Lamotrigine

Anticonvulsant, Mood stabilizer, Sodium channel blocker

Lamotrigine

Lamictal (IR), Lamictal XR, Lamictal ODT

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Summary

Classes

Anticonvulsant, Mood stabilizer, Sodium channel blocker

Pharmacy

Starting dose

Slow titration is essential to mitigate Stevens-Johnson syndrome risk. Standard adult: 25 mg PO daily for 2 weeks, then 50 mg daily for 2 weeks, then 100 mg daily for 1 week, then 200 mg daily target. Double the rate if on enzyme inducers (carbamazepine, phenytoin); halve the rate if on valproate

Preparations

IR tablets 25, 100, 150, 200 mg; chewable dispersible tablets 2, 5, 25 mg; ODT 25, 50, 100, 200 mg; XR tablets 25, 50, 100, 200, 250, 300 mg

US FDA Max

400 mg/day (bipolar monotherapy); 700 mg/day (epilepsy with enzyme-inducing comedication)

Pharmacology

Routes

Oral

Onset

Antiepileptic effect within days at therapeutic level; mood-stabilizing effect emerges over weeks

Duration

24 hours (often divided BID at higher doses)

Half-life

~25-33 hours alone; ~15 hours with enzyme inducers; ≥60 hours with valproate (UGT inhibition)

Bioavailability

~98% (oral)

Pregnancy

Among the safest mood stabilizers in pregnancy with reassuring monotherapy registry data, in sharp contrast to valproate. Estrogen-containing contraceptives accelerate lamotrigine metabolism, requiring dose adjustments at start and stop of contraception

Legal status

Rx-only in US. Carries the FDA Boxed Warning for serious skin reactions including Stevens-Johnson syndrome and toxic epidermal necrolysis, with the risk concentrated in the first 2-8 weeks of therapy and elevated by rapid titration

Purported mechanism

Voltage-gated sodium channel blocker in the inactivated state, reducing high-frequency repetitive neuronal firing and consequently reducing presynaptic glutamate release. The mood-stabilizing mechanism is incompletely characterized but is plausibly the same glutamatergic dampening applied to limbic circuits.▲0▼ Metabolized predominantly by UGT1A4 glucuronidation (not CYP), which is why valproate doubles exposure (UGT inhibition) and carbamazepine, phenytoin, rifampin halve exposure (UGT induction). The HLA-B*15:02 allele substantially elevates SJS risk in Asian populations; CPIC and FDA support pre-treatment HLA-B*15:02 testing in at-risk patients.