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

genzyme corporation - alemtuzumab (unii: 3a189dh42v) (alemtuzumab - unii:3a189dh42v) - alemtuzumab 12 mg in 1.2 ml - lemtrada is indicated for the treatment of relapsing forms of multiple sclerosis (ms), to include relapsing-remitting disease and active secondary progressive disease, in adults. because of its safety profile, the use of lemtrada should generally be reserved for patients who have had an inadequate response to two or more drugs indicated for the treatment of ms [see warnings and precautions (5)] . limitations of use lemtrada is not recommended for use in patients with clinically isolated syndrome (cis) because of its safety profile [see warnings and precautions (5)]. lemtrada is contraindicated in patients: - with known hypersensitivity or anaphylactic reactions to alemtuzumab or any of the excipients in lemtrada - who are infected with human immunodeficiency virus (hiv) because lemtrada causes prolonged reductions of cd4+ lymphocyte counts - with active infection risk summary there are no adequate data on the developmental risk associated with the use of lemtrada in pregnant women. lemtrada was embryolethal in pregnant hucd52 transgenic mice when administered during organogenesis [see animal data] . auto-antibodies may develop after administration of lemtrada. placental transfer of anti-thyroid antibodies resulting in neonatal graves' disease has been reported. 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. there is a pregnancy surveillance program for lemtrada. if lemtrada exposure occurs during pregnancy, healthcare providers and patients are encouraged to report pregnancies by calling 1-800-745-4447, option 2. clinical considerations lemtrada induces persistent thyroid disorders [see warnings and precautions (5.8)] . untreated hypothyroidism in pregnant women increases the risk for miscarriage and may have effects on the fetus including mental retardation and dwarfism. in mothers with graves' disease, maternal thyroid stimulating hormone receptor antibodies can be transferred to a developing fetus and can cause neonatal graves' disease. in a patient who developed graves' disease after treatment with alemtuzumab, placental transfer of anti-thyrotropin receptor antibodies resulted in neonatal graves' disease with thyroid storm in her infant who was born 1 year after alemtuzumab dosing [see warnings and precautions (5.1)] . data animal data when lemtrada was administered to pregnant hucd52 transgenic mice during organogenesis (gestation days [gd] 6–10 or gd 11–15) at doses of 3 or 10 mg/kg iv, no teratogenic effects were observed. however, there was an increase in embryolethality (increased postimplantation loss and the number of dams with all fetuses dead or resorbed) in pregnant animals dosed during gd 11–15. in a separate study in pregnant hucd52 transgenic mice, administration of lemtrada during organogenesis (gd 6–10 or gd 11–15) at doses of 3 or 10 mg/kg iv, decreases in b- and t-lymphocyte populations were observed in the offspring at both doses tested. in pregnant hucd52 transgenic mice administered lemtrada at doses of 3 or 10 mg/kg/day iv throughout gestation and lactation, there was an increase in pup deaths during the lactation period at 10 mg/kg. decreases in t- and b-lymphocyte populations and in antibody response were observed in offspring at both doses tested. risk summary there are no data on the presence of alemtuzumab in human milk, the effects on the breastfed infant, or the effects of the drug on milk production. alemtuzumab was detected in the milk of lactating hucd52 transgenic mice administered lemtrada [see animal data]. the developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for lemtrada and any potential adverse effects on the breastfed child from lemtrada or from the underlying maternal conditions. data animal data alemtuzumab was detected in the milk of lactating hucd52 transgenic mice following intravenous administration of lemtrada at a dose of 10 mg/kg on postpartum days 8–12. serum levels of alemtuzumab were similar in lactating mice and offspring on postpartum day 13 and were associated with evidence of pharmacological activity (decrease in lymphocyte counts) in the offspring. contraception before initiation of lemtrada treatment, women of childbearing potential should be counselled on the potential for a serious risk to the fetus. to avoid in utero exposure to lemtrada, women of childbearing potential should use effective contraceptive measures when receiving a course of treatment with lemtrada and for 4 months following that course of treatment [see use in specific populations (8.1)] . infertility in hucd52 transgenic mice, administration of lemtrada prior to and during the mating period resulted in adverse effects on sperm parameters in males and reduced number of corpora lutea and implantations in females [see nonclinical toxicology (13.1)] . safety and effectiveness in pediatric patients less than 17 years of age have not been established. use of lemtrada is not recommended in pediatric patients due to the risks of autoimmunity, infusion reactions, and stroke, and because it may increase the risk of malignancies (thyroid, melanoma, lymphoproliferative disorders, and lymphoma) [see warnings and precautions (5.1, 5.2, 5.3, 5.4)] . clinical studies of lemtrada did not include sufficient numbers of patients aged 65 and over to determine whether they respond differently than younger patients.

