Idarubicin - CAS 58957-92-9

Idarubicin - CAS 58957-92-9 Catalog number: BADC-00327

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Idarubicin is an anthracycline antibiotic and a DNA topoisomerase II (topo II) inhibitor for MCF-7 cells with IC50 of 3.3 ng/mL.

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BADC-00327 -- $--
Idarubicin is an anthracycline antibiotic and a DNA topoisomerase II (topo II) inhibitor for MCF-7 cells with IC50 of 3.3 ng/mL.
IMI30; IMI-30; IMI 30; NSC256439; NSC-256439; NSC 256439; 4-DMDR; IDA; 4-Demethoxydaunomycin;(7S,9S)-9-acetyl-7-(((2R,4S,5S,6S)-4-amino-5-hydroxy-6-methyltetrahydro-2H-pyran-2-yl)oxy)-6,9,11-trihydroxy-7,8,9,10-tetrahydrotetracene-5,12-dione;
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Mechanism Of Action
Idarubicin has antimitotic and cytotoxic activity through a number of proposed mechanisms of action: Idarubicin 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.
Idarubicin is an antineoplastic in the anthracycline class. General properties of drugs in this class include: interaction with DNA in a variety of different ways including intercalation (squeezing between the base pairs), DNA strand breakage and inhibition with the enzyme topoisomerase II. Most of these compounds have been isolated from natural sources and antibiotics. However, they lack the specificity of the antimicrobial antibiotics and thus produce significant toxicity. The anthracyclines are among the most important antitumor drugs available. Doxorubicin is widely used for the treatment of several solid tumors while daunorubicin and idarubicin are used exclusively for the treatment of leukemia. Idarubicin may also inhibit polymerase activity, affect regulation of gene expression, and produce free radical damage to DNA. Idarubicin possesses an antitumor effect against a wide spectrum of tumors, either grafted or spontaneous. The anthracyclines are cell cycle-nonspecific.
In Vitro
Idarubicin is a clinically effective synthetic anthracycline analog used in the treatment of several human neoplasms. Anthracyclines have the potential to undergo bioactivation by flavoenzymes to free radicals and thus exert their cytotoxic actions. The plasmid DNA experiments demonstrated that idarubicin could undergo bioreduction by P450 reductase with the resulting formation of DNA strand breaks. The antioxidant enzymes SOD and catalase, and hydroxyl radical scavengers, DMSO and thiourea, afforded significant levels of protection against idarubicin-induced DNA strand breaks. These findings suggested that DNA damage by idarubicin occurs through a mechanism which involves its redox cycling with P450 reductase to generate reactive oxygen species (ROS). The extent of DNA damage by idarubicin was found to increase with increasing concentrations of drug or enzyme as well as with increasing incubation time. The capacity of idarubicin to induce DNA damage under above incubation conditions was compared with that of a model compound, mitomycin C. Finally, enzyme assays carried out with purified P450 reductases revealed that idarubicin exhibited about two-fold higher rate of reduction than mitomycin C.
In Vivo
Idarubicin loading in ONCOZENE DEE agents was > 99% at 10 minutes. Time to reach 75% of the release plateau level was 37 minutes ± 6 for DC Bead DEE agents and 170 minutes ± 19 for ONCOZENE DEE agents both loaded with idarubicin 10 mg/mL. After transarterial chemoembolization with idarubicin-loaded ONCOZENE DEE agents, three partial responses and one complete response were observed with only two asymptomatic grade 3 biologic adverse events. Median time to maximum concentration for idarubicin in patients was 10 minutes, and mean maximum concentration was 4.9 µg/L ± 1.7. Mean area under the concentration-time curve from 0-24 hours was equal to 29.5 µg.h/L ± 20.5.
Clinical Trial Information
NCT NumberCondition Or DiseasePhaseStart DateSponsorStatus
NCT01305135High Grade Myelodysplastic Syndrome LesionsPhase 12017-06-07Groupe Francophone des MyelodysplasiesCompleted
NCT03444649AMLPhase 12018-09-11University Hospital Inselspital, BerneWithdrawn (IMP will not be further developed)
NCT00878722Acute Myeloid LeukemiaPhase 1, Phase 22015-07-28OnxeoCompleted
NCT02277847Acute Myeloid LeukemiaPhase 42014-10-29Guangdong Provincial People's HospitalUnknown Verified October 2014 by Guangdong Provincial People's Hospital. Recruitment status was Enrolling by invitation
NCT01518556Leukemia, Myeloid, AcutePhase 12019-08-20Konkuk University Medical CenterRecruiting
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1.FLAG Regimen with or without Idarubicin in Children with Relapsed/Refractory Acute Leukemia: Experience from a Turkish Pediatric Hematology Center.
