JohnBoy2000
Bluelighter
- Joined
- May 11, 2016
- Messages
- 2,468
So drugs taken orally pass through the liver before being taken to the brain.
Correct me any time here, cause I'm just stringing together pieces of information.
The liver - from what I understand - is where by far the greatest concentration of CYP enzymes resides.
Thus - say there was a drug that was known to inhibition CYP2D6 - being taken in conjunction with another drug that is a sensitive subject of this enzyme.
Could drug interference be reduced or avoided by dosing with a time gap consistent with the Tmax of the drug dosed first?
So say one was taking Fluoxetine with - Desipramine; just by example.
Fluoxetine is a potent CYP2D6 inhibitor - desipramine's major metabolic pathway is CYP2D6.
Dosed together - the plasma levels of desipramine are going to soar.
But say desipramine is dosed 5 to 8 hours (the Tmax of fluoxetine) after fluoxetine - thus, presumably, most or all of the fluoxetine has passed through the liver - thus there would be less potential for the desipramine metabolism to be inhibited by the fluoxetine.
Does that make any sense?
Does it work like that - or no?
Correct me any time here, cause I'm just stringing together pieces of information.
The liver - from what I understand - is where by far the greatest concentration of CYP enzymes resides.
Thus - say there was a drug that was known to inhibition CYP2D6 - being taken in conjunction with another drug that is a sensitive subject of this enzyme.
Could drug interference be reduced or avoided by dosing with a time gap consistent with the Tmax of the drug dosed first?
So say one was taking Fluoxetine with - Desipramine; just by example.
Fluoxetine is a potent CYP2D6 inhibitor - desipramine's major metabolic pathway is CYP2D6.
Dosed together - the plasma levels of desipramine are going to soar.
But say desipramine is dosed 5 to 8 hours (the Tmax of fluoxetine) after fluoxetine - thus, presumably, most or all of the fluoxetine has passed through the liver - thus there would be less potential for the desipramine metabolism to be inhibited by the fluoxetine.
Does that make any sense?
Does it work like that - or no?