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Doxorubicin hydrochloride

产品编号 T1020 CAS 25316-40-9

别名: Adriamycin, Doxorubicin (Adriamycin) HCl, Hydroxydaunorubicin hydrochloride, 盐酸多柔比星, 盐酸阿霉素, NSC 123127

Doxorubicin hydrochloride (Adriamycin) 属于蒽环类抗生素，是人类 DNA 拓扑异构酶 I/II 抑制剂 (IC50=0.8/2.67 μM)。Doxorubicin hydrochloride 具有细胞毒性和抗肿瘤活性。Doxorubicin hydrochloride 可降低 AMPK 及其下游靶蛋白乙酰辅酶 A 羧化酶的磷酸化，还可诱导凋亡和自噬。

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Doxorubicin hydrochloride Chemical Structure

Doxorubicin hydrochloride, CAS 25316-40-9

规格	价格/CNY	货期
5 mg	￥ 155	现货
10 mg	￥ 274	现货
25 mg	￥ 455	现货
50 mg	￥ 756	现货
100 mg	￥ 1,347	现货
200 mg	￥ 2,150	现货
500 mg	￥ 3,850	现货
1 g	￥ 4,210	现货
1 mL * 10 mM (in DMSO)	￥ 328	现货

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其他形式的 Doxorubicin hydrochloride:

Doxorubicin
询价

选择批次

纯度: 99.36%

COA DATASHEET SDS HPLC HNMR

纯度: 99.13%

COA DATASHEET SDS HNMR HPLC

纯度: 98.59%

COA DATASHEET SDS HPLC HNMR

纯度: 98.15%

COA DATASHEET SDS HNMR HPLC

COA DATASHEET SDS HNMR

COA DATASHEET SDS LCMS HNMR

纯度: 98%

COA DATASHEET SDS HNMR

纯度: 98%

COA DATASHEET SDS HNMR

纯度: 98%

COA DATASHEET SDS HNMR

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天然产物信息

生物活性

化学信息

存储 & 溶解度

参考文献

相关产品

植物来源	天然产物 > 其他（植物来源） > 其他

产品描述	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.
靶点活性	Topo I:0.8 μM (IC50), Topo II:2.67 μM (IC50)
体外活性	方法：人乳腺癌细胞 MCF10A、BT474、MCF-7 和 T47D 用 Doxorubicin hydrochloride (0.1-10 μM) 处理 48 h，使用 MTT 方法检测细胞生长抑制情况。结果：Doxorubicin hydrochloride 剂量依赖性地抑制 MCF10A、BT474、MCF-7 和 T47D 细胞生长，IC50 分别为 2.51 µM、1.14 µM、0.69 µM 和 8.53 µM。[1] 方法：牛主动脉内皮细胞 BAECs 和人卵巢畸胎瘤细胞 PA-1 用 Doxorubicin (0.5 μM) 处理 1-16 h，使用 Flow Cytometry 方法检测细胞凋亡情况，使用 caspase-3 assay kit 检测 caspase-3 的活性。结果：Doxorubicin 时间依赖性地诱导 BAECs 和 PA-1 细胞的凋亡及 caspase-3 激活。[2] 方法：犬乳腺癌细胞 CIPp 用 Doxorubicin (EC50(20h)=12.08 μM) 处理 3-48 h，使用 qRT-PCR 方法检测靶基因表达情况。结果：Doxorubicin 诱导多药耐药性 (MDR) 相关基因 P-gp 和 BCRP 的 mRNA 表达水平上调。[3]
体内活性	方法：为检测体内抗肿瘤活性，将 Doxorubicin hydrochloride (1 mg/kg/4 天) 和 lovastatin (5 mg/kg/天) 腹腔注射给携带鼠黑色素瘤肿瘤 B16F10 的 B6D2F1 小鼠，持续两周。结果：与单独作用的任一药物相比，Doxorubicin hydrochloride 和 lovastatin 联合治疗的敏感性显著增加，lovastatin 增强了 Doxorubicin hydrochloride 的抗肿瘤活性。[4] 方法：为研究 Doxorubicin 对癌症患者的急性和长期认知障碍，将 Doxorubicin hydrochloride (25 mg/kg) 单剂量腹腔注射给 B6C3F1J 小鼠。结果：Doxorubicin hydrochloride 全身治疗在 24 h 内改变了与认知功能相关的关键细胞核中的谷氨酸神经传递，对空间学习和记忆没有持久影响。[5]
细胞实验	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].
动物实验	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].

