Last reviewed 2026-04-20 · How we verify

Idamycin Pfs (IDARUBICIN)

Idarubicin works by binding to DNA topoisomerase 2-alpha, preventing the enzyme from unwinding DNA and leading to cell death.

Idarubicin (Idamycin Pfs) is a marketed anthracycline antibiotic used primarily for the treatment of Acute Myeloid Leukemia (AML), with a key composition patent expiring in 2028. Its mechanism of action, which involves binding to DNA topoisomerase 2-alpha, provides a strong therapeutic effect, distinguishing it from other same-class drugs such as doxorubicin, daunorubicin, epirubicin, mitoxantrone, and valrubicin, many of which are off-patent and available as generics. The primary risk to Idarubicin's market position is the significant competition from these off-patent generics, which may erode market share and revenue.

At a glance

Mechanism of action

Mechanism of Action. Idarubicin hydrochloride is DNA-intercalating analog of daunorubicin which has an inhibitory effect on nucleic acid synthesis and interacts with the enzyme topoisomerase II. The absence of methoxy group at position of the anthracycline structure gives the compound high lipophilicity which results in an increased rate of cellular uptake compared with other anthracyclines.

Approved indications

• Acute Myeloid Leukemia (AML)

Boxed warnings

• WARNING: CARDIOMYOPATHY, SECONDARY MALIGNANCIES, and EXTRAVASATION AND TISSUE NECROSIS • Cardiomyopathy: IDAMYCIN PFS can cause myocardial damage, including acute left ventricular failure, during or after termination of therapy. The risk of cardiomyopathy is increased in patients who have received prior anthracyclines or who have pre-existing cardiac disease. Assess left ventricular cardiac function prior to initiation of IDAMYCIN PFS and during and after treatment [see Warnings and Precautions (5.1) ] . • Secondary Malignancies: Secondary acute myelogenous leukemia (AML) and myelodysplastic syndrome (MDS) occur at a higher incidence in patients treated with anthracyclines, including IDAMYCIN PFS [see Warnings and Precautions (5.2) ] . • Extravasation and Tissue Necrosis: Extravasation of IDAMYCIN PFS during administration can result in local tissue injury and necrosis. Immediately terminate the infusion of IDAMYCIN PFS and institute the recommended management procedures [see Dosage and Administration (2.6) and Warnings and Precautions (5.3) ] . WARNING: CARDIOMYOPATHY, SECONDARY MALIGNANCIES, and EXTRAVASATION AND TISSUE NECROSIS See full prescribing information for complete boxed warning. • Cardiomyopathy: Myocardial damage leading to congestive heart failure can occur with IDAMYCIN PFS. Assess left ventricular cardiac function prior to initiation of IDAMYCIN PFS and during and after treatment. (5.1) • Secondary Malignancies: Secondary acute myelogenous leukemia (AML) and myelodysplastic syndrome (MDS) occur at a higher incidence in patients treated with anthracyclines, including IDAMYCIN PFS. (5.2) • Extravasation of IDAMYCIN PFS during administration can result in local tissue injury and necrosis. Immediately discontinue the IDAMYCIN PFS infusion if extravasation occurs. ( 2.6 , 5.3 )

Common side effects

• Infection
• Nausea/Vomiting
• Alopecia
• Abdominal Pain/Diarrhea
• Hemorrhage
• Mucositis
• Dermatologic
• Mental Status Changes
• Pulmonary Disorders
• Fever
• Headache
• Cardiac Disorder

Key clinical trials

• Standard-dose vs Intermediate-dose Cytarabine Induction in the Treatment of Acute Myeloid Leukemia With RUNX1-RUNX1T1 (PHASE3)
• Testing the Addition of an Anti-cancer Drug, Navtemadlin, to the Usual Treatments (Cytarabine and Idarubicin) in Patients With Acute Myeloid Leukemia (PHASE1)
• BLAST MRD AML-1: BLockade of PD-1 Added to Standard Therapy to Target Measurable Residual Disease in Acute Myeloid Leukemia 1- A Randomized Phase 2 Study of Anti-PD-1 Pembrolizumab in Combination With Intensive Chemotherapy as Frontline Therapy in Patients With Acute Myeloid Leukemia (PHASE2)
• CPX-351 vs Intensive Chemotherapy in Patients With de Novo Intermediate or Adverse Risk AML Stratified by Genomics (PHASE2)
• VAG Versus Standard Chemotherapy With FLT3 Inhibitor in Adult Patients With FLT3-Mutated AML (PHASE3)
• Trial to Compare Efficacy and Safety of Chemotherapy/Quizartinib vs Chemotherapy/Placebo in Adults FMS-like Tyrosine Kinase 3 (FLT3) Wild-type Acute Myeloid Leukemia (AML) (PHASE2)
• Venetoclax, Azacitidine, and Mitoxantrone Hydrochloride Liposome Versus Idarubicin and Cytarabine in Newly Diagnosed AML (PHASE3)
• A Multicenter RCT of "3+7" vs Venetoclax + CACAG in Newly Diagnosed Mid/High-Risk AML Patients (PHASE2)

Primary sources

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