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Daunorubicin - CAS 20830-81-3

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Category
ADCs
Product Name
Daunorubicin
Catalog Number
20830-81-3
Synonyms
RP13057
CAS Number
20830-81-3
Description
Daunorubicin(RP13057) inhibits both DNA and RNA synthesis and inhibits DNA synthesis with Ki of 0.02 μM.
Molecular Weight
527.52
Molecular Formula
C27H29NO10
COA
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MSDS
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Tag
ADCs Cytotoxin
Structure
CAS 20830-81-3 Daunorubicin
Specification
Purity
>98%
Application
ADCs Cytotoxin
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Reference Reading
1. Adsorptive Stripping Voltammetric Determination of Low Levels of Daunorubicin
Joseph Wang,* Meng Shan Lin and Vince Villa. ANALYST, SEPTEMBER 1987, VOL. 112
The anthracycline antibiotic daunorubicin is a widely used anticancer drug, owing to its clinical efficacy against a wide range of malignancies. This drug was the first compound to show therapeutic effects in the treatment of leukaemia in man. The cytotoxic activity of daunorubicin against cancerous cells is hampered by dose-related cardiotoxic effects. Conse-quently, a highly sensitive analytical method is essential for the evaluation and administration of this drug. Various analytical methods have been employed for this purpose, including fluorescence, radioimmunoassayn and liquid chromatographic techniques. The complex redox activity of daunorubicin, and related anthracycline antibiotics, was investigated by Rao et aZ. who discussed the redox process in relation to the antineoplastic activity of these drugs. Anthracycline antibiotics contain two electroactive moieties: a reducible quinone group and an oxidisable hydroquinone centre. The reduction of the quinone group was used for polarographic measurements of the structurally similar anthracycline, Adriamycin, down to micromolar concentrations and for measuring the binding of anthracyclines to DNA. Trace amounts of daunorubicin have not yet been determined by voltammetric procedures.
2. Overview on in vitro and in vivo investigations of nanocomposite based cancer diagnosis and therapeutics
A. P. Subramanian, S. K. Jaganathan* and Eko Supriyanto. RSC Adv.,2015, 5, 72638–72652
Nanocomposite made of nano Fe3O4 and polylactide nanofibers loaded with daunorubicin to cause the induction of cell death of leukemia cancer cells was reported. The number of viable cells decreased when treated with the daunorubicin loaded nanocomposite. The cellular uptake was demonstrated by the inter-cellular green fluorescence emitted by the daunorubicin drug. The cell inhibition with the 9.93 *10-7 and 1.99 * 10-6 mol L-1 daunorubicin concentrations in the presence of Fe3O4 nanoparticles or PLA nanofibers produced no significant difference fromthat of the cell treated with daunorubicin alone. However, for daunorubicin concentrations at 9.93 * 10-7 and 1.99 * 10-6 mol L-1, the inhibition rates increased to 31% and 46% for the cell system cultured with daunorubicin and Fe3O4–PLA. Chen et al. developed a poly(lactic acid) (PLA) based nanocomposites for targeted drug delivery of daunorubicin to the leukemia K562 cells.
3. PEG–PLGA–PLL nanoparticles in combination with gambogic acid for reversingmultidrug resistance of K562/A02 cells to daunorubicin
Peipei Xu, Ruju Wang, Jian Li, Jian Ouyanga and Bing Chen*. RSC Adv.,2015, 5,61051–61059
Daunorubicin (DNR) is an effective chemotherapeutic agent which is widely used to treat leukaemia. However, DNR lacks specificity to cancer cells and can induce severe side effects. The development of MDR to DNR also hampered the clinical application of DNR. Therefore, new strategies are needed to overcome drug resistance and selectively deliver chemotherapeutic drugs to the tumour area with the aim of improving therapeutic efficacy.
4. Suitability of porous silicon microparticles for the long-term delivery of redox-active therapeutics
Elizabeth C. Wu, Jennifer S. Andrew, Alex Buyanin, Joseph M. Kinsellac and Michael J. Sailor*. Chem. Commun., 2011, 47, 5699–5701
Therefore, in using pSi as a drug delivery carrier, the redox chemistry of the material with the drug of interest must be considered, especially for molecules that are easily reduced. Anthracyclines such as doxorubicin and daunorubicin have been found to be effective against a wide range of human malignant neoplasms, but they display dose-limiting cardiotoxicity. This toxicity has been attributed to the in vivo reduction of the quinine moiety on the drug to a semiquinone free radical. The semiquinone can disproportionate to the hydroquinone, and further degradation of the compound can occur, potentially generating reactive oxygen radicals such as superoxide or hydroxyl radicals that can lead to DNA damage. Due to their structural similarity to benzoquinone, it is likely that anthracycline drugs will also undergo a redox reaction with a pSi host. Indeed, prior work on daunorubicin-loaded hydrosilylated pSi microparticles reported an uncharacterized degradation reaction in this reductive environment.
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