IGALMI
Clinical safety rating: caution
Comprehensive clinical and safety monograph for IGALMI (IGALMI).
Selective alpha-2 adrenergic receptor agonist; reduces sympathetic outflow from the central nervous system, resulting in decreased agitation and sedation.
| Metabolism | Primarily metabolized by CYP3A4 and CYP2D6; also undergoes glucuronidation. |
| Excretion | Approximately 75% of the dose is excreted renally as unchanged drug, with the remainder eliminated via biliary/fecal routes (approximately 20%) and minor metabolic clearance. |
| Half-life | Terminal elimination half-life is 2.5 to 3.5 hours in healthy subjects, with prolonged half-life in patients with hepatic impairment (up to 5-7 hours) or renal impairment (up to 6-8 hours). |
| Protein binding | Approximately 40-50% bound to plasma proteins, primarily albumin and alpha-1-acid glycoprotein. |
| Volume of Distribution | Volume of distribution is approximately 1.5-2.0 L/kg, indicating extensive tissue distribution. |
| Bioavailability | Sublingual bioavailability is approximately 55-65% due to first-pass metabolism; intravenous administration yields 100% bioavailability. |
| Onset of Action | Sublingual administration: Onset of sedation occurs within 15-20 minutes, with peak clinical effect by 30-45 minutes. |
| Duration of Action | Duration of sedative effect is approximately 1-2 hours following single sublingual dose, with clinical monitoring recommended for at least 2 hours due to risk of hypotension and bradycardia. |
Sublingual: 120 mcg to 180 mcg as a single dose, administered under the tongue, one time. Maximum single dose: 180 mcg.
| Dosage form | FILM |
| Renal impairment | No dose adjustment required for mild to moderate renal impairment. Not studied in severe renal impairment (eGFR <30 mL/min/1.73 m2) or end-stage renal disease. |
| Liver impairment | Mild hepatic impairment (Child-Pugh A): no adjustment. Moderate hepatic impairment (Child-Pugh B): consider lower dose (120 mcg) due to increased exposure. Severe hepatic impairment (Child-Pugh C): not recommended. |
| Pediatric use | Safety and efficacy not established in pediatric patients (<18 years). |
| Geriatric use | Initiate at 120 mcg dose; monitor for hypotension, orthostatic hypotension, and somnolence, as elderly patients may be more sensitive. |
| 1st trimester | Consult provider |
| 2nd trimester | Consult provider |
| 3rd trimester | Consult provider |
Clinical note
Comprehensive clinical and safety monograph for IGALMI (IGALMI).
| Breastfeeding | Excretion into human milk unknown. M/P ratio not established. Due to high protein binding (94%), transfer likely low. Consider benefits of breastfeeding vs potential infant sedation or hypotension; monitor infant for lethargy, bradycardia, or feeding difficulties. |
| Teratogenic Risk | IGALMI (dexmedetomidine) sublingual film: In animal studies, no evidence of teratogenicity at clinically relevant doses. However, human data are insufficient to establish risk. First trimester: Theoretical risk due to alpha-2 adrenergic agonism; use only if benefit outweighs risk. Second/third trimester: Prolonged use may cause fetal bradycardia or hypotension; avoid during labor due to risk of maternal sedation and neonatal respiratory depression. |
■ FDA Black Box Warning
None.
| Serious Effects |
["Hypersensitivity to dexmedetomidine or any component","Advanced heart block (unless paced)","Uncontrolled hypotension or hypovolemia"]
| Precautions | ["Hypotension, orthostatic hypotension, bradycardia, and syncope","QT interval prolongation","Somnolence and sedation","Risk of falls","Withdrawal reactions after abrupt discontinuation","Hepatic impairment"] |
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| Fetal Monitoring | Monitor maternal blood pressure, heart rate, and sedation level (Ramsay Sedation Scale). Fetal: Heart rate monitoring (non-stress test or biophysical profile) if prolonged therapy during pregnancy; assess for bradycardia. Neonatal: Observe for respiratory depression, bradycardia, and hypotonia after delivery if used near term. |
| Fertility Effects | No human data. Animal studies: No impairment of fertility at clinically relevant doses. Theoretical: alpha-2 agonism may alter hypothalamic-pituitary-gonadal axis; however, no evidence of significant reproductive toxicity. |