Active half-life of steroids and esters

Plasmin is inactivated by proteins such as α2-macroglobulin and α2-antiplasmin . The mechanism of plasmin inactivation involves the cleavage of an α2-macroglobulin at the bait region (a segment of the aM that is particularly susceptible to proteolytic cleavage) by plasmin. This initiates a conformational change such that the α2-macroglobulin collapses about the plasmin. In the resulting α2-macroglobulin-plasmin complex, the active site of plasmin is sterically shielded, thus substantially decreasing the plasmin's access to protein substrates. Two additional events occur as a consequence of bait region cleavage, namely (i) a h-cysteinyl-g-glutamyl thiol ester of the α2-macroglobulin becomes highly reactive and (ii) a major conformational change exposes a conserved COOH-terminal receptor binding domain. The exposure of this receptor binding domain allows the α2-macroglobulin protease complex to bind to clearance receptors and be removed from circulation.

Also I say the post about steady state and it is correct in saying it usually take about 4 to 5 doses to reach a steady state. Steady state is the point where a doctor would look for pharmacotherapuetic effects. Is it working for the patient and creating the desired effect? Slow release or controlled release help a person receive a dose over an extended period of time without having to take multiple pills because the body hasn't had a chance to degraded it. Look up hepatic first pass. All drugs taken orally pass through the liver and are degraded. Slow release/ extend release allows you to keep a more consistent dose through out the day

Active half-life of steroids and esters

active half-life of steroids and esters

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