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

pfizer australia pty ltd - paracetamol, quantity: 500 mg - injection, solution - excipient ingredients: hydrochloric acid; sodium citrate dihydrate; sodium acetate trihydrate; glucose monohydrate; sodium hydroxide; glacial acetic acid; water for injections - for the relief of mild to moderate pain and the reduction of fever where an intravenous route of administration is considered clinically necessary.

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

pfizer laboratories div pfizer inc - celecoxib (unii: jcx84q7j1l) (celecoxib - unii:jcx84q7j1l) - celecoxib 50 mg - celebrex is indicated for the management of the signs and symptoms of oa [see clinical studies (14.1) ]. for the management of the signs and symptoms of ra [see clinical studies (14.2) ]. for the management of the signs and symptoms of jra in patients 2 years and older [see clinical studies (14.3) ]. for the management of the signs and symptoms of as [see clinical studies (14.4) ]. for the management of acute pain in adults [see clinical studies (14.5) ]. for the management of primary dysmenorrhea [see clinical studies (14.5) ]. celebrex is contraindicated in the following patients: risk summary use of nsaids, including celebrex, can cause premature closure of the fetal ductus arteriosus and fetal renal dysfunction leading to oligohydramnios and, in some cases, neonatal renal impairment. because of these risks, limit dose and duration of celebrex use between about 20 and 30 weeks of gestation and avoid celebrex use at about 30 weeks of gestation and later in pregnancy (see error! hyperlink reference not valid. , error! hyperlink reference not valid. ). premature closure of fetal ductus arteriosus use of nsaids, including celebrex, at about 30 weeks gestation or later in pregnancy increases the risk of premature closure of the fetal ductus arteriosus. oligohydramnios/neonatal renal impairment use of nsaids at about 20 weeks gestation or later in pregnancy has been associated with cases of fetal renal dysfunction leading to oligohydramnios, and in some cases, neonatal renal impairment. data from observational studies regarding other potential embryofetal risks of nsaid use in women in the first or second trimesters of pregnancy are inconclusive. in animal reproduction studies, embryo-fetal deaths and an increase in diaphragmatic hernias were observed in rats administered celecoxib daily during the period of organogenesis at oral doses approximately 6 times the maximum recommended human dose (mrhd) of 200 mg twice daily. in addition, structural abnormalities (e.g., septal defects, ribs fused, sternebrae fused and sternebrae misshapen) were observed in rabbits given daily oral doses of celecoxib during the period of organogenesis at approximately 2 times the mrhd (see error! hyperlink reference not valid. ). based on animal data, prostaglandins have been shown to have an important role in endometrial vascular permeability, blastocyst implantation, and decidualization. in animal studies, administration of prostaglandin synthesis inhibitors such as celecoxib, resulted in increased pre- and post-implantation loss. prostaglandins also have been shown to have an important role in fetal kidney development. in published animal studies, prostaglandin synthesis inhibitors have been reported to impair kidney development when administered at clinically relevant doses. 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 premature closure of fetal ductus arteriosus: avoid use of nsaids in women at about 30 weeks gestation and later in pregnancy, because nsaids, including celebrex, can cause premature closure of the fetal ductus arteriosus (see error! hyperlink reference not valid. ). oligohydramnios/neonatal renal impairment: if an nsaid is necessary at about 20 weeks gestation or later in pregnancy, limit the use to the lowest effective dose and shortest duration possible. if celebrex treatment extends beyond 48 hours, consider monitoring with ultrasound for oligohydramnios. if oligohydramnios occurs, discontinue celebrex and follow up according to clinical practice (see error! hyperlink reference not valid. ). labor or delivery there are no studies on the effects of celebrex during labor or delivery. in animal studies, nsaids, including celecoxib, inhibit prostaglandin synthesis, cause delayed parturition, and increase the incidence of stillbirth. data human data the available data do not establish the presence or absence of developmental toxicity related to the use of celebrex. premature closure of fetal ductus arteriosus: published literature reports that the use of nsaids at about 30 weeks of gestation and later in pregnancy may cause premature closure of the fetal ductus arteriosus. oligohydramnios/neonatal renal impairment: published studies and postmarketing reports describe maternal nsaid use at about 20 weeks gestation or later in pregnancy associated with fetal renal dysfunction leading to oligohydramnios, and in some cases, neonatal renal impairment. these adverse outcomes are seen, on average, after days to weeks of treatment, although oligohydramnios has been infrequently reported as soon as 48 hours after nsaid initiation. in many cases, but not all, the decrease in amniotic fluid was transient and reversible with cessation of the drug. there have been a limited number of case reports of maternal nsaid use and neonatal renal dysfunction without oligohydramnios, some of which were irreversible. some cases of neonatal renal dysfunction required treatment with invasive procedures, such as exchange transfusion or dialysis. methodological limitations of these postmarketing studies and reports include lack of a control group; limited information regarding dose, duration, and timing of drug exposure; and concomitant use of other medications. these limitations preclude establishing a reliable estimate of the risk of adverse fetal and neonatal outcomes with maternal nsaid use. because the published safety data on neonatal outcomes involved mostly preterm infants, the generalizability of certain reported risks to the full-term infant exposed to nsaids through maternal use is uncertain. animal data celecoxib at oral doses ≥150 mg/kg/day (approximately 2 times the human exposure at 200 mg twice daily