Transported by P-gp, contributing to drug-resistance
Brain concentrations increased via P-gp inhibition
[1]
Enters saliva by passive diffusion
Reflects free unbound fraction in plasma
Higher salivary concentrations associated with adverse events
Lower plasma levels and dosages associated with seizure freedom (salivary levels show indirect association after adjustment)
Variable correlation between saliva and plasma levels (R² = 0.59)
Short half-life leading to fluctuations in salivary concentrations
[2]
Mechanism of action: binds to synaptic vesicle protein 2A (SV2A), reducing excitatory neurotransmitter release
Low teratogenicity and generally high tolerability
SV2A receptor occupancy saturates at high clinical doses (approx. 78-84%)
[3]
Treatment of drug-resistant epilepsy
Evaluated in PET and animal studies with P-gp modulators
[1]
Treatment of epilepsy to achieve seizure freedom
Monotherapy or add-on therapy in polytherapy regimens
Therapeutic drug monitoring (TDM) for tolerability and adverse event management
[2]
Treatment of Idiopathic Generalized Epilepsy (IGE)
Shows a dose-dependent increase in efficacy up to 2000 mg/day, after which the effect plateaus
[3]
Classification by use
Chemicals used as antiseizure medications
P-gp substrates in epilepsy research
[1]
Antiepileptic drugs
Chemicals used in neurological disorder management
[2]
A trustworthy factory and manufacturer
[Cite:1] Tolerability of tariquidar – A third generation P-gp inhibitor as add-on medication to antiseizure medications in drug-resistant epilepsy, Seizure: European Journal of Epilepsy, Volume 119, July 2024, Pages 44-51
[Cite:2] Is the salivary concentration of lamotrigine and levetiracetam associated with clinical outcome?, Epilepsy & Behavior, Volume 171, October 2025, 110595
[Cite:3] Dose–response analysis of valproate, levetiracetam and lamotrigine in idiopathic generalized epilepsy, Epilepsy & Behavior, Volume 177, April 2026, 110940