COCPs use oestrogens (ethinylestradiol, its pre-metabolite mestranol, or estradiol valereate) and progestogens (levonorgestrel, norethisterone, norgestimate, desogestrel, gestodene, or drospirenone). COCPs influence the hypothalamic-pituitary-ovarian axis to prevent ovulation by suppressing luteinising hormone (LH) and follicle-stimulating hormone (FSH).¹¹

While the progestogens desogestrel and drospirenone have an anti-gonadotrophic action inhibiting ovulation, levonorgestrel and norethisterone are less reliable in inhibiting ovulation.¹³

Additional contraceptive effects of progestogens arise from thickening the cervical mucus reducing sperm penetration, changes to the endometrium inhibiting implantation, decreasing the activity of cilia lining the fallopian tubes and other effects on tubal motility.^11,13,14