Non-CYP metabolism. Side effects such as nausea and vomiting may be potentially porphyrinogenic through reduction in caloric intake.

Plerixafor is a small-molecule bicyclam derivative.

Plerixafor is a CXCR4 chemokine-receptor antagonist, used with granulocyte colony-stimulating factor (G-CSF) to mobilise stem cells for collection and subsequent autologous transplantation in patients with non-Hodgkins lymphoma or multiple myeloma. It is administered as a subcutaneous injection. Common adverse reactions of plerixafor that can be confused with an acute porphyric attack are diarrhoea, nausea, constipation, vomiting, abdominal pain, insomnia and musculoskeletal pain. Side effects such as nausea and vomiting may be potentially porphyrinogenic through reduction in caloric intake.

Plerixafor is mainly excreted unchanged through the kidneys. Plerixafor was metabolically stable and not subject to hepatic metabolism in in vitro metabolism studies conducted with human liver microsomes and hepatocytes. Concentrations of plerixafor that inhibit enzyme activity by 50% (IC50) for all isozymes (CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP3A4/5, CYP2A6, CYP2B6, CYP 2C8, and CYP2E1) were >100 μM with and without preincubation, indicating that plerixafor is neither a direct nor a mechanism based inhibitor of the major CYP enzymes. In in vitro studies with human hepatocytes, plerixafor doses did not induce CYP1A2, CYP2B6, and CYP3A4 enzymes.