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Journal articles on the topic 'Doxorubicin'

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Published: 4 June 2021

Last updated: 30 July 2024

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1

Rahmani, Talia Putri, Yahdiana Harahap, and Denni Joko Purwanto. "A review of the relationship between Doxorubicin and Doxorubicinol, CBR1 polymorphism, and cardiotoxicity." Pharmacy Education 24, no. 6 (June 14, 2024): 105–15. http://dx.doi.org/10.46542/pe.2024.246.105115.

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Background: Doxorubicin is a chemotherapy drug given to breast cancer patients. However, its administration is limited by its cardiotoxicity. The CBR1 enzyme in the liver catalyses doxorubicin to doxorubicinol, which also contributes to its cardiotoxicity. The polymorphism of the CBR1 enzyme affects doxorubicin and doxorubicinol levels in the body. Objective: To review the effect of CBR1 polymorphisms on the levels of doxorubicin and doxorubicinol after administration of doxorubicin. Methods: Relevant studies from selected databases were examined; Three main studies with 20 support studies were reviewed. Results: The recommended methods were the analysis of doxorubicin and doxorubicinol levels using the Dried Blood Spot biosampling technique, which uses the ultra-high-performance liquid chromatography-tandem mass spectrometry (LCMS/MS), and the evaluation of the genetic profile of CBR1 using Polymerase Chain Reaction. Conclusion: Four CBR1 genetic polymorphisms have been shown to reduce doxorubicinol levels in the body, which is associated with decreased CBR1 activity and expression. Thus, the conversion of doxorubicin to doxorubicinol is reduced. Therefore, individuals who experience CBR1 polymorphisms have a lower risk of cardiotoxicity after the administration of doxorubicin.

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2

Fan, L., J. Y. Guo, C. I. Wong, R. Lim, H. L. Yap, Y. M. Khoo, P. Iau, B. C. Goh, H. S. Lee, and S. C. Lee. "Genetic variants in human carbonyl reductase 3 (CBR3) and their influence on doxorubicin pharmacokinetics in Asian breast cancer patients." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 2505. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.2505.

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2505 Background: Human carbonyl reductase 3 (CBR3) is one of the main metabolizing enzymes to extensively reduce doxorubicin to its major active metabolite, doxorubicinol in normal and tumor tissues. Recently, the CBR3 958G>A (V244M) genetic variant has been described to alter function in vitro. We postulate that CBR3 genetic variants could contribute to the inter-individual variability of doxorubicin pharmacokinetics in breast cancer patients. Methods: We studied 101 female breast cancer patients (66 Chinese, 26 Malay, 7 Indian and 2 of other ethnic origins) who were treated with doxorubicin at 75mg/m2 every 3 weeks. Comprehensive sequencing of the 3 exons of CBR3, including the splice-site junctions was performed. Plasma concentrations of doxorubicin and doxorubicinol were analyzed during the first doxorubicin cycle. Results: Five CBR3 coding region variants (239G>A, 483C>T, 507C>T, 598G>A and 958G>A) were detected, of which 239G>A, 598G>A and 958G>A were non-synonymous. 598G>A was novel, and was found in 1 Malay patient who was heterozygous. The genotype distributions of 239G>A and 958G>A were 36%/30%/34%, and 40%/36%/24% respectively for GG/AG/AA. The 239GG variant was associated with significantly higher AUC of doxorubicinol and AUC ratio of doxorubicinol to doxorubicin than the AG and AA variants (AUC of doxorubicinol 2.18±1.37ug/ml*h (GG) vs 2.04±2.11ug/ml*h (AG), p=0.05, and 1.55±0.61ug/ml*h (AA), p=0.004; AUC ratio of doxorubicinol to doxorubicin 1.90±1.29 (GG) vs 1.72±1.34 (AG), p=0.025, and 1.45±0.67 (AA), p=0.006). Patients with the 958AA variant had significantly higher AUC of doxorubicinol than those with the 958GG variant (2.29±1.60ug/ml*h vs 1.56±0.60ug/ml*h, p=0.009). The 239GG variant was more common in our population than in Caucasians (36% vs 20%. p=0.027), while the 958AA variant was more common than reported in Caucasians (24% vs 8%, p=0.014) and Japanese (24% vs 7%, p=0.016). Conclusions: CBR3 genetic variants may influence the pharmacokinetics of doxorubicin and its major metabolite doxorubicinol. Inter-ethnic differences in frequencies of CBR3 genetic variants exist and may account for differences in pharmacokinetics and pharmacodynamics of doxorubicin between different populations. No significant financial relationships to disclose.

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3

Choi, Won-Gu, Dong Kyun Kim, Yongho Shin, Ria Park, Yong-Yeon Cho, Joo Young Lee, Han Chang Kang, and Hye Suk Lee. "Liquid Chromatography–Tandem Mass Spectrometry for the Simultaneous Determination of Doxorubicin and its Metabolites Doxorubicinol, Doxorubicinone, Doxorubicinolone, and 7-Deoxydoxorubicinone in Mouse Plasma." Molecules 25, no. 5 (March 10, 2020): 1254. http://dx.doi.org/10.3390/molecules25051254.

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Doxorubicin, an anthracycline antitumor antibiotic, acts as a cancer treatment by interfering with the function of DNA. Herein, liquid chromatography-tandem mass spectrometry was for the first time developed and validated for the simultaneous determination of doxorubicin and its major metabolites doxorubicinol, doxorubicinone, doxorubicinolone, and 7-deoxydoxorubicinone in mouse plasma. The liquid–liquid extraction of a 10 μL mouse plasma sample with chloroform:methanol (4:1, v/v) and use of the selected reaction monitoring mode led to less matrix effect and better sensitivity. The lower limits of quantification levels were 0.5 ng/mL for doxorubicin, 0.1 ng/mL for doxorubicinol, and 0.01 ng/mL for doxorubicinone, doxorubicinolone, and 7-deoxydoxorubicinone. The standard curves were linear over the range of 0.5–200 ng/mL for doxorubicin; 0.1–200 ng/mL for doxorubicinol; and 0.01–50 ng/mL for doxorubicinone, doxorubicinolone, and 7-deoxydoxorubicinone in mouse plasma. The intra and inter-day relative standard deviation and relative errors for doxorubicin and its four metabolites at four quality control concentrations were 0.9–13.6% and –13.0% to 14.9%, respectively. This method was successfully applied to the pharmacokinetic study of doxorubicin and its metabolites after intravenous administration of doxorubicin at a dose of 1.3 mg/kg to female BALB/c nude mice.

