . safety and effectiveness have been established in pediatric patients 3 months and older for the prophylaxis of organ rejection of allogeneic kidney, heart or liver transplants. use of mycophenolate mofetil in this population is supported by evidence from adequate and well-controlled studies of mycophenolate mofetil in adults with additional data from one open-label, pharmacokinetic and safety study of mycophenolate mofetil in pediatric patients after receiving allogeneic kidney transplant (100 patients, 3 months to 18 years of age) [see dosage and administration (2.2), adverse reactions (6.1), clinical pharmacology (12.3), clinical studies (14.1)] . use of mycophenolate mofetil in pediatric heart transplant and liver transplant patients is supported by adequate and well-controlled studies and pharmacokinetic data in adult heart transplant and liver transplant patients. additional supportive data include pharmacokinetic data in pediatric kidney transplant and pediatric liver transplant patients (8 liver transplant patients, 9 months to 5 years of age, in an open-label, pharmacokinetic and safety study) and published evidence of clinical efficacy and safety in pediatric heart transplant and pediatric liver transplant patients [see dosage and administration (2.3, 2.4), adverse reactions (6.1), clinical pharmacology (12.3), clinical studies (14.1)] . clinical studies of mycophenolate mofetil 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 geriatric and younger patients. in general, dose selection for a geriatric patient should take into consideration the presence of decreased hepatic, renal or cardiac function and of concomitant drug therapies [see adverse reactions (6.1), drug interactions (7)] . no dosage adjustments are needed in kidney transplant patients experiencing delayed graft function postoperatively but patients should be carefully monitored [see clinical pharmacology (12.3)] . in kidney transplant patients with severe chronic impairment of the graft (gfr < 25 ml/min/1.73 m 2 ), no dose adjustments are necessary; however, doses greater than 1 g administered twice a day should be avoided. no data are available for heart or liver transplant patients with severe chronic renal impairment. mycophenolate mofetil may be used for heart or liver transplant patients with severe chronic renal impairment if the potential benefits outweigh the potential risks. no dosage adjustments are recommended for kidney transplant patients with severe hepatic parenchymal disease. however, it is not known whether dosage adjustments are needed for hepatic disease with other etiologies [see clinical pharmacology (12.3)] . no data are available for heart transplant patients with severe hepatic parenchymal disease.

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

golden state medical supply, inc. - valproic acid (unii: 614oi1z5wi) (valproic acid - unii:614oi1z5wi) - valproic acid 250 mg - valproic acid capsules are indicated as monotherapy and adjunctive therapy in the treatment of patients with complex partial seizures that occur either in isolation or in association with other types of seizures. valproic acid capsules are indicated for use as sole and adjunctive therapy in the treatment of simple and complex absence seizures, and adjunctively in patients with multiple seizure types which include absence seizures. simple absence is defined as very brief clouding of the sensorium or loss of consciousness accompanied by certain generalized epileptic discharges without other detectable clinical signs. complex absence is the term used when other signs are also present. see warnings and precaution (5.1) for statement regarding fatal hepatic dysfunction. because of the risk to the fetus of decreased iq, neural tube defects, and other major congenital malformations, which may occur very early in pregnancy, valproate should not be administered to a woman of childbearing potential unle

