Features and properties of mavacamten
Alternative names | Camzyos; HCM 1; MAVA-Bristol Myers Squibb/MyoKardia; MYK-461; SAR-439152 |
Class | Cardiovascular therapies; Ethylamines; Heart failure therapies; Pyrimidinones; Small molecules |
Mechanism of action | Cardiac myosin inhibitors |
Route of administration | Oral |
Pharmacodynamics | Stabilizes cardiac myosin; decreases the number of myosin heads that can enter “on actin” states and reduces the probability of systolic and diastolic cross-bridge formation. Reduces LVOT obstruction, LV mass, LA volume and NT-proBNP levels |
Pharmacokinetics | Median Tmax 1 h, 97–98% plasma protein bound. Extensively metabolized in the liver, primarily via CYP2C19 (74%), CYP3A4 (18%) and CYP2C9 (8%); elimination depends on polymorphic CYP2C19 status (mean AUC∞ ↑241%, mean Cmax ↑ 47%, t1/2 ↑ to 23 days in CYP2C19 poor metabolizers). Mainly excreted in urine |
Adverse events | |
Most frequent | Dizziness, syncope |
Occasional | Reversible ↓ in LVEF to < 50% |
ATC codes | |
WHO ATC code | C01E-B24 (Mavacamten) |
EphMRA ATC code | C1 (Cardiac Therapy) |
Chemical name | 3-(1-methylethyl)-6-[[(1S)-1-phenylethyl]amino]-2,4(1H,3H)-pyrimidinedione |