Adult and pediatric patients 2 years and older with neurofibromatosis type 1 (NF1) who have symptomatic, inoperable plexiform neurofibromas.
Adults: 2 mg orally twice daily. Pediatric patients: dosed by body surface area. Continue until disease progression or unacceptable toxicity.
Capsules: 2 mg; Oral Solution: 0.4 mg/mL
None listed in the prescribing information.
Dermatitis Acneiform (72%), Nausea (42%), Vomiting (36%), Diarrhea (34%), Paronychia (30%), Fatigue (28%), Dry Skin (24%), Increased CPK (20%)
Consult the complete prescribing information for a comprehensive list of adverse reactions and their frequencies.
Strong CYP1A2 Inhibitors: Avoid; may increase mirdametinib exposure.
Strong CYP1A2 Inducers: Avoid; may reduce efficacy.
Consult the full prescribing information for pregnancy-related considerations.
Refer to prescribing information for lactation guidance.
Pediatric safety and efficacy information is detailed in the full label.
Dose modifications for organ impairment are specified in the complete prescribing information.
Mirdametinib is a highly selective, non-ATP-competitive allosteric inhibitor of MEK1/MEK2. Inhibition of MEK in the RAS-MAPK pathway reduces proliferation of neoplastic cells in plexiform neurofibromas driven by NF1 loss-of-function mutations.
Tmax: 1-3 hours. Protein binding: ~97%. Metabolized by CYP1A2 and UGTs. Half-life: ~5 hours. Elimination: feces 76%, urine 18%.
Clinical efficacy and safety data supporting the approval are available in the full prescribing information and from the clinical trials listed below.
Gomekli has FDA-approved indications across the following cancer types covered on CancerDrugEvidence:
Gomekli (mirdametinib) is an FDA-approved oncology agent. Refer to the full prescribing information for complete indication details.
Refer to the full prescribing information for dosing schedules, administration instructions, and dose modifications.
Mirdametinib is a highly selective, non-ATP-competitive allosteric inhibitor of MEK1/MEK2. Inhibition of MEK in the RAS-MAPK pathway reduces proliferation of neoplastic cells in plexiform neurofibromas driven by NF1 loss-of-function mutations.
Dermatitis Acneiform (72%), Nausea (42%), Vomiting (36%), Diarrhea (34%), Paronychia (30%), Fatigue (28%), Dry Skin (24%), Increased CPK (20%) Dermatitis Acneiform 72% Nausea 42% Vomiting 36% Diarrhea 34% Paronychia 30% Fatigue 28% Dry Skin 24% Increased CPK 20%