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Bioflavonoids
Published in Hafiz Ansar Rasul Suleria, Megh R. Goyal, Masood Sadiq Butt, Phytochemicals from Medicinal Plants, 2019
Muhammad Sajid Arshad, Urooj Khan, Ali Imran, Hafiz Ansar Rasul Suleria
Dexrazoxane is a cardioprotective agent approved by the FDA for anthracycline-induced cardiotoxicity. Previously, it was thought that dexrazoxane provides cardioprotective effects from anthracyclines primarily through the metal-chelating activity of its intracellular hydrolysis products in the myocardium. This activity involves chelation of free iron and iron bound in anthracycline complexes, thereby preventing the formation of cardiotoxic reactive oxygen radicals.25 It could also act as a catalytic inhibitor of DNA topoisomerase II.41 It has recently been suggested that the explanation is the interaction with the topoisomerase IIb isoform108. HIF activation is another mechanism that contributes to the protective effect of dexrazoxane against anthracycline cardiotoxicity.99
Survivorship: Pediatric cancer survivors
Published in Susan F. Dent, Practical Cardio-Oncology, 2019
Shahnawaz Amdani, Neha Bansal, Emma Rachel Lipshultz, Michael Jacob Adams, Steven E. Lipshultz
Dexrazoxane acts by chelating iron, thus preventing myocardial damage secondary to reactive oxygen species (71,112,143,144). Dexrazoxane also reduces doxorubicin-induced DNA damage, perhaps by the formation of Top2-DNA covalent complexes (145).
Therapeutic Uses and Side Effects
Published in Fazal-I-Akbar Danish, Ahmed Ehsan Rabbani, Pharmacology in 7 Days for Medical Students, 2018
Fazal-I-Akbar Danish, Ahmed Ehsan Rabbani
The most distinctive side effect of these anthracyclines is cardiotoxicity (arrhythmias; cardiomyopathy; CHF). It can be avoided by ‘rescue therapy’ with dexrazoxane. As we know that anthracyclines generate free radicals, which in turn block the synthesis of RNA and DNA. Dexrazoxane administration inhibits free radical formation and thus prevents cardiotoxicity.
In vivo and in vitro protective effects of shengmai injection against doxorubicin-induced cardiotoxicity
Published in Pharmaceutical Biology, 2022
Peng Zhou, Ge Gao, Chun-chun Zhao, Jing-ya Li, Jian-fei Peng, Shu-shu Wang, Rui Song, Hui Shi, Liang Wang
Dexrazoxane is the only FDA-approved cardioprotective medication for DOX. Dexrazoxane may ameliorate cardiotoxicity and protect heart function by inhibiting both apoptosis and necroptosis in cardiomyocyte injury caused by DOX (Zhang et al. 2021). Although dexrazoxane protects the heart from the cardiotoxicity of DOX, it can also produce side effects such as decreased appetite, nausea, and vomiting, myeloid inhibition, neurotoxic phlebitis, and diarrhoea in the clinic (Lue et al. 2018). Dexrazoxane was used as a positive control in this study to assess the effect of SMI on DOX cardiac toxicity. SMI has been shown in recent studies to improve heart function, protect myocardial cells, and increase myocardial energy, as well as to be beneficial in the treatment of heart diseases such as myocardial infarction, myocardial ischaemia-reperfusion injury, heart failure, diabetic cardiomyopathy, and myocarditis (Cao et al. 2020).
Pharmacological strategies to overcome treatment resistance in acute myeloid leukemia: increasing leukemic drug exposure by targeting the resistance factor SAMHD1 and the toxicity factor Top2β
Published in Expert Opinion on Drug Discovery, 2021
The backbone of AML therapy has for almost half a century been an anthracycline combined with ara-C. While this combination therapy enabled cure for a previously lethal disease, mortality for AML remains unacceptably high. This discrepancy is suggestive of treatment resistance, i.e. certain properties that stand in the way for therapy to eradicate the disease in a subset of patients. While new developments with the advent of innovative drugs against AML certainly contribute to a better prognosis for AML, a main task for the hematological community remains to improve existing standard therapies by alleviating treatment resistance, i.e. remove obstacles that impede standard AML therapy to establish cure. One paradigm to do so is to find ways to increase the intraleukemic concentration of the active metabolites of the administered antineoplastic agents. For anthracyclines, I suggest to evaluate whether the escalation of anthracycline doses, made possible by protection of the dose-limiting organ, the heart, through addition of dexrazoxane, can overrun different resistance mechanisms. For ara-C, I suggest the evaluation of adding a functional SAMHD1 ara-CTPase inhibitor, namely hydroxyurea, to ara-C courses. If those strategies are able to reduce mortality without an unacceptable increase of toxicity, they might stand the chance to be considered for future standard-of-care of newly diagnosed patients with AML. When aiming to combine both strategies, the safety and compatibility of combining hydroxyurea with dexrazoxane would first have to be evaluated though.
Pegylated liposomal doxorubicin as neoadjuvant therapy for stage II–III locally advanced breast cancer
Published in Journal of Chemotherapy, 2020
Jia Yao, Shaobo Pan, Xiao Fan, Xue Jiang, Yuhong Yang, Jing Jin, Yu Liu
The advantages of PLD being less cardiotoxic than non-liposomal, anthracyclines have been demonstrated.12,22,23 In our study, none of the patients developed congestive heart failure and there was no significant difference in ECG abnormalities or LEVF decline between the two groups. This conclusion may be related to our routine use of a cardioprotective agent in EPI group, dexrazoxane. Dexrazoxane has been proven as a well-tolerated and effective cardioprotectant when administered with anthracycline-containing chemotherapy.24,25 Dexrazoxane is now included in both clinical practice guidelines and in treatment protocols. For example, both ESMO and ASCO recommend dexrazoxane for specific patients at risk of cardiotoxicity.26,27