How is a new protein molecule different in its ultimate effects from heparin? For instance, how does it prevent clots inside vessels and not at the surface?
No one is sure right now how the new protein prevents clots in vessels and not at the skin. The current model is that there are redundant pathways which can cause clotting at the skin, while there may only be one relevant one in vessels. Thus, if the new protein blocks that one, there’s still a functioning mechanism remaining to help clots form at the skin. The biochemical details of this are extremely murky right now… As for aspirin–it acts by inhibiting the ezyme cyclooxegenase. Cyclooxegenase is involved in the biosynthesis of thromboxane A2, which is a potent stimulator of platelets. When stimulated by throboxane A2, platelets become “activated” and initiate a cascade of biochemical events which result in clotting. The properties of a molecule that make it a good orally active drug include small size (molecular weight less than 500 grams/mole) and what might be called a “medium greasy” nature–i.e., it must be soluble in water (to dissolve in the stomach in the first place) and
Related Questions
- Can I share a ticket with someone else? For instance, if I purchase a 3 day Park Hopper can 3 different people use it on the same day to get in?
- Why does the protein look so different from the molecule? Where are the atoms and/or bonds in the protein?
- Ive seen molecules displayed with heatmaps in other packages. Whats different about Glowing Molecule?