as measured by auc0–24 ), caused an increased incidence of ventricular septal defects, a rare event, and fetal alterations, such as ribs fused, sternebrae fused and sternebrae misshapen when rabbits were treated throughout organogenesis. a dose-dependent increase in diaphragmatic hernias was observed when rats were given celecoxib at oral doses ≥30 mg/kg/day (approximately 6 times human exposure based on the auc0–24 at 200 mg twice daily for ra) throughout organogenesis. in rats, exposure to celecoxib during early embryonic development resulted in pre-implantation and post-implantation losses at oral doses ≥50 mg/kg/day (approximately 6 times human exposure based on the auc0–24 at 200 mg twice daily for ra). celecoxib produced no evidence of delayed labor or parturition at oral doses up to 100 mg/kg in rats (approximately 7-fold human exposure as measured by the auc0–24 at 200 mg twice daily). the effects of celebrex on labor and delivery in pregnant women are unknown. risk summary limited data from 3 published reports that included a total of 12 breastfeeding women showed low levels of celebrex in breast milk. the calculated average daily infant dose was 10 to 40 mcg/kg/day, less than 1% of the weight-based therapeutic dose for a two-year old-child. a report of two breastfed infants 17 and 22 months of age did not show any adverse events. caution should be exercised when celebrex is administered to a nursing woman. the developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for celebrex and any potential adverse effects on the breastfed infant from the celebrex or from the underlying maternal condition. infertility females based on the mechanism of action, the use of prostaglandin-mediated nsaids, including celebrex, may delay or prevent rupture of ovarian follicles, which has been associated with reversible infertility in some women. published animal studies have shown that administration of prostaglandin synthesis inhibitors has the potential to disrupt prostaglandin mediated follicular rupture required for ovulation. small studies in women treated with nsaids have also shown a reversible delay in ovulation. consider withdrawal of nsaids, including celebrex, in women who have difficulties conceiving or who are undergoing investigation of infertility. celebrex is approved for relief of the signs and symptoms of juvenile rheumatoid arthritis in patients 2 years and older. safety and efficacy have not been studied beyond six months in children. the long-term cardiovascular toxicity in children exposed to celebrex has not been evaluated and it is unknown if long-term risks may be similar to that seen in adults exposed to celebrex or other cox-2 selective and non-selective nsaids [see boxed warning, warnings and precautions (5.5), and clinical studies (14.3) ]. the use of celecoxib in patients 2 years to 17 years of age with pauciarticular, polyarticular course jra or in patients with systemic onset jra was studied in a 12-week, double-blind, active controlled, pharmacokinetic, safety and efficacy study, with a 12-week open-label extension. celecoxib has not been studied in patients under the age of 2 years, in patients with body weight less than 10 kg (22 lbs), and in patients with active systemic features. patients with systemic onset jra (without active systemic features) appear to be at risk for the development of abnormal coagulation laboratory tests. in some patients with systemic onset jra, both celecoxib and naproxen were associated with mild prolongation of activated partial thromboplastin time (aptt) but not prothrombin time (pt). when nsaids including celecoxib are used in patients with systemic onset jra, monitor patients for signs and symptoms of abnormal clotting or bleeding, due to the risk of disseminated intravascular coagulation. patients with systemic onset jra should be monitored for the development of abnormal coagulation tests [see dosage and administration (2.4), warnings and precautions (5.15), adverse reactions (6.1), animal toxicology (13.2), clinical studies (14.3) ]. alternative therapies for treatment of jra should be considered in pediatric patients identified to be cyp2c9 poor metabolizers [see poor metabolizers of cyp2c9 substrates (8.8) ]. elderly patients, compared to younger patients, are at greater risk for nsaid-associated serious cardiovascular, gastrointestinal, and/or renal adverse reactions. if the anticipated benefit for the elderly patient outweighs these potential risks, start dosing at the low end of the dosing range, and monitor patients for adverse effects [see warnings and precautions (5.1, 5.2, 5.3, 5.6, 5.14) ]. of the total number of patients who received celebrex in pre-approval clinical trials, more than 3,300 were 65–74 years of age, while approximately 1,300 additional patients were 75 years and over. no substantial differences in effectiveness were observed between these subjects and younger subjects. in clinical studies comparing renal function as measured by the gfr, bun and creatinine, and platelet function as measured by bleeding time and platelet aggregation, the results were not different between elderly and young volunteers. however, as with other nsaids, including those that selectively inhibit cox-2, there have been more spontaneous post-marketing reports of fatal gi events and acute renal failure in the elderly than in younger patients [see warnings and precautions (5.2, 5.6) ]. the daily recommended dose of celebrex capsules in patients with moderate hepatic impairment (child-pugh class b) should be reduced by 50%. the use of celebrex in patients with severe hepatic impairment is not recommended [see dosage and administration (2.7) and clinical pharmacology (12.3) ]. celebrex is not recommended in patients with severe renal insufficiency [see warnings and precautions (5.6) and clinical pharmacology (12.3) ]. in patients who are known or suspected to be poor cyp2c9 metabolizers (i.e., cyp2c9*3/*3), based on genotype or previous history/experience with other cyp2c9 substrates (such as warfarin, phenytoin) administer celebrex starting with half the lowest recommended dose. alternative management should be considered in jra patients identified to be cyp2c9 poor metabolizers [see dosage and administration (2.7) and clinical pharmacology (12.5) ].