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4

Tonetti, M., A. B. Astroff, W. Satterfield, A. De Flora, U. Benatti, and J. R. DeLoach. "Pharmacokinetic properties of doxorubicin encapsulated in glutaraldehyde-treated canine erythrocytes." American Journal of Veterinary Research 52, no. 10 (October 1, 1991): 1630–35. http://dx.doi.org/10.2460/ajvr.1991.52.10.1630.

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SUMMARY Canine erythrocytes were loaded with the antineoplastic drug doxorubicin and then treated with 0.16% glutaraldehyde. This procedure has been previously shown to slow down the efflux of doxorubicin from erythrocytes and to result in the selective targeting of the carrier erythrocytes to liver. Three dogs were treated each with 2 different schedules of iv bolus administration of doxorubicin (0.4 mg/kg of body weight): free drug and doxorubicin encapsulated in glutaraldehyde-treated erythrocytes. The 2 treatments yielded consistent differences in the plasma pharmacokinetic properties of doxorubicin and of its only metabolite, doxorubicinol. A triphasic exponential decay of doxorubicin plasma concentrations was observed on injection of the free drug. Conversely, in the case of erythrocyte-encapsulated doxorubicin, 4 phases of plasma concentrations of doxorubicin were found. The plasma concentrations of doxorubicinol, after a steady increase during the first hour, followed patterns of decay comparable to those of the parent drug. On the basis of the kinetic variables calculated with the 2 administration schedules, area under curve concentrations of plasma doxorubicin were 136 μg·h/L (free infusion) and 734 μ-g·h/L (erythrocyte-encapsulated drug). Significant alterations of hematologic and hematochemical factors were not observed in the 3 dogs during and after the 2 treatments. On the basis of our findings, doxorubicin-loaded and glutaraldehyde-treated erythrocytes may potentially be used in the treatment of systemic and hepatic tumors in dogs.

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5

Bartlett, N. L., B. L. Lum, G. A. Fisher, N. A. Brophy, M. N. Ehsan, J. Halsey, and B. I. Sikic. "Phase I trial of doxorubicin with cyclosporine as a modulator of multidrug resistance." Journal of Clinical Oncology 12, no. 4 (April 1994): 835–42. http://dx.doi.org/10.1200/jco.1994.12.4.835.

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PURPOSE To study the effects of cyclosporine (CsA), a modulator of multidrug resistance (MDR), on the pharmacokinetics and toxicities of doxorubicin. PATIENTS AND METHODS Nineteen patients with incurable malignancies entered this phase I trial. Initially patients received doxorubicin alone (60 or 75 mg/m2) as a 48-hour continuous intravenous (i.v.) infusion. Patients whose tumors did not respond received CsA as a 2-hour loading dose of 6 mg/kg and a 48-hour continuous infusion of 18 mg/kg/d with doxorubicin. Target CsA levels were 3,000 to 4,800 ng/mL (2.5 to 4.0 mumol/L). Doxorubicin doses were reduced to 40% of the prior dose without CsA, and then escalated until myelosuppression equivalent to that resulting from doxorubicin alone was observed. Doxorubicin pharmacokinetics were analyzed with and without CsA. RESULTS Thirteen patients received both doxorubicin alone and the combination of doxorubicin and CsA. Mean CsA levels were more than 2,000 ng/mL for all cycles and more than 3,000 ng/mL for 68% of cycles. Dose escalation of doxorubicin with CsA was stopped at 60% of the doxorubicin alone dose, as four of five patients at this dose level had WBC nadirs equivalent to those seen with doxorubicin alone. Nonhematologic toxicities were mild. Reversible hyperbilirubinemia occurred in 68% of doxorubicin/CsA courses. The addition of CsA to doxorubicin increased grade 1 and 2 nausea (87% v 47%) and vomiting (50% v 10%) compared with doxorubicin alone. There was no significant nephrotoxicity. Paired pharmacokinetics were studied in 12 patients. The addition of CsA increased the dose-adjusted area under the curve (AUC) of doxorubicin by 55%, and of its metabolite doxorubicinol by 350%. CONCLUSION CsA inhibits the clearance of both doxorubicin and doxorubicinol. Equivalent myelosuppression was observed when the dose of doxorubicin with CsA was 60% of the dose of doxorubicin without CsA. Understanding these pharmacokinetic interactions is essential for the design and interpretation of clinical trials of MDR modulation, and should be studied with more potent MDR modulators.

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Darrabie, Marcus D., Antonio Jose Luis Arciniegas, Jose Gabriel Mantilla, Rajashree Mishra, Miguel Pinilla Vera, Lucia Santacruz, and Danny O. Jacobs. "Exposing cardiomyocytes to subclinical concentrations of doxorubicin rapidly reduces their creatine transport." American Journal of Physiology-Heart and Circulatory Physiology 303, no. 5 (September 1, 2012): H539—H548. http://dx.doi.org/10.1152/ajpheart.00108.2012.

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Doxorubicin is commonly used to treat leukemia, lymphomas, and solid tumors, such as soft tissue sarcomas or breast cancer. A major side effect of doxorubicin therapy is dose-dependent cardiotoxicity. Doxorubicin's effects on cardiac energy metabolism are emerging as key elements mediating its toxicity. We evaluated the effect of doxorubicin on [14C]creatine uptake in rat neonatal cardiac myocytes and HL-1 murine cardiac cells expressing the human creatine transporter protein. A significant and irreversible decrease in creatine transport was detected after an incubation with 50–100 nmol/l doxorubicin. These concentrations are well below peak plasma levels (5 μmol/l) and within the ranges (25–250 nmol/l) for steady-state plasma concentrations reported after the administration of 15–90 mg/m2 doxorubicin for chemotherapy. The decrease in creatine transport was not solely because of increased cell death due to doxorubicin's cytotoxic effects. Kinetic analysis showed that doxorubicin decreased Vmax, Km, and creatine transporter protein content. Cell surface biotinylation experiments confirmed that the amount of creatine transporter protein present at the cell surface was reduced. Cardiomyocytes rely on uptake by a dedicated creatine transporter to meet their intracellular creatine needs. Our findings show that the cardiomyocellular transport capacity for creatine is substantially decreased by doxorubicin administration and suggest that this effect may be an important early event in the pathogenesis of doxorubicin-mediated cardiotoxicity.