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

genzyme corporation - eliglustat (unii: dr40j4wa67) (eliglustat - unii:dr40j4wa67) - eliglustat 84 mg - cerdelga is indicated for the long-term treatment of adult patients with gaucher disease type 1 (gd1) who are cyp2d6 extensive metabolizers (ems), intermediate metabolizers (ims), or poor metabolizers (pms) as detected by an fda-cleared test [see dosage and administration (2.1)] . limitations of use : - patients who are cyp2d6 ultra-rapid metabolizers (urms) may not achieve adequate concentrations of cerdelga to achieve a therapeutic effect [see clinical studies (14)] . - a specific dosage cannot be recommended for those patients whose cyp2d6 genotype cannot be determined (indeterminate metabolizers) [see clinical studies (14)] . cerdelga is contraindicated in the following patients based on cyp2d6 metabolizer status due to the risk of cardiac arrhythmias from prolongation of the pr, qtc, and/or qrs cardiac intervals. ems - taking a strong or moderate cyp2d6 inhibitor concomitantly with a strong or moderate cyp3a inhibitor [see drug interactions (7.1)] - moderate or severe hepatic impairment [see use in specific populations (8.7)] - mild hepatic impairment and taking a strong or moderate cyp2d6 inhibitor [see use in specific populations (8.7)] ims - taking a strong or moderate cyp2d6 inhibitor concomitantly with a strong or moderate cyp3a inhibitor [see drug interactions (7.1)] - taking a strong cyp3a inhibitor [see drug interactions (7.1)] - any degree of hepatic impairment [see use in specific populations (8.7)] pms - taking a strong cyp3a inhibitor [see drug interactions (7.1)] - any degree of hepatic impairment [see use in specific populations (8.7)] risk summary available data on cerdelga use in pregnant women includes 20 pregnancies that occurred during the clinical development program and a small number of post-marketing case reports. these data are not sufficient to assess drug-associated risks major birth defects, miscarriage, or adverse maternal or fetal outcomes. in animal reproduction studies in pregnant rats administered oral eliglustat during organogenesis, a spectrum of various developmental abnormalities were observed at doses 6 times the recommended human dose. no adverse developmental outcomes were observed with oral administration of eliglustat to pregnant rabbits at dose levels 10 times the recommended human dose [see data] . the estimated background risk of major birth defects and miscarriage in the indicated population is unknown. all pregnancies have a background risk of birth defect, loss or other adverse outcomes. in the u.s. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively. clinical considerations disease-associated maternal and/or embryo/fetal risk women with gaucher disease type 1 have an increased risk of spontaneous abortion, especially if disease symptoms are not treated and controlled pre-conception and during a pregnancy. pregnancy may exacerbate existing gaucher disease type 1 symptoms or result in new disease manifestations. gaucher disease type 1 manifestations may lead to adverse pregnancy outcomes including, hepatosplenomegaly which can interfere with the normal growth of a pregnancy and thrombocytopenia which can lead to increased bleeding and possible hemorrhage. data animal data reproduction studies have been performed in pregnant rats at oral doses up to 120 mg/kg/day (about 6 times the recommended human dose based on body surface area) and in pregnant rabbits at oral doses up to 100 mg/kg/day (about 10 times the recommended human dose based on body surface area) following administration of eliglustat during the period of organogenesis (gestation days 6 to 17 in the rat and 6 to 18 in the rabbit). in rats, at 120 mg/kg/day (about 6 times the recommended human dose based on body surface