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Doxorubicin hydrochloride

Catalog No. T1020 CAS 25316-40-9

Synonyms: Adriamycin, Doxorubicin (Adriamycin) HCl, Hydroxydaunorubicin hydrochloride, NSC 123127

Doxorubicin hydrochloride (Adriamycin) belongs to the anthracycline class of antibiotics and is an inhibitor of human DNA topoisomerase I/II (IC50=0.8/2.67 μM). Doxorubicin hydrochloride exhibits cytotoxicity and antitumor activity. Doxorubicin hydrochloride reduces the phosphorylation of AMPK and its downstream target protein acetyl coenzyme A carboxylase, and induces apoptosis and autophagy.

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Doxorubicin hydrochloride Chemical Structure

Doxorubicin hydrochloride, CAS 25316-40-9

Pack Size	Availability	Price/USD
25 mg	In stock	$ 34.00
50 mg	In stock	$ 48.00
100 mg	In stock	$ 68.00
200 mg	In stock	$ 98.00
500 mg	In stock	$ 187.00
1 g	In stock	$ 276.00
1 mL * 10 mM (in DMSO)	In stock	$ 50.00

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Purity: 99.36%

Purity: 99.13%

Purity: 98.59%

Purity: 98.15%

Purity: 98%

Biological Description

Chemical Properties

Storage & Solubility Information

Description	Doxorubicin hydrochloride (Adriamycin) belongs to the anthracycline class of antibiotics and is an inhibitor of human DNA topoisomerase I/II (IC50=0.8/2.67 μM). Doxorubicin hydrochloride exhibits cytotoxicity and antitumor activity. Doxorubicin hydrochloride reduces the phosphorylation of AMPK and its downstream target protein acetyl coenzyme A carboxylase, and induces apoptosis and autophagy.
Targets&IC50	Topo I:0.8 μM (IC50), Topo II:2.67 μM (IC50)
In vitro	METHODS: Human breast cancer cells MCF10A, BT474, MCF-7 and T47D were treated with Doxorubicin hydrochloride (0.1-10 μM) for 48 h, and cell growth inhibition was detected by MTT. RESULTS: Doxorubicin hydrochloride dose-dependently inhibited the growth of MCF10A, BT474, MCF-7 and T47D cells with IC50s of 2.51 µM, 1.14 µM, 0.69 µM and 8.53 µM, respectively. [1] METHODS: Bovine aortic endothelial cells BAECs and human ovarian teratoma cells PA-1 were treated with Doxorubicin (0.5 μM) for 1-16 h. Apoptosis was detected by Flow Cytometry, and caspase-3 activity was detected by caspase-3 assay kit. RESULTS: Doxorubicin induced apoptosis and caspase-3 activation in BAECs and PA-1 cells in a time-dependent manner. [2] METHODS: Canine breast cancer cells CIPp were treated with Doxorubicin (EC50(20h)=12.08 μM) for 3-48 h. The expression of target genes was detected by qRT-PCR. RESULTS: Doxorubicin induced up-regulation of the mRNA expression levels of multidrug resistance (MDR)-related genes P-gp and BCRP. [3]
In vivo	METHODS: To detect antitumor activity in vivo, Doxorubicin hydrochloride (1 mg/kg/4 days) and lovastatin (5 mg/kg/day) were intraperitoneally injected into B6D2F1 mice bearing murine melanoma tumor B16F10 for two weeks. RESULTS: The combination of Doxorubicin hydrochloride and lovastatin showed a significant increase in sensitivity compared to either drug alone. lovastatin enhanced the antitumor activity of Doxorubicin hydrochloride. [4] METHODS: To investigate the acute and long-term cognitive deficits of Doxorubicin in cancer patients, a single dose of Doxorubicin hydrochloride (25 mg/kg) was administered intraperitoneally to B6C3F1J mice. RESULTS: Systemic treatment with Doxorubicin hydrochloride altered glutamatergic neurotransmission in the nucleus of key cells associated with cognitive function within 24 h. There were no lasting effects on spatial learning and memory. [5]