Yılmaz Bengoa Ş, Ataseven E, Kızmazoğlu D, Demir Yenigürbüz F, Erdem M, Ören H. Turk J Haematol. 2016 Apr 18. doi: 10.4274/Tjh.2015.0411. [Epub ahead of print]
in English, TurkishGİRİŞ ve AMAÇ: Relaps/refrakter akut lösemili çocuklarda daha yüksek sağkalımı sağlayabilecek en uygun tedavi yaklaşımı halen bilinmemektedir. Gelişmekte olan ülkelerde bu hasta grubunda etkin olduğu iyi bilinen ve yakın zamanda geliştirilmiş bazı ilaçlara ulaşımda güçlük yaşanmaktadır. Biz relaps/refrakter akut lenfoblastik lösemili (ALL) ve akut miyeloid lösemili (AML) çocuklarda idarubisin (IDA) eklenmiş veya eklenmemiş, fludarabin, yüksek doz sitarabin ve granülosit koloni stimüle edici faktör (FLAG tedavisi) kombinasyonunun etkinliğini değerlendirdik. YÖNTEM ve GEREÇLER: Çalışmaya Eylül 2007 ve Mayıs 2015 arasında merkezimizde izlenen, IDA eklenmiş veya eklenmemiş FLAG tedavisi verilen, 18 relaps/refrakter akut lösemili çocuk dahil edilmiştir. Birincil sonlanım noktası kemoterapi sonrası alınan kemik iliği örneğinin remisyon durumu ve ikinci sonlanım noktası ise hematopoetik kök hücre nakli (HKHN) sonrası sağkalım süresi olarak belirlenmiştir.
2.Fludarabine, idarubicin, and cytarabine regimen together with TKI followed by haploidentical hematopoietic stem cell transplantation, a success for relapsed Ph+ acute lymphoblastic leukemia.
Sang W1, Wang Y1, Zhang C1, Yan D1, Niu M1, Yang C2, Liu X3, Sun C1, Zhang Z1, Loughran TP Jr4, Xu K1. Clin Case Rep. 2016 Mar 4;4(4):390-5. doi: 10.1002/ccr3.438. eCollection 2016.
In this report, a case of relapsed Ph+ ALL was remedied by reinduction, and consolidation regimen of TKI and Flu+ Ara-C+ IDA (FLAI) combination, followed by haploidentical SCT. Results suggest that FLAI together with TKI and subsequently with haploidentical SCT could be applied for relapsed Ph+ ALL.
3.Aptamer targeting of the elongation factor 1A impairs hepatocarcinoma cells viability and potentiates bortezomib and idarubicin effects.
Bruna S1, Rosella F2, Barbara D1, Gabriele B1, Gabriele P3, Mario G2, Fabrizio Z3, Gabriele G4. Int J Pharm. 2016 Apr 16. pii: S0378-5173(16)30315-5. doi: 10.1016/j.ijpharm.2016.04.031. [Epub ahead of print]
The high morbidity and mortality of hepatocellular carcinoma (HCC) is mostly due to the limited efficacy of the available therapeutic approaches. Here we explore the anti-HCC potential of an aptamer targeting the elongation factor 1A (eEF1A), a protein implicated in the promotion of HCC. As delivery methods, we have compared the effectiveness of cationic liposome and cholesterol-mediated approaches. A75 nucleotide long aptamer containing GT repetition (GT75) was tested in three HCC cell lines, HepG2, HuH7 and JHH6. When delivered by liposomes, GT75 was able to effectively reducing HCC cells viability in a dose and time dependent fashion. Particular sensitive were JHH6 where increased apoptosis with no effects on cell cycle were observed. GT75 effect was likely due to the interference with eEF1A activity as neither the mRNA nor the protein levels were significantly affected. Notably, cholesterol-mediated delivery of GT75 abrogated its efficacy due to cellular mis-localization as proven by fluorescence and confocal microscopic analysis.
4.Pentoxifylline affects idarubicin binding to DNA.
Gołuński G1, Borowik A1, Lipińska A2, Romanik M1, Derewońko N2, Woziwodzka A1, Piosik J3. Bioorg Chem. 2016 Apr;65:118-25. doi: 10.1016/j.bioorg.2016.02.005. Epub 2016 Feb 20.
Anticancer drug idarubicin - derivative of doxorubicin - is commonly used in treatment of numerous cancer types. However, in contrast to doxorubicin, its biophysical properties are not well established yet. Additionally, potential direct interactions of idarubicin with other biologically active aromatic compounds, such as pentoxifylline - representative of methylxanthines - were not studied at all. Potential formation of such hetero-aggregates may result in sequestration of the anticancer drug and, in consequence, reduction of its biological activity. This work provide description of the idarubicin biophysical properties as well as assess influence of pentoxifylline on idarubicin interactions with DNA. To achieve these goals we employed spectrophotometric methods coupled with analysis with the appropriate mathematical models as well as flow cytometry and Ames test. Obtained results show influence of pentoxifylline on idarubicin binding to DNA and are well in agreement with the data previously published for other aromatic ligands.

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