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Daunorubicin
Clinical data
Trade namesCerubidine, others
AHFS/Drugs.comMonograph
MedlinePlusa682289
Pregnancy
category
Routes of
administration		Intravenous
ATC code
Legal status
Legal status
Pharmacokinetic data
MetabolismLiver
Elimination half-life26.7 hours (metabolite)
ExcretionBile duct and urinary
Identifiers
  • (8S,10S)-8-Acetyl-10-[(2S,4S,5S,6S)-
    4-amino-5-hydroxy-6-methyl-oxan-
    2-yl]oxy-6,8,11-trihydroxy-1-methoxy-
    9,10-dihydro-7H-tetracene-5,12-dione
CAS Number
PubChem CID
IUPHAR/BPS
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
CompTox Dashboard (EPA)
ECHA InfoCard100.040.048 Edit this at Wikidata
Chemical and physical data
FormulaC27H29NO10
Molar mass527.526 g·mol−1
3D model (JSmol)
  • C[C@H]1[C@H]([C@H](C[C@@H](O1)O[C@H]2C[C@@](Cc3c2c(c4c(c3O)C(=O)c5cccc(c5C4=O)OC)O)(C(=O)C)O)N)O
  • InChI=1S/C27H29NO10/c1-10-22(30)14(28)7-17(37-10)38-16-9-27(35,11(2)29)8-13-19(16)26(34)21-20(24(13)32)23(31)12-5-4-6-15(36-3)18(12)25(21)33/h4-6,10,14,16-17,22,30,32,34-35H,7-9,28H2,1-3H3/t10-,14-,16-,17-,22+,27-/m0/s1 checkY
  • Key:STQGQHZAVUOBTE-VGBVRHCVSA-N checkY
  (verify)

Daunorubicin, also known as daunomycin, is a chemotherapy medication used to treat cancer.[2] Specifically it is used for acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), chronic myelogenous leukemia (CML), and Kaposi's sarcoma.[2] It is administered by injection into a vein.[2] A liposomal formulation known as liposomal daunorubicin also exists.[2]

Common side effects include hair loss, vomiting, bone marrow suppression, and inflammation of the inside of the mouth.[2] Other severe side effects include heart disease and tissue death at the site of injection.[2] Use in pregnancy may harm the fetus.[2] Daunorubicin is in the anthracycline family of medication.[3] It works in part by blocking the function of topoisomerase II.[2]

Daunorubicin was approved for medical use in the United States in 1979.[2] It is on the World Health Organization's List of Essential Medicines.[4] It was originally isolated from bacteria of the Streptomyces type.[5]

Medical uses

[edit]

It slows or stops the growth of cancer cells in the body. Treatment is usually performed together with other chemotherapy drugs (such as cytarabine), and its administration depends on the type of tumor and the degree of response.[citation needed]

In addition to its major use in treating acute myeloid leukemia, daunorubicin is also used to treat neuroblastoma. Daunorubicin has been used with other chemotherapy agents to treat the blastic phase of chronic myelogenous leukemia.[citation needed]

Daunorubicin is also used as the starting material for semi-synthetic manufacturing of doxorubicin, epirubicin and idarubicin.[citation needed]

Mechanism of action

[edit]

Similar to doxorubicin, daunorubicin interacts with DNA by intercalation and inhibition of macromolecular biosynthesis.[6][7] This inhibits the progression of the enzyme topoisomerase II, which relaxes supercoils in DNA; without action of topoisomerase II, these DNA supercoils interfere in transcription of DNA. Daunorubicin stabilizes the topoisomerase II complex after it has broken the DNA chain for replication, preventing the DNA double helix from being resealed and thereby stopping the process of replication. On binding to DNA, daunomycin intercalates, with its daunosamine residue directed toward the minor groove. It has the highest preference for two adjacent G/C base pairs flanked on the 5' side by an A/T base pair. Crystallography shows that daunomycin induces a local unwinding angle of 8°, and other conformational disturbances of adjacent and second-neighbour base pairs.[8] It can also induce histone eviction from chromatin upon intercalation.[9][10]