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7

Maureen Okwudiri Onyebuenyi, Nsikak-Abasi Udokang, Ita Sunday Out, and Gbaranor Barina Kekii. "Assessment of the ameliorative potential of A. cepa and its fractions on doxorubicin-induced cardiotoxicity in Wistar rats." Open Access Research Journal of Biology and Pharmacy 9, no. 3 (December 30, 2023): 021–40. http://dx.doi.org/10.53022/oarjbp.2023.9.2.0057.

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The assessment of the ameliorative potentials of A. cepa and its fractions on doxorubicin-induced cardiotoxicity in Wistar rats was evaluated in this study. 45 Wistar rats of both sexes were randomly divided into 9 groups of 5 animals each; as follows: group I, served as control and received 10 ml/kg body weight of 0.9% saline, group II, 10mg/kg body weight of doxorubicin, group III, 4 mg/kg body weight of vitamin E plus Dox. Group IV, 1000mg/kg body weight of crude extracts of A. cepa plus Dox. Group V, 1000mg/kg body weight of n-hexane fraction of A. cepa plus Dox. Group VI, 1000mg/kg body weight of DCM fraction of A. cepa plus Dox. Group VII, 1000mg/kg body weight of EA fraction of A.cepa plus Dox. Group VIII, 1000mg/kg body weight of methanol fraction of A. cepa plus Dox, and group IX, combinations of 1000mg/kg, 4mg/kg 10mg/kg body weight of crude extract of A. cepa, vitamin E and Dox respectively for 16 days. Groups I and II treatments lasted 14 days, while treatments for groups III-VIII lasted 16 days (making 14 day for respective treatments and addition 2 days for doxorubin administered once 48 hourly) before sacrificing. All substances in this study were administered orally except doxorubicin that was done intravenously. The results showed that doxorubicn administration (group II) significantly (p<0.05) elevated troponin and NO levels; CK and LDH activities, compared to the control group indicating cardiotoxicity. This cardiotoxic effect of doxorubincin was significantly reversed by administration of vitamin E, crude extract, DCM, n-hexane to groups III, IV, V and VI respectively. A significant (p<0.05) reduction of only NO was recorded with EA fraction, compared with group II (dox). Methanol fraction (group VIII) further escalated doxorubicin-induced cardiotoxicity with a significantly (p<0.05) elevated myoglobulin and NO levels and CK activity. But the combined treatment with vitamin E, Crude extract and dox significantly (p<0.05) reduced cardiotoxic markers in this study except myoglobulin where a significant (p<0.05) elevation was recorded. It can be concluded that fresh A. cepa leaves extract possesses cardio-protective properties and may be a suitable cardio-protector against drug-induced cardiotoxicity in crude extract form, fractions of DCM and n-hexane but definitely not with methanol fraction as shown in this study.

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8

Gergely, Szabolcs, Csaba Hegedűs, Petra Lakatos, Katalin Kovács, Renáta Gáspár, Tamás Csont, and László Virág. "High Throughput Screening Identifies a Novel Compound Protecting Cardiomyocytes from Doxorubicin-Induced Damage." Oxidative Medicine and Cellular Longevity 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/178513.

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Antracyclines are effective antitumor agents. One of the most commonly used antracyclines is doxorubicin, which can be successfully used to treat a diverse spectrum of tumors. Application of these drugs is limited by their cardiotoxic effect, which is determined by a lifetime cumulative dose. We set out to identify by high throughput screening cardioprotective compounds protecting cardiomyocytes from doxorubicin-induced injury. Ten thousand compounds of ChemBridge’s DIVERSet compound library were screened to identify compounds that can protect H9C2 rat cardiomyocytes against doxorubicin-induced cell death. The most effective compound proved protective in doxorubicin-treated primary rat cardiomyocytes and was further characterized to demonstrate that it significantly decreased doxorubicin-induced apoptotic and necrotic cell death and inhibited doxorubicin-induced activation of JNK MAP kinase without having considerable radical scavenging effect or interfering with the antitumor effect of doxorubicin. In fact the compound identified as 3-[2-(4-ethylphenyl)-2-oxoethyl]-1,2-dimethyl-1H-3,1-benzimidazol-3-ium bromide was toxic to all tumor cell lines tested even without doxorubicine treatment. This benzimidazole compound may lead, through further optimalization, to the development of a drug candidate protecting the heart from doxorubicin-induced injury.

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9

Harahap, Yahdiana, Maria Juanita, and Baitha Palanggatan Maggadani. "ANALYTICAL METHOD VALIDATION OF DOXORUBICIN AND DOXORUBICINOL IN VOLUMETRIC ABSORPTIVE MICROSAMPLING BY LIQUID CHROMATOGRAPHY-TANDEM MASS SPECTROMETRY." Journal of Southwest Jiaotong University 56, no. 5 (October 30, 2021): 424–32. http://dx.doi.org/10.35741/issn.0258-2724.56.5.38.

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Doxorubicin is a broad-spectrum anthracycline antibiotic which has antineoplastic activity. Doxorubicin can cause cardiotoxic effects due to the formation of doxorubicinol as its main metabolite. One of the latest bio sampling methods, Volumetric Absorptive Microsampling (VAMS), has various advantages which include blood sampling by finger-prick, hematocrit does not influence it, and it can be stored at room temperature. This study aims to determine the optimum analysis conditions and sample preparation method in VAMS with daunorubicin as an internal standard, and to develop sensitive, specific measurements as well as validate the analytical method using Ultra High Performance Liquid Chromatography-Tandem Mass Spectrometry (UPLC-MS/MS). Analytical quantification analysis using mass spectrometry with a mass analyzer type is a triple quadrupole with a positive type of electrospray ionization (ESI). The separation was carried out with the Acquity® UPLC BEH C18 column (2.1 x 100 mm; 1.7 μm), with a flow rate of 0.2 mL/min, and gradient elution using 0.1% formic acid in water and 0.1% formic acid in acetonitrile for 7 minutes. Multiple reaction monitoring (MRM) values were set at m/z 544.22 > 396.9 for doxorubicin; m/z 546.22 > 398.9 for doxorubicinol; and m/z 528.5 > 362.95 for daunorubicin. Sample preparation used protein precipitation with methanol as the extracting solution, the drying time of the VAMS was 2 hours, and the sonication time was 30 minutes. LLOQ values obtained were 8 ng/mL for doxorubicin and 3 ng/mL for doxorubicinol with the linearity of 0.9904 for doxorubicin and 0.9902 for doxorubicinol.