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

pfizer laboratories div pfizer inc - nafarelin acetate (unii: 8enz0qjw4h) (nafarelin - unii:1x0094v6jv) - nafarelin 2 mg in 1 ml - (for endometriosis, see reverse side ) synarel is indicated for treatment of central precocious puberty (cpp) (gonadotropin-dependent precocious puberty) in children of both sexes. the diagnosis of central precocious puberty (cpp) is suspected when premature development of secondary sexual characteristics occurs at or before the age of 8 years in girls and 9 years in boys, and is accompanied by significant advancement of bone age and/or a poor adult height prediction. the diagnosis should be confirmed by pubertal gonadal sex steroid levels and a pubertal lh response to stimulation by native gnrh. pelvic ultrasound assessment in girls usually reveals enlarged uterus and ovaries, the latter often with multiple cystic formations. magnetic resonance imaging or ct-scanning of the brain is recommended to detect hypothalamic or pituitary tumors, or anatomical changes associated with increased intracranial pressure. other causes of sexual precocity, such as congenital adrenal hyperplasia, testotoxicosis, testicular

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

pfizer laboratories div pfizer inc - ritlecitinib tosylate (unii: eag4t1459k) (ritlecitinib - unii:2oye00pc25) - litfulo is a kinase inhibitor indicated for the treatment of severe alopecia areata in adults and adolescents 12 years and older. limitations of use : not recommended for use in combination with other jak inhibitors, biologic immunomodulators, cyclosporine or other potent immunosuppressants. litfulo is contraindicated in patients with known hypersensitivity to ritlecitinib or any of its excipients [see warnings and precautions (5.6)] .       if a patient becomes pregnant while receiving litfulo, healthcare providers should report litfulo exposure by calling 1-877-390-2940. risk summary available data from clinical trials with litfulo use in pregnant women are insufficient to identify a drug-associated risk of major birth defects, miscarriage or other adverse maternal or fetal outcomes. in animal reproduction studies, oral administration of ritlecitinib to pregnant rats and rabbits during organogenesis caused fetotoxicity and fetal malformations at exposures 49 and 55 times the maximum recommended human dose (mrhd) based on area under the curve (auc) comparison, respectively (see animal data) . the background risks of major birth defects and miscarriage for the indicated population are unknown. all pregnancies carry some risk of birth defects, loss, or other adverse outcomes. the estimated background risks in the u.s. general population of major birth defects and miscarriages are 2-4% and 15-20% of clinically recognized pregnancies, respectively. data animal data in an embryo-fetal development study in pregnant rats, oral administration of ritlecitinib from gestation days 6 to 17 decreased fetal body weights and caused fetal skeletal malformations (malformed vertebrae and ribs) and variations (delayed ossification) at doses ≥175 mg/kg/day (49 times the mrhd based on auc comparison). maternal toxicity (lower body weights) was noted at 325 mg/kg/day (102 times the mrhd based on auc comparison). there was no developmental toxicity at 75 mg/kg/day (16 times the mrhd based on auc comparison). in an embryo-fetal development study in pregnant rabbits, oral administration of ritlecitinib from gestation days 7 to 19 decreased mean fetal body weights and increased visceral malformations (malpositioned kidneys), skeletal malformations (supernumerary sternebrae, absent thoracic arch, and/or fused thoracic centra), and skeletal variations (delayed ossification) at 75 mg/kg/day (55 times the mrhd based on auc comparison). there was no developmental toxicity at doses up to 25 mg/kg/day (12 times the mrhd based on auc comparison). in a pre- and