History

[edit]
See also: Anthracycline § History, Doxorubicin § History, and History of cancer chemotherapy

In the 1950s, an Italian research company, Farmitalia Research Laboratories, began an organized effort to isolate anticancer compounds from soil-based microbes. A soil sample was isolated from the area surrounding the Castel del Monte, a 13th-century castle in Apulia. A new strain of Streptomyces peucetius which produced a red pigment was isolated, and an antibiotic was produced from this bacterium that was found to have good activity against murine tumors. Since a group of French researchers discovered the same compound at about the same time, the two teams named the compound daunorubicin, combining the name Dauni, a pre-Roman tribe that occupied the area of Italy where the compound was isolated, with the French word for ruby, rubis, describing the color.[11][12][13] Clinical trials began in the 1960s, and the drug saw success in treating acute leukemia and lymphoma.

However, by 1967, it was recognized that daunorubicin could produce fatal cardiac toxicity.[14]

In 2015–16, a team at Ohio State University "showed that, by carefully manipulating strands of viral DNA, an origami structure with complex folds can be created in just 10 minutes. Incredibly, these structures are only 100 nanometers across – that’s 1,000 times smaller than the width of a human hair. Small volumes of daunorubicin can be wrapped up in these minuscule pods, which can then be released into a leukemia cell-filled environment."[15][16][unreliable medical source?]

Route of administration

[edit]

Daunorubicin should only be administered in a rapid intravenous infusion. It should not be administered intramuscularly or subcutaneously, since it may cause extensive tissue necrosis. It should also never be administered intrathecally (into the spinal canal), as this will cause extensive damage to the nervous system and may lead to death. Daunorubicin has been used intravitreally (inside the eye) for the purposes of preventing proliferative vitreoretinopathy, a common complication following retinal detachment surgery, but has not been found to be effective and is not used for any other ophthalmic purposes at this time.[17]

References

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Daunorubicin

View on Grokipedia
from Grokipedia
Daunorubicin is an anthracycline antibiotic derived from the bacterium Streptomyces peucetius, serving as a potent antineoplastic agent primarily used in chemotherapy to treat various forms of leukemia. It functions by intercalating into DNA, inhibiting topoisomerase II, and disrupting DNA and RNA synthesis, which leads to apoptosis in rapidly dividing cancer cells. Chemically, it has the molecular formula C27H29NO10 and appears as an orange-red powder, often administered as the hydrochloride salt via intravenous injection. Discovered in the early during a search for soil-derived antibiotics, daunorubicin was isolated from peucetius and represents the first identified for anticancer activity. It received FDA approval in 1979 for remission induction in acute nonlymphocytic leukemia in adults and acute lymphocytic leukemia in children, typically in combination with cytarabine as part of the standard "7+3" regimen. Additional indications include, in liposomal formulations like Vyxeos (combined with cytarabine), for therapy-related or AML with myelodysplasia-related changes since 2017. While highly effective, daunorubicin carries significant risks, including dose-limiting that can lead to congestive , particularly at cumulative doses exceeding 400–550 mg/m², as well as myelosuppression, , alopecia, and potential for secondary malignancies. It is metabolized primarily in the liver to the active but less cytotoxic daunorubicinol via aldo-keto reductase enzymes, with elimination occurring through biliary (40%) and urinary (25%) routes; dosage adjustments are required for hepatic or renal impairment. Contraindications include and preexisting heart disease, and it is classified as D due to fetal harm risks.

