The newer progestogens desogestrel, norgestimate, gestodene, dienogest and nomegestrol share the common property of having weak or no androgenic effects, but there is great variation between agents in their pharmacokinetic properties and hormonal activities. Both desogestrel (acting as 3-keto-desogestrel) and norgestimate (acting mainly through levonorgestrel) are prodrugs. While nomegestrol is derived from 19-norprogesterone, the other compounds are 19-nortestosterone derivatives: desogestrel, norgestimate and gestodene belong to the subgroup of 13-ethyl-gonanes with an ethinyl group at C17 alpha, and dienogest represents an estrane (13-methyl-gonane) with a cyanomethyl group at C17 alpha. Both dienogest and nomegestrol have antiandrogenic properties. In proportion to the dose, the highest serum concentrations are observed after intake of gestodene. When combined with ethinylestradiol, gestodene and 3-keto-desogestrel accumulate in serum during daily treatment because of slowed-down elimination. This is probably caused both by binding to sex hormone-binding globulin (SHBG) and by inhibition of inactivating enzymes. Dienogest does not accumulate in serum, although at a dose of 2 mg very high serum concentrations of dienogest are reached. The most potent progestogens are gestodene and desogestrel, while the effect of dienogest and nomegestrol on endometrium and cervix is less, even though in a similar range. As the ovulation-inhibiting effect is brought about not only by receptor-mediated interactions but also by a direct inhibition of steroid biosynthesis, dienogest and nomegestrol are much less effective than gestodene, desogestrel and norgestimate. Ethinylated progestogens, particularly gestodene, have been demonstrated to inhibit cytochrome P450 enzymes. Both gestodene and desogestrel may moderately reduce SHBG levels and counteract the stimulating effect of ethinylestradiol on hepatic serum proteins, while dienogest and nomegestrol have no influence. Compared with progestogens with androgenic properties which may restrict the stimulatory action of ethinylestradiol on haemostatic parameters, the newer progestogens do not seem to be superior with respect to haemostasis. There are no data on the direct effect of the compounds on the arterial and venous vessel wall. Due to the less pronounced antagonism on ethinylestradiol-induced changes in lipid metabolism, the newer progestogens appear to be beneficial rather than deleterious, although atherosclerosis was probably not promoted by the older formulations because of the direct effect of ethinylestradiol on the arterial wall. There is no evidence for a lesser impact of the newer progestogens on carbohydrate metabolism, which is mostly impaired by the estrogen component in oral contraceptives. Formulations containing the newer progestogens are, however, preferable in patients with hyperandrogenaemia, the symptoms of which may be improved by the suppression of total and free testosterone and an increase in SHBG; an additional beneficial effect of the antiandrogenic properties of dienogest or nomegestrol remains to be proven.