Doxorubicin
Übersicht
Beschreibung
Doxorubicin, auch bekannt unter seinem Handelsnamen Adriamycin, ist ein Chemotherapeutikum, das zur Behandlung verschiedener Krebsarten eingesetzt wird, darunter Brustkrebs, Blasenkrebs, Kaposi-Sarkom, Lymphom und akute lymphatische Leukämie . Es gehört zur Klasse der Anthracycline und wirkt, indem es die Funktion der DNA stört, was letztendlich das Wachstum und die Proliferation von Krebszellen hemmt .
Wirkmechanismus
Target of Action
Doxorubicin, a widely used drug in cancer chemotherapy, is known to bind to DNA-associated enzymes and intercalate with DNA base pairs . It targets multiple molecular targets to produce a range of cytotoxic effects .
Mode of Action
This compound exerts its effect through DNA intercalation , which eventually leads to DNA damage and the generation of reactive oxygen species . It inhibits the enzyme topoisomerase II , causing DNA damage and induction of apoptosis . It also intercalates at points of local uncoiling of the double helix .
Biochemical Pathways
This compound influences various biochemical pathways. It activates molecular signals from AMPK (AMP-activated protein kinase inducing apoptosis) to influence the Bcl-2/Bax apoptosis pathway . By altering the Bcl-2/Bax ratio, downstream activation of different caspases can occur, resulting in apoptosis . This compound also induces ferroptosis , a major form of cell death in its cytotoxicity .
Pharmacokinetics
Various parenteral this compound formulations, such as liposomes, polymeric micelles, polymeric nanoparticles, and polymer-drug conjugates, have been developed to increase its therapeutic efficacy .
Result of Action
The molecular and cellular effects of this compound’s action include the generation of reactive oxygen species, DNA damage, inhibition of topoisomerase II, and induction of apoptosis . It also induces apoptosis and necrosis in healthy tissue, causing toxicity in the brain, liver, kidney, and heart .
Action Environment
Environmental factors can influence the action, efficacy, and stability of this compoundRather, the level of orthophosphate salt is the main factor influencing the initial burst effect and drug release . Moreover, hypoxic areas of tumors are characterized by acidification, which is likely the environmental factor influencing the accumulation of this compound .
Wissenschaftliche Forschungsanwendungen
Doxorubicin hat eine breite Palette an Anwendungen in der wissenschaftlichen Forschung, insbesondere in den Bereichen Chemie, Biologie, Medizin und Industrie. In der Medizin wird es ausgiebig als Chemotherapeutikum zur Behandlung verschiedener Krebsarten eingesetzt. Die Forschung konzentriert sich auf die Verbesserung seiner Wirksamkeit und die Reduzierung seiner Nebenwirkungen durch die Entwicklung neuartiger Arzneimittelverabreichungssysteme wie Liposomen, Nanopartikel und polymerer Mizellen .
In der Biologie wird this compound verwendet, um die Mechanismen der DNA-Schädigung und -Reparatur sowie die zellulären Reaktionen auf oxidativen Stress zu untersuchen. In der Chemie dient es als Modellverbindung zur Untersuchung der Wechselwirkungen zwischen kleinen Molekülen und DNA .
5. Wirkmechanismus
This compound entfaltet seine Wirkung, indem es sich in die DNA interkaliert und so die Wirkung der Topoisomerase II hemmt, einem Enzym, das an der DNA-Replikation beteiligt ist. Dies führt zur Entstehung reaktiver Sauerstoffspezies und nachfolgender DNA-Schäden, was letztendlich zum Zelltod führt . This compound beeinflusst auch verschiedene molekulare Ziele und Signalwege, darunter den Bcl-2/Bax-Apoptose-Signalweg, der eine entscheidende Rolle bei der Regulierung des Zelltods spielt .
Ähnliche Verbindungen:
- Daunorubicin
- Epirubicin
- Idarubicin
- Mitoxantron
Vergleich: this compound ist unter diesen Verbindungen einzigartig aufgrund seines breiten Wirkungsspektrums gegen verschiedene Krebsarten und seiner Fähigkeit, sich in die DNA zu interkalieren. Obwohl Daunorubicin strukturell this compound ähnlich ist, hat es eine andere Seitenkette, die seine pharmakokinetischen Eigenschaften beeinflusst . Epirubicin und Idarubicin sind ebenfalls Anthracycline, haben aber unterschiedliche Toxizitätsprofile und klinische Anwendungen . Mitoxantron, obwohl kein Anthracyclin, weist einige strukturelle Ähnlichkeiten auf und wird in ähnlichen klinischen Situationen eingesetzt .