Medical Uses

Indications

Daunorubicin is approved by the FDA for use in remission induction therapy for (ANLL), including (AML), in adults when administered in combination with other chemotherapeutic agents. It is also indicated for remission induction in (ALL) in both adults and children, typically combined with and , where it has been shown to increase complete remission rates from 47% to 83% in adults. In protocols, daunorubicin plays a key role in achieving complete remission by targeting rapidly proliferating leukemic cells during the induction phase, with complete remission rates of 53-65% in AML when used with cytarabine. For (CML) in the blastic phase, daunorubicin is commonly incorporated into intensive regimens, such as those combining it with high-dose cytarabine, to induce hematologic responses and potentially achieve a second chronic phase. The liposomal formulation Vyxeos (daunorubicin and cytarabine in a fixed 1:5 molar ratio) is FDA-approved for newly diagnosed therapy-related (t-AML) or AML with myelodysplasia-related changes (AML-MRC) in adults (2017) and in pediatric patients aged 1 year and older (2021). Daunorubicin has historical use in the treatment of advanced , particularly in pediatric patients, where early studies demonstrated partial responses in disseminated disease when administered at doses of 1 mg/kg every other day. Off-label applications include select solid tumors where are applicable due to their activity against rapidly dividing cells.

Combination Therapy

Daunorubicin is commonly administered in combination with cytarabine as part of the standard 7+3 induction regimen for newly diagnosed acute myeloid leukemia (AML), involving continuous cytarabine infusion at 100-200 mg/m²/day for 7 days and daunorubicin at 45-60 mg/m²/day intravenously for 3 days. This protocol aims to achieve rapid remission by synergistically targeting leukemic cells during induction therapy. In (ALL), daunorubicin is frequently combined with and (or dexamethasone) during the induction phase, typically dosed at 25-60 mg/m² of daunorubicin alongside weekly at 1.4 mg/m² and at 40-60 mg/m²/day for 4-6 weeks. For high-risk (APL), a subtype of AML, daunorubicin is integrated with all-trans (ATRA) and often , using daunorubicin at 45 mg/m²/day for 3-4 days alongside ATRA at 45 mg/m²/day to induce differentiation and in promyelocytes. The rationale for these combinations lies in addressing multi-drug resistance mechanisms, such as efflux pumps, and targeting complementary aspects of the : daunorubicin intercalates DNA to inhibit topoisomerase II during S and G2 phases, while cytarabine incorporates into DNA to block chain elongation in , and disrupts in M phase. This multi-target approach reduces the likelihood of resistant clones emerging compared to monotherapy. Clinical trials demonstrate superior outcomes with these regimens over daunorubicin monotherapy; for instance, the 7+3 protocol yields complete remission rates of 60-80% in AML patients under 60 years, with overall survival improvements of 10-20% at 5 years versus single-agent , as shown in randomized studies comparing standard and intensified dosing. In ALL, adding daunorubicin to and increases remission rates from approximately 50% to over 80%, with enhanced event-free survival. Similarly, ATRA-daunorubicin combinations in high-risk APL achieve cure rates exceeding 80%, significantly higher than chemotherapy alone.

Pharmacology

Mechanism of Action

Daunorubicin is an anthracycline-class antibiotic originally isolated from the soil bacterium Streptomyces peucetius. Its molecular structure features a planar anthraquinone ring system fused to a tetracyclic ring and a daunosamine sugar moiety, which contributes to its ability to interact with nucleic acids. This structural arrangement enables daunorubicin to bind DNA through intercalation, where the planar anthraquinone chromophore inserts between adjacent base pairs, primarily at GC-rich sequences such as CpG steps or sites flanked by AT bases. Intercalation distorts the DNA helix by unwinding it locally by approximately 10°, which inhibits the activity of DNA and RNA polymerases, thereby blocking nucleic acid synthesis and replication. In addition to intercalation, daunorubicin exerts its cytotoxic effects by poisoning DNA topoisomerase II (Topo II), an enzyme essential for resolving DNA supercoils during replication and transcription. The drug stabilizes the transient DNA-Topo II cleavable complex, preventing the religation of DNA strands and resulting in persistent double-strand breaks that trigger arrest and . This Topo II inhibition is concentration-dependent, acting as a poison at clinically relevant doses to amplify DNA damage. Daunorubicin also generates (ROS) through redox cycling of its moiety, which can oxidize cellular components and further induce independently of direct DNA interactions. Moreover, it promotes eviction from open regions, deregulating and contributing to cytotoxicity even in cells lacking Topo II activity. This effect is a shared property of and enhances the drug's antitumor activity.