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Bagdasaryan, Alina A., Vladimir N. Chubarev, Elena A. Smolyarchuk, Vladimir N. Drozdov, Ivan I. Krasnyuk, Junqi Liu, Ruitai Fan, Edmund Tse, Evgenia V. Shikh, and Olga A. Sukocheva. "Pharmacogenetics of Drug Metabolism: The Role of Gene Polymorphism in the Regulation of Doxorubicin Safety and Efficacy." Cancers 14, no. 21 (November 4, 2022): 5436. http://dx.doi.org/10.3390/cancers14215436.

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Breast cancer (BC) is the prevailing malignancy and major cause of cancer-related death in females. Doxorubicin is a part of BC neoadjuvant and adjuvant chemotherapy regimens. The administration of anthracycline derivates, such as doxorubicin, may cause several side effects, including hematological disfunction, gastrointestinal toxicity, hepatotoxicity, nephrotoxicity, and cardiotoxicity. Cardiotoxicity is a major adverse reaction to anthracyclines, and it may vary depending on individual differences in doxorubicin pharmacokinetics. Determination of specific polymorphisms of genes that can alter doxorubicin metabolism was shown to reduce the risk of adverse reactions and improve the safety and efficacy of doxorubicin. Genes which encode cytochrome P450 enzymes (CYP3A4 and CYP2D6), p-glycoproteins (ATP-binding cassette (ABC) family members such as Multi-Drug Resistance 1 (MDR1) protein), and other detoxifying enzymes were shown to control the metabolism and pharmacokinetics of doxorubicin. The effectiveness of doxorubicin is defined by the polymorphism of cytochrome p450 and p-glycoprotein-encoding genes. This study critically discusses the latest data about the role of gene polymorphisms in the regulation of doxorubicin’s anti-BC effects. The correlation of genetic differences with the efficacy and safety of doxorubicin may provide insights for the development of personalized medical treatment for BC patients.

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11

Natale, Ronald B., Alain C. Mita, Edward M. Wolin, Brenda Laabs, Hillary Dinh, Scott Wieland, Daniel Levitt, and Monica M. Mita. "Pharmacokinetic study of aldoxorubicin in solid tumor patients." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): e13572-e13572. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e13572.

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e13572 Background: Aldoxorubicin consists of doxorubicin conjugated to a pH sensitive linker that binds covalently to circulating albumin. Previous studies demonstrated that aldoxorubicin can be administered at doses up to 350 mg/m2 (260 mg/m2doxorubicin equivalents, DE) every 21 days for up to 8 cycles. We have investigated aldoxorubicin pharmacokinetics, including albumin-bound and free doxorubicin and doxorubicinol after administration of 2 dose levels of aldoxorubicin in patients with advanced solid tumors. Methods: Patients with solid tumors and no standard therapy were eligible. Other entry criteria: ECOG PS 0-2, LVEF > 45% of predicted normal for the site, adequate hematological status. Patients were administered either 230 mg/m2 aldoxorubicin (165 mg/m2 DE) or 350 mg/m2 aldoxorubicin (260 mg/m2 DE) iv over 30 minutes on day 1 of cycles 1 and 3. Blood samples were taken prior to administration and at multiple time points up to 72 hr post administration. Serum concentrations of albumin-bound doxorubicin, unbound doxorubicin and doxorubicinol were analyzed. Results: As of January 31, 7 subjects have been entered in the study. 6 subjects have received 230 mg/m2 aldoxorubicin and 1 subject has received 350 mg/m2 aldoxorubicin. No serious adverse events have been reported. Grade 3 or 4 adverse events include neutropenia, thrombocytopenia and anemia. A minor response (20% decrease) was observed in one subject (230 mg/m2aldoxorubicin) with small cell lung cancer who had received 3 prior chemotherapy regimens. For the 230 mg/m2 cohort during cycle 1, median results for albumin-bound doxorubicin include Cmax= 64 µg/mL, tmax= 0.25 hr, t1/2= 19.7 hr, AUC t-∞= 1500 h*µg/mL, CLpred= 0.153 L/h/m2, Vss pred= 3.91 L/m2. Results were similar for cycle 3. Free doxorubicin accounted for only 0.8% of total doxorubicin detected, and doxorubicinol less than 0.0007% of total drug. Results from the 350 mg/m2 cohort are pending. Data from all 12 subjects will be available at presentation. Conclusions: Aldoxorubicin binds rapidly to albumin and is cleared slowly from the circulation. It possess a relatively narrow volume of distribution. These characteristics distinguish aldoxorubicin from published PK data for doxorubicin. Clinical trial information: NCT01706835.

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Veleti, Kowmudi, Hemanth Kumar, Nazia Begum, Sharath Kondra, and Prashanth Nallavelli. "Protective Effect of Beta-Caryophyllene on Doxorubicin Induced Multiple Organ Toxicity in Rats." INTERNATIONAL JOURNAL OF APPLIED PHARMACEUTICAL SCIENCES AND RESEARCH 5, no. 02 (April 1, 2020): 22–29. http://dx.doi.org/10.21477/ijapsr.5.2.1.

