Doxorubicin (Adriamycin) HCl

For research use only. Not for use in humans.

Licensed by Pfizer 製品コードS1208 別名:NSC 123127, DOX, Doxorubicin hydrochloride, Hydroxydaunorubicin HCl

Doxorubicin (Adriamycin) HCl化学構造

CAS No. 25316-40-9

Doxorubicin (Adriamycin, NSC 123127, DOX, Hydroxydaunorubicin) HCl is an antibiotic agent that inhibits DNA topoisomerase II and induces DNA damage, mitophagy and apoptosis in tumor cells. Doxorubicin reduces basal phosphorylation of AMPK. Doxorubicin is used in the concomitant treatment of HIV-infected patients but is found to be at high risk of HBV reactivation.

サイズ 価格(税別)  
10mM (1mL in DMSO) JPY 21400
JPY 16900
JPY 36800
JPY 113200
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製品安全説明書

Antineoplastic and Immunosuppressive Antibiotics阻害剤の選択性比較

生物活性

製品説明 Doxorubicin (Adriamycin, NSC 123127, DOX, Hydroxydaunorubicin) HCl is an antibiotic agent that inhibits DNA topoisomerase II and induces DNA damage, mitophagy and apoptosis in tumor cells. Doxorubicin reduces basal phosphorylation of AMPK. Doxorubicin is used in the concomitant treatment of HIV-infected patients but is found to be at high risk of HBV reactivation.
ターゲット
AMPK [6]
()
Topo II [1]
(Tumor cells)
体外試験

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]

細胞データ
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
L1210 MlfiSpVv[3Srb36gRZN{[Xl? M2WxRmlvcGmkaYTpc44hd2ZiUl7BJJN6dnSqZYPpd{B4cXSqIFXEOVAhd2ZiMD61PEDPxE1? NWW1TJRuRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxNEmwOVM3Lz52OUC1N|Y9N2F-
Yoshida sarcoma M3;6fWZ2dmO2aX;uJGF{e2G7 MWTJcohq[mm2aX;uJI9nKFt|SG3U[HIhcW6lb4Lwc5JifGmxbjD3bZRpKEmFNUCgc4YhOC5yMjFOwG0> MUi8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8yOzJ{OUi2K|4yOzJ{OUi2QE9iRg>?
CHO MVPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYq5eYlEUUN3ME2wMlA3KM7:TR?= NWrqNXpDRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMUO1OFc2OCd-MUO1OFc2ODxxYU6=