Zusammenfassend lässt sich sagen, dass this compound ein wichtiges Chemotherapeutikum mit einem breiten Anwendungsspektrum in der wissenschaftlichen Forschung und Medizin ist. Sein einzigartiger Wirkmechanismus und sein breites Wirkungsspektrum machen es zu einem wichtigen Werkzeug im Kampf gegen Krebs.
Biochemische Analyse
Biochemical Properties
Doxorubicin plays a crucial role in biochemical reactions by interacting with several key biomolecules. It intercalates between DNA base pairs, disrupting the DNA structure and inhibiting the activity of topoisomerase II, an enzyme essential for DNA replication and transcription . This interaction leads to the generation of reactive oxygen species, causing oxidative damage to cellular components . Additionally, this compound binds to various proteins, including histones and transcription factors, further affecting gene expression and cellular function .
Cellular Effects
This compound exerts profound effects on various types of cells and cellular processes. It induces DNA damage, leading to cell cycle arrest and apoptosis . In cancer cells, this compound triggers the activation of apoptotic pathways, including the Bcl-2/Bax pathway, resulting in programmed cell death . The compound also impairs mitochondrial function, leading to the generation of reactive oxygen species and further promoting cell death . In addition to its cytotoxic effects, this compound influences cell signaling pathways, gene expression, and cellular metabolism, contributing to its overall anticancer activity .
Molecular Mechanism
The molecular mechanism of this compound involves several key processes. Upon entering the cell, this compound intercalates into DNA, disrupting the DNA structure and inhibiting the activity of topoisomerase II . This inhibition prevents the relaxation of supercoiled DNA, leading to the accumulation of DNA breaks and ultimately cell death . This compound also generates reactive oxygen species, causing oxidative damage to cellular components, including lipids, proteins, and DNA . Furthermore, this compound induces the activation of apoptotic pathways, including the Bcl-2/Bax pathway, resulting in programmed cell death .
Temporal Effects in Laboratory Settings
In laboratory settings, the effects of this compound change over time. The compound is relatively stable, but its efficacy can decrease due to degradation and the development of drug resistance . Long-term exposure to this compound can lead to chronic cardiotoxicity, characterized by mitochondrial dysfunction and oxidative stress . In vitro and in vivo studies have shown that this compound’s cytotoxic effects are time-dependent, with prolonged exposure leading to increased cell death and tissue damage .
Dosage Effects in Animal Models
The effects of this compound vary with different dosages in animal models. At low doses, this compound induces apoptosis in cancer cells without causing significant toxicity to normal tissues . At high doses, this compound can cause severe cardiotoxicity, characterized by mitochondrial damage, oxidative stress, and cell death . Threshold effects have been observed, with a narrow therapeutic window between effective and toxic doses . Studies in animal models have highlighted the importance of dose optimization to minimize adverse effects while maintaining anticancer efficacy .
Metabolic Pathways
This compound is involved in several metabolic pathways, including one-electron reduction, two-electron reduction, and deglycosidation . The compound is metabolized by enzymes such as cytochrome P450 reductase and aldo-keto reductase, leading to the formation of active and inactive metabolites . These metabolic pathways influence the pharmacokinetics and toxicity of this compound, affecting its overall efficacy and safety . Additionally, this compound can alter metabolic flux and metabolite levels, further impacting cellular function .
Transport and Distribution
This compound is transported and distributed within cells and tissues through various mechanisms. The compound is taken up by cells via passive diffusion and active transport, involving transporters such as P-glycoprotein . Once inside the cell, this compound is distributed to different organelles, including the nucleus, mitochondria, and lysosomes . The localization and accumulation of this compound within specific cellular compartments influence its cytotoxic effects and overall efficacy .
Subcellular Localization
The subcellular localization of this compound plays a critical role in its activity and function. This compound primarily localizes to the nucleus, where it intercalates into DNA and inhibits topoisomerase II . Additionally, this compound accumulates in mitochondria, leading to mitochondrial dysfunction and the generation of reactive oxygen species . The compound can also be found in lysosomes, where it contributes to lysosomal membrane permeabilization and cell death . Targeting signals and post-translational modifications may direct this compound to specific compartments, influencing its subcellular distribution and activity .