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The major limiting factor in doxorubicin’s long-term administration is the development of cumulative dosedependent cardiomyopathy and congestive heart failure. Also, doxorubicin causes deterioration in hepato-renal function. It significantly increases the levels of blood urea nitrogen, creatinine, alanine transaminase, and aspartate transaminase distortion in normal renal and hepatic histology. The present study was undertaken to find out the protective role of beta-caryophyllene (BCP), an anti-oxidant against doxorubicin-induced multiple organ toxicities in experimental animals. In this study, male Wistar rats were divided into four groups. The first group, control group, was administered with vehicle (2.5% tween 20); the second group received doxorubicin (15 mg/kg intraperitoneally at a single dose), third and fourth groups (treatment groups) received BCP plus doxorubicin (15 mg/kg) at doses of 100 mg/kg and 200 mg/kg respectively. BCP was given orally for 15 days and doxorubicin was given on 13th day of treatment. Cardiac function was assessed by measuring electrocardiogram changes and cardiac biomarkers—doxorubicin-induced significant lengthening of QT-interval and ST-elevation, which was completely prevented by BCP treatment. Doxorubicin caused oxidative stress as indicated by a significant decrease in reduced superoxide dismutase, glutathione level, and catalase activity with an increase in malondialdehyde compared to control. Doxorubicin and BCP significantly reversed these values compared to doxorubicin in heart, kidney, and liver. The histopathological examination has also shown signs of toxicity in doxorubicin treated groups, and healing effect was noticed in treatment groups.

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Rodvold, K. A., D. A. Rushing, and D. A. Tewksbury. "Doxorubicin clearance in the obese." Journal of Clinical Oncology 6, no. 8 (August 1988): 1321–27. http://dx.doi.org/10.1200/jco.1988.6.8.1321.

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A study was carried out to examine the effect, if any, of obesity on doxorubicin pharmacokinetics. Body weight was found to be significantly related to doxorubicin clearance (r = -.75; P less than .001) and elimination half-life (r = .62; P = .003). Thus, the contribution of obesity on pharmacokinetics of antineoplastic agents should be taken into consideration in the analysis of clinical data with respect to toxicity and tumor response. Twenty-one patients were studied with their first course of doxorubicin (50 to 70 mg/m2) administered as a 60-minute intravenous (IV) infusion. Patients were divided into three groups on the basis of percentage of ideal body weight (IBW): normal (less than 115% IBW), mildly obese (115% to 130% IBW), and obese (greater than 130% IBW). Blood samples were collected up to 48 hours after the infusion and analyzed for doxorubicin and its metabolite, doxorubicinol, by high performance liquid chromatography. Doxorubicin area under the curve (AUC) was greater in obese than in normal patients (2,209 v 1,190 ng h/mL; P less than .05), yielding correspondingly reduced systemic clearance of the agent in obese patients (891 v 1,569 mL/min; P less than .001). The mean elimination half-life (T1/2) was 20.4 hours in the obese patients and 13.0 hours in the normal patients. The apparent volume of distribution (Vss) was not significantly different among the three groups of patients, indicating that the prolonged T1/2 in the obese patients is due to the reduction in clearance. The AUC and T1/2 of doxorubicinol were similar among all patient groups.

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Korga, Agnieszka, Magdalena Iwan, Dariusz Matosiuk, Marzena Rzadkowska, Elzbieta Szacon, Ewelina Humeniuk, Marcin Sysa, Marta Ostrowska, and Jaroslaw Dudka. "New tirapazamine derivatives protect cardiomyocytes from doxorubicin toxicity." Current Issues in Pharmacy and Medical Sciences 33, no. 1 (March 1, 2020): 1–5. http://dx.doi.org/10.2478/cipms-2020-0001.

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AbstractDoxorubicin cardiotoxicity is caused by various mechanisms, most importantly by oxidative stress originating in the mitochondria. Tirapazamine is a hypoxia-activated anticancer experimental drug. Both drugs in normoxia conditions undergo univalent reduction, thus tirapazamine may compete with doxorubicin in univalent reduction enzyme uptake. Herein, tirapazamine derivatives consisted of drug molecules and alkyl chain-connected triphenylphosphine cations that bring about an accumulation in mitochondria. The aim of this study was to evaluate the interaction of newly synthesized tirapazamine derivatives with doxorubicin in rat cardiomyocytes via an vitro model. In the work, H9C2 cells were incubated with combinations of doxorubicin, tirapazamine and seven variants of tirapazamine derivatives. After 24 hours, cell viability was assessed using MTT assay and the results were confirmed by microscopic observation. Tirapazamine in all tested concentrations did not revealed significant protective activity to cardiomyocytes treated with doxorubicine. However, tirapazamine derivatives diminished the cytotoxic effect of doxorubicin regardless of concentration and alkyl chain length. Tirapazamine derivatives have shown protective effects in relation to cardiomyocytes treated with doxorubicin and the mechanism of this phenomenon must be confirmed.

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&NA;. "Doxorubicin see Daunorubicin/doxorubicin." Reactions Weekly &NA;, no. 373 (October 1991): 6. http://dx.doi.org/10.2165/00128415-199103730-00027.

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&NA;. "Doxorubicin see Cisplatin/doxorubicin." Reactions Weekly &NA;, no. 291 (March 1990): 7. http://dx.doi.org/10.2165/00128415-199002910-00023.

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&NA;. "Doxorubicin see Daunorubicin/doxorubicin." Reactions Weekly &NA;, no. 292 (March 1990): 5. http://dx.doi.org/10.2165/00128415-199002920-00016.

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&NA;. "Doxorubicin see Daunorubicin/doxorubicin." Reactions Weekly &NA;, no. 348 (April 1991): 7. http://dx.doi.org/10.2165/00128415-199103480-00031.

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Dragojevic, Sonja, Jung Su Ryu, Michael E. Hall, and Drazen Raucher. "Targeted Drug Delivery Biopolymers Effectively Inhibit Breast Tumor Growth and Prevent Doxorubicin-Induced Cardiotoxicity." Molecules 27, no. 11 (May 24, 2022): 3371. http://dx.doi.org/10.3390/molecules27113371.