postnatal development study in rats, oral administration of ritlecitinib from gestation day 6 through lactation day 20 had no effects on pre- and postnatal development at doses up to 75 mg/kg/day (14 times the mrhd based on auc comparison). at 175 mg/kg/day (41 times the mrhd based on auc comparison), ritlecitinib caused adverse lower postnatal survival and lower offspring body weights, which correlated with delayed sexual maturation in both sexes. bred females in the f1 generation also exhibited lower mean numbers of corpora lutea at 175 mg/kg/day. risk summary there are no data on the presence of ritlecitinib in human milk, the effects on the breastfed infant, or the effects on milk production. ritlecitinib is present in the milk of lactating rats (see data) . when a drug is present in animal milk, it is likely that it will be present in human milk. because of the serious adverse effects in adults, including risks of serious infection and malignancy, advise women not to breastfeed during treatment with litfulo and for approximately 14 hours after the last dose (approximately 6 elimination half-lives). data after a single oral 30 mg/kg dose of ritlecitinib to lactating rats, ritlecitinib concentrations in milk over time were higher than those in plasma. the mean milk to plasma auc ratio was 2.2. the safety and effectiveness of litfulo for the treatment of alopecia areata have been established in pediatric patients ages 12 years and older. a total of 181 pediatric patients ages 12 to <18 years were enrolled in alopecia areata clinical trials, with 105 pediatric patients ages 12 to <18 years with alopecia areata randomized in a pivotal, double-blind, placebo-controlled trial (trial aa-i). efficacy was consistent between the pediatric patients and adults [see clinical studies (14)] . the adverse reaction profile in the pediatric patients was similar to adults. the safety and efficacy of litfulo have not been established in pediatric patients under 12 years of age. no dose adjustment is required for patients ≥65 years of age. a total of 28 patients enrolled in alopecia areata trials were 65 years of age and older, and none were 75 years of age and older. clinical trials of litfulo did not include sufficient numbers of patients 65 years of age and older to determine whether they respond differently from younger adult patients. as there is a higher incidence of infections in the elderly population in general, caution should be used when treating the elderly. no dose adjustment is required in patients with mild (child pugh a) or moderate (child pugh b) hepatic impairment. litfulo is not recommended in patients with severe (child pugh c) hepatic impairment [see dosage and administration (2.3) and clinical pharmacology (12.3)] .

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

pfizer laboratories div pfizer inc - glasdegib (unii: k673dmo5h9) (glasdegib - unii:k673dmo5h9) - daurismo is indicated, in combination with low-dose cytarabine, for the treatment of newly-diagnosed acute myeloid leukemia (aml) in adult patients who are ≥75 years old or who have comorbidities that preclude use of intensive induction chemotherapy. none. risk summary based on its mechanism of action and findings in animal embryo-fetal developmental toxicity studies, daurismo can cause fetal harm when administered to a pregnant woman [see clinical pharmacology (12.1)] . there are no clinical data on the use of daurismo in pregnant women to inform of a drug-associated risk of major birth defects and miscarriage. daurismo is not recommended for use during pregnancy. conduct pregnancy testing in female patients of reproductive potential prior to initiating treatment with daurismo. report pregnancy exposures to pfizer at 1-800-438-1985. in animal embryo-fetal developmental toxicity studies, repeat-dose oral administration of daurismo during organogenesis at maternal exposures that were less than the human exposu