area), eliglustat increased the number of late resorptions, dead fetuses and post implantation loss, reduced fetal body weight, and caused fetal cerebral variations (dilated cerebral ventricles), fetal skeletal variations (poor bone ossification) and fetal skeletal malformations (abnormal number of ribs or lumbar vertebra). eliglustat-related effects on fetal rats were observed in association with signs of maternal toxicity. eliglustat did not cause fetal harm in rabbits at oral doses up to 100 mg/kg/day (about 10 times the recommended human dose based on body surface area). mild maternal toxicity was observed at the 100 mg/kg/day dose. in a pre and postnatal development study in rats (dosed daily from gestation day 6 to postpartum day 21), eliglustat did not show any significant adverse effects on pre and postnatal development at doses up to 100 mg/kg/day (about 5 times the recommended human dose based on body surface area). risk summary there are no human data available on the presence of eliglustat in human milk, the effects on the breastfed infant, or the effects on milk production. eliglustat and its metabolites were present in the milk of lactating rats [see data] . when a drug is present in animal milk, it is likely that the drug will be present in human milk. the developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for cerdelga and any potential adverse effects on the breastfed child from cerdelga or from the underlying maternal condition. data in a milk excretion study in the rat, a single oral dose of 30 mg/kg [14 c]-labeled eliglustat was administered to lactating female rats at day 11 postpartum. approximately 0.23% of the administered radioactivity was excreted into the milk within 24 hours of dose administration. the concentration in the milk at 24 hours post dose was 16.3-fold higher than the plasma concentration. safety and effectiveness in pediatric patients have not been established. clinical studies of cerdelga did not include sufficient numbers of subjects aged 65 and over to determine whether they respond differently from younger subjects. clinical experience has not identified differences in responses between the elderly and younger patients. use cerdelga in patients with renal impairment based on the patient's cyp2d6 metabolizer status [see clinical pharmacology (12.3)] . ems - avoid cerdelga in patients with end-stage renal disease (esrd) (estimated creatinine clearance (eclcr) less than 15 ml/min not on dialysis or requiring dialysis). - no dosage adjustment is recommended in patients with mild, moderate, or severe renal impairment (eclcr at least 15 ml/min). ims and pms - avoid cerdelga in patients with any degree of renal impairment. use cerdelga in patients with hepatic impairment based on cyp2d6 metabolizer status and concomitant use of cyp2d6 or cyp3a inhibitors [see clinical pharmacology (12.3)] . ems - cerdelga is contraindicated in patients with [see contraindications (4)] : severe (child-pugh class c) hepatic impairment moderate (child-pugh class b) hepatic impairment mild (child-pugh class a) hepatic impairment taking a strong or moderate cyp2d6 inhibitor - severe (child-pugh class c) hepatic impairment - moderate (child-pugh class b) hepatic impairment - mild (child-pugh class a) hepatic impairment taking a strong or moderate cyp2d6 inhibitor - reduce dosage frequency of cerdelga 84 mg to once daily [see dosage and administration (2.3)] in patients with mild hepatic impairment taking: a weak cyp2d6 inhibitor a strong, moderate, or weak cyp3a inhibitor - a weak cyp2d6 inhibitor - a strong, moderate, or weak cyp3a inhibitor - no dosage adjustment is recommended in patients with mild hepatic impairment, unless otherwise specified above. ims and pms - cerdelga is contraindicated in patients with any degree of hepatic impairment [see contraindications (4)] .

