30 SECONDS LIMITED (NZ) - search results

Australia - English - APVMA (Australian Pesticides and Veterinary Medicines Authority)

30 seconds spray & walk away hose end lichen, moss & algae killer

30 seconds limited (nz) - benzalkonium chloride - soluble concentrate - benzalkonium chloride ammonium-quaternary active 350.0 g/l - fungicide

Australia - English - APVMA (Australian Pesticides and Veterinary Medicines Authority)

30 seconds works over time roof treatment concentrate lichen, moss & algae killer

Australia - English - APVMA (Australian Pesticides and Veterinary Medicines Authority)

30 seconds rapid clean outdoor cleaner concentrate algae, moss, mould and mildew remover

Australia - English - APVMA (Australian Pesticides and Veterinary Medicines Authority)

30 seconds spray & walk away ready to use lichen, moss & algae killer for control of lichen, moss mould and algae on paths, decks, driveways, fences and other hard surfaces

Australia - English - APVMA (Australian Pesticides and Veterinary Medicines Authority)

30 seconds roof treatment lichen, moss & algae killer ready to use spray & walk away

Australia - English - APVMA (Australian Pesticides and Veterinary Medicines Authority)

30 seconds spray and walk away concentrate lichen, moss & algae killer

Australia - English - APVMA (Australian Pesticides and Veterinary Medicines Authority)

30 seconds outdoor cleaner - ready to use for the removal of algae, moss, mould, mildew from exterior surfaces

New Zealand - English - Medsafe (Medicines Safety Authority)

humulin 30/70

eli lilly and company (nz) limited - insulin, human, recombinant dna origin 100 [iu] (as 70% isophane insulin and 30% regular insulin) - suspension for injection - 100 iu/ml - active: insulin, human, recombinant dna origin 100 [iu] (as 70% isophane insulin and 30% regular insulin) excipient: dibasic sodium phosphate heptahydrate glycerol hydrochloric acid as 10% solution for ph adjustment metacresol phenol protamine sulfate sodium hydroxide as 10% solution for ph adjustment water for injection zinc oxide - humulin is indicated for the treatment of insulin-requiring diabetes mellitus

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

metformin hydrochloride tablet, extended release

aurobindo pharma limited - metformin hydrochloride (unii: 786z46389e) (metformin - unii:9100l32l2n) - metformin hydrochloride 500 mg - metformin hydrochloride extended-release tablets are indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. metformin hydrochloride extended-release tablets are contraindicated in patients with: - severe renal impairment (egfr below 30 ml/min/1.73 m2 ) [see warnings and precautions (5.1) ]. - hypersensitivity to metformin. - acute or chronic metabolic acidosis, including diabetic ketoacidosis, with or without coma. risk summary limited data with metformin hydrochloride extended-release tablets in pregnant women are not sufficient to determine a drug-associated risk for major birth defects or miscarriage. published studies with metformin use during pregnancy have not reported a clear association with metformin and major birth defect or miscarriage risk [see data]. there are risks to the mother and fetus associated with poorly controlled diabetes mellitus in pregnancy [see clinical considerations]. no adverse developmental effects were ob