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

pfizer laboratories div pfizer inc - abrocitinib (unii: 73sm5sf3or) (abrocitinib - unii:73sm5sf3or) - cibinqo is indicated for the treatment of adults and pediatric patients 12 years of age and older with refractory, moderate-to-severe atopic dermatitis whose disease is not adequately controlled with other systemic drug products, including biologics, or when use of those therapies is inadvisable. limitations of use cibinqo is not recommended for use in combination with other jak inhibitors, biologic immunomodulators, or other immunosuppressants. cibinqo is contraindicated in patients taking antiplatelet therapies, except for low-dose aspirin (≤81 mg daily), during the first 3 months of treatment [see warnings and precautions (5.6), drug interactions (7.2), and clinical pharmacology (12.2)].             pregnancy exposure registry there is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to cibinqo during pregnancy. pregnant women exposed to cibinqo and health care providers are encouraged to call 1-877-311-3770. risk summary available data from pregnancies reported in clinical trials with cibinqo are not sufficient to establish a drug‑associated risk for major birth defects, miscarriage, or other adverse maternal or fetal outcomes. in animal reproduction studies, oral administration of abrocitinib to pregnant rats and rabbits during organogenesis at exposure 11 or 4 times the maximum recommended human dose (mrhd) based on auc comparison, respectively, resulted in maternal dystocia and skeletal variations in rats and no adverse effects in rabbits (see data ). the background risks of major birth defects and miscarriage for the indicated population are unknown. all pregnancies carry some risk of birth defects, loss, or other adverse outcomes. the background risks in the u.s. general population of major birth defects and miscarriages are 2–4% and 15–20% of clinically recognized pregnancies, respectively. data animal data in an embryofetal development study, abrocitinib was administered orally to pregnant rats at doses of 10, 30, or 60 mg/kg/day during the period of organogenesis. no fetal malformations were observed. abrocitinib increased the incidence of skeletal variations of short 13th ribs at 30 mg/kg/day (11 times the mrhd based on auc comparison). increased embryofetal lethality and additional skeletal variations (cervical arches with reduced ventral processes, thickened ribs, and unossified metatarsals) were noted at 60 mg/kg/day (17 times the mrhd based on auc comparison). in an embryofetal development study, abrocitinib was administered orally to pregnant rabbits at doses of 10, 30, or 75 mg/kg/day during the period of organogenesis. no abrocitinib-related maternal or developmental toxicity was noted at doses up to 75 mg/kg/day (4 times the mrhd based on auc comparison). in a prenatal and postnatal development study, abrocitinib was administered orally to pregnant rats at doses of 10, 30, and 60 mg/kg/day beginning on gestation day 6 and continuing through lactation day 20. dystocia with prolonged parturition and reduced offspring body weights were noted at 30 mg/kg/day (11 times the mrhd based on auc comparison). postnatal survival was markedly decreased at 60 mg/kg/day (17 times the mrhd based on auc comparison). no maternal toxicity was observed at 10 mg/kg/day (2.4 times the mrhd based on auc comparison). no abrocitinib-related effects on postnatal developmental, neurobehavioral, or reproductive performance of offspring was noted at doses up to 30 mg/kg/day (11 times the mrhd based on auc comparison). risk summary there are no data on the presence of abrocitinib in human milk, the effects on the breast-fed infant, or the effects on milk production. abrocitinib was secreted in 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. because of the serious adverse findings in adults, including risks of serious infections, malignancy, and thrombosis, advise women not to breastfeed during treatment with cibinqo and for one day after the last dose (approximately 5–6 elimination half-lives). data animal data lactating female rats were orally administered a single dose of 10 mg/kg abrocitinib on lactation day 12. abrocitinib auc was approximately 5 times greater in milk than in plasma.       