Suitable for use in IA. Each laboratory should determine an optimum working titer for use in its particular application. Other applications have not been tested but use in such assays should not necessarily be excluded.
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Background
Doxorubicin has demonstrated effectiveness in the treatment of several types of cancer. It is commonly used in the management of breast cancer, bladder cancer, Kaposi's sarcoma, lymphoma, and acute lymphocytic leukemia. It is often administered in combination with other chemotherapy agents to enhance its therapeutic outcomes. Additionally, doxorubicin has shown promise in the treatment of multiple myeloma, ovarian cancer, thyroid cancer, and soft tissue sarcoma. The primary mechanism of action of doxorubicin involves its interference with the function of DNA. By binding to DNA and inhibiting its replication and transcription, doxorubicin prevents cancer cells from proliferating and ultimately leads to their death. Moreover, doxorubicin generates free radicals and causes DNA damage, further contributing to its cytotoxic effects. However, research into the pharmacological mechanism of action of doxorubicin has been challenging due to difficulties in determining its concentrations in tissues or cell types within the bone marrow. This hampers the analysis of its effects on the human or mouse genome and changes in protein expression. To overcome these limitations, the use of the Mouse Anti-Doxorubicin Monoclonal Antibody specific to doxorubicin can significantly advance cancer research. This antibody can recognize both conserved chemical analogs and derivatives, making it valuable for antibody-based chemical and bioassays.
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References
Doxorubicin, DNA torsion, and chromatin dynamics
Biochimica et Biophysica Acta (BBA)-Reviews on Cancer
Doxorubicin is one of the most important anti-cancer chemotherapeutic drugs, being widely used for the treatment of solid tumors and acute leukemias. The action of doxorubicin and other anthracycline drugs has been intensively investigated during the last several decades, but the mechanisms that have been proposed for cell killing remain disparate and controversial. In this review, we examine the proposed models for doxorubicin action from the perspective of the chromatin landscape, which is altered in many types of cancer due to recurrent mutations in chromatin modifiers. We highlight recent evidence for effects of anthracyclines on DNA torsion and chromatin dynamics that may underlie basic mechanisms of doxorubicin-mediated cell death and suggest new therapeutic strategies for cancer treatment.
Molecular Mechanisms of Cardiotoxicity: A Review on Major Side-effect of Doxorubicin
Doxorubicin is among the most powerful drugs used for the treatment of both adult and child cancers. Doxorubicin is a major cause of chemotherapy-induced cardiotoxicity that is a restricting factor for an optimum dose of the drug for treatment of the cancer patients. Many studies have explored pathophysiology and mechanisms of doxorubicin-induced cardiotoxicity. Cellular and animal experiments proposed that doxorubicin-induced cardiotoxicity mechanism is multifactorial. Oxidative stress has been considered as the primary cause of cardiotoxicity. Although there is no effective treatment for doxorubicin-induced cardiotoxicity currently but many investigations are being done to discover prevention treatments whereas no specific treatment has been approved. Studies have shown that reactive oxygen species and topoisomerase 2b are molecular targets for cardioprotection. Therapeutic imaging methods and cardio-biomarkers may be helpful in the improvement of rapid detection of cardiac damage. In this review, effects of doxorubicin on DNA damage, free radical generation, mitochondrial damage, cell death, and other parameters have been studied.
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