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

golden state medical supply, inc. - ketoconazole (unii: r9400w927i) (ketoconazole - unii:r9400w927i) - ketoconazole 200 mg - ketoconazole tablets are not indicated for treatment of onychomycosis, cutaneous dermatophyte infections, or candida infections. ketoconazole tablets should be used only when other effective antifungal therapy is not available or tolerated and the potential benefits are considered to outweigh the potential risks. ketoconazole tablets are indicated for the treatment of the following systemic fungal infections in patients who have failed or who are intolerant to other therapies: blastomycosis, coccidioidomycosis, histoplasmosis, chromomycosis, and paracoccidioidomycosis. ketoconazole tablets should not be used for fungal meningitis because it penetrates poorly into the cerebrospinal fluid. coadministration of a number of cyp3a4 substrates such as dofetilide, quinidine, cisapride and pimozide is contraindicated with ketoconazole tablets. coadministration with ketoconazole can cause elevated plasma concentrations of these drugs and may increase or prolong both therapeutic and adverse effects to such an extent that a potentially serious adverse reaction may occur. for example, increased plasma concentrations of some of these drugs can lead to qt prolongation and sometimes resulting in life-threatening ventricular tachyarrhythmias including occurrences of torsades de pointes, a potentially fatal arrhythmia. (see precautions: drug interactions.) coadministration of ketoconazole tablets with lurasidone is contraindicated since it may result in an increase in lurasidone exposure and the potential for serious adverse reactions (see precautions: drug interactions). additionally, the following other drugs are contraindicated with ketoconazole tablets: methadone, disopyramide, dronedarone, ergot alkaloids such as dihydroergotamine, ergometrine, ergotamine, methylergometrine, irinotecan, lurasidone, oral midazolam, alprazolam, triazolam, felodipine, nisoldipine, ranolazine, tolvaptan, eplerenone, lovastatin, simvastatin and colchicine. (see precautions: drug interactions.) coadministration of ketoconazole tablets with oral midazolam, oral triazolam or alprazolam has resulted in elevated plasma concentrations of these drugs. this may potentiate and prolong hypnotic and sedative effects, especially with repeated dosing or chronic administration of these agents. concomitant administration of ketoconazole tablets with oral triazolam, oral midazolam or alprazolam is contraindicated. (see precautions: drug interactions.) coadministration of cyp3a4 metabolized hmg-coa reductase inhibitors such as simvastatin, and lovastatin is contraindicated with ketoconazole tablets. (see precautions: drug interactions.) concomitant administration of ergot alkaloids such as dihydroergotamine and ergotamine with ketoconazole tablets is contraindicated. (see precautions: drug interactions.) the use of ketoconazole tablets is contraindicated in patients with acute or chronic liver disease. ketoconazole tablets usp, 200 mg is contraindicated in patients who have shown hypersensitivity to the drug.

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

golden state medical supply, inc. - dalfampridine (unii: bh3b64okl9) (dalfampridine - unii:bh3b64okl9) - dalfampridine extended-release tablets are indicated as a treatment to improve walking in adult patients with multiple sclerosis (ms). this was demonstrated by an increase in walking speed [see clinical studies (14)]. the use of dalfampridine extended-release tablets are contraindicated in the following conditions: - history of seizure [see warnings and precautions (5.1)] - moderate or severe renal impairment (crcl≤50 ml/min) [see warnings and precautions (5.2)] - history of hypersensitivity to dalfampridine or 4-aminopyridine; reactions have included anaphylaxis [see warnings and precautions (5.4)] risk summary there are no adequate data on the developmental risk associated with use of dalfampridine extended-release tablets in pregnant women. administration of dalfampridine to animals during pregnancy and lactation resulted in decreased offspring viability and growth at clinically relevant doses [see data]. 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. the background risk of major birth defects and miscarriage for the indicated population is unknown. data animal data oral administration of dalfampridine to pregnant rats and rabbits throughout organogenesis resulted in no evidence of developmental toxicity in either species. the highest doses tested (10 mg/kg/day in rats, 5 mg/kg/day in rabbits), which were associated with maternal toxicity, are approximately 5 times the mrhd on a body surface area (mg/m 2 ) basis. oral administration of dalfampridine (0, 1, 3, and 9 to 6 mg/kg/day; high dose reduced during the second week of dosing) to female rats throughout pregnancy and lactation resulted in decreased offspring viability at the highest dose tested and decreased body weight in offspring at the mid and high doses. the no-effect dose for pre-and postnatal developmental toxicity in rats (1 mg/kg/day) is less than the mrhd on a mg/m 2 basis. risk summary there are no data on the presence of dalfampridine in human milk, the effects of dalfampridine on the breastfed infant, or the effects on milk production. the developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for dalfampridine and any potential adverse effects on the breastfed infant from dalfampridine or from the underlying maternal condition. safety and effectiveness in patients younger than 18 years of age have not been established. clinical studies of dalfampridine extended-release tablets did not include sufficient numbers of subjects aged 65 and over to determine whether they respond differently than younger subjects. a population pk analysis showed that dalfampridine clearance modestly decreased with increasing age, but not sufficiently to necessitate a modification of dose with age. other reported clinical experience has identified no differences in responses between the elderly and younger patients. dalfampridine is known to be substantially excreted by the kidneys and the risk of adverse reactions, including seizures, is greater with increasing exposure of dalfampridine. because elderly patients are more likely to have decreased renal function, it is particularly important to know the estimated creatinine clearance (crcl) in these patients [see warnings and precautions (5.2)]. clearance of dalfampridine is decreased in patients with renal impairment and is significantly correlated with creatinine clearance (crcl) [see clinical pharmacology (12.3)] . dalfampridine extended-release tablets are contraindicated in patients with moderate or severe renal impairment (crcl ≤50 ml/min) [see contraindications (4)]. the risk of seizures in patients with mild renal impairment (crcl 51 to 80 ml/min) is unknown, but dalfampridine plasma levels in these patients may approach those seen at a dose of 15 mg twice daily, a dose that may be associated with an increased risk of seizures. if unknown, estimated creatinine clearance should be calculated prior to initiating treatment with dalfampridine extended-release tablets [see dosage and administration (2.3)and warnings and precautions (5.2)] .

