Last update 06 Dec 2024
Dexrazoxane Hydrochloride
Last update 06 Dec 2024
Overview
Basic Info
Drug Type Small molecule drug |
Synonyms dexrazoxane, Topotect, Totect + [13] |
Target |
Mechanism Top II inhibitors(Topoisomerase II inhibitors) |
Therapeutic Areas |
Inactive Indication |
Originator Organization |
Inactive Organization |
Drug Highest PhaseApproved |
First Approval Date US (26 May 1995), |
RegulationAccelerated Approval (US), Orphan Drug (AU), Orphan Drug (US) |
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Structure
Molecular FormulaC11H17ClN4O4 |
InChIKeyBIFMNMPSIYHKDN-FJXQXJEOSA-N |
CAS Registry149003-01-0 |
Related
52
Clinical Trials associated with Dexrazoxane HydrochlorideProspective Treatment of Types I, II and III Pleuropulmonary Blastoma (PPB)
ANTICIPATE: Prevention of ANThracycline-Induced Cardiac Dysfunction by Dexrazoxane In PATients With diffusE Large B-cell Lymphoma: a Phase III National Multicenter Prospective Randomized Open-label Trial
A Phase II, Single Arm, Open Label, Study on the Safety, Efficacy, Pharmacokinetics & Pharmacodynamics of Quizartinib + Chemotherapy and as Single-agent After High Dose Therapy in Newly Diagnosed Pediatric FLT3-ITD+ and NPM1wt AML Patients
100 Clinical Results associated with Dexrazoxane Hydrochloride
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100 Translational Medicine associated with Dexrazoxane Hydrochloride
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100 Patents (Medical) associated with Dexrazoxane Hydrochloride
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847
Literatures (Medical) associated with Dexrazoxane Hydrochloride01 Feb 2025CARDIOLOGY CLINICS
Cardiotoxicity of Anthracyclines
Review
Author: Hoeger, Christopher W. ; Ariza, Abul ; Asnani, Aarti ; Balough, Elizabeth ; Hoeger, Christopher W
Anthracycline chemotherapy is associated with cardiotoxicity, predominantly manifesting as left ventricular systolic dysfunction within the first year of treatment. Early detection is possible through biomarkers and cardiovascular imaging before clinical symptoms develop. Comprehensive cardiovascular risk assessment is essential for all patients prior to anthracycline therapy to stratify their risk of cardiotoxicity. Preventive measures, including cardiovascular risk optimization, as well as anthracycline dose adjustments, the use of liposomal anthracyclines, and dexrazoxane in high-risk patients, are crucial to mitigate the risk of cardiotoxicity. Long-term follow-up and cardiovascular risk optimization are critical for cancer survivors to optimize cardiovascular outcomes.
01 Dec 2024TOXICOLOGY
Knock-down of FOXO3, GATA2, NFE2L2 and AHR promotes doxorubicin-induced cardiotoxicity in human cardiomyocytes
Article
Author: Asensio, J Ochoteco ; van den Beucken, T ; Caiment, F ; Faber, J G
Recent advances in cancer therapy have substantially increased survival rates among patients, yet the prolonged effect of current treatment regimens with anthracyclines (ACs) often include severe long-term complications, notably in the form of anthracycline-induced cardiotoxicity (AIC). Despite known associations between AC treatment and AIC, a comprehensive understanding of the underlying molecular pathways remains elusive. This gap is highlighted by the scarcity of reliable therapeutic interventions, with dexrazoxane being the sole FDA-approved drug to mitigate AIC risks. This study aims at elucidating the transcriptional response of human cardiomyocytes (hCMs) to AC exposure by analyzing a previously generated RNA-sequencing dataset of cardiac spheroids subjected to clinically relevant doses of ACs. The analysis revealed a robust transcriptional response identified across various time points. We aimed at identifying important transcription factors (TFs) mediating AIC by employing predictive algorithms to highlight key TFs for further experimental validation. Using shRNA constructs, we further assessed the impact of these TFs on hCM response to doxorubicin (DOX) and revealed that these TFs had a notable impact on hCM survival upon DOX exposure. TFs FOXO3, GATA2, AHR and NFE2L2 were further investigated for their role in AIC including cell viability, DOX uptake, DNA damage repair and induction of apoptosis through Cleaved-Caspase 3. Our study demonstrated that eliminating FOXO3 and GATA2 made hCMs more vulnerable to DOX and the lack of GATA2, NFE2L2 and AHR led to significantly higher intracellular levels of DOX. Additionally, FOXO3 played a role in the repair of hCM DNA damage as we observed markedly enhanced levels of CDKN1A. We also noted significant increases in DNA damage through COMET-assays when FOXO3, GATA2, NFE2L2 and AHR were absent. Furthermore, we investigated the clinical relevance by comparing our results with those from a study based on hiPSC-CMs derived from patients with doxorubicin-induced cardiotoxicity, identifying overlapping TFs and their regulatory roles in critical cellular processes like the cell cycle and DNA repair. This approach not only advances the understanding of the molecular mechanisms behind AIC but also opens possible windows for new therapeutic approaches to mitigate the negative side-effects from patient AC treatment.