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The anticancer agent doxorubicin(dox) has been widely used in the treatment of a variety of hematological malignancies and solid tumors. Despite doxorubicin’s efficiency in killing tumor cells, severe damage to healthy tissues, along with cardiotoxicity, limits its clinical use. To overcome these adverse side effects, improve patient safety, and enhance therapeutic efficacy, we have designed a thermally responsive biopolymer doxorubicin carrier that can be specifically targeted to tumor tissue by locally applying mild hyperthermia (41 °C). The developed drug vehicle is composed of the following: a cell penetrating peptide (SynB1) to promote tumor and cellular uptake; thermally responsive Elastin-like polypeptide (ELP); and the (6-maleimidocaproyl) hydrazone derivative of doxorubicin (DOXO-EMCH) containing a pH-sensitive hydrazone linker that releases doxorubicin in the acidic tumor environment. We used the in vivo imaging system, IVIS, to determine biodistribution of doxorubicin-delivered ELP in MDA-MB-231 xenografts in nude mice. Tumor bearing mice were treated with a single IV injection of 10 mg/kg doxorubicin equivalent dose with free doxorubicin, thermally responsive SynB1 ELP 1-DOXO, and a thermally nonresponsive control biopolymer, SynB1 ELP 2-DOXO. Following a 2 h treatment with hyperthermia, tumors showed a 2-fold higher uptake when treated with SynB1 ELP 1-DOXO compared to free doxorubicin. Accumulation of the thermally non-responsive control SynB1 ELP2 –DOXO was comparable to free doxorubicin, indicating that an increase in dox accumulation with ELP is due to aggregation in response to thermal targeting. Higher levels of SynB1 ELP1–DOXO and SynB1 ELP2 –DOXO with respect to free doxorubicin were observed in kidneys. Fluorescence intensity from hearts of animals treated with SynB1 ELP1–DOXO show a 5-fold decrease in accumulation of doxorubicin than the same dose of free doxorubicin. SynB1-ELP1-DOXO biopolymers demonstrated a 6-fold increase in tumor/heart ratio in comparison to free doxorubicin, indicating preferential accumulation of the drug in tumors. These results demonstrate that thermally targeted polymers are a promising therapy to enhance tumor targeting and uptake of anticancer drugs and to minimize free drug toxicity in healthy tissues, representing a great potential for clinical application.

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Sara A. Al-Kenany and Nada N. Al-Shawi. "Protective Effect of Cafestol on Doxorubicin-induced Genotoxicity in Rats." Iraqi Journal of Pharmaceutical Sciences ( P-ISSN 1683 - 3597 E-ISSN 2521 - 3512) 32, Suppl. (November 1, 2023): 16–25. http://dx.doi.org/10.31351/vol32isssuppl.pp16-25.

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Doxorubicin is an efficient antineoplastic agent that has a broad antitumour spectrum; however, its genotoxic adverse effects on normal cells can be produced through oxidative damage, and this limits its clinical application. Cafestol is a naturally-occurring diterpene in unfiltered coffee with noteworthy antioxidant, antimutagenic and anti-inflammatory activities. The present study aimed to investigate the possible protective effect of cafestol against doxorubicin-induced chromosomal and DNA damage in rat bone marrow cells. Wistar Albino rats of both sexes were administered cafestol (5mg/kg body weight once daily for 14 consecutive days) by oral gavage alone or with doxorubicin which was injected as a single dose (90 mg/kg intraperitoneally at day 14) to induce toxicity. The bone marrow was harvested 24 hours after doxorubicin’s injection in all groups for the assessment of structural chromosomal aberration, micronucleus, and comet assays. The result showed that rats in the doxorubicin-only group exhibited a significant decrease (P<0.05) in mitotic index with a significant elevation (P<0.05) in the % DNA in Tail, micronucleus appearance and total structural chromosomal aberrations compared to those of the negative control group; while oral administration of cafestol 14 days prior to doxorubicin, significantly-reduced the % DNA in Tail, micronucleus appearance, and the total number of chromosomal aberrations (P<0.05), and improved the mitotic index compared to rats intraperitoneally-injected with doxorubicin alone. This study revealed that cafestol has protective effects against the genotoxicity induced by doxorubicin.

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&NA;. "Doxorubicin see Dactinomycin/doxorubicin/vincristine." Reactions Weekly &NA;, no. 333 (January 1991): 7. http://dx.doi.org/10.2165/00128415-199103330-00029.

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Laksmiani, Ni Putu Linda, Ratna Asmah Susidarti, and Edy Meiyanto. "Brazilein Increased Cytotoxic Activity of Doxorubicin on MCF-7/DOX Cells." Indonesian Journal of Cancer Chemoprevention 6, no. 2 (January 31, 2017): 58. http://dx.doi.org/10.14499/indonesianjcanchemoprev6iss2pp58-63.

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Brazilein is a compound obtained in a large amount from the dried heartwood of Secang (Caesalpinia sappan L.). Brazilein has strong cytotoxic effect in several cancer cell lines. This research was designed to evaluate the cytotoxic effect of brazilein and its combination with a chemotherapy agent, doxorubicin on MCF-7/DOX breast cancer cells. In the cytotoxicity assay, MCF-7/DOX cells were cultured in the presence of brazilein solely and in combination with doxorubicin for 24 hours and cell viability was evaluated by using MTT assay. MTT assay showed a dose-dependent inhibition of cell proliferation with IC50 value of 37 µM. Brazilein increased doxorubicin’s cytotoxic activity on MCF-7/DOX cells. Both of single treatment with different concentration of brazilein 12.5 and 25 mM or doxorubicin 0.8 and 1 mM gave cell viability percentage above 80%, but combination of them led to decrease the cell viability percentage significantly. Based on this research, it can be concluded that brazilein is potential to be developed as a co-chemotherapy agent on breast cancer cell that have been resistant to doxorubicin. Futher study must be held to evaluate its molecular mechanism.Keywords : brazilein, doxorubicin, MCF-7/DOX, cytotoxic.

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Chen, Robert W., Katrin Tiemann, Jessica Alluin, Stephen Forman, and John Rossi. "siRNAs Against Cyclin D1/D2 Improves Cytotoxicity of Chemotherapy In Mantle Cell Lymphoma." Blood 116, no. 21 (November 19, 2010): 1816. http://dx.doi.org/10.1182/blood.v116.21.1816.1816.

