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Doxorubicin hydrochloride

カタログ番号 T1020   CAS 25316-40-9
別名: Adriamycin, Doxorubicin (Adriamycin) HCl, Hydroxydaunorubicin hydrochloride, DOX 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
パッケージサイズ 在庫状況 単価(税別) キャンペーン価格
サンプルについてお問い合わせ
25 mg 在庫あり ¥ 8,000 6,500
50 mg 在庫あり ¥ 11,000 9,000
100 mg 在庫あり ¥ 16,000 13,000
200 mg 在庫あり ¥ 22,500 18,000
500 mg 在庫あり ¥ 43,000 34,500
1 g 在庫あり ¥ 63,500 51,000
1 mL * 10 mM (in DMSO) 在庫あり ¥ 11,500 9,500
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生物学的特性に関する説明
化学的特性
保存条件 & 溶解度情報
説明 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.
ターゲット&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]
細胞研究 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].
動物実験 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].
別名 Adriamycin, Doxorubicin (Adriamycin) HCl, Hydroxydaunorubicin hydrochloride, DOX hydrochloride, NSC 123127
分子量 579.99
分子式 C27H29NO11·HCl
CAS No. 25316-40-9

保存条件

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

溶解度情報

DMSO: 55 mg/mL (94.83 mM)

H2O: 29 mg/mL (50 mM)

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

引用文献

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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関連化合物ライブラリー

この製品は下記化合物ライブラリに含まれています:
Microbial Natural Product Library FDA-Approved Kinase Inhibitor Library Anti-Cancer Drug Library Natural Product Library for HTS Kinase Inhibitor Library Anti-Cancer Approved Drug Library Anti-Cancer Active Compound Library Anti-Cancer Clinical Compound Library Traditional Chinese Medicine Monomer Library EMA Approved Drug Library

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投与量変換

You can also refer to dose conversion for different animals. 詳細

In vivo投与量計算 (透明溶液)

ステップ1: 以下の情報を入力してください
投与量
mg/kg
動物の平均体重
g
動物あたりの投与量
ul
動物数
溶媒の組成を入力してください
% DMSO
%
% Tween 80
% ddH2O
計算する リセット

計算器

モル濃度計算機
希釈計算機
再構成計算
分子量計算機
=
X
X

モル度計算機では以下の計算が可能です

  • 既知の体積と濃度の溶液を調製するために必要な化合物の質量
  • 質量が既知の化合物を目的の濃度まで溶解させるのに必要な溶液の量
  • 特定の体積の中に既知の質量の化合物を入れて得られる溶液の濃度
参考例

モル濃度計算機を使用したモル濃度計算の例
化合物の分子量が197.13g/molである場合、10mlの水に10mMのストック溶液を作るのに必要な化合物の質量はどれくらいですか?
[分子量(MW)]の欄に[197.13]と入力してください
[濃度]ボックスに10と入力し、正しい単位(millimolar)を選択します
[容量]ボックスに10と入力し、正しい単位(milliliter)を選択します
計算を押します
答えの19.713mgが質量欄に表示されます

X
=
X

溶液を作るのに必要な希釈率の計算

溶液の調製に必要な希釈率の算出
希釈計算機は、既知の濃度の原液をどのように希釈するかを計算することができる便利なツールです。V1を計算するためにC1、C2&V2を入力します。

参考例

Tocrisの希釈計算器を用いた希釈計算の一例
50μMの溶液を20ml作るためには、10mMの原液を何ml必要ですか?
C1V1=C2V2という式を用いて、C1=10mM、C2=50μM、V2=20ml、V1を未知数とします。
濃度(開始)ボックスに10を入力し正しい単位(millimolar)を選択してください
濃度(終了)ボックスに50を入力し正しい単位(millimolar)を選択してください
体積(終了)ボックスに20を入力し正しい単位(millimolar)を選択してください
計算を押します
100 microliter (0.1 ml) という答えが体積(開始)ボックスに表示されます。

=
/

バイアルを再構成するのに必要な溶媒の量を計算する.

再構成計算機を使えば、バイアルを再構成するための試薬の量をすぐに計算することができます.
試薬の質量と目標濃度を入力するだけで計算します。

g/mol

化合物の化学式を入力して、そのモル質量や元素組成を計算します

Tヒント:化学式は大文字と小文字を区別します。: C10H16N2O2 c10h16n2o2

化合物のモル質量(分子量)を計算する手順:
化学物質のモル質量を計算するには、その化学式を入力し、「計算」をクリックしてください。.
分子質量、分子量、モル質量、モル重量の定義:
分子質量(分子量)とは、物質の1分子の質量であり、統一された原子質量単位(u)で表されます。(1uは炭素12の1原子の質量の1/12に等しい)
モル質量(molar weight)とは、ある物質の1モルの質量のことで、単位はg/molです。

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技術サポート

Please see Inhibitor Handling Instructions for more frequently ask questions. Topics include: how to prepare stock solutions, how to store products, and cautions on cell-based assays & animal experiments, etc.

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 Mitochondrial Autophagy Bacterial Inhibitor DOX hydrochloride Hepatitis B virus ADC Payload ADC Cytotoxin Hydroxydaunorubicin inhibit NSC-123127 AMP-activated protein kinase Hydroxydaunorubicin Hydrochloride NSC 123127 NSC123127 inhibitor