01 Dec 2024CELL BIOCHEMISTRY AND BIOPHYSICS
Cardioprotective effect of Robinin ameliorates Endoplasmic Reticulum Stress and Apoptosis in H9c2 cells
Article
Author: Abhirami, N ; Ayyappan, Janeesh Plakkal
Robinin is one of the glycosyloxyflavones that has been less explored for its therapeutic application, especially in the field of CVD. Herein, we explored the cardioprotective efficacy of Robinin by using H2O2 and Doxorubicin (DOX) - treated H9c2 cells as an in vitro model. H2O2 and DOX treatment resulted in severe cellular damage to the cardiomyocytes, which was followed by apoptosis. Apoptosis and nuclear morphology were analysed through Hoechst 33342 and AO/EB staining. qPCR was employed to detect the expression of apoptosis as well as ERS-related markers. Reactive oxygen species (ROS) generation was observed using DCFH-DA staining and FACS analysis. Signaling pathways involved were analysed using Western blot. Robinin pre-treatment considerably decreased the apoptotic rate by boosting the endogenous anti-oxidative activity and lowering the activity of Malonaldehyde and Lactate dehydrogenase enzyme. Robinin also inhibited the generation of ROS. Robinin reduced the expression of ERS-associated genes and proteins, thereby decreasing apoptosis-related proteins. Upon comparing the cardioprotective effect of Robinin with a known cardioprotective agent Dexrazoxane (DEX) it was revealed that DEX has more cardioprotective effect against DOX than H2O2-induced stress, while Robinin showed a significant protective effect against both H2O2 and DOX induced stress.
3
News (Medical) associated with Dexrazoxane Hydrochloride11 Aug 2023
AcquisitionLicense out/in
10 Aug 2023
AcquisitionRadiation Therapy
09 Feb 2019
Accelerated ApprovalOrphan DrugFast TrackBreakthrough TherapyDrug Approval
100 Deals associated with Dexrazoxane Hydrochloride
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External Link
| KEGG | Wiki | ATC | Drug Bank |
|---|---|---|---|
| D07807 | Dexrazoxane Hydrochloride |
R&D Status
Approved
10 top approved records. to view more data
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| Indication | Country/Location | Organization | Date |
|---|---|---|---|
| Extravasation of Diagnostic and Therapeutic Materials | EU | 27 Jul 2006 | |
| Extravasation of Diagnostic and Therapeutic Materials | IS | 27 Jul 2006 | |
| Extravasation of Diagnostic and Therapeutic Materials | LI | 27 Jul 2006 | |
| Extravasation of Diagnostic and Therapeutic Materials | NO | 27 Jul 2006 | |
| Cytoprotective Agent | CN | 29 May 2006 | |
| Cardiomyopathies | US | 26 May 1995 | |
| Metastatic breast cancer | US | 26 May 1995 |
Developing
10 top R&D records. to view more data