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Abstract Abstract 1816 Introduction: Mantle cell lymphoma is an aggressive B cell neoplasm with a median survival of 3 years. Cyclin D1 overexpression is the genetic hallmark of MCL and regulates cell cycle progression. However, the significance of cyclin D1 in the pathogenesis and treatment of MCL still remains to be defined. The aim of this study is to determine whether down regulation of cyclin D1 with siRNA will lead to enhanced therapeutic effect of chemotherapy in MCL. We used siRNA technology in three well characterized MCL cell lines, and tested traditional chemotherapy agents (doxorubicin and etoposide) as a model system. Material and Methods: We designed three different siRNA targeting cyclin D1 (si-224, 391, 778), one siRNA against cyclin D2 (si-D2), and a dual targeting siRNA against both cyclin D1 and D2 (si-D1/D2). The siRNAs used were 27 mer asymetric duplexes with a 2nd 3′ overhang. Granta-519 cells were transfected by lipofection (Lipofectamin RNAimax, Invitrogen), Z-138 and Jeko-1 cells were transfected with electroporation (BioRad). Western Blot analysis and real time PCR were performed to examine the down regulatory efficiency of the siRNAs on cyclin D1 mRNA and protein. Chemotherapeutics doxorubicin and etoposide were tested for enhancement of cytotoxicity by siRNA. The effect on cell viability of cyclin D1 reduction in combination with chemotherapeutics was analyzed by MTS assay. Results: We achieved cyclin D1 mRNA and protein down regulation in all 3 MCL cell lines, although the efficiency of knockdown varied among the siRNAs and the cell lines of interests. (Table 1) Si-224 has the best activity in Granta-519 while si-778 has the best activity in Jeko-1. We determined the cytotoxic effect of chemotherapy alone as well as in combination with siRNAs by MTS assays. The combination of chemotherapeutic with our siRNAs decreased the IC50 of both doxorubicine and etoposide. In Granta 519, si-224 decreased the IC 50 of doxorubicin by 32% and etoposide by 28%. In Jeko-1, si-778 decreased the IC 50 of doxorubicin by 49% but no effect on etoposide was seen. The magnitude of cyclin D1 down regulation seems to correlates with the percentages changes in IC 50. Klier et al previously reported that knockdown of cyclin D1 leads to an upregulation of cyclin D2 in MCL. Hence we mixed si-224 as well as si-778 targeting cyclin D1 with a si-D2 against cyclin D2 in combination with doxorubicine and etoposide in Granta-519. We also designed a dual-targeting siRNA against CCND1 and CCND2 (si-D1/D2). Targeting both cyclin D1 and D2 decreased the IC 50 of doxorubicin further than targeting cyclin D1 alone. Si224/D2 decreased the IC 50 of doxorubicin by 57% (si-224 alone 32%) and etoposide by 39% (si-224 alone 28%), and si778/D2 decreased the IC 50 of doxorubicine by 58% (si-778 alone 49%). The dual-targeting siRNA showed a decrease in IC 50 of doxorubicin by 45% and etoposide by 48%. Conclusions: Down regulation of cyclin D1 in MCL with siRNA improves the IC 50 of chemotherapeutic agents. Dual inhibition of both cyclin D1 and D2 further enhances the cytotoxic effect of doxorubicine and etoposide. Besides being a cell cycle regulator, cyclin D1 also seems to regulate chemosensitivity in MCL. Footnotes: This work was supported by grants from the Tower Cancer Research Foundation and Tim Nesvig Lymphoma Research Fund and Fellowship, Think Cure, Keck-foundation, SPORE. Disclosures: No relevant conflicts of interest to declare.

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Rahman, Khalil Ur, Shuo Yang, Nasir Azam, Zhen Yuan, Jiawen Yu, Chunhui Zhao, and Bin Feng. "Mir-153-3p Modulates the Breast Cancer Cells’ Chemosensitivity to Doxorubicin by Targeting KIF20A." Cancers 15, no. 6 (March 11, 2023): 1724. http://dx.doi.org/10.3390/cancers15061724.

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Breast cancer is considered the solid tumor most sensitive to chemotherapy. However, it can become resistant to various chemotherapeutic drugs, including doxorubicin, which triggers cell death by intercalation between DNA bases, free radical formation, and topoisomerase II inhibition. When drug resistance develops, several miRNAs are dysregulated, suggesting that miRNAs may play a significant role in resistance formation. In the current study, we investigated how doxorubicin sensitivity of breast cancer cells is affected by miR-153-3p and its target gene. The MTT method was used to determine the chemo-sensitizing effect of miR-153-3p on doxorubicin in MCF-7 and MDA-MB-231 cell lines. Results of Western blot and dual luciferase confirmed that miR-153-3p targets KIF20A and decreases its expression. Transwell and flow cytometry experiments showed that miR-153-3p and doxorubicin together had higher effects on MCF-7 and MDA-MB-231 cell proliferation, migration, and invasion, as well as increasing apoptosis and arresting cells in the G1 phase. Proteins related to apoptosis and the cell cycle exhibited the same tendency. Intracellular vesicle formation was inhibited and RAB26 was also downregulated by treatment with miR-153-3p alone or in combination with doxorubicin. Doxorubicin’s ability to suppress tumors may be enhanced by miR-153-3p, according to in vivo studies. According to our findings, miR-153-3p has a direct effect on KIF20A and may regulate the formation of intracellular vesicles, which in turn makes breast cancer cells more susceptible to doxorubicin.

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Syahputra, Rony Abdi, Urip Harahap, Yahdiana Harahap, Andayana Puspitasari Gani, Aminah Dalimunthe, Amer Ahmed, and Satirah Zainalabidin. "Vernonia amygdalina Ethanol Extract Protects against Doxorubicin-Induced Cardiotoxicity via TGFβ, Cytochrome c, and Apoptosis." Molecules 28, no. 11 (May 24, 2023): 4305. http://dx.doi.org/10.3390/molecules28114305.

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Doxorubicin (DOX) has been extensively utilized in cancer treatment. However, DOX administration has adverse effects, such as cardiac injury. This study intends to analyze the expression of TGF, cytochrome c, and apoptosis on the cardiac histology of rats induced with doxorubicin, since the prevalence of cardiotoxicity remains an unpreventable problem due to a lack of understanding of the mechanism underlying the cardiotoxicity result. Vernonia amygdalina ethanol extract (VAEE) was produced by soaking dried Vernonia amygdalina leaves in ethanol. Rats were randomly divided into seven groups: K- (only given doxorubicin 15 mg/kgbw), KN (water saline), P100, P200, P400, P4600, and P800 (DOX 15 mg/kgbw + 100, 200, 400, 600, and 800 mg/kgbw extract); at the end of the study, rats were scarified, and blood was taken directly from the heart; the heart was then removed. TGF, cytochrome c, and apoptosis were stained using immunohistochemistry, whereas SOD, MDA, and GR concentration were evaluated using an ELISA kit. In conclusion, ethanol extract might protect the cardiotoxicity produced by doxorubicin by significantly reducing the expression of TGF, cytochrome c, and apoptosis in P600 and P800 compared to untreated control K- (p < 0.001). These findings suggest that Vernonia amygdalina may protect cardiac rats by reducing the apoptosis, TGF, and cytochrome c expression while not producing the doxorubicinol as doxorubicin metabolite. In the future, Vernonia amygdalina could be used as herbal preventive therapy for patient administered doxorubicin to reduce the incidence of cardiotoxicity.