Vorbereitungsmethoden
Synthesewege und Reaktionsbedingungen: Doxorubicin wird aus Daunorubicin, einem anderen Anthracyclin-Antibiotikum, synthetisiert. Die Synthese umfasst mehrere Schritte, darunter Glykosylierung, Oxidation und Methylierung. Das Schlüsselzwischenprodukt bei der Synthese ist Daunorubicin, das einer Hydroxylierung unterzogen wird, um this compound zu bilden .
Industrielle Produktionsmethoden: Die industrielle Produktion von this compound erfolgt typischerweise durch Fermentation unter Verwendung des Bakteriums Streptomyces peucetius. Dem Fermentationsprozess folgen Extraktions- und Reinigungsschritte zur Isolierung von this compound. Fortschrittliche Techniken wie Remote Loading und PEGylation werden eingesetzt, um die Stabilität und Wirksamkeit von this compound-Liposomen zu verbessern .
Analyse Chemischer Reaktionen
Arten von Reaktionen: Doxorubicin unterliegt verschiedenen chemischen Reaktionen, darunter Oxidation, Reduktion und Substitution. Es ist bekannt, dass es an DNA-assoziierte Enzyme bindet und sich in DNA-Basenpaare interkaliert, was zu DNA-Schäden führt .
Häufige Reagenzien und Bedingungen: Häufige Reagenzien, die bei den Reaktionen mit this compound verwendet werden, umfassen Oxidationsmittel, Reduktionsmittel und verschiedene Lösungsmittel. Die Bedingungen für diese Reaktionen beinhalten typischerweise kontrollierte Temperaturen und pH-Werte, um die Stabilität der Verbindung zu gewährleisten .
Hauptprodukte, die gebildet werden: Die Hauptprodukte, die aus den Reaktionen von this compound gebildet werden, umfassen seine Metaboliten, die über den Urin und den Kot ausgeschieden werden. Diese Metaboliten werden durch Prozesse wie Hydroxylierung und Glykosylierung gebildet .
Vergleich Mit ähnlichen Verbindungen
- Daunorubicin
- Epirubicin
- Idarubicin
- Mitoxantrone
Comparison: Doxorubicin is unique among these compounds due to its broad spectrum of activity against various cancers and its ability to intercalate with DNA. While daunorubicin is structurally similar to this compound, it has a different side chain, which affects its pharmacokinetic properties . Epirubicin and idarubicin are also anthracyclines but have different toxicity profiles and clinical applications . Mitoxantrone, although not an anthracycline, shares some structural similarities and is used in similar clinical settings .
Eigenschaften
IUPAC Name |
(7S,9S)-7-[(2R,4S,5S,6S)-4-amino-5-hydroxy-6-methyloxan-2-yl]oxy-6,9,11-trihydroxy-9-(2-hydroxyacetyl)-4-methoxy-8,10-dihydro-7H-tetracene-5,12-dione |
Source
|
|---|---|---|
| Source | PubChem | |
| URL | https://pubchem.ncbi.nlm.nih.gov | |
| Description | Data deposited in or computed by PubChem | |
InChI |
InChI=1S/C27H29NO11/c1-10-22(31)13(28)6-17(38-10)39-15-8-27(36,16(30)9-29)7-12-19(15)26(35)21-20(24(12)33)23(32)11-4-3-5-14(37-2)18(11)25(21)34/h3-5,10,13,15,17,22,29,31,33,35-36H,6-9,28H2,1-2H3/t10-,13-,15-,17-,22+,27-/m0/s1 |
Source
|
| Source | PubChem | |
| URL | https://pubchem.ncbi.nlm.nih.gov | |
| Description | Data deposited in or computed by PubChem | |
InChI Key |
AOJJSUZBOXZQNB-TZSSRYMLSA-N |
Source
|
| Source | PubChem | |
| URL | https://pubchem.ncbi.nlm.nih.gov | |
| Description | Data deposited in or computed by PubChem | |
Canonical SMILES |
CC1C(C(CC(O1)OC2CC(CC3=C2C(=C4C(=C3O)C(=O)C5=C(C4=O)C(=CC=C5)OC)O)(C(=O)CO)O)N)O |
Source
|
| Source | PubChem | |
| URL | https://pubchem.ncbi.nlm.nih.gov | |
| Description | Data deposited in or computed by PubChem | |
Isomeric SMILES |
C[C@H]1[C@H]([C@H](C[C@@H](O1)O[C@H]2C[C@@](CC3=C2C(=C4C(=C3O)C(=O)C5=C(C4=O)C(=CC=C5)OC)O)(C(=O)CO)O)N)O |
Source
|
| Source | PubChem | |
| URL | https://pubchem.ncbi.nlm.nih.gov | |
| Description | Data deposited in or computed by PubChem | |
Molecular Formula |
C27H29NO11 |
Source
|
| Source | PubChem | |
| URL | https://pubchem.ncbi.nlm.nih.gov | |
| Description | Data deposited in or computed by PubChem | |
Related CAS |
25316-40-9 (hydrochloride) |
Source
|
| Record name | Doxorubicin [USAN:INN:BAN] | |
| Source | ChemIDplus | |
| URL | https://pubchem.ncbi.nlm.nih.gov/substance/?source=chemidplus&sourceid=0023214928 | |
| Description | ChemIDplus is a free, web search system that provides access to the structure and nomenclature authority files used for the identification of chemical substances cited in National Library of Medicine (NLM) databases, including the TOXNET system. | |
