aced126
Bluelighter
- Joined
- May 18, 2015
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- 1,047
http://www.ncbi.nlm.nih.gov/pubmed/18991468
In that study they take some measurements to determine pharmacokinetic properties of lisdexamphetamine.
They administer a 70mg oral dose, but measure that average peak plasma concentration is 58ng/ml.
There's ~5000ml blood in humans, and 10^6 nanograms in 1 mg, so that works out to be 0.29mg peak concentration. This seems very low. If I iv administered even 10 times less than the oral dose, I would still have 7mg in my blood instantly, several times higher than the oral peak plasma concentration. This occured 1 hour after administration.
If this is because most of the lisdex has been metabolised to dex already (at t=1 hour), then what even is the point of having the prodrug substitution if it has barely any amphetamine to release after only 1 hour? I've got to be missing something
In that study they take some measurements to determine pharmacokinetic properties of lisdexamphetamine.
They administer a 70mg oral dose, but measure that average peak plasma concentration is 58ng/ml.
There's ~5000ml blood in humans, and 10^6 nanograms in 1 mg, so that works out to be 0.29mg peak concentration. This seems very low. If I iv administered even 10 times less than the oral dose, I would still have 7mg in my blood instantly, several times higher than the oral peak plasma concentration. This occured 1 hour after administration.
If this is because most of the lisdex has been metabolised to dex already (at t=1 hour), then what even is the point of having the prodrug substitution if it has barely any amphetamine to release after only 1 hour? I've got to be missing something