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

genzyme corporation - vandetanib (unii: yo460oq37k) (vandetanib - unii:yo460oq37k) - vandetanib 100 mg - caprelsa is indicated for the treatment of symptomatic or progressive medullary thyroid cancer in patients with unresectable locally advanced or metastatic disease. use caprelsa in patients with indolent, asymptomatic or slowly progressing disease only after careful consideration of the treatment related risks of caprelsa. do not use in patients with congenital long qt syndrome [see boxed warning] . risk summary based on its mechanism of action and findings in animals, caprelsa can cause fetal harm when administered to a pregnant woman. there are no available human data on caprelsa use in pregnant women to inform a drug-associated risk. vandetanib is embryotoxic, fetotoxic, and induced fetal malformations in rats at exposures less than or equal to those expected at the recommended human dose of 300 mg/day. advise patients of the potential risk to a fetus. in the u.s. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively. data animal data in reproductive toxicity studies, administration of vandetanib to female rats prior to mating and through the first week of pregnancy at a dose of 25 mg/kg/day (approximately equal to the human exposure at the 300 mg clinical dose based on cmax ), there were increases in pre-implantation loss and post-implantation loss resulting in a reduction in the number of live embryos. during organogenesis, vandetanib caused an increase in post-implantation loss, including occasional total litter loss at a dose of 25 mg/kg/day. at doses greater than 10 mg/kg/day (approximately 0.4 times the human cmax at the 300 mg clinical dose) treatment with vandetanib resulted in increases in late embryofetal death and decreases in fetal birth weight. a no-effect level for malformations was not identified in this study. administration of vandetanib at doses greater than or equal to 1 mg/kg/day (approximately 0.03 times the human cmax at the 300 mg clinical dose) resulted in dose dependent increases in both malformations of the heart vessels and skeletal variations including delayed ossification of the skull, vertebrae, and sternum, indicating delayed fetal development. in a rat prenatal and postnatal development study, at doses (1 and 10 mg/kg/day) producing mild maternal toxicity during gestation and/or lactation, vandetanib decreased pup survival and reduced postnatal pup growth. reduced postnatal pup growth was associated with a delay in physical development. risk summary there are no data on the presence of vandetanib or its metabolites in human milk, the effects on the breastfed child or on milk production. vandetanib was present in the milk of lactating rats (see data) . because of the potential for serious adverse reactions from caprelsa in breastfed children, advise lactating women not to breastfeed during treatment with caprelsa and for 4 months after the last dose. data animal data in nonclinical studies, vandetanib was excreted in rat milk and found in plasma of pups following dosing to lactating rats. vandetanib transfer in breast milk resulted in relatively constant exposure in pups due to the long half-life of the drug. pregnancy testing verify the pregnancy status of females of reproductive potential prior to initiating treatment with caprelsa [see use in specific populations (8.1)] . contraception caprelsa can cause fetal harm when administered to a pregnant woman [see use in specific populations (8.1)] . females advise females of reproductive potential to use effective contraception during treatment with caprelsa and for 4 months after the last dose. males advise males with female partners of reproductive potential to use effective contraception during treatment with caprelsa and for 4 months after the last dose. infertility there are no data on the effect of caprelsa on human fertility. results from animal studies indicate that vandetanib can impair male and female fertility [see nonclinical toxicology (13.1)] . safety and efficacy of caprelsa in pediatric patients have not been established. the mtc study of caprelsa did not include sufficient numbers of patients aged 65 years and over to determine whether they respond differently compared to younger patients. vandetanib exposure is increased in patients with impaired renal function. reduce the starting dose to 200 mg in patients with moderate (creatinine clearance ≥30 to <50 ml/min) renal impairment [see dosage and administration (2.1), warnings and precautions (5.12), and clinical pharmacology (12.3)] . vandetanib is not recommended for use in patients with severe renal impairment (clearance below 30 ml/min) [see warnings and precautions (5.12)] . patients with end-stage renal disease requiring dialysis were not studied [see adverse reactions (6.1)] . the pharmacokinetics of caprelsa were evaluated after a single dose of 800 mg in subjects with mild (n=8), moderate (n=7), and severe (n=6) hepatic impairment and normal hepatic function (n=5). subjects with mild (child-pugh class a), moderate (child-pugh class b), and severe (child-pugh class c) hepatic impairment had comparable mean auc and clearance values to those with normal hepatic function. there are limited data in patients with liver impairment (serum bilirubin greater than 1.5 times the upper limit of normal). caprelsa is not recommended for use in patients with moderate and severe hepatic impairment, as safety and efficacy have not been established [see dosage and administration (2.1) and warnings and precautions (5.13)] .