DSSTOX Substance ID |
DTXSID8021480 |
Source
|
| Record name | Doxorubicin | |
| Source | EPA DSSTox | |
| URL | https://comptox.epa.gov/dashboard/DTXSID8021480 | |
| Description | DSSTox provides a high quality public chemistry resource for supporting improved predictive toxicology. | |
Molecular Weight |
543.5 g/mol |
Source
|
| Source | PubChem | |
| URL | https://pubchem.ncbi.nlm.nih.gov | |
| Description | Data deposited in or computed by PubChem | |
Physical Description |
Solid |
Source
|
| Record name | Doxorubicin | |
| Source | Human Metabolome Database (HMDB) | |
| URL | http://www.hmdb.ca/metabolites/HMDB0015132 | |
| Description | The Human Metabolome Database (HMDB) is a freely available electronic database containing detailed information about small molecule metabolites found in the human body. | |
| Explanation | HMDB is offered to the public as a freely available resource. Use and re-distribution of the data, in whole or in part, for commercial purposes requires explicit permission of the authors and explicit acknowledgment of the source material (HMDB) and the original publication (see the HMDB citing page). We ask that users who download significant portions of the database cite the HMDB paper in any resulting publications. | |
Solubility |
Soluble, 2% sol in water; soluble in aqueous alcohols; moderately soluble in anhydrous methanol; insoluble in non-polar organic solvents, 1.18e+00 g/L |
Source
|
| Record name | Doxorubicin | |
| Source | DrugBank | |
| URL | https://www.drugbank.ca/drugs/DB00997 | |
| Description | The DrugBank database is a unique bioinformatics and cheminformatics resource that combines detailed drug (i.e. chemical, pharmacological and pharmaceutical) data with comprehensive drug target (i.e. sequence, structure, and pathway) information. | |
| Explanation | Creative Common's Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/legalcode) | |
| Record name | DOXORUBICIN | |
| Source | Hazardous Substances Data Bank (HSDB) | |
| URL | https://pubchem.ncbi.nlm.nih.gov/source/hsdb/3070 | |
| Description | The Hazardous Substances Data Bank (HSDB) is a toxicology database that focuses on the toxicology of potentially hazardous chemicals. It provides information on human exposure, industrial hygiene, emergency handling procedures, environmental fate, regulatory requirements, nanomaterials, and related areas. The information in HSDB has been assessed by a Scientific Review Panel. | |
| Record name | Doxorubicin | |
| Source | Human Metabolome Database (HMDB) | |
| URL | http://www.hmdb.ca/metabolites/HMDB0015132 | |
| Description | The Human Metabolome Database (HMDB) is a freely available electronic database containing detailed information about small molecule metabolites found in the human body. | |
| Explanation | HMDB is offered to the public as a freely available resource. Use and re-distribution of the data, in whole or in part, for commercial purposes requires explicit permission of the authors and explicit acknowledgment of the source material (HMDB) and the original publication (see the HMDB citing page). We ask that users who download significant portions of the database cite the HMDB paper in any resulting publications. | |
Mechanism of Action |
Doxorubicin has antimitotic and cytotoxic activity through a number of proposed mechanisms of action: Doxorubicin forms complexes with DNA by intercalation between base pairs, and it inhibits topoisomerase II activity by stabilizing the DNA-topoisomerase II complex, preventing the religation portion of the ligation-religation reaction that topoisomerase II catalyzes., Doxorubicin hydrochloride is an antineoplastic antibiotic with pharmacologic actions similar to those of daunorubicin. Although the drug has anti-infective properties, its cytotoxicity precludes its use as an anti-infective agent. The precise and/or principal mechanism(s) of the antineoplastic action of doxorubicin is not fully understood. It appears that the cytotoxic effect of the drug results from a complex system of multiple modes of action related to free radical formation secondary to metabolic activation of the doxorubicin by electron reduction, intercalation of the drug into DNA, induction of DNA breaks and chromosomal aberrations, and alterations in cell membranes induced by the drug. Evidence from in vitro studies in cells treated with doxorubicin suggests that apoptosis (programmed cell death) also may be involved in the drug's mechanism of action. These and other mechanisms (chelation of metal ions to produce drug-metal complexes) also may contribute to the cardiotoxic effects of the drug., Doxorubicin undergoes enzymatic 1- and 2-electron reduction to the corresponding semiquinone and dihydroquinone. 