| Leukemia, Myelocytic, Acute
Mylotarg vs Trisenox
Side-by-side clinical, coverage, and cost comparison for leukemia, myelocytic, acute.Deep comparison between: Mylotarg vs Trisenox with Prescriber.AI
AI compares prescribing info and payer-specific access barriers across 1,200+ formularies. Here's a preview of what prescribers are already asking.Safety signalsTrisenox has a higher rate of injection site reactions vs Mylotarg based on FDA-approved prescribing information
Coverage gaps3 major payers require step therapy for Trisenox but not Mylotarg, including UnitedHealthcare
Sign up to reveal the full AI analysis
Category
Mylotarg
Trisenox
At A Glance
IV infusion
CD33-directed antibody-drug conjugate (ADC)
Intravenous
Daily
Arsenical antineoplastic
Indications
- Leukemia, Myelocytic, Acute
- Leukemia, Myelocytic, Acute
Dosing
Leukemia, Myelocytic, Acute - newly-diagnosed, combination regimen Adults: Induction 3 mg/m2 (up to one 4.5 mg vial) IV on Days 1, 4, and 7 with daunorubicin and cytarabine; Consolidation 3 mg/m2 IV on Day 1 with daunorubicin and cytarabine. Pediatric patients 1 month and older: 3 mg/m2 (BSA >=0.6 m2) or 0.1 mg/kg (BSA <0.6 m2) IV.
Leukemia, Myelocytic, Acute - newly-diagnosed, single-agent Adults: Induction 6 mg/m2 IV on Day 1 and 3 mg/m2 on Day 8; Continuation 2 mg/m2 IV on Day 1 every 4 weeks for up to 8 cycles.
Leukemia, Myelocytic, Acute - relapsed or refractory Adults and pediatric patients 2 years and older: 3 mg/m2 (up to one 4.5 mg vial) IV on Days 1, 4, and 7 as a single course.
Acute Promyelocytic Leukemia (newly-diagnosed low-risk) Induction: 0.15 mg/kg/day IV daily in combination with tretinoin until bone marrow remission, not to exceed 60 days. Consolidation: 0.15 mg/kg/day IV daily for 5 days per week during weeks 1-4 of each 8-week cycle for 4 cycles in combination with tretinoin.
Acute Promyelocytic Leukemia (relapsed or refractory) Induction: 0.15 mg/kg/day IV daily until bone marrow remission, not to exceed 60 days. Consolidation: 0.15 mg/kg/day IV daily for 25 doses over a period of up to 5 weeks, beginning 3 to 6 weeks after completion of induction.
Contraindications
- Known hypersensitivity to gemtuzumab ozogamicin, its components, or any excipient (reactions have included anaphylaxis)
- Hypersensitivity to arsenic
Adverse Reactions
Most common Infection, febrile neutropenia, hemorrhage, thrombocytopenia, neutropenia, decreased appetite, hyperglycemia, mucositis, transaminase increased, fatigue, nausea
Serious Hepatotoxicity including veno-occlusive disease (VOD), infusion-related reactions, hemorrhage, prolonged thrombocytopenia, prolonged neutropenia
Postmarketing Neutropenic colitis (including fatal events), fungal lung infections (Pulmonary mycosis, Pneumocystis jirovecii pneumonia), Stenotrophomonas bacterial infection, hemorrhagic cystitis, interstitial pneumonia
Most common (>=30%) Nausea, cough, fatigue, pyrexia, headache, abdominal pain, vomiting, tachycardia, diarrhea, dyspnea, hypokalemia, leukocytosis, hyperglycemia, hypomagnesemia, insomnia, dermatitis, edema, QTc prolongation, rigors, sore throat, arthralgia, paresthesia, pruritus
Serious Differentiation syndrome, cardiac conduction abnormalities, QTc prolongation, encephalopathy, hepatotoxicity, hyperleukocytosis, atrial dysrhythmias, hyperglycemia
Postmarketing Ventricular tachycardia, torsade de pointes, atrioventricular block, congestive heart failure, deafness, pancytopenia, bone marrow necrosis, peripheral neuropathy, seizures, confusion, encephalopathy, Wernicke's encephalopathy, posterior reversible encephalopathy syndrome, toxic epidermal necrolysis, rhabdomyolysis, melanoma, pancreatic cancer, squamous cell carcinoma
Pharmacology
Gemtuzumab ozogamicin is a CD33-directed antibody-drug conjugate (ADC) that binds CD33-expressing tumor cells, undergoes internalization of the ADC-CD33 complex, and releases N-acetyl gamma calicheamicin dimethyl hydrazide intracellularly via hydrolytic linker cleavage; the activated calicheamicin derivative induces double-strand DNA breaks, leading to cell cycle arrest and apoptotic cell death.
The mechanism of action is not completely understood. Arsenic trioxide causes morphological changes and DNA fragmentation characteristic of apoptosis in promyelocytic leukemia cells and causes damage or degradation of the PML-RAR-alpha fusion protein.
Enter your patient's insuranceCheck specific coverage details for your patient.
Most Common Insurance
Anthem BCBS
Mylotarg
- Covered on 5 commercial plans
- PA (10/12) · Step Therapy (4/12) · Qty limit (0/12)
Trisenox
- Covered on 5 commercial plans
- PA (9/12) · Step Therapy (0/12) · Qty limit (0/12)
UnitedHealthcare
Mylotarg
- Covered on 4 commercial plans
- PA (1/8) · Step Therapy (0/8) · Qty limit (0/8)
Trisenox
- Covered on 4 commercial plans
- PA (0/8) · Step Therapy (0/8) · Qty limit (0/8)
Humana
Mylotarg
- Covered on 0 commercial plans
- PA (2/3) · Step Therapy (0/3) · Qty limit (0/3)
Trisenox
- Covered on 0 commercial plans
- PA (2/3) · Step Therapy (0/3) · Qty limit (0/3)
Coverage data sourced from MMIT. Updated monthly.
Savings
Cost estimate not availableAssistance Fund: Acute Myeloid Leukemia
Commercial or private insurance
Medicare, Medicaid, VA, TRICARE
Cost estimate not availableHealthWell: Acute Myeloid Leukemia
Commercial or private insurance
Medicare, Medicaid, VA, TRICARE
Compare Other Drugs
Let us handle your prior authsJust enter your patient's info and we'll:
- Verify eligibility with the payer.
- Pull the right PA forms directly from the payer.
- Submit, track & send live updates to your dashboard.
Free to start · HIPAA compliant
Next Steps for Your Patient
MylotargView full Mylotarg profile
TrisenoxView full Trisenox profile
Clinical data sourced from FDA-approved labeling. Coverage data via MMIT. Updated monthly.