Mycophenolic acid
Mycophenolic acid glucuronide

• Monitor theraputic levels of Mycophenolic acid (MPA)
• Evaluate toxicity

Red serum vial/tube, 5 mL

1. Allow specimen to clot
2. Spin within two (2) hours of sample collection
3. Transfer separated serum to a Transfer vial/tube with cap - 12mL (LabCorp), labelled as serum

Transfer vial/tube with cap - 12mL (LabCorp)

Lavender (EDTA), 4mL

Immediately following collection, mix sample thoroughly by gentle inverting 8 - 10 times to prevent clotting

1. Spin within two (2) hours of sample collection
2. Transfer plasma to a Transfer vial/tube with cap - 12mL (LabCorp), labelled as EDTA plasma

Ambient (preferred) - 14 days

Refrigerated - 14 days

Frozen - 14 days

Freeze/thaw cycles - stable x 3

• Gel-barrier (SST) tube

Liquid chromatography/tandem mass spectrometry (LC/MS-MS)

Mycophenolic acid: 1.0 - 3.5 µg/mL
Mycophenolic acid glucuronide: 15 - 125 µg/mL

Monitor theraputic levels; evaluate toxicity Mycophenolic acid (MPA) is the active metabolite of the prodrug, mycophenolate mofetil (MMF). Absorption of the prodrug is rapid following oral administration to the extent that detectable levels are not seen. Similar effects are observed after cessation of I.V. administration. Once formed, MPA undergoes metabolism to form the pharmacologic- ally inactive phenolic glucuronide metabolite, MPAG. In vivo, MPAG is converted to MPA via enterohepatic recircula- tion, which results in a secondary peak in the plasma concentration time profile. MPA and MPAG are 92% and 87% protein bound, respectively, at usual clinical concentrations.

Recent reports have suggested that there could be a potential pharmacokinetic drug interaction between MPA and the calcineurin inhibitors. Several groups have observed that, in combination with cyclosporine, MPA serum concentrations are lower, and the MPAG serum concentrations are higher than in combination with tacrolimus. MPA has also been implicated as an adjuvant with highly active antiretroviral therapy (HAART) due to the selective inhibition of the conversion of inosine 5'-monophosphate to xanthosine 5'-monophosphate by the enzyme, inosine 5'-mono- phosphate dehydrogenase (IMPDH). Blocking this enzyme in lymphocytes depletes guanosine triphosphate (GTP) and deoxyguanosine triphosphate (dGTP) pools. This depletion of dGTP pools inhibits the activation of T lymphocytes, therebylimiting the availability of target cells for HIV.