Comparative Pharmacology
Head-to-head clinical analysis: FINGOLIMOD HYDROCHLORIDE versus GILENYA.
Peer-Reviewed Evidence
Head-to-head clinical analysis: FINGOLIMOD HYDROCHLORIDE versus GILENYA.
FINGOLIMOD HYDROCHLORIDE vs GILENYA
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Sphingosine 1-phosphate receptor modulator; binds to S1P receptors (S1P1, S1P3, S1P4, S1P5) on lymphocytes, causing receptor internalization and preventing egress from lymph nodes, thereby reducing circulating lymphocyte counts.
Fingolimod is a sphingosine 1-phosphate receptor modulator. It is phosphorylated to fingolimod-phosphate, which binds to S1P receptors 1, 3, 4, and 5. It blocks lymphocyte egress from lymph nodes by acting as a functional antagonist at S1P1 receptors, reducing peripheral blood lymphocyte count and central nervous system inflammation.
0.5 mg orally once daily
0.5 mg orally once daily, with or without food
None Documented
None Documented
Terminal elimination half-life is approximately 6–9 days; due to extensive tissue distribution, steady-state is reached within 1–2 months of daily dosing.
The terminal elimination half-life of fingolimod is approximately 6–9 days (mean 8.4 days). Due to the prolonged half-life, steady-state is achieved after 1–2 months of daily dosing, and lymphopenia may persist for up to 2 months after treatment cessation.
Primarily hepatic metabolism (CYP4F2) with subsequent biliary/fecal elimination (81% of total clearance); renal excretion accounts for <2.5% of unchanged drug.
Fingolimod is primarily eliminated via fecal excretion (81%) and to a lesser extent via renal excretion (<1% as unchanged drug). Biliary excretion accounts for a minor portion. The major metabolic pathway is via CYP4F2-mediated hydroxylation, followed by glucuronidation and elimination in feces.
Category C
Category C
Sphingosine 1-Phosphate Receptor Modulator
Sphingosine 1-Phosphate Receptor Modulator