Cell Research	To analyze the effect of Bcl-2 expression on the viability of HUVECs treated with Dox, cells were co-transfected with 200 ng of the pEGFP-spectrin expression plasmid together with 200 ng of either pCDNA3-hBcl-2 or the control pCMVβ-galactosidase expression vector (33). The pGL3 Basic vector (2.1 μg) was added as a DNA carrier in a total volume of 0.140 ml, and transfection was performed by the calcium phosphate procedure in 35-mm tissue culture dishes. After treatment, the cells were washed with PBS, fixed with 3.7% formaldehyde for 15 min, and washed for a further 10 min with 50 mM NH4Cl blocking solution in PBS. Cells were then washed with PBS, permeabilized with a 0.1% Triton X-100 for 10 min, washed again with PBS, and stained with 1 μg/ml 4′,6-diamidino-2-phenyl-indole solution for 2 min. The cells were examined under a fluorescence microscope, and GFP-positive cells were scored after counting a minimum of 1000 total cells for each condition. The efficiency of transfection in Bcl-2- and β-galactosidase-expressing cells, determined in aliquots of transfected cells just before the addition of Dox, was similar (10–12%) [1].
Animal Research	Athymic male nude mice (3-4 weeks old) are used. PC3 cells (4×106) are injected subcutaneously into the flanks of mice. Animals bearing tumors are randomly assigned to treatment groups (five or six mice per group) and treatment initiated when xenografts reached volumes of about 100 mm3. Tumors are measured using digital calipers and volume calculated using the formula: Volume=Width2×Length×0.52, where width represents the shorter dimension of the tumor. Treatments are administered as indicated using vehicle (PBS containing 0.1% BSA), Doxorubicin (2-8 mg/kg), Apo2L/TRAIL (500 μg/animal), or a combination of 4 mg/kg Doxorubicin followed by 500 μg Apo2L/TRAIL. Doxorubicin is administered systemically whereas Apo2L/TRAIL is given either intratumorally or systemically. All treatments are given once. Mice are monitored daily for signs of adverse effects (listlessness and scruffy appearance). Treatments seemed to be well tolerated. The mean±SEM is calculated for each data point. Differences between treatment groups are analyzed by the student t-test. Differences are considered significant when P<0.05 [3]. Altogether, 29 male Wistar rats (weight 306 ± 18.6 g) were used in the study. Animals were divided into three groups: control (group C; n = 10; 306.4 ± 17.2 g), animals treated with DOX (group DOX; n = 10; 305.0 ± 24.9 g) and animals treated with L-DOX (group L-DOX; n = 9; 306.7 ± 15.0 g). Vehiculum (aqua pro injection), DOX and L-DOX were applied to group C, DOX and L-DOX, respectively, by single intraperitoneal injection; concentration of both DOX and L-DOX was 5 mg/kg, similar to the concentrations used in human treatment protocols. All animals were sacrificed 24 h after drug application. Thoracotomy was performed, hearts were excised and samples were obtained separately from the free wall of the left atrium (LA), left ventricle (LV), right atrium (RA) and right ventricle (RV).Samples were placed into RNA later preservation solution and stored at -80 C until further analysis [4].

Synonyms	Adriamycin, Doxorubicin (Adriamycin) HCl, Hydroxydaunorubicin hydrochloride, NSC 123127
Molecular Weight	579.99
Formula	C27H29NO11·HCl
CAS No.	25316-40-9

Storage

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

Solubility Information

DMSO: 29 mg/mL (50 mM)

H2O: 29 mg/mL (50 mM)