Pharmacokinetics

Daunorubicin is not orally bioavailable due to poor gastrointestinal absorption and extensive first-pass metabolism, necessitating intravenous administration for clinical use, which achieves 100% bioavailability. Following intravenous injection, daunorubicin exhibits rapid tissue penetration with wide distribution throughout the body, accumulating to highest concentrations in organs such as the spleen, kidneys, liver, lungs, and heart. It demonstrates high plasma protein binding, primarily to albumin, at approximately 63%. The volume of distribution is large, ranging from 1006 to 1725 L/m², reflecting extensive extravascular distribution. Daunorubicin crosses the placenta but minimally penetrates the blood-brain barrier. Metabolism of daunorubicin occurs primarily in the liver and other tissues through reduction by aldo-keto reductases, yielding the daunorubicinol, which retains similar to the parent compound. Additional involvement of enzymes, particularly , contributes to its and clearance. Within 30 minutes of administration, about 40% of plasma daunorubicin is converted to daunorubicinol, increasing to 60% by 4 hours. Elimination of daunorubicin follows a biphasic pattern, with an initial distribution of approximately 1 to 2 hours for the parent and a terminal elimination of 18.5 hours; the daunorubicinol has a longer of about 26.7 hours. occurs mainly via the hepatobiliary route, with approximately 40% eliminated in feces through biliary , and about 9 to 25% via renal clearance in , primarily as metabolites. In special populations, pharmacokinetic adjustments are recommended for hepatic or renal impairment to mitigate risks; for example, reduce the dose by 25% if serum is 1.2 to 3 mg/dL or by 50% if greater than 3 mg/dL or serum exceeds 3 mg/dL. Elderly patients require cautious monitoring and potentially lower doses due to increased susceptibility, while obese individuals may need PK monitoring as can influence clearance and distribution.

Side Effects

Common Side Effects

Daunorubicin therapy commonly induces gastrointestinal adverse effects, including and , which occur in more than 10% of patients and are typically mild and reversible. , manifesting as sores in the and on the , develops 3–7 days after administration and affects a significant proportion of patients, while and are reported occasionally. Hematologic toxicity is a dose-limiting effect, with myelosuppression occurring in all patients receiving therapeutic doses, leading to , , and . The nadir of neutropenia typically peaks 10–14 days post-dose, with recovery occurring by 21–24 days. Management involves regular monitoring of complete blood counts and prophylactic use of growth factors to mitigate risk from neutropenia. Dermatologic effects include reversible alopecia, which develops in most patients, often resulting in total . Hyperpigmentation may occur, particularly in previously irradiated areas, though it is less frequent. Other common side effects encompass and fever, which are frequently observed during treatment. Mild infusion reactions, such as chills or flushing, can arise but are rare. Supportive care, including antiemetics for and , is standard to alleviate these effects. In indications like pediatric , these adverse reactions are closely monitored due to the intravenous route's potential for local irritation.