infertility females based on the findings in rats, oral administration of cibinqo may impair female fertility. impaired fertility in female rats was reversible 1 month after cessation of abrocitinib oral administration [see nonclinical toxicology (13.1)] . the safety and effectiveness of cibinqo in pediatric patients 12 years of age and older with atopic dermatitis have been established. in trials trial-ad-1 and trial-ad-2, 124 pediatric subjects 12 to less than 18 years old weighing 25 kg or more with moderate-to-severe atopic dermatitis were enrolled and randomized to receive either cibinqo 100 mg (n=51), 200 mg (n=48), or matching placebo (n=25) in monotherapy. additional 284 pediatric subjects 12 to less than 18 years of age weighing 25 kg or more with moderate-to-severe atopic dermatitis, were enrolled and randomized to receive either cibinqo 100 mg (n=95) or 200 mg (n=94) or matching placebo (n=95) in combination with topical corticosteroids in trial-ad-4. efficacy and adverse reaction profile were comparable between the pediatric patients and adults [see clinical studies (14) and adverse reactions (6.1)] . the safety and effectiveness of cibinqo have not been established in pediatric patients below 12 years of age. juvenile animal toxicity data in a juvenile animal toxicity study, abrocitinib was administered orally to juvenile rats at doses of 5, 25, and 75 mg/kg/day from postnatal day 10 (approximately equivalent to a human infant) through postnatal day 63 (approximately equivalent to an adolescent). abrocitinib caused a reversible, dose‑related decrease in the primary spongiosa in the metaphysis of the proximal tibia and distal femur and adverse effects on bone development at all dose levels. abrocitinib caused irreversible dose-related small or misshapen femoral heads at doses ≥5 mg/kg/day (0.8 times the mrhd based on auc comparison); irreversibly decreased femur size and caused paw malrotation and limb impairment at doses ≥25 mg/kg/day (7.2 times the mrhd based on auc comparison); and fractures at 75 mg/kg/day (27 times the mrhd based on auc comparison). in a follow-up study, abrocitinib (25 mg/kg/day, at least 4.5 times the mrhd based on auc comparison) was orally administered to juvenile rats from postnatal day (pnd) 10, 15, 21, or 30 through pnd day 63. administration beginning pnd 10 caused adverse macroscopic and microscopic bone findings consistent with the previous juvenile animal study. however, administration beginning pnd 15 (approximately equivalent to a 6- to 12-month old infant) caused non-adverse reversible microscopic bone findings. no bone findings were noted when administration began on pnd 21 or 30 (approximately equivalent to 2- and 6-year old children, respectively). a total of 145 (4.6%) subjects 65 years of age and older, while 25 (0.8%) were 75 years of age and older, were enrolled in cibinqo clinical trials. clinical trials of cibinqo did not include sufficient numbers of subjects 65 years of age and older to determine whether they respond differently from younger adult subjects. a higher proportion of subjects 65 years of age and older discontinued from clinical trials compared to younger subjects. among all subjects exposed to cibinqo, including the long-term extension trial, confirmed alc <500/mm3 occurred only in subjects 65 years of age and older. a higher proportion of subjects 65 years of age and older had platelet counts <75,000/mm3 . the incidence rate of herpes zoster in subjects 65 years of age and older treated with cibinqo (7.40 per 100 patient-years) was higher than that of subjects 18 to less than 65 years of age (3.44 per 100 patient-years). in patients with severe (egfr <30 ml/min) and moderate (egfr 30–59 ml/min) renal impairment, the combined exposure (aucinf,u ) of abrocitinib and its two active metabolites, m1 and m2, is increased compared to patients with normal renal function (egfr ≥90 ml/min) [see clinical pharmacology (12.3)]. this may increase the risk of adverse reactions such as infections. cibinqo is not recommended for use in patients with severe renal impairment and esrd including those on renal replacement therapy [see dosage and administration (2.3)]. a dosage reduction in patients with moderate renal impairment is recommended. no dosage adjustment is required in patients with mild renal impairment (egfr 60–89 ml/min) [see dosage and administration (2.3)] . cibinqo has not been studied in subjects on renal replacement therapy. in phase 3 clinical trials, cibinqo was not evaluated in subjects with atopic dermatitis with baseline creatinine clearance values less than 40 ml/min. avoid use of cibinqo in patients with severe (child pugh c) hepatic impairment. in clinical trials, cibinqo was not evaluated in subjects with severe (child pugh c) hepatic impairment. dosage adjustment is not required in patients with mild (child pugh a) or moderate (child pugh b) hepatic impairment based on similar combined exposure (aucinf,u ) of abrocitinib and its two active metabolites, m1 and m2 compared to patients with normal hepatic function [see clinical pharmacology (12.3)] . in patients who are cyp2c19 poor metabolizers, the auc of abrocitinib is increased compared to cyp2c19 normal metabolizers due to reduced metabolic clearance. dosage reduction of cibinqo is recommended in patients who are known or suspected to be cyp2c19 poor metabolizers based on genotype or previous history/experience with other cyp2c19 substrates [see dosage and administration (2.4) and clinical pharmacology (12.5)] .