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

genzyme corporation - teriflunomide (unii: 1c058ikg3b) (teriflunomide - unii:1c058ikg3b) - teriflunomide 7 mg - aubagio® is indicated for the treatment of relapsing forms of multiple sclerosis (ms), to include clinically isolated syndrome, relapsing-remitting disease, and active secondary progressive disease, in adults. aubagio is contraindicated in/with: - patients with severe hepatic impairment [see warnings and precautions (5.1)] . - pregnant women and females of reproductive potential not using effective contraception. aubagio may cause fetal harm [see warnings and precautions (5.2, 5.3) and use in specific populations (8.1)] . - patients with a history of a hypersensitivity reaction to teriflunomide, leflunomide, or to any of the inactive ingredients in aubagio. reactions have included anaphylaxis, angioedema, and serious skin reactions [see warnings and precautions (5.5)]. - coadministration with leflunomide [see clinical pharmacology (12.3)]. risk summary aubagio is contraindicated for use in pregnant women and females of reproductive potential not using effective contraception because of the potential for fetal harm based on animal data [see contraindications (4) and warnings and precautions (5.2)] . in animal reproduction studies in rat and rabbit, oral administration of teriflunomide during organogenesis caused teratogenicity and embryolethality at plasma exposures (auc) lower than that at the maximum recommended human dose (mrhd) of 14 mg/day [see data]. available human data from pregnancy registries, clinical trials, pharmacovigilance cases, and published literature are too limited to draw any conclusions, but they do not clearly indicate increased birth defects or miscarriage associated with inadvertent teriflunomide exposure in the early first trimester when followed by an accelerated elimination procedure [see clinical considerations and data] . there are no human data pertaining to exposures later in the first trimester or beyond. in the us general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2%–4% and 15%–20%, respectively. the background risk of major birth defects and miscarriage in the indicated population is unknown. there is a pregnancy surveillance program for aubagio. if aubagio exposure occurs during pregnancy, healthcare providers and patients are encouraged to report pregnancies by calling 1-800-745-4447, option 2. clinical considerations fetal/neonatal adverse reactions lowering the plasma concentration of teriflunomide by instituting an accelerated drug elimination procedure as soon as pregnancy is detected may decrease the risk to the fetus from aubagio. the accelerated drug elimination procedure includes verification that the plasma teriflunomide concentration is less than 0.02 mg/l [see warnings and precautions (5.3) and clinical pharmacology (12.3)]. data human data available human data are limited. prospectively reported data (from clinical trials and postmarketing reports) from >150 pregnancies in patients treated with teriflunomide and >300 pregnancies in patients treated with leflunomide have not demonstrated an increased rate of congenital malformations or miscarriage following teriflunomide exposure in the early first trimester when followed by an accelerated elimination procedure. specific patterns of major congenital malformations in humans have not been observed. limitations of these data include an inadequate number of reported pregnancies from which to draw conclusions, the short duration of drug exposure in reported pregnancies, which precludes a full evaluation of the fetal risks, incomplete reporting, and the inability to control for confounders (such as underlying maternal disease and use of concomitant medications). animal data when teriflunomide (oral doses of 1, 3, or 10 mg/kg/day) was administered to pregnant rats throughout the period of organogenesis, high incidences of fetal malformation (primarily craniofacial, and axial and appendicular skeletal defects) and fetal death were observed at doses not associated with maternal toxicity. adverse effects on fetal development were observed following dosing at various stages throughout organogenesis. maternal plasma exposure at the no-effect level (1.0 mg/kg/day) for fetal developmental toxicity in rats was less than that in humans at the maximum recommended human dose (mrhd, 14 mg/day). administration of teriflunomide (oral doses of 1, 3.5, or 12 mg/kg/day) to pregnant rabbits throughout organogenesis resulted in high incidences of fetal malformation (primarily craniofacial, and axial and appendicular skeletal defects) and fetal death at doses associated with minimal maternal toxicity. maternal plasma exposure at the no-effect dose (1.0 mg/kg/day) for fetal developmental toxicity in rabbits was less than that in humans at the mrhd. in studies in which teriflunomide (oral doses of 0.05, 0.1, 0.3, 0.6, or 1.0 mg/kg/day) was administered to rats during gestation and lactation, decreased growth, eye and skin abnormalities, and high incidences of malformation (limb defects) and postnatal death were observed in the offspring at doses not associated with maternal toxicity. maternal plasma exposure at the no-effect dose for prenatal and postnatal developmental toxicity in rats (0.10 mg/kg/day) was less than that in humans at the mrhd. in animal reproduction studies of leflunomide, embryolethality and teratogenic effects were observed in pregnant rat and rabbit at or below clinically relevant plasma teriflunomide exposures (auc). in published reproduction studies in pregnant mice, leflunomide