References and Literature

1. Wen SH, et al. Sulbactam-enhanced cytotoxicity of doxorubicin in breast cancer cells. Cancer Cell Int. 2018 Sep 4;18:128. 2. Wang S, et al. Doxorubicin induces apoptosis in normal and tumor cells via distinctly different mechanisms. intermediacy of H(2)O(2)- and p53-dependent pathways. J Biol Chem. 2004 Jun 11;279(24):25535-43. 3. Levi M, et al. Doxorubicin treatment modulates chemoresistance and affects the cell cycle in two canine mammary tumour cell lines. BMC Vet Res. 2021 Jan 18;17(1):30. 4. Feleszko W, et al. Lovastatin potentiates antitumor activity of doxorubicin in murine melanoma via an apoptosis-dependent mechanism. Int J Cancer. 2002 Jul 1;100(1):111-8. 5. Thomas TC, et al. Acute treatment with doxorubicin affects glutamate neurotransmission in the mouse frontal cortex and hippocampus. Brain Res. 2017 Oct 1;1672:10-17. 6. Zhang L, Feng M, Wang X, et al. Peptide Szeto‑Schiller 31 ameliorates doxorubicin‑induced cardiotoxicity by inhibiting the activation of the p38 MAPK signaling pathway[J]. International Journal of Molecular Medicine. 2021, 47(4): 1-11 7. Hu Y, Liu J, Lu J, et al. sFRP1 protects H9c2 cardiac myoblasts from doxorubicin-induced apoptosis by inhibiting the Wnt/PCP-JNK pathway[J]. Acta Pharmacologica Sinica. 2020: 1-8. 8. Zuo Z, Shen J X, Pan Y, et al. Weighted gene correlation network analysis (WGCNA) detected loss of MAGI2 promotes chronic kidney disease (CKD) by podocyte damage[J]. Cellular Physiology and Biochemistry. 2018;51(1):244-261. 9. Tang K, Zhang X, Guo Y. Identification of the dietary supplement capsaicin as an inhibitor of Lassa virus entry[J]. Acta Pharmaceutica Sinica B. 2020. 10. Lu J, Li J, Hu Y, et al. Chrysophanol protects against doxorubicin-induced cardiotoxicity by suppressing cellular PARylation[J]. Acta Pharmaceutica Sinica B. 2018 Nov

Citations

1. Wang B, Jin Y, Liu J, et al.EP1 activation inhibits doxorubicin-cardiomyocyte ferroptosis via Nrf2.Redox Biology.2023: 102825. 2. Li J, Sun Y, Zhao X, et al.Radiation induces IRAK1 expression to promote radioresistance by suppressing autophagic cell death via decreasing the ubiquitination of PRDX1 in glioma cells.Cell Death & Disease.2023, 14(4): 1-16. 3. Yue Y, Li H, Wang X, et al.Intelligent Responsive Nanoparticles with Multilevel Triggered Drug Penetration for Tumor Photochemotherapy.ACS Applied Materials & Interfaces.2023 4. Rizwan A, Gulfam M, Jo S H, et al.Gelatin-based NIR and reduction-responsive injectable hydrogels cross-linked through IEDDA click chemistry for drug delivery application.European Polymer Journal.2023: 112019. 5. Bi X, Zhang M, Zhou J, et al.Phosphorylated Hsp27 promotes adriamycin resistance in breast cancer cells through regulating dual phosphorylation of c-Myc.Cellular Signalling.2023: 110913. 6. Wang H, Shi J, Tang B, et al.Forecast and verification of the active compounds and latent targets of Guyuan decoction in treating frequently relapsing nephrotic syndrome based on network pharmacology.Renal Failure.2023, 45(1): 2184654. 7. Hu Y, Liu J, Lu J, et al. sFRP1 protects H9c2 cardiac myoblasts from doxorubicin-induced apoptosis by inhibiting the Wnt/PCP-JNK pathway. Acta Pharmacologica Sinica. 2020: 1-8. 8. Wang H, Wang Q, Cai G, et al. Nuclear TIGAR mediates an epigenetic and metabolic autoregulatory loop via NRF2 in cancer therapeutic resistance. Acta Pharmaceutica Sinica B. 2021 9. Lü Z, Li X, Li K, et al. Nitazoxanide and related thiazolides induce cell death in cancer cells by targeting the 20S proteasome with novel binding modes. Biochemical Pharmacology. 2022: 114913. 10. Zhang L, Feng M, Wang X, et al. Peptide Szeto‑Schiller 31 ameliorates doxorubicin‑induced cardiotoxicity by inhibiting the activation of the p38 MAPK signaling pathway. International Journal of Molecular Medicine. 2021, 47(4): 1-11