Philippines - English - FDA (Food And Drug Administration)

gold life distributor phils, inc. - thiamine mononitrate (vitamin b1) , pyridoxine hydrochloride (vitamin b6) , cyanocobalamin (vitamin b12) - tablet - 100mg/5mg/50mcg

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

golden state medical supply, inc. - dextroamphetamine sulfate (unii: jj768o327n) (dextroamphetamine - unii:tz47u051fi), dextroamphetamine saccharate (unii: g83415v073) (dextroamphetamine - unii:tz47u051fi), amphetamine aspartate monohydrate (unii: o1zpv620o4) (amphetamine - unii:ck833kgx7e), amphetamine sulfate (unii: 6dpv8nk46s) (amphetamine - unii:ck833kgx7e) - dextroamphetamine saccharate, amphetamine aspartate monohydrate, dextroamphetamine sulfate and amphetamine sulfate extended-release capsules are indicated for the treatment of attention deficit hyperactivity disorder (adhd) in adults and pediatric patients 6 years and older. dextroamphetamine saccharate, amphetamine aspartate monohydrate, dextroamphetamine sulfate and amphetamine sulfate extended-release capsules administration is contraindicated in patients: - known to be hypersensitive to amphetamine, or other components of dextroamphetamine saccharate, amphetamine aspartate monohydrate, dextroamphetamine sulfate and amphetamine sulfate extended-release capsules. hypersensitivity reactions such as angioedema and anaphylactic reactions have been reported in patients treated with other amphetamine products [see adverse reactions ( 6.2 )] - taking monoamine oxidase inhibitors (maois), or within 14 days of stopping maois (including maois such as linezolid or intravenous methylene blue), because of an increased risk of hypertensive crisis [see warnings and precautions ( 5. 8 ), drug interactions ( 7.1 )] pregnancy exposure registry there is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to dextroamphetamine saccharate, amphetamine aspartate monohydrate, dextroamphetamine sulfate and amphetamine sulfate extended-release capsules during pregnancy. healthcare providers are encouraged to register patients by calling the national pregnancy registry for psychostimulants at 1-866-961-2388 or visiting online at https://womensmentalhealth.org/clinical-and-research-programs/pregnancyregistry/othermedications/. risk summary available data from published epidemiologic studies and postmarketing reports on use of prescription amphetamine in pregnant women have not identified a drug-associated risk of major birth defects and miscarriage (see data ). adverse pregnancy outcomes, including premature delivery and low birth weight, have been seen in infants born to mothers taking amphetamines during pregnancy (see clinical considerations ) . no apparent effects on morphological development were observed in embryo-fetal development studies, with oral administration of amphetamine to rats and rabbits during organogenesis at doses 2 and 12 times, respectively, the maximum recommended human dose (mrhd) of 20 mg/day given to adolescents, on a mg/m 2 basis. however, in a pre-  and postnatal development study, amphetamine ( d- to l- ratio of 3:1) administered orally to pregnant rats during gestation and lactation caused a decrease in pup survival and a decrease in pup body weight that correlated with a delay in developmental landmarks at clinically relevant doses of amphetamine. in addition, adverse effects on reproductive performance were observed in pups whose mothers were treated with amphetamine. long-term neurochemical and behavioral effects have also been reported in animal developmental studies using clinically relevant doses of amphetamine (see data ) . the estimated background risk of major birth defects and miscarriage for the indicated population is unknown. all pregnancies have a background risk of birth defect, loss, or other adverse outcomes. in the u.s. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2 to 4% and 15 to 20%, respectively. clinical considerations fetal/neonatal adverse reactions amphetamines, such as dextroamphetamine saccharate, amphetamine aspartate monohydrate, dextroamphetamine sulfate and amphetamine sulfate extended-release capsules, cause vasoconstriction and thereby may decrease placental perfusion. in addition, amphetamines can stimulate uterine contractions, increasing the risk of premature delivery. infants born to mothers taking amphetamines during pregnancy have an increased risk of premature delivery and low birth weight. monitor infants born to mothers taking amphetamines for symptoms of withdrawal such as feeding