The mechanism of action of the active substance is based on its role as an antagonist of human oxytocin at the receptor level. As a result, there is a reduction in myometrial tone and a decrease in the frequency of uterine contractions. In summary, uterine quiescence is induced.
Pharmacokinetic studies have shown that in women receiving the active substance by infusion (300 μg/min) for 6–12 hours, mean steady-state plasma concentrations of 442 ng/ml were achieved within 1 hour.
Atosiban is 46–48% bound to plasma proteins. The mean volume of distribution was approximately 18.3 ± 6.8 litres. The active substance does not penetrate into erythrocytes.
There are two metabolites of the active substance formed by cleavage of the peptide bond between ornithine and proline. The larger fragment retains activity as an oxytocin receptor antagonist but is 10 times less potent than the parent compound.
Small quantities of atosiban are found in the urine, whereas 50-fold greater amounts are present as metabolite. The amount of drug excreted in faeces is unknown.
⚠️ Warnings
The safety and efficacy of the active substance have not been studied in women with renal or hepatic impairment, or with abnormal placental position. Clinical data on the use of the compound in multiple pregnancies and in women at 24 to 27 weeks of gestation are very limited. Monitoring of foetal heart rate and uterine contractile activity is recommended during treatment with the active substance. Monitoring of postpartum blood loss is recommended, although clinical experience does not suggest that uterine contraction is adversely affected following delivery after atosiban administration.