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| Indication | Highest Phase | Country/Location | Organization | Date |
|---|---|---|---|---|
| Hemorrhage | Phase 3 | DK | 01 Apr 2002 | |
| Hemorrhage | Phase 3 | DE | 01 Apr 2002 | |
| Hemorrhage | Phase 3 | IT | 01 Apr 2002 | |
| Hemorrhage | Phase 3 | NL | 01 Apr 2002 | |
| Hemorrhage | Phase 3 | PL | 01 Apr 2002 | |
| Bronchitis | Phase 3 | DK | 01 Jun 2001 |
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Clinical Result
Clinical Result
Indication
Phase
Evaluation
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Not Applicable | - | bqjnnajnni(eyhgdwknnp) = fcorwyviwr zspiumxvvq (jvcbensmud ) View more | - | 07 Dec 2024 | |||
Non-initiators of Dexrazoxane | bqjnnajnni(eyhgdwknnp) = oydhmpqflo zspiumxvvq (jvcbensmud ) View more | ||||||
Not Applicable | 142 | Anthracycline + Dexrazoxane | wbmyoklpba(hsxgokeioj) = syfwjutbef siorjxpfwp (zkwhffnrah ) | Positive | 31 May 2023 | ||
Anthracycline only | wbmyoklpba(hsxgokeioj) = rmcqadywrb siorjxpfwp (zkwhffnrah ) View more | ||||||
Not Applicable | - | 195 | (yrgaugowqh) = bokegsopod yhouakabln (rxbubyntrz ) | - | 20 Jan 2023 | ||
Doxorubicin with Dexrazoxane | - | ||||||
Not Applicable | 263 | wovcybfcqh(okfwjoqwze) = xlvryefxbx bzlisvcygf (omzjxzpbtm ) View more | - | 03 Dec 2022 | |||
wovcybfcqh(okfwjoqwze) = nxcothkmks bzlisvcygf (omzjxzpbtm ) View more | |||||||
Not Applicable | - | 1,308 | Doxorubicin with dexrazoxane | (xufwytkilw): HR = 1.07 (95% CI, 0.78 - 1.47) View more | - | 15 Feb 2022 | |
Doxorubicin without dexrazoxane | |||||||
Phase 3 | 236 | Therapeutic Conventional Surgery (Very Low-risk Group) | fgibetlbtp(cfchvuoweg) = orfhvvodin pkbcjtccuo (eirgkfoxci, bjvcxxfyus - gcdhkjcici) View more | - | 28 Dec 2021 | ||
(Low-risk Group (Regimen T)) | fgibetlbtp(cfchvuoweg) = bebbdfxclu pkbcjtccuo (eirgkfoxci, zchgxtmobt - eehimkjyhp) View more | ||||||
Not Applicable | 2,375 | gcbdffrtva(oatgdnxfii): OR = 1.15 (95% CI, 0.57 - 2.31), P-Value = 0.7 View more | - | 29 Jun 2021 | |||
No drug or placebo | |||||||
Not Applicable | 173 | kxmsabxjwe(cunxsjfrlp) = drojijfubm zukcgntaqu (nslbfrzgkv, 6.0 - 18.0) View more | Positive | 25 May 2020 | |||
kxmsabxjwe(cunxsjfrlp) = cwqhxijsiy zukcgntaqu (nslbfrzgkv, 6.0 - 28.2) View more | |||||||
Phase 2 | 46 | (Arm A: VACdxr With ImmTher) | qbsbfcscjl(wdhjlumuwt) = vspwkxtopq uachtlkfil (fblxqqwldj, uykzzmckvb - pqodtgwlce) View more | - | 29 Jan 2020 | ||
(Arm B: VACdxr) | qbsbfcscjl(wdhjlumuwt) = xpatycheui uachtlkfil (fblxqqwldj, nsmdcedyae - zczwgylrgo) View more | ||||||
Phase 1 | 1 | xnqmbglsxc(sddgtiklho) = dxtfhpbohd mimljcades (cbsfwdgkbh, bnuuvjabek - eocbtxkckq) View more | - | 19 Feb 2019 |
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