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

pfizer australia pty ltd - tobramycin, quantity: 80 mg - injection, solution - excipient ingredients: sodium hydroxide; sodium metabisulfite; phenol; water for injections; sulfuric acid; disodium edetate - for the treatment of serious infections of the following type where they are caused by susceptible organisms: skin and skin structure infections including burns, bone infections; gastrointestinal infections including peritonitis; central nervous system infections including meningitis, septicaemia and neonatal sepsis; lower respiratory tract infections including pneumonia, bronchopneumonia, and acute bronchitis; complicated and recurrent urinary tract infections such as pyelonephritis and cystitis.,aminoglycosides, including tobramycin, should not be used in uncomplicated initial episodes of urinary tract infection unless the causative organisms are not susceptible to other less toxic antibiotics.,tobramycin can be used in serious staphylococcal infections for which penicillin or other less toxic drugs are contraindicated and where susceptibility testing and clinical judgement indicate its use. if susceptibility tests show a resistance to tobramycin in the causative organisms other appropriate therapy should be instituted.,note that bacterial cultures should bo obtained before and during treatment to isolate and identify etiologic organisms and to test their susceptibility to tobramycin. if the organisms are resistant, other appropriate therapy should be instituted. in patients in whom gram-negative septicaemia, neonatal sepsis or meningitis is suspected, including those in whom concurrent therapy with a penicillin or cefalosporin and an aminoglycoside may be indicated, tobramycin therapy may be initiated before results of susceptibility studies are obtained. the decision to continue tobramycin therapy should be based upon the results of susceptibility studies, the severity of infection and the important additional concepts discussed in the product information leaflet.

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

pfizer australia pty ltd - tobramycin, quantity: 80 mg - injection, solution - excipient ingredients: water for injections; disodium edetate; sodium hydroxide; sulfuric acid - for the treatment of serious infections of the following type where they are caused by susceptible organisms: skin and skin structure infections including burns, bone infections; gastrointestinal infections including peritonitis; central nervous system infections including meningitis, septicaemia and neonatal sepsis; lower respiratory tract infections including pneumonia, bronchopneumonia, and acute bronchitis; complicated and recurrent urinary tract infections such as pyelonephritis and cystitis.,aminoglycosides, including tobramycin, should not be used in uncomplicated initial episodes of urinary tract infection unless the causative organisms are not susceptible to other less toxic antibiotics.,tobramycin can be used in serious staphylococcal infections for which penicillin or other less toxic drugs are contraindicated and where susceptibility testing and clinical judgement indicate its use. if susceptibility tests show a resistance to tobramycin in the causative organisms other appropriate therapy should

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

pfizer australia pty ltd - sodium bicarbonate, quantity: 8.4 g - injection, intravenous infusion - excipient ingredients: disodium edetate; water for injections - 1. metabolic acidosis in severe renal disease, uncontrolled diabetes, circulatory insufficiency due to shock or severe dehydration, extracorporeal circulation of blood, cardiac arrest and severe primary lactic acidosis where a rapid increase in plasma total co2 content is crucial. treatment of metabolic acidosis should be concurrent with measures designed to control the cause of the acidosis. 2.urinary alkalinisation in the treatment of certain drug intoxications (ie barbiturates, salicylates, lithium, methyl alcohol) and in the haemolytic reactions requiring alkalinisation of the urine to diminish nephrotoxicity of blood pigments. urinary alkalinisation is also used in methotrexate therapy to prevent nephrotoxicity. 3.severe diarrhoea which is often accompanied by a significant loss of bicarbonate.

New Zealand - English - Medsafe (Medicines Safety Authority)

pfizer new zealand limited - varenicline tartrate 0.85mg equivalent to 0.5 mg varenicline;  ;   - film coated tablet - 0.5 mg - active: varenicline tartrate 0.85mg equivalent to 0.5 mg varenicline     excipient: calcium hydrogen phosphate colloidal silicon dioxide croscarmellose sodium magnesium stearate microcrystalline cellulose opadry clear ys-2-19114-a opadry white ys-1-18202 - an aid to smoking cessation