Примери за използване на Postnatal toxicity на Английски и техните преводи на Български
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A pre- and postnatal toxicity study was not performed with reteplase.
There are no studies of foetal, developmental,perinatal or postnatal toxicity.
Preclinical data on postnatal toxicity of adalimumab are not available(see section 5.3).
However, tenofovir disoproxil reduced the viability index and weight of pups in a peri and postnatal toxicity study at maternally toxic doses.
A peri/postnatal toxicity study in rats revealed no significant effects at therapeutically relevant doses.
Carcinogenicity studies, and standard assessments of fertility and postnatal toxicity, were not performed with LIFMIOR due to the development of neutralising antibodies in rodents.
Non-clinical data reveal no special hazard for humans based on repeated dose toxicity, local tolerance, female fertility,embryo-foetal and postnatal toxicity.
Preclinical data on postnatal toxicity and fertility effects of adalimumab are not available(see section 5.3).
Non-clinical data reveal no special hazard for humans based on conventional studies of safety pharmacology, acute and repeated dose toxicity, local tolerance, fertility,embryo-foetal and postnatal toxicity(up to the end of the lactation period).
Preclinical data about peri- and postnatal toxicity of etanercept and of effects of etanercept on fertility and general reproductive performance are not available.
Non-clinical data obtained with the mock-up vaccine using a H5N1 vaccine strain reveal no special hazard for humans based on conventional studies of safety pharmacology, acute and repeated dose toxicity, local tolerance, female fertility,embryo-fetal and postnatal toxicity(up to the end of the lactation period).
Preclinical data about peri- and postnatal toxicity of etanercept and of effects of etanercept on fertility and general.
Non-clinical data obtained with a version of Arepanrix containing 3.75 µg HA derived from A/Indonesia/05/2005(H5N1) reveal no special hazard for humans based on conventional studies of safety pharmacology, acute and repeated dose toxicity, local tolerance, female fertility,embryo-fetal and postnatal toxicity(up to the end of the lactation period).
Preclinical data about peri- and postnatal toxicity of etanercept and of effects of etanercept on fertility and general reproductive performance are not available.
In prenatal/postnatal toxicity studies in the rat, duloxetine induced adverse behavioural effects in the offspring at exposures below maximum clinical exposure(AUC).
Carcinogenicity studies, and standard assessments of fertility and postnatal toxicity, were not performed with etanercept due to the development of neutralising antibodies in rodents.
In pre/postnatal toxicity study in the rat, duloxetine induced adverse behavioural effects in the offspring at systemic exposure levels below maximum clinical exposure(AUC).
Neither carcinogenicity studies, nora standard assessment of fertility and postnatal toxicity, were performed with adalimumab due to the lack of appropriate models for an antibody with limited cross-reactivity to rodent TNF and to the development of neutralising antibodies in rodents.
In pre- and postnatal toxicity studies in rats, reduced weight gain of offspring was observed at maternal exposures approximately 4-times the maximal clinical exposure to empagliflozin.
Preclinical data about peri- and postnatal toxicity of etanercept and of effects of etanercept on fertility and general reproductive performance are not available.
In prenatal/postnatal toxicity studies in the rat, duloxetine induced adverse behavioural effects in the offspring at exposures below maximum clinical exposure(AUC).
Carcinogenicity studies, andstandard assessment of fertility and postnatal toxicity, were not performed with adalimumab due to the lack of appropriate models for an antibody with limited cross-reactivity to rodent TNF and the development of neutralizing antibodies in rodents.
In prenatal/ postnatal toxicity studies in the rat, duloxetine induced adverse behavioural effects in the offspring at exposures below maximum clinical exposure(AUC).
In prenatal/postnatal toxicity studies, pregabalin induced offspring developmental toxicity in rats at exposures> 2 times the maximum recommended human exposure.
A peri- and postnatal toxicity study performed in rabbits with thalidomide administered at doses up to 500 mg/kg/day resulted in abortions, increased stillbirths and decreased pup viability during lactation.
In the pre- and postnatal toxicity study with linagliptin in rats, reduced weight gain in offspring was observed at maternal exposures approximately 1,500-times the maximal clinical exposure to linagliptin.
Mortality was the dose-limiting toxicity in juvenile rats in which dosing was initiated on postnatal day(PND) 7 or PND21 and was observed at exposures that were respectively 125- or 12-fold lower compared with the exposure at which mortality was observed in adult rats, suggesting an increasing sensitivity to toxicity with decreasing age.
Studies in animals have shown toxicity with respect to postnatal development(see section 5.3).
In a pre- and postnatal development toxicity study in rats, abnormal delivery and nursing conditions were observed at maternally toxic doses, and the number of stillbirths was increased in offspring.
In a pre- and postnatal development toxicity study in monkeys, no related increase in pregnancy loss was observed at exposures up to 85 times the human exposure at the recommended dose.