Atosiban Acetate

Atosiban binds to oxytocin receptors that sit in the membrane of the myometrium (the uterine muscle). By doing so, it stops oxytocin from raising the production of inositol triphosphate. Without that rise, the stored calcium in the sarcoplasmic reticulum isn't released, and the voltage gated calcium channels don't open afterwards. Calcium inside the cell therefore doesn't increase, and the uterine muscle doesn't contract. The contractions become less frequent and the uterus settles into a quiet state (uterine quiescence).

More recently, atosiban has been found to act as a biased ligand at oxytocin receptors. It blocks Gq coupling, which explains the inhibition of the inositol triphosphate pathway thought to be responsible for the effect on uterine contraction. But it acts as an agonist of Gi coupling. This agonism produces a pro-inflammatory effect in the human amnion by activating the pro-inflammatory signal tranducer NF-κB. It is thought that this makes atosiban less effective than agents that do not cause inflammation, because inflammatory mediators are known to play a role in the induction of labour.