Doxorubicin (DOX) HCl

製品コードS1208 バッチS120813

化学情報

	Synonyms	Adriamycin, NSC 123127, Hydroxydaunorubicin HCl	Storage (From the date of receipt)	3 years -20°C powder 1 years -80°C in solvent
	化学式	C₂₇H₂₉NO₁₁.HCl
	分子量	579.98	CAS No.	25316-40-9
Solubility (25°C)*	体外	DMSO	100 mg/mL (172.41 mM)
		Water	100 mg/mL (172.41 mM)
		Ethanol	Insoluble
* <1 mg/ml means slightly soluble or insoluble. * Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

溶剤液（一定の濃度）を調合する

生物活性

製品説明	ドキソルビチン塩酸塩 (Doxorubicin (Adriamycin, NSC 123127, DOX, Hydroxydaunorubicin) HCl) は抗生物質の一種であり、DNA トポイソメラーゼ (topoisomerase) II を阻害することで DNA 損傷を引き起こし、がん細胞中においてマイトファジー (mitophagy) およびアポトーシス (apoptosis) を誘導します。ドキソルビシンは AMPK の基底状態におけるリン酸化を減弱します。また、ドキソルビシンは HIV 感染患者の併用療法において使用されますが、同時に HBV 再活性化のリスクを伴うことが分かっています。This product may precipitate when dissolved in PBS solution. It is recommended to prepare the stock solution in pure water and dilute with either pure water or saline to obtain the working solution.
in vitro	Doxorubicin, an antibiotic anthracycline, is commonly considered to exert its anti-tumor activity at two fundamental levels, altering DNA and producing free radicals to trigger apoptosis of cancer cells through DNA damage. Doxorubicin can block the synthesis of DNA by intercalating into the DNA strand, and inhibits DNA topoisomerase II (TOP2). Doxorubicin is most effective when cells are rapidly proliferating and expressing high levels of TOP2. Additionally, Doxorubicin can trigger apoptosis by producing ceramide (which prompts apoptosis by activating p53 or other downstream pathways such as JNK), the degradation of Akt by serine threonine proteases, the mitochondrial release of cytochrome c, increased FasL (death receptor Fas/CD95 ligand) mRNA production, and a greater production of free radicals. ^[2] Pre-treatment with GSNO (nitrosoglutathione) suppresses the resistance in the doxorubicin-resistant breast cancer cell line MCF7/Dx, accompanied by enhanced protein glutathionylation and accumulation of doxorubicin in the nucleus. ^[3] Doxorubicin induced G2/M checkpoint arrest are attributed to elevated cyclin G2 (CycG2) expression and phospho-modification of proteins in the ataxia telangiectasia mutated (ATM) and ATM and Rad3-related (ATR) signaling pathways. ^[5] Doxorubicin inhibits AMP-activated protein kinase (AMPK), resulting in SIRT1 dysfunction, p53 accumulation, and increased cell death in mouse embryonic fibroblasts (MEFs) and cardiomyocytes, which can be further sensitized by pre-inhibition of AMPK. ^[6] Doxorubicin elicits a marked heat shock response, and that either inhibition or silencing of heat shock proteins enhance the Doxorubicin apoptotic effect in neuroblastoma cells. Nanomolar Doxorubicin treatment of neuroblastoma cells causes dose-dependent over-ubiquitination of a specific set of proteins in the absence of measurable inhibition of proteasome, and loss of activity of ubiquitinated enzymes such as lactate dehydrogenase and α-enolase, the protein ubiquination patterns of which is similar to those with proteasome inhibitor Bortezomib, indicating that Doxorubicin may also exert its effect by damaging proteins. ^[8]
in vivo	In vivo, Doxorubicin in combination with adenoviral MnSOD (AdMnSOD) plus 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) has the greatest effect in decreasing the volumes of MB231 tumors and prolonging survival of mice. ^[1] Although its use is limited by the chronic and acute toxic side effects it produces, Doxorubicin is essential in treating breast and oesophageal carcinomas, solid tumours in childhood, osteosarcomas, Kaposi's sarcoma, soft tissue sarcomas, and Hodgkin and non-Hodgkin lymphomas. ^[2]

製品説明

ドキソルビチン塩酸塩 (Doxorubicin (Adriamycin, NSC 123127, DOX, Hydroxydaunorubicin) HCl) は抗生物質の一種であり、DNA トポイソメラーゼ (topoisomerase) II を阻害することで DNA 損傷を引き起こし、がん細胞中においてマイトファジー (mitophagy) およびアポトーシス (apoptosis) を誘導します。ドキソルビシンは AMPK の基底状態におけるリン酸化を減弱します。また、ドキソルビシンは HIV 感染患者の併用療法において使用されますが、同時に HBV 再活性化のリスクを伴うことが分かっています。This product may precipitate when dissolved in PBS solution. It is recommended to prepare the stock solution in pure water and dilute with either pure water or saline to obtain the working solution.