7-Deoxyaglycones are formed enzymatically by 1-electron reduction, and the resulting semiquinone free radical reacts with oxygen to produce the hydroxyl radical in a cascade of reactions; this radical may lead to cell death by reacting with DNA, RNA, cell membranes, and proteins. The dihydroquinone that results from 2-electron reduction of doxorubicin also can be formed by the reaction of 2 semiquinones. In the presence of oxygen, dihydroquinone reacts to form hydrogen peroxide, and in its absence, loses its sugar and gives rise to the quinone methide, a monofunctional alkylating agent with low affinity for DNA. The contribution of dihydroquinone and the quinone methide to the cytotoxicity of doxorubicin is unclear. Experimental evidence indicates that doxorubicin forms a complex with DNA by intercalation between base pairs, causing inhibition of DNA synthesis and DNA-dependent RNA synthesis by the resulting template disordering and steric obstruction. Doxorubicin also inhibits protein synthesis. Doxorubicin is active throughout the cell cycle including the interphase., Several anthracycline-induced effects may contribute to the development of cardiotoxicity. In animals, anthracyclines cause a selective inhibition of cardiac muscle gene expression for ?-actin, troponin, myosin light-chain 2, and the M isoform of creatine kinase, which may result in myofibrillar loss associated with anthracycline-induced cardiotoxicity. Other potential causes of anthracycline-induced cardiotoxicity include myocyte damage from calcium overload, altered myocardial adrenergic function, release of vasoactive amines, and proinflammatory cytokines. Limited data indicate that calcium-channel blocking agents (eg, prenylamine) or beta-adrenergic blocking agents may prevent calcium overload ... It has been suggested that the principal cause of anthracycline-induced cardiotoxicity is associated with free radical damage to DNA., Anthracyclines intercalate DNA, chelate metal ions to produce drug-metal complexes, and generate oxygen free radicals via oxidation-reduction reactions. Anthracyclines contain a quinone structure that may undergo reduction via NADPH-dependent reactions to produce a semiquinone free radical that initiates a cascade of oxygen-free radical generation. It appears that the metabolite, doxorubicinol, may be the moiety responsible for cardiotoxic effects, and the heart may be particularly susceptible to free-radical injury because of relatively low antioxidant concentrations. ... Chelation of metal ions, particularly iron, by the drug results in a doxorubicin-metal complex that catalyzes the generation of reactive oxygen free radicals, and the complex is a powerful oxidant that can initiate lipid peroxidation in the absence of oxygen free radicals. This reaction is not blocked by free-radical scavengers, and probably is the principal mechanism of anthracycline-induced cardiotoxicity., The effect of doxorubicin on reactive oxygen metb in rat heart was investigated. It produced oxygen radicals in heart homogenate, sarcoplasmic reticulum, mitochondria, and cytosol, the major sites of cardiac damage. Superoxide prodn in heart sarcosomes and the mitochondrial fraction was incr. Apparently, free radical formation by doxorubicin, which occurs in the same myocardial compartments that are subject to drug-induced tissue injury, may damage the heart by exceeding the oxygen radical detoxifying capacity of cardiac mitochondria and sarcoplasmic reticulum. |
Source
|
| Record name | Doxorubicin | |
| Source | DrugBank | |
| URL | https://www.drugbank.ca/drugs/DB00997 | |
| Description | The DrugBank database is a unique bioinformatics and cheminformatics resource that combines detailed drug (i.e. chemical, pharmacological and pharmaceutical) data with comprehensive drug target (i.e. sequence, structure, and pathway) information. | |