Serious Side Effects

Daunorubicin poses significant risks of severe toxicities that can be life-threatening, necessitating vigilant monitoring and preventive strategies during . The most prominent is , characterized by dose-dependent that may culminate in congestive . This arises from free radical generation and preferential accumulation of the daunorubicinol in myocardial tissue. In adults, the cumulative lifetime dose is capped at 400–550 mg/, with a reduction to 300–400 mg/ recommended for patients with prior mediastinal ; lower limits apply for children (300 mg/ for those over 2 years or 10 mg/kg for those under 2 years). Cardiac function should be assessed via baseline and serial echocardiograms to detect subclinical left ventricular dysfunction early, allowing for dose adjustments or discontinuation. Extravasation represents another critical hazard, as daunorubicin's vesicant nature can induce severe local tissue and ulceration if the drug leaks into surrounding tissues. Immediate intervention is essential: must be halted, the site aspirated if feasible, cold compresses applied to the affected area for 15–20 minutes every 6 hours for the first 24–48 hours, and antidotes such as administered systemically or topical (DMSO) applied to limit damage and promote healing. Preventive measures include using central venous access and monitoring sites closely during administration. Daunorubicin therapy elevates the risk of secondary malignancies, particularly therapy-related , stemming from its intercalation into DNA and induction of chromosomal damage. Long-term follow-up with hematologic monitoring is advised for early detection in survivors. As a potent teratogen, daunorubicin carries an FDA D designation, signifying evidence of fetal harm based on human data, including congenital malformations and growth retardation; it is strictly contraindicated in , with effective contraception required for patients of childbearing potential. Additional severe effects include , manifesting as acute reactions with and , which demands immediate discontinuation and supportive care such as epinephrine administration. may also occur, especially in high-burden hematologic malignancies, leading to , renal failure, and electrolyte derangements; prophylaxis with hydration, , or is recommended for at-risk patients.

Administration

Route of Administration

Daunorubicin is administered exclusively via the intravenous route to ensure effective delivery and minimize risks associated with its vesicant properties. The primary method involves over 10 to 30 minutes into the tubing of a rapidly flowing intravenous line, which helps reduce peak plasma concentrations and thereby lowers the risk of compared to bolus administration. Two main formulations are available: conventional daunorubicin , which is a direct solution, and liposomal formulations such as Vyxeos (daunorubicin and cytarabine in a 1:5 molar ratio), designed for specific indications to provide sustained release and mitigate peak-related toxicities such as . DaunoXome (liposomal daunorubicin citrate) is used for advanced HIV-associated . For preparation, the conventional form is typically diluted in 0.9% normal saline or 5% dextrose in (D5W) to a concentration of 1 mg/mL or less before ; a central venous line is preferred over peripheral access due to the drug's potential to cause severe tissue damage if occurs. Vyxeos is administered as a 90-minute without further dilution. Administration by intramuscular, subcutaneous, intrathecal, or oral routes is strictly prohibited, as these can lead to severe local from tissue irritation or in the case of intrathecal use. Improper handling, such as , requires immediate cessation of infusion and application of local protocols to manage potential ulceration. Infusion-related may occur but is generally managed with supportive care. Unopened vials of daunorubicin injection should be stored under at 2°C to 8°C (36°F to 46°F) and protected from by retaining them in the original carton until use; reconstituted solutions are stable for up to 48 hours under or 24 hours at , also shielded from . Liposomal formulations follow similar storage guidelines to maintain stability.

Dosage

Daunorubicin is typically administered as part of induction for (AML), with a standard dose of 45 to 60 mg/m² per day intravenously for 3 days, often in combination with cytarabine at 100 mg/m² per day for 7 days in the initial course. For patients aged 60 years or older, the dose is commonly reduced to 30 mg/m² per day for the same schedule to minimize toxicity risks. Subsequent courses may shorten the cytarabine duration to 5 days while maintaining the daunorubicin schedule, with up to three cycles administered until remission is achieved. For Vyxeos in therapy-related AML or AML with myelodysplasia-related changes, the dose is 44 mg/m² daunorubicin and 100 mg/m² cytarabine IV on days 1, 3, and 5 for induction (two cycles), followed by consolidation. In pediatric patients, dosing for AML induction is typically 50 mg/m² per day for 3 days (or on days 1, 3, 5), reflecting protocols to balance efficacy and risk. For obese patients, dosing should be calculated using actual body weight rather than ideal body weight to ensure appropriate exposure without excessive reduction. The lifetime cumulative dose limit for daunorubicin is 400 to 550 mg/m² in adults and 300 mg/m² in children over 2 years of age, with reductions (e.g., to 400 mg/m² in adults with prior mediastinal radiation) based on cardiac risk factors; this limit is determined based on ongoing assessments of cardiac function to prevent irreversible . Dose adjustments are required for hepatic dysfunction: reduce by 25% if serum is 1.2-3 mg/dL, and by 50% if exceeding 3 mg/dL or in cases of biliary obstruction, to account for impaired clearance. No dose adjustment is necessary for renal impairment, as daunorubicin is primarily eliminated via biliary excretion. Monitoring during therapy includes weekly complete blood counts (CBC) to assess for myelosuppression and guide dose timing, along with baseline and periodic evaluations of cardiac via or multigated acquisition (MUGA) scan to detect early signs of . These protocols may vary slightly based on specific regimens, such as those incorporating cytarabine.