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

prasugrel tablet, film coated

aurobindo pharma limited - prasugrel hydrochloride (unii: g89jq59i13) (prasugrel - unii:34k66tbt99) - prasugrel 5 mg - prasugrel tablets are indicated to reduce the rate of thrombotic cv events (including stent thrombosis) in patients with acute coronary syndrome (acs) who are to be managed with percutaneous coronary intervention (pci) as follows: - patients with unstable angina (ua) or non-st-elevation myocardial infarction (nstemi). - patients with st-elevation myocardial infarction (stemi) when managed with primary or delayed pci. prasugrel tablets have been shown to reduce the rate of a combined endpoint of cardiovascular death, nonfatal myocardial infarction (mi), or nonfatal stroke compared to clopidogrel. the difference between treatments was driven predominantly by mi, with no difference on strokes and little difference on cv death [see clinical studies (14) ] . prasugrel tablets are contraindicated in patients with active pathological bleeding such as peptic ulcer or intracranial hemorrhage (ich) [see warnings and precautions (5.1) and adverse reactions (6.1)] . prasugrel tablets are contraindicated in patients with a history of prior transient ischemic attack (tia) or stroke. in triton-timi 38 (tr ial to assess i mprovement in t herapeutic outcomes by o ptimizing platelet inhibition with prasugrel), patients with a history of tia or ischemic stroke (>3 months prior to enrollment) had a higher rate of stroke on prasugrel tablets (6.5%; of which 4.2% were thrombotic stroke and 2.3% were intracranial hemorrhage [ich]) than on clopidogrel (1.2%; all thrombotic). in patients without such a history, the incidence of stroke was 0.9% (0.2% ich) and 1.0% (0.3% ich) with prasugrel tablets and clopidogrel, respectively. patients with a history of ischemic stroke within 3 months of screening and patients with a history of hemorrhagic stroke at any time were excluded from triton-timi 38. patients who experience a stroke or tia while on prasugrel tablets generally should have therapy discontinued [see adverse reactions (6.1) and clinical studies (14)] . prasugrel tablets are contraindicated in patients with hypersensitivity (e.g., anaphylaxis) to prasugrel or any component of the product [see adverse reactions (6.2)] . risk summary there are no data with prasugrel use in pregnant women to inform a drug-associated risk. no structural malformations were observed in animal reproductive and developmental toxicology studies when rats and rabbits were administered prasugrel during organogenesis at doses of up to 30 times the recommended therapeutic exposures in humans [see data] . due to the mechanism of action of prasugrel, and the associated identified risk of bleeding, consider the benefits and risks of prasugrel and possible risks to the fetus when prescribing prasugrel to a pregnant woman [see boxed warning and warnings and precautions (5.1, 5.3)]. the background risk of major birth defects and miscarriage for the indicated population is unknown. the background risk in the u.s. general population of major birth defects is 2 to 4% and of miscarriage is 15 to 20% of clinically recognized pregnancies. data animal data in embryo-fetal developmental toxicology studies, pregnant rats and rabbits received prasugrel at maternally toxic oral doses equivalent to more than 40 times the human exposure. a slight decrease in fetal body weight was observed, but there were no structural malformations in either species. in prenatal and postnatal rat studies, maternal treatment with prasugrel had no effect on the behavioral or reproductive development of the offspring at doses greater than 150 times the human exposure. risk summary there is no information regarding the presence of prasugrel in human milk, the effects on the breastfed infant, or the effects on milk production. metabolites of prasugrel were found in rat milk [see data] . the developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for prasugrel and any potential adverse effects on the breastfed child from prasugrel or from the underlying maternal condition. data animal data following a 5 mg/kg oral dose of [14 c]-prasugrel to lactating rats, metabolites of prasugrel were detected in the maternal milk and blood. safety and effectiveness in pediatric patients have not been established. in a randomized, placebo-controlled trial, the primary objective of reducing the rate of vaso-occlusive crisis (painful crisis or acute chest syndrome) in pediatric patients, aged 2 to less than 18 years, with sickle cell anemia was not met. in triton-timi 38, 38.5% of patients were ≥65 years of age and 13.2% were ≥75 years of age. the risk of bleeding increased with advancing age in both treatment groups, although the relative risk of bleeding (prasugrel compared with clopidogrel) was similar across age groups. patients ≥75 years of age who received prasugrel 10 mg had an increased risk of fatal bleeding events (1.0%) compared to patients who received clopidogrel (0.1%). in patients ≥75 years of age, symptomatic intracranial hemorrhage occurred in 7 patients (0.8%) who received prasugrel and in 3 patients (0.3%) who received clopidogrel. because of the risk of bleeding, and because effectiveness is uncertain in patients ≥75 years of age [see clinical studies (14)] , use of prasugrel is generally not recommended in these patients, except in high-risk situations (diabetes and past history of myocardial infarction) where its effect appears to be greater and its use may be considered [see warnings and precautions (5.1), clinical pharmacology (12.3), and clinical studies (14)] . in triton-timi 38, 4.6% of patients treated with prasugrel had body weight <60 kg. individuals with body weight <60 kg had an increased risk of bleeding and an increased exposure to the active metabolite of prasugrel [see dosage and administration (2), warnings and precautions (5.1), and clinical pharmacology (12.3)] . consider lowering the maintenance dose to 5 mg in patients <60 kg. the effectiveness and safety of the 5 mg dose have not been prospectively studied [see dosage and administration (2) and clinical pharmacology (12.3)] . no dosage adjustment is necessary for patients with renal impairment. there is limited experience in patients with end-stage renal disease, but such patients are generally at higher risk of bleeding [see warnings and precautions (5.1) and clinical pharmacology (12.3)] . no dosage adjustment is necessary in patients with mild to moderate hepatic impairment (child-pugh class a and b). the pharmacokinetics and pharmacodynamics of prasugrel in patients with severe hepatic disease have not been studied, but such patients are generally at higher risk of bleeding [see warnings and precautions (5.1) and clinical pharmacology (12.3)] . in healthy subjects, patients with stable atherosclerosis, and patients with acs receiving prasugrel, there was no relevant effect of genetic variation in cyp2b6, cyp2c9, cyp2c19, or cyp3a5 on the pharmacokinetics of prasugrel’s active metabolite or its inhibition of platelet aggregation.