Ah - I understand these passages such that they describe the passage of the intact LDX molecule into the bloodstream, and I don't see mention of the lysine-amphetamine cleavage action. This describes what part of the intestine is able to pull the whole LDX molecule into the blood. Note the distinction between absorption and metabolism. Later passages:
LDX was not metabolized in vitro by SGF, SIF, or trypsin, [so] any conversion of LDX to d-amphetamine in the GI tract in vivo is likely to be minimal. [...,] consistent with a model of absorption of predominantly intact LDX with subsequent enzymatic conversion to active d-amphetamine and l-lysine.
LDX was metabolized to d-amphetamine in rat and human whole blood but not in plasma. [Red blood cells] are responsible for the presystemic conversion of LDX to d-amphetamine.
LDX was metabolized to d-amphetamine by human RBCs but not by other blood fractions, such as white blood cells or platelets. Moreover, RBCs had a very high capacity for the metabolism of LDX. The rate of metabolism was not substantially reduced until concentrations of RBCs were reduced to 10% of normal hematocrit. Lysis of the RBCs also had little impact on the rate of metabolism of LDX, and nor did EDTA (a calcium chelator that inhibits the activity of calcium-dependent enzymes).
In conclusion, LDX is absorbed as the intact prodrug and converted to inactive l-lysine and active d-amphetamine primarily in the blood by RBCs.
LDX was not metabolized in vitro by SGF, SIF, or trypsin, [so] any conversion of LDX to d-amphetamine in the GI tract in vivo is likely to be minimal. [...,] consistent with a model of absorption of predominantly intact LDX with subsequent enzymatic conversion to active d-amphetamine and l-lysine.
LDX was metabolized to d-amphetamine in rat and human whole blood but not in plasma. [Red blood cells] are responsible for the presystemic conversion of LDX to d-amphetamine.
LDX was metabolized to d-amphetamine by human RBCs but not by other blood fractions, such as white blood cells or platelets. Moreover, RBCs had a very high capacity for the metabolism of LDX. The rate of metabolism was not substantially reduced until concentrations of RBCs were reduced to 10% of normal hematocrit. Lysis of the RBCs also had little impact on the rate of metabolism of LDX, and nor did EDTA (a calcium chelator that inhibits the activity of calcium-dependent enzymes).
In conclusion, LDX is absorbed as the intact prodrug and converted to inactive l-lysine and active d-amphetamine primarily in the blood by RBCs.
It's fascinating isn't it? :)
I find the effect to be very very different.
Here's a graph of plasma concentration of free dextroamphetamine, time release capsules, and molecular-braked lisdexamfetamine: https://farm1.staticflickr.com/727/23028958560_2ae3ddc5bd_o....