was embryolethal and increased the incidence of malformations (craniofacial, axial skeletal, heart and great vessel). supplementation with exogenous uridine reduced the teratogenic effects in pregnant mice, suggesting that the mode of action (inhibition of mitochondrial enzyme dihydroorotate dehydrogenase) is the same for therapeutic efficacy and developmental toxicity. at recommended doses in humans, teriflunomide and leflunomide result in a similar range of plasma concentrations of teriflunomide. risk summary there are no data on the presence of aubagio in human milk, the effects on the breastfed infant, or the effects on milk production. teriflunomide was detected in rat milk following a single oral dose. because of the potential for adverse reactions in a breastfed infant from aubagio, women should not breastfeed during treatment with aubagio. pregnancy testing exclude pregnancy prior to initiation of treatment with aubagio in females of reproductive potential. advise females to notify their healthcare provider immediately if pregnancy occurs or is suspected during treatment [see warnings and precautions (5.2, 5.3) and use in specific populations (8.1)]. contraception females females of reproductive potential should use effective contraception while taking aubagio. if aubagio is discontinued, use of contraception should be continued until it is verified that plasma concentrations of teriflunomide are less than 0.02 mg/l (0.02 mcg/ml, the level expected to have minimal fetal risk, based on animal data). females of reproductive potential who wish to become pregnant should discontinue aubagio and undergo an accelerated elimination procedure. effective contraception should be used until it is verified that plasma concentrations of teriflunomide are less than 0.02 mg/l (0.02 mcg/ml) [see warnings and precautions (5.2, 5.3) and use in specific populations (8.1)] . males aubagio is detected in human semen. animal studies to specifically evaluate the risk of male mediated fetal toxicity have not been conducted. to minimize any possible risk, men not wishing to father a child and their female partners should use effective contraception. men wishing to father a child should discontinue use of aubagio and either undergo an accelerated elimination procedure or wait until verification that the plasma teriflunomide concentration is less than 0.02 mg/l (0.02 mcg/ml) [see warnings and precautions (5.3)]. safety and effectiveness in pediatric patients have not been established. effectiveness of aubagio for the treatment of relapsing form of multiple sclerosis in pediatric patients (10 to 17 years of age) was not established in an adequate and well-controlled clinical study in 166 patients (109 patients received once-daily doses of aubagio and 57 patients received placebo) for up to 96 weeks. pancreatitis has been reported in adults in the postmarketing setting, but appears to occur at higher frequency in the pediatric population. in this pediatric study, cases of pancreatitis were reported in 1.8% (2/109) of patients who received aubagio compared to no patients in the placebo group. all patients in the pediatric trial recovered or were recovering after treatment discontinuation and accelerated elimination procedure [see warnings and precautions (5.11)] . additionally, elevated or abnormal blood creatine phosphokinase was reported in 6.4% of pediatric patients who received aubagio compared to no patients in the placebo group. juvenile animal toxicity data oral administration of teriflunomide (0, 0.3, 3, or 6 mg/kg/day) to young rats on postnatal days 21 to 70 resulted in suppression of immune function (t-cell dependent antibody response) at the mid and high doses, and adverse effects on male reproductive organs (reduced sperm count) and altered neurobehavioral function (increased locomotor activity) at the high dose. at the no-effect dose (0.3 mg/kg/day) for developmental toxicity in juvenile rats, plasma exposures were less than those in pediatric patients at the doses of aubagio tested in the clinical study. clinical studies of aubagio did not include patients over 65 years old. no dosage adjustment is necessary for patients with mild and moderate hepatic impairment. the pharmacokinetics of teriflunomide in severe hepatic impairment has not been evaluated. aubagio is contraindicated in patients with severe hepatic impairment [see contraindications (4), warnings and precautions (5.1), and clinical pharmacology (12.3)] . no dosage adjustment is necessary for patients with mild, moderate, and severe renal impairment [see clinical pharmacology (12.3)] .

Panama - English - Ministerio de Salud (Dirección Nacional de Farmacia Y Drogas)

genzyme corporation - hilano - hilano....8mg

Panama - English - Ministerio de Salud (Dirección Nacional de Farmacia Y Drogas)

genzyme corporation - hilano - hilano....8.0mg

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

genzyme corporation - clofarabine (unii: 762rdy0y2h) (clofarabine - unii:762rdy0y2h) - clofarabine 1 mg in 1 ml

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

genzyme corporation - autologous cultured chondrocytes (unii: d5p3k3v822) (autologous cultured chondrocytes - unii:d5p3k3v822) - autologous cultured chondrocytes 1.2e+007

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

genzyme corporation - alglucosidase alfa (unii: dti67o9503) (alglucosidase alfa - unii:dti67o9503) - alglucosidase alfa 5 mg in 1 ml

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

genzyme corporation - mipomersen sodium (unii: 18eay4870e) (mipomersen - unii:9gj8s4gu0m) - mipomersen sodium 200 mg in 1 ml