I am not going to go into the politics of Friday's Supreme Court decision on abortion, and I need to start out by saying that I will reserve the right to delete comments to this post that are only politics-based flaming on the subject. But there is a drug regulation part of this story that could become increasingly important. This is of course the practice of "medication abortion", which is most commonly done through taking mifepristone (also known as RU-486) and misoprostol. Mifepristone became available in the US in 2000, and has over the years become the route for about half the abortions in the country, on a steadily rising trend that will surely continue. First the biology, then the regulatory affairs. Mifepristone is a competitive antagonist at the progesterone steroid receptor, a very potent one indeed (IC 50 of about 25 picomolar) and it thus blocks progesterone's effects. It's an antagonist at some other steroid receptors as well (antiglucocorticoid and antiandrogen), but at potencies 100x to 1000x lower. Since we're talking nuclear receptors here, the terms "agonist" and "antagonist" (which were imported from G-protein coupled receptors) don't really fit all that well, though: mifepristone is an antagonist if it's competing with progesterone, but by itself (no progesterone around) it might be better described as a partial agonist, which is a pretty roomy category with the steroid receptors and the nuclear hormone receptors in general. But in the case of pregnancy, there is most definitely progesterone around (it's essential), and mifepristone shuts down its effects. That stops the maintenance of the uterine lining and starts its shedding process, detaching the embryo. After mifepristone treatment, misoprostol (a prostaglandin analog) dilates the cervix and induces muscle contractions, clearing the uterus. (Misoprostol itself can also induce an abortion, but it's more effective in combination with mifepristone). This whole process is basically what…