History

Discovery and Development

Daunorubicin was isolated in the late from a strain of the soil bacterium Streptomyces peucetius collected near Castel del Monte in , , by researchers at the Italian pharmaceutical company Farmitalia. The compound, initially named daunomycin, was derived from the Dauni, an ancient pre-Roman tribe inhabiting the region, while the suffix "rubicin" reflected its ruby-red color, a naming convention also seen in the French term rubidomycin used by parallel researchers at who isolated the same substance independently. By 1964, the identity of daunomycin and rubidomycin was confirmed, leading to the unified name daunorubicin. Early preclinical studies demonstrated daunorubicin's antitumor activity in animal models, notably against L1210 mouse leukemia, where it inhibited and showed potent cytotoxic effects and . These findings prompted the initiation of clinical trials in during the early 1960s, focusing on leukemia patients. The first remissions were reported in 1962 by Jean Bernard in for (ALL) and in 1964 by Clarence Tan in the United States for both ALL and (AML), marking significant progress in inducing temporary disease control. Key milestones in the included the identification of daunorubicin's cardiac toxicity in 1967, observed during pediatric treatments and linked to cumulative dosing by Tan and colleagues, which prompted dose-limiting strategies. Concurrently, efforts to mitigate toxicity and broaden led to the synthesis of analogs; in 1969, Farmitalia researcher Arcamone isolated (adriamycin) from a mutant strain of S. peucetius, enhancing the class's therapeutic potential.

Regulatory Approval

Daunorubicin was first approved for clinical use in Italy during the 1960s by Farmitalia, following its isolation from Streptomyces peucetius caesius and initial clinical trials in the mid-1960s. In the United States, the Food and Drug Administration (FDA) granted initial approval on December 19, 1979, for daunorubicin hydrochloride (Cerubidine) as part of combination chemotherapy for remission induction in acute nonlymphocytic leukemia (ANLL) in adults and for induction of remission in acute lymphocytic leukemia (ALL) in children and adults. The World Health Organization (WHO) included daunorubicin on its first Model List of Essential Medicines in 1977, recognizing its importance for treating acute leukemias, and it has remained on the list in subsequent updates. A liposomal formulation, daunorubicin citrate injection (DaunoXome), received FDA approval on April 8, 1996, for first-line cytotoxic therapy in patients with advanced HIV-associated . Internationally, daunorubicin has been approved in the through national authorizations since the late 1970s or early , with variations in formulations; for instance, liposomal daunorubicin availability differs by . In , approved daunorubicin for acute leukemias around the same period as the U.S., with generic versions listed in the Drug Product Database since the . Post-marketing surveillance led to significant label updates, including the addition of warnings in the for severe , including congestive , and for the risk of secondary acute myelogenous following long-term use. Daunorubicin became available as a after patent expiration in the late , broadening access while maintaining these safety warnings in regulatory labels worldwide. As of 2025, no major revisions to approvals for pediatric use or new combinations have occurred for the standard formulation, though the liposomal combination Vyxeos (daunorubicin and cytarabine) received FDA approval in 2017 for specific AML subtypes.

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