| Explanation | Creative Common's Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/legalcode) | |
| Record name | DOXORUBICIN | |
| Source | Hazardous Substances Data Bank (HSDB) | |
| URL | https://pubchem.ncbi.nlm.nih.gov/source/hsdb/3070 | |
| Description | The Hazardous Substances Data Bank (HSDB) is a toxicology database that focuses on the toxicology of potentially hazardous chemicals. It provides information on human exposure, industrial hygiene, emergency handling procedures, environmental fate, regulatory requirements, nanomaterials, and related areas. The information in HSDB has been assessed by a Scientific Review Panel. | |
Impurities |
(8S,10S)-10[(3-amino-2,3,6-trideoxy-alpha-levo-lyxo-hexopyranosyl)oxy]-8-(2-bromo-1,1-dimethoxyethyl)-6,8,11-trihydroxy-1-methoxy-7,8,9,10-tetrahydrotetracene-5,12-dione, (8S,10S)-10[(3-amino-2,3,6-trideoxy-alpha-levo-lyxo-hexopyranosyl)oxy]-8-(bromoacetyl)-6,8,11-trihydroxy-1-methoxy-7,8,9,10-tetrahydrotetracene-5,12-dione, Daunorubicin, Doxorubicinone |
Source
|
| Record name | DOXORUBICIN | |
| Source | Hazardous Substances Data Bank (HSDB) | |
| URL | https://pubchem.ncbi.nlm.nih.gov/source/hsdb/3070 | |
| Description | The Hazardous Substances Data Bank (HSDB) is a toxicology database that focuses on the toxicology of potentially hazardous chemicals. It provides information on human exposure, industrial hygiene, emergency handling procedures, environmental fate, regulatory requirements, nanomaterials, and related areas. The information in HSDB has been assessed by a Scientific Review Panel. | |
Color/Form |
Red, crystalline solid | |
CAS No. |
23214-92-8 |
Source
|
| Record name | Doxorubicin | |
| Source | CAS Common Chemistry | |
| URL | https://commonchemistry.cas.org/detail?cas_rn=23214-92-8 | |
| Description | CAS Common Chemistry is an open community resource for accessing chemical information. Nearly 500,000 chemical substances from CAS REGISTRY cover areas of community interest, including common and frequently regulated chemicals, and those relevant to high school and undergraduate chemistry classes. This chemical information, curated by our expert scientists, is provided in alignment with our mission as a division of the American Chemical Society. | |
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| Record name | Doxorubicin [USAN:INN:BAN] | |
| Source | ChemIDplus | |
| URL | https://pubchem.ncbi.nlm.nih.gov/substance/?source=chemidplus&sourceid=0023214928 | |
| Description | ChemIDplus is a free, web search system that provides access to the structure and nomenclature authority files used for the identification of chemical substances cited in National Library of Medicine (NLM) databases, including the TOXNET system. | |
| Record name | Doxorubicin | |
| Source | DrugBank | |
| URL | https://www.drugbank.ca/drugs/DB00997 | |
| Description | The DrugBank database is a unique bioinformatics and cheminformatics resource that combines detailed drug (i.e. chemical, pharmacological and pharmaceutical) data with comprehensive drug target (i.e. sequence, structure, and pathway) information. | |
| Explanation | Creative Common's Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/legalcode) | |
| Record name | Doxorubicin | |
| Source | EPA DSSTox | |
| URL | https://comptox.epa.gov/dashboard/DTXSID8021480 | |
| Description | DSSTox provides a high quality public chemistry resource for supporting improved predictive toxicology. | |
| Record name | Doxorubicin | |
| Source | European Chemicals Agency (ECHA) | |
| URL | https://echa.europa.eu/substance-information/-/substanceinfo/100.041.344 | |
| Description | The European Chemicals Agency (ECHA) is an agency of the European Union which is the driving force among regulatory authorities in implementing the EU's groundbreaking chemicals legislation for the benefit of human health and the environment as well as for innovation and competitiveness. | |
| Explanation | Use of the information, documents and data from the ECHA website is subject to the terms and conditions of this Legal Notice, and subject to other binding limitations provided for under applicable law, the information, documents and data made available on the ECHA website may be reproduced, distributed and/or used, totally or in part, for non-commercial purposes provided that ECHA is acknowledged as the source: "Source: European Chemicals Agency, http://echa.europa.eu/". Such acknowledgement must be included in each copy of the material. ECHA permits and encourages organisations and individuals to create links to the ECHA website under the following cumulative conditions: Links can only be made to webpages that provide a link to the Legal Notice page. | |