difficulties, irritability, agitation, and excessive drowsiness. data animal data amphetamine (d- to l- enantiomer ratio of 3:1) had no apparent effects on embryofetal morphological development or survival when administered orally to pregnant rats and rabbits throughout the period of organogenesis at doses of up to 6 and 16 mg/kg/day, respectively. these doses are approximately 2 and 12 times, respectively, the maximum recommended human dose (mrhd) of 20 mg/day given to adolescents, on a mg/m 2 basis. fetal malformations and death have been reported in mice following parenteral administration of d-amphetamine doses of 50 mg/kg/day (approximately 10 times the mrhd given to adolescents on a mg/m 2 basis) or greater to pregnant animals. administration of these doses was also associated with severe maternal toxicity. a study was conducted in which pregnant rats received daily oral doses of amphetamine (d- to l-enantiomer ratio of 3:1) of 2, 6, and 10 mg/kg from gestation day 6 to lactation day 20. these doses are approximately 0.8, 2, and 4 times the mrhd of 20 mg/day given to adolescents, on a mg/m 2 basis. all doses caused hyperactivity and decreased weight gain in the dams. a decrease in pup survival was seen at all doses. a decrease in pup body weight was seen at 6 and 10 mg/kg which correlated with delays in developmental landmarks, such as preputial separation and vaginal opening. increased pup locomotor activity was seen at 10 mg/kg on day 22 postpartum but not at 5 weeks postweaning. when pups were tested for reproductive performance at maturation, gestational weight gain, number of implantations, and number of delivered pups were decreased in the group whose mothers had been given 10 mg/kg. a number of studies from the literature in rodents indicate that prenatal or early postnatal exposure to amphetamine (d- or d, l-) at doses similar to those used clinically can result in long-term neurochemical and behavioral alterations. reported behavioral effects include learning and memory deficits, altered locomotor activity, and changes in sexual function. risk summary based on limited case reports in published literature, amphetamine (d- or d, l-) is present in human milk, at relative infant doses of 2 to 13.8% of the maternal weight-adjusted dosage and a milk/plasma ratio ranging between 1.9 and 7.5. there are no reports of adverse effects on the breastfed infant. long-term neurodevelopmental effects on infants from amphetamine exposure are unknown. it is possible that large dosages of amphetamine might interfere with milk production, especially in women whose lactation is not well established. because of the potential for serious adverse reactions in nursing infants, advise patients that breastfeeding is not recommended during treatment with dextroamphetamine saccharate, amphetamine aspartate monohydrate, dextroamphetamine sulfate and amphetamine sulfate extended-release capsules. the safety and effectiveness of dextroamphetamine saccharate, amphetamine aspartate monohydrate, dextroamphetamine sulfate and amphetamine sulfate extended-release capsules have been established in pediatric patients with adhd 6 years of age and older. the safety and efficacy of dextroamphetamine saccharate, amphetamine aspartate monohydrate, dextroamphetamine sulfate and amphetamine sulfate extended-release capsules in pediatric patients less than 6 years of age have not been established. long-term effects of amphetamines in pediatric patients have not been well established. long-term growth suppression growth should be monitored during treatment with stimulants, including dextroamphetamine saccharate, amphetamine aspartate monohydrate, dextroamphetamine sulfate and amphetamine sulfate extended-release capsules, and pediatric patients aged 6 to 17 years who are not growing or gaining weight as expected may need to have their treatment interrupted [see warnings and precautions ( 5.5)] . juvenile animal toxicity data juvenile rats treated with mixed amphetamine salts early in the postnatal period through sexual maturation demonstrated transient changes in motor activity. learning and memory was impaired at approximately 6 times the maximum recommended human dose (mrhd) given to children on a mg/m 2 basis. no recovery was seen following a drug-free period. a delay in sexual maturation was observed at a dose approximately 6 times the mrhd given to children on a mg/m 2 basis, although there was no effect on fertility. in a juvenile developmental study, rats received daily oral doses of amphetamine (d to l enantiomer