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Karwt, Rawdah, Oksana V. Bondar, Mikhail V. Pugachev, Tharaa Mohammad, Aisylu S. Kadyrova, Roman S. Pavelyev, Saleh Alrhmoun, Oleg I. Gnezdilov, and Yurii G. Shtyrlin. "Anticancer Potential of Pyridoxine-Based Doxorubicin Derivatives: An In Vitro Study." Life 14, no. 3 (February 20, 2024): 282. http://dx.doi.org/10.3390/life14030282.

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Doxorubicin (DOX) is a prevalent anticancer agent; however, it is unfortunately characterized by high cardiotoxicity, myelosuppression, and multiple other side effects. To overcome DOX limitations, two novel pyridoxine-derived doxorubicin derivatives were synthesized (DOX-1 and DOX-2). In the present study, their antitumor activity and mechanism of action were investigated. Of these two compounds, DOX-2, in which the pyridoxine fragment is attached to the doxorubicin molecule via a C3 linker, revealed higher selectivity against specific cancer cell types compared to doxorubicin and a promising safety profile for conditionally normal cells. However, the compound with a C1 linker (DOX-1) was not characterized by selectivity of antitumor action. It was revealed that DOX-2 obstructs cell cycle progression, induces apoptosis via the mitochondrial pathway without the development of necrosis, and showcases antioxidant capabilities, underlining its cell-regulatory roles. In contrast to doxorubicin’s DNA-centric mechanism, DOX-2 does not interact with nuclear DNA. Given these findings, DOX-2 presents a new promising direction in cancer therapeutics, which is deserving of further in vivo exploration.

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&NA;. "Doxorubicin." Reactions Weekly &NA;, no. 1377 (November 2011): 17. http://dx.doi.org/10.2165/00128415-201113770-00051.

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&NA;. "Doxorubicin." Reactions Weekly &NA;, no. 1379 (November 2011): 16. http://dx.doi.org/10.2165/00128415-201113790-00058.

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&NA;. "Doxorubicin." Reactions Weekly &NA;, no. 1389 (February 2012): 21. http://dx.doi.org/10.2165/00128415-201213890-00071.

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&NA;. "Doxorubicin." Reactions Weekly &NA;, no. 1393 (March 2012): 19. http://dx.doi.org/10.2165/00128415-201213930-00062.

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&NA;. "Doxorubicin." Reactions Weekly &NA;, no. 1393 (March 2012): 19. http://dx.doi.org/10.2165/00128415-201213930-00064.

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&NA;. "Doxorubicin." Reactions Weekly &NA;, no. 1395 (March 2012): 20. http://dx.doi.org/10.2165/00128415-201213950-00067.

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&NA;. "Doxorubicin." Reactions Weekly &NA;, no. 1396 (April 2012): 21. http://dx.doi.org/10.2165/00128415-201213960-00073.

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34

&NA;. "Doxorubicin." Reactions Weekly &NA;, no. 1161 (July 2007): 10. http://dx.doi.org/10.2165/00128415-200711610-00029.

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&NA;. "Doxorubicin." Reactions Weekly &NA;, no. 1163 (August 2007): 11. http://dx.doi.org/10.2165/00128415-200711630-00033.

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&NA;. "Doxorubicin." Reactions Weekly &NA;, no. 1167 (September 2007): 13. http://dx.doi.org/10.2165/00128415-200711670-00037.

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&NA;. "Doxorubicin." Reactions Weekly &NA;, no. 1185 (January 2008): 13. http://dx.doi.org/10.2165/00128415-200811850-00037.

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&NA;. "Doxorubicin." Reactions Weekly &NA;, no. 1361 (July 2011): 18–19. http://dx.doi.org/10.2165/00128415-201113610-00063.

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&NA;. "Doxorubicin." Reactions Weekly &NA;, no. 1366 (August 2011): 14. http://dx.doi.org/10.2165/00128415-201113660-00050.

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&NA;. "Doxorubicin." Reactions Weekly &NA;, no. 537 (February 1995): 6. http://dx.doi.org/10.2165/00128415-199505370-00017.

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&NA;. "Doxorubicin." Reactions Weekly &NA;, no. 553 (June 1995): 6. http://dx.doi.org/10.2165/00128415-199505530-00025.

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&NA;. "Doxorubicin." Reactions Weekly &NA;, no. 555 (June 1995): 5. http://dx.doi.org/10.2165/00128415-199505550-00014.

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&NA;. "Doxorubicin." Reactions Weekly &NA;, no. 425 (October 1992): 7. http://dx.doi.org/10.2165/00128415-199204250-00025.

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&NA;. "Doxorubicin." Reactions Weekly &NA;, no. 428 (November 1992): 6. http://dx.doi.org/10.2165/00128415-199204280-00023.

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&NA;. "Doxorubicin." Reactions Weekly &NA;, no. 431 (December 1992): 8. http://dx.doi.org/10.2165/00128415-199204310-00032.

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&NA;. "Doxorubicin." Reactions Weekly &NA;, no. 433 (January 1993): 8. http://dx.doi.org/10.2165/00128415-199304330-00032.

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&NA;. "Doxorubicin." Reactions Weekly &NA;, no. 439 (February 1993): 7. http://dx.doi.org/10.2165/00128415-199304390-00032.

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&NA;. "Doxorubicin." Reactions Weekly &NA;, no. 450 (May 1993): 8. http://dx.doi.org/10.2165/00128415-199304500-00032.

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&NA;. "Doxorubicin." Reactions Weekly &NA;, no. 613 (August 1996): 8. http://dx.doi.org/10.2165/00128415-199606130-00018.

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&NA;. "Doxorubicin." Reactions Weekly &NA;, no. 687 (February 1998): 7–8. http://dx.doi.org/10.2165/00128415-199806870-00014.

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