| Record name | DOXORUBICIN | |
| Source | FDA Global Substance Registration System (GSRS) | |
| URL | https://gsrs.ncats.nih.gov/ginas/app/beta/substances/80168379AG | |
| Description | The FDA Global Substance Registration System (GSRS) enables the efficient and accurate exchange of information on what substances are in regulated products. Instead of relying on names, which vary across regulatory domains, countries, and regions, the GSRS knowledge base makes it possible for substances to be defined by standardized, scientific descriptions. | |
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| Record name | DOXORUBICIN | |
| Source | Hazardous Substances Data Bank (HSDB) | |
| URL | https://pubchem.ncbi.nlm.nih.gov/source/hsdb/3070 | |
| Description | The Hazardous Substances Data Bank (HSDB) is a toxicology database that focuses on the toxicology of potentially hazardous chemicals. It provides information on human exposure, industrial hygiene, emergency handling procedures, environmental fate, regulatory requirements, nanomaterials, and related areas. The information in HSDB has been assessed by a Scientific Review Panel. | |
| Record name | Doxorubicin | |
| Source | Human Metabolome Database (HMDB) | |
| URL | http://www.hmdb.ca/metabolites/HMDB0015132 | |
| Description | The Human Metabolome Database (HMDB) is a freely available electronic database containing detailed information about small molecule metabolites found in the human body. | |
| Explanation | HMDB is offered to the public as a freely available resource. Use and re-distribution of the data, in whole or in part, for commercial purposes requires explicit permission of the authors and explicit acknowledgment of the source material (HMDB) and the original publication (see the HMDB citing page). We ask that users who download significant portions of the database cite the HMDB paper in any resulting publications. | |
Melting Point |
229-231 °C, 230 °C, MELTING POINT: 205 °C WITH DECOMP; PKA: 8.22; ALMOST ODORLESS; HYGROSCOPIC /HYDROCHLORIDE/, 204 - 205 °C |
Source
|
| Record name | Doxorubicin | |
| Source | DrugBank | |
| URL | https://www.drugbank.ca/drugs/DB00997 | |
| Description | The DrugBank database is a unique bioinformatics and cheminformatics resource that combines detailed drug (i.e. chemical, pharmacological and pharmaceutical) data with comprehensive drug target (i.e. sequence, structure, and pathway) information. | |
| Explanation | Creative Common's Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/legalcode) | |
| Record name | DOXORUBICIN | |
| Source | Hazardous Substances Data Bank (HSDB) | |
| URL | https://pubchem.ncbi.nlm.nih.gov/source/hsdb/3070 | |
| Description | The Hazardous Substances Data Bank (HSDB) is a toxicology database that focuses on the toxicology of potentially hazardous chemicals. It provides information on human exposure, industrial hygiene, emergency handling procedures, environmental fate, regulatory requirements, nanomaterials, and related areas. The information in HSDB has been assessed by a Scientific Review Panel. | |
| Record name | Doxorubicin | |
| Source | Human Metabolome Database (HMDB) | |
| URL | http://www.hmdb.ca/metabolites/HMDB0015132 | |
| Description | The Human Metabolome Database (HMDB) is a freely available electronic database containing detailed information about small molecule metabolites found in the human body. | |
| Explanation | HMDB is offered to the public as a freely available resource. Use and re-distribution of the data, in whole or in part, for commercial purposes requires explicit permission of the authors and explicit acknowledgment of the source material (HMDB) and the original publication (see the HMDB citing page). We ask that users who download significant portions of the database cite the HMDB paper in any resulting publications. | |
Retrosynthesis Analysis
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Feasible Synthetic Routes
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