Preterm labour is the most significant cause of perinatal morbidity and mortality, causing significant socioeconomic consequences for individuals, families and society. Our previous work has demonstrated that cAMP enhances the ability of progesterone to repress IL1B driven COX2 expression in myometrium. The fetal membranes, specifically the amnion, have a potentially significant role in the initiation of labour. Labour being a pro-inflammatory state, potentially could be delayed with the modulation of this inflammatory process. We demonstrated that treatment of primary amnion cell cultures with P4 significantly reduces the IL1B driven COX2 response and that the addition of a cAMP agonist significantly enhances this effect.