别名	Adriamycin, Doxorubicin (Adriamycin) HCl, Hydroxydaunorubicin hydrochloride, 盐酸多柔比星, 盐酸阿霉素, NSC 123127
化合物与蛋白结合的复合物	CRYSTAL STRUCTURE OF FOUR MORPHOLINO-DOXORUBICIN ANTICANCER DRUGS COMPLEXED WITH D(CGTACG) AND D(CGATCG): IMPLICATIONS IN DRUG-DNA CROSSLINK
分子量	579.99
分子式	C27H29NO11·HCl
CAS No.	25316-40-9

存储

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

溶解度

DMSO: 29 mg/mL (50 mM)

H2O: 29 mg/mL (50 mM)

溶液配制表

可选溶剂	浓度体积质量	1 mg	5 mg	10 mg	25 mg
DMSO / H2O	1 mM	1.7242 mL	8.6208 mL	17.2417 mL	43.1042 mL
	5 mM	0.3448 mL	1.7242 mL	3.4483 mL	8.6208 mL
	10 mM	0.1724 mL	0.8621 mL	1.7242 mL	4.3104 mL
	20 mM	0.0862 mL	0.431 mL	0.8621 mL	2.1552 mL
	50 mM	0.0345 mL	0.1724 mL	0.3448 mL	0.8621 mL

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摩尔浓度计算器

稀释计算器

配液计算器

分子量计算器

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参考文献

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

文献引用

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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对于不同动物的给药剂量换算，您也可以参考 更多...

体内实验配液计算器

请在以下方框中输入您的动物实验信息后点击计算，可以得到母液配置方法和体内配方的制备方法：比如您的给药剂量是10 mg/kg，每只动物体重20 g，给药体积100 μL，一共给药动物10 只，您使用的配方为5% DMSO+30% PEG300+5% Tween 80+60% ddH2O。那么您的工作液浓度为2 mg/mL。

母液配置方法：2 mg 药物溶于 50 μL DMSO (母液浓度为 40 mg/mL)，如您需要配置的浓度超过该产品的溶解度，请先与我们联系。

体内配方的制备方法：取 50 μL DMSO 主液，加入 300 μL PEG300，混匀澄清，再加 50 μL Tween 80，混匀澄清，再加 600 μL ddH2O, 混匀澄清。

第一步：请输入动物实验的基本信息

剂量

mg/kg

每只动物体重

给药体积

μL

动物数量

第二步：请输入动物体内配方组成，不同的产品配方组成不同，如有配方需求，可先联系我们提供正确的体内配方。

% DMSO+

% +

% Tween 80+

% ddH₂O

%DMSO+

计算重置

计算结果如下:

工作液浓度: mg/ml;

母液配置方法: mg 药物溶于 μL DMSO (母液浓度为 mg/mL)，如您需要配置的浓度超过该产品的溶解度，请先与我们联系。

体内配方的制备方法：取 μL DMSO 主液，加入 μL PEG300，混匀澄清，再加 μL Tween 80，混匀澄清，再加 μL ddH₂O, 混匀澄清。

备注:

要按顺序从左向右依次添加助溶剂。可配合物理方法，如涡流、超声波或热水浴使之帮助溶解。

技术支持

您可能有的问题的答案可以在抑制剂处理说明中找到，包括如何准备库存溶液，如何存储产品，以及基于细胞的分析和动物实验需要特别注意的问题。

Keywords

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

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Doxorubicin hydrochloride

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