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 uterine muscle tone as well as the frequency of uterine contractions. In summary, uterine quiescence is induced.
Pharmacokinetic studies have shown that in women who received the active substance by infusion (300 μg/min) for 6–12 hours, mean steady-state 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 red blood cells.
There are two metabolites of the active substance formed by cleavage of the peptide bond between ornithine and proline. The larger fragment of the compound remains active as an oxytocin receptor antagonist but is 10 times less potent than the parent molecule.
Small amounts of atosiban are found in urine, whereas a 50-fold greater amount is present as a 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 positioning. Clinical data on the use of the compound in multiple pregnancies and in women with a gestational age of 24 to 27 weeks are very limited. Monitoring of foetal heart rate and uterine contractile activity is recommended during treatment with the active substance. It is recommended to monitor postpartum blood loss, although clinical experience does not suggest that uterine contraction after delivery is impaired following administration of atosiban.
