Raloxifene is a selective estrogen receptor modulator approved for prevention and treatment of osteoporosis in postmenopausal women. Raloxifene has an estrogen-agonistic effect on bone, although it is unclear how this effect comes about. It has been proven that raloxifene decreases levels of both bone formation markers and bone resorption markers in postmenopausal women. Moreover, it preserves the bone mineral density at most skeletal sites in these women. Raloxifene decreases the serum levels of low-density lipoprotein cholesterol and total cholesterol. In breast tissue, raloxifene is an estrogen antagonist. It decreases the risk of breast cancer in postmenopausal women. In contrast to estrogen and tamoxifen, raloxifene does not increase the risk of uterine cancer and it does not cause endometrial proliferation. Raloxifene is rapidly absorbed after oral administration, but its bioavailability is only 2% because of an extensive first-past effect. The maximum plasma concentration of 0.5 ng/ml is reached after 6 hours. Raloxifene is more than 95% bound to plasma proteins and the apparent volume of distribution is 2,348 l/kg. The clearance is 40 - 60 l/kg x h and the half-life of raloxifene after multiple dosing is 32.5 h. Less than 0.2% of an oral dose is excreted unchanged in the urine and less than 6% is excreted in urine as glucuronide conjugates. Serious adverse event caused by raloxifene is a 3-fold increase in the risk of thromboembolic events.