in vitro

Doxorubicin, an antibiotic anthracycline, is commonly considered to exert its anti-tumor activity at two fundamental levels, altering DNA and producing free radicals to trigger apoptosis of cancer cells through DNA damage. Doxorubicin can block the synthesis of DNA by intercalating into the DNA strand, and inhibits DNA topoisomerase II (TOP2). Doxorubicin is most effective when cells are rapidly proliferating and expressing high levels of TOP2. Additionally, Doxorubicin can trigger apoptosis by producing ceramide (which prompts apoptosis by activating p53 or other downstream pathways such as JNK), the degradation of Akt by serine threonine proteases, the mitochondrial release of cytochrome c, increased FasL (death receptor Fas/CD95 ligand) mRNA production, and a greater production of free radicals. ^[2]

Pre-treatment with GSNO (nitrosoglutathione) suppresses the resistance in the doxorubicin-resistant breast cancer cell line MCF7/Dx, accompanied by enhanced protein glutathionylation and accumulation of doxorubicin in the nucleus. ^[3]

Doxorubicin induced G2/M checkpoint arrest are attributed to elevated cyclin G2 (CycG2) expression and phospho-modification of proteins in the ataxia telangiectasia mutated (ATM) and ATM and Rad3-related (ATR) signaling pathways. ^[5]

Doxorubicin inhibits AMP-activated protein kinase (AMPK), resulting in SIRT1 dysfunction, p53 accumulation, and increased cell death in mouse embryonic fibroblasts (MEFs) and cardiomyocytes, which can be further sensitized by pre-inhibition of AMPK. ^[6]

Doxorubicin elicits a marked heat shock response, and that either inhibition or silencing of heat shock proteins enhance the Doxorubicin apoptotic effect in neuroblastoma cells. Nanomolar Doxorubicin treatment of neuroblastoma cells causes dose-dependent over-ubiquitination of a specific set of proteins in the absence of measurable inhibition of proteasome, and loss of activity of ubiquitinated enzymes such as lactate dehydrogenase and α-enolase, the protein ubiquination patterns of which is similar to those with proteasome inhibitor Bortezomib, indicating that Doxorubicin may also exert its effect by damaging proteins. ^[8]

in vivo

In vivo, Doxorubicin in combination with adenoviral MnSOD (AdMnSOD) plus 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) has the greatest effect in decreasing the volumes of MB231 tumors and prolonging survival of mice. ^[1]

Although its use is limited by the chronic and acute toxic side effects it produces, Doxorubicin is essential in treating breast and oesophageal carcinomas, solid tumours in childhood, osteosarcomas, Kaposi's sarcoma, soft tissue sarcomas, and Hodgkin and non-Hodgkin lymphomas. ^[2]

プロトコル(参考用のみ)

細胞アッセイ	細胞株	ID8 cells
	濃度	5 uM
	反応時間	24 h
	実験の流れ	Parental ID8 or erastin-resistant ID8 cells were treated with different concentrations of doxorubicin for 24 hours.
動物実験	動物モデル	Female athymic nude mice injected s.c. with MB231 cells
	投薬量	3 mg/kg/day
	投与方法	Delivered intratumorly

参考

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カスタマーフィードバック

: Data from [Cancer Res, 2014, 74, 298-308]

: Data from [Data independently produced by PLoS One, 2014, 9, e94309]

: Data independently produced by , 2014, Dr Milica Pesic from Institute for Biological Research

Selleckの高級品が、幾つかの出版された研究調査結果（以下を含む）で使われた：

A novel role for the ROS-ATM-Chk2 axis mediated metabolic and cell cycle reprogramming in the M1 macrophage polarization [ Redox Biol, 2024, 70:103059]	PubMed: 38316066
An oncolytic vaccinia virus encoding hyaluronidase reshapes the extracellular matrix to enhance cancer chemotherapy and immunotherapy [ J Immunother Cancer, 2024, 12(3)e008431]	PubMed: 38458640
Neutrophil extracellular traps mediate cardiomyocyte ferroptosis via the Hippo-Yap pathway to exacerbate doxorubicin-induced cardiotoxicity [ Cell Mol Life Sci, 2024, 81(1):122]	PubMed: 38456997
miR-218-5p and doxorubicin combination enhances anticancer activity in breast cancer cells through Parkin-dependent mitophagy inhibition [ Cell Death Discov, 2024, 10(1):149]	PubMed: 38514650
EFNB1 levels determine distinct drug response patterns guiding precision therapy for B-cell neoplasms [ iScience, 2024, 27(1):108667]	PubMed: 38155773
Cooperative sensing of mitochondrial DNA by ZBP1 and cGAS promotes cardiotoxicity [ Cell, 2023, 186(14):3013-3032.e22]	PubMed: 37352855
SRCAP mutations drive clonal hematopoiesis through epigenetic and DNA repair dysregulation [ Cell Stem Cell, 2023, 10.1016/j.stem.2023.09.011]	PubMed: 37863054
A CRISPR-drug perturbational map for identifying compounds to combine with commonly used chemotherapeutics [ Nat Commun, 2023, 14(1):7332]	PubMed: 37957169
High-throughput deconvolution of 3D organoid dynamics at cellular resolution for cancer pharmacology with Cellos [ Nat Commun, 2023, 14(1):8406.]	PubMed: 38114489
Executioner caspases restrict mitochondrial RNA-driven Type I IFN induction during chemotherapy-induced apoptosis [ Nat Commun, 2023, 14(1):1399]	PubMed: 36918588

長期の保管のために-20°Cの下で製品を保ってください。

人間や獣医の診断であるか治療的な使用のためにでない。

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