ratio of 3:1) of 2, 6, or 20 mg/kg on days 7 to 13 of age; from day 14 to approximately day 60 of age these doses were given b.i.d. for total daily doses of 4, 12, or 40 mg/kg. the latter doses are approximately 0.6, 2, and 6 times the mrhd of 30 mg/day, given to children on a mg/m 2 basis. postdosing hyperactivity was seen at all doses; motor activity measured prior to the daily dose was decreased during the dosing period but the decreased motor activity was largely absent after an 18 day drug-free recovery period. performance in the morris water maze test for learning and memory was impaired at the 40 mg/kg dose, and sporadically at the lower doses, when measured prior to the daily dose during the treatment period; no recovery was seen after a 19 day drug-free period. a delay in the developmental milestones of vaginal opening and preputial separation was seen at 40 mg/kg but there was no effect on fertility. dextroamphetamine saccharate, amphetamine aspartate monohydrate, dextroamphetamine sulfate and amphetamine sulfate extended-release capsules have not been studied in the geriatric population. due to reduced clearance of amphetamines in patients with severe renal impairment (gfr 15 to <30 ml/min/1.73 m 2 ), the recommended dose should be reduced. dextroamphetamine saccharate, amphetamine aspartate monohydrate, dextroamphetamine sulfate and amphetamine sulfate extended-release capsules are not recommended in patients with esrd (gfr <15 ml/min/1.73 m 2 ) [see dosage and administration ( 2.6 ), clinical pharmacology ( 12.3 )]. d-amphetamine is not dialyzable. dextroamphetamine saccharate, amphetamine aspartate monohydrate, dextroamphetamine sulfate and amphetamine sulfate extended-release capsules contain amphetamine, a schedule ii controlled substance. dextroamphetamine saccharate, amphetamine aspartate monohydrate, dextroamphetamine sulfate and amphetamine sulfate extended-release capsules 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)] . dextroamphetamine saccharate, amphetamine aspartate monohydrate, dextroamphetamine sulfate and amphetamine sulfate extended-release capsules 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 healthcare 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 amphetamine 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 dextroamphetamine saccharate, amphetamine aspartate monohydrate, dextroamphetamine sulfate and amphetamine sulfate extended-release capsules, 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. physical dependence dextroamphetamine saccharate, amphetamine aspartate monohydrate, dextroamphetamine sulfate and amphetamine sulfate extended-release capsules 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 dextroamphetamine saccharate, amphetamine aspartate monohydrate, dextroamphetamine sulfate and amphetamine sulfate extended-release capsules include dysphoric mood; depression; fatigue; vivid, unpleasant dreams; insomnia or hypersomnia; increased appetite; and psychomotor retardation or agitation. tolerance dextroamphetamine saccharate, amphetamine aspartate monohydrate, dextroamphetamine sulfate and amphetamine sulfate extended-release capsules 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).

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

golden state medical supply, inc. - clomipramine hydrochloride (unii: 2lxw0l6gwj) (clomipramine - unii:nuv44l116d) - clomipramine hydrochloride capsules usp are indicated for the treatment of obsessions and compulsions in patients with obsessive-compulsive disorder (ocd). the obsessions or compulsions must cause marked distress, be time-consuming, or significantly interfere with social or occupational functioning, in order to meet the dsm-iii-r (circa 1989) diagnosis of ocd. obsessions are recurrent, persistent ideas, thoughts, images, or impulses that are ego-dystonic. compulsions are repetitive, purposeful, and intentional behaviors performed in response to an obsession or in a stereotyped fashion, and are recognized by the person as excessive or unreasonable. the effectiveness of clomipramine for the treatment of ocd was demonstrated in multicenter, placebo-controlled, parallel-group studies, including two 10-week studies in adults and one 8-week study in children and adolescents 10 to 17 years of age. patients in all studies had moderate-to-severe ocd (dsm-iii), with mean baseline ratings on the yale-brown obsessive com

Australia - English - Department of Health (Therapeutic Goods Administration)

pacific applied health pty ltd - olea europaea,propolis -