11. Lu J, Li J, Hu Y, et al. Chrysophanol protects against doxorubicin-induced cardiotoxicity by suppressing cellular PARylation. Acta Pharmaceutica Sinica B. 2018 Nov 12. Zuo Z, Shen J X, Pan Y, et al. Weighted gene correlation network analysis (WGCNA) detected loss of MAGI2 promotes chronic kidney disease (CKD) by podocyte damage. Cellular Physiology and Biochemistry. 2018;51(1):244-261 13. Wang Y, Wu Y, Chen Y, et al. Nanoliter Centrifugal Liquid Dispenser Coupled with Superhydrophobic Microwell Array Chips for High-Throughput Cell Assays. Micromachines. 2018 Jun 6;9(6) 14. Yıldızhan K, Huyut Z, Altındağ F. Involvement of TRPM2 Channel on Doxorubicin-Induced Experimental Cardiotoxicity Model: Protective Role of Selenium. Biological Trace Element Research. 2022: 1-12. 15. Tang K, Zhang X, Guo Y. Identification of the dietary supplement capsaicin as an inhibitor of Lassa virus entry. Acta Pharmaceutica Sinica B. 2020 16. Liang C, Yu X, Xiong N, et al. Pictilisib Enhances the Antitumor Effect of Doxorubicin and Prevents Tumor-Mediated Bone Destruction by Blockade of PI3K/AKT Pathway. Frontiers in oncology. 2020, 10. 17. Yıldızhan K, Huyut Z, Altındağ F Involvement of TRPM2 Channel on Doxorubicin‑Induced Experimental Cardiotoxicity Model: Protective Role of Selenium. Biological Trace Element Research. 2022: 1-12 18. Zhong Y, Li M, Zhang X, et al. Dissecting Chemical Composition and Cardioprotective Effects of Fuzhengkangfu Decoction against Doxorubicin-Induced Cardiotoxicity by LC–MS and Bioinformatics Approaches. ACS Omega. 2020 19. Gaweł, Agata M., et al. Analysis of the Role of FRMD5 in the Biology of Papillary Thyroid Carcinoma. International Journal of Molecular Sciences. 22.13 (2021): 6726. 20. Xu H, You H, Gong J, et al.Discovery of Zidovudine as a cardiomyocyte protectant for doxorubicin-induced toxicity through high-throughput phenotypic drug screening.Fundamental Research.2023 21. Hou Z, Ren Y, Zhang X, et al.EP300-ZNF384 transactivates IL3RA to promote the progression of B-cell acute lymphoblastic leukemia.Cell Communication and Signaling.2024, 22(1): 211.

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This product is contained In the following compound libraries：

Microbial Natural Product Library EMA Approved Drug Library Drug Repurposing Compound Library Anti-Cancer Approved Drug Library Anti-Cancer Active Compound Library FDA-Approved Kinase Inhibitor Library Kinase Inhibitor Library Anti-Cancer Clinical Compound Library Anti-Cancer Drug Library Bioactive Compound Library

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Keywords

Doxorubicin hydrochloride 25316-40-9 Apoptosis Autophagy Chromatin/Epigenetic DNA Damage/DNA Repair Microbiology/Virology PI3K/Akt/mTOR signaling Proteases/Proteasome Topoisomerase HIV Protease HBV Antibacterial Antibiotic AMPK Mitophagy Doxorubicin Doxorubicin Hydrochloride Adriamycin Human immunodeficiency virus Doxorubicin (Adriamycin) HCl HIV Hydroxydaunorubicin hydrochloride Mitochondrial Autophagy Bacterial Inhibitor Hepatitis B virus ADC Payload ADC Cytotoxin Hydroxydaunorubicin inhibit NSC-123127 AMP-activated protein kinase Hydroxydaunorubicin Hydrochloride NSC 123127 NSC123127 inhibitor

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