Doxorubicin (Hydroxydaunorubicin) hydrochloride是一种具有细胞毒性的蒽环类抗生素，是一种抗癌化疗试剂。Doxorubicin hydrochloride 是一种有效的人类 DNA topoisomerase I 和 topoisomerase II 抑制剂，IC50 分别为 0.8 μM 和 2.67 μM。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 (apoptosis) 和自噬。
Doxorubicin hydrochloride Chemical Structure
CAS No. : 25316-40-9
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10 mM * 1 mL in DMSO
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生物活性
Doxorubicin (Hydroxydaunorubicin) hydrochloride, a cytotoxic anthracycline antibiotic, is an anti-cancer chemotherapy agent. Doxorubicin hydrochloride is a potent human DNA topoisomerase I and topoisomerase II inhibitor with IC50s of 0.8 μM and 2.67 μM, respectively. Doxorubicin hydrochloride reduces basal phosphorylation of AMPK and its downstream target acetyl-CoA carboxylase. Doxorubicin hydrochloride induces apoptosis and autophagy[1][2][3].
IC50 & Target[1][2][3]
Topoisomerase II
2.67 μM (IC50)
Daunorubicins/Doxorubicins
Topoisomerase I
0.8 μM (IC50)
HIV-1
体外研究 (In Vitro)
Doxorubicin hydrochloride (1-8 µM; 24 and 48 hours) decreases the viability of MCF-10F, MCF-7 and MDA-MB-231 cells in a time- and dose-dependent manner[4]. Doxorubicin hydrochloride (1 μM; 3 and 24 hours) results in Hct-116 human colon carcinoma cells reduction in G0/G1 phase and accumulation in G2 phase[5]. Doxorubicin hydrochloride (1 μM for MCF-10F and MDA-MB-231 cells, 4 μM for MCF-7 cells; 48 hours) induces apoptosis by upregulating Bax, caspase-8 and caspase-3 and downregulation of Bcl-2 protein expression[4].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Viability Assay[4]
Cell Line:
Breast cancer cell lines MCF-10F, MCF-7 and MDA-MB-231
Concentration:
0, 1, 2, 4 and 8 μM
Incubation Time:
24 and 48 hours
Result:
IC50 was 1 μM for both MCF-10F and MDA-MB-231 cell lines. IC50 was 4 μM for MCF-7 cell line.
Cell Cycle Analysis[5]
Cell Line:
Hct-116 human colon carcinoma cells
Concentration:
1 μM
Incubation Time:
3 hours and 24 hours
Result:
Both, bolus (3 h) and continuous (24 h) incubation led to a significant reduction of cells in G0/G1 and accumulation in G2 phase.
Western Blot Analysis[4]
Cell Line:
Breast cancer cell lines MCF-10F, MCF-7 and MDA-MB-231
Concentration:
1 μM for MCF-10F and MDA-MB-231 cells, 4 μM for MCF-7 cells
Incubation Time:
48 hours
Result:
Bax protein expression was upregulated in MCF-10F and MDA-MB-231 cell lines but MCF-7 cells did not show any significant increase. Caspase-8 gene expression was upregulated in MCF-10F, but it was downregulated in MCF-7 and MDA-MB-231 cells.
体内研究 (In Vivo)
Treatment with Doxorubicin (2 mg/kg) or Zoledronic acid (100 μg/kg) alone does not statistically significantly decrease final tumor volume compared with saline. Mice treated with Doxorubicin plus Zoledronic acid have statistically significantly smaller final tumor volumes than those treated with Doxorubicin alone[6].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Female MF1 nu/nu mice bearing MDA-G8 breast tumor xenograft (6-week-old)[6]
Moderate inhibition of subcutaneous tumor growth in mice that were treated with 2 mg/kg Doxorubicin alone or with 100 μg/kg Zoledronic acid alone compared to the saline control. Mice treated with Zoledronic acid and Doxorubicin together had statistically significant smaller mean tumor volumes on day 42 than those treated with Doxorubicin alone.
Clinical Trial
分子量
579.98
Formula
C27H30ClNO11
CAS 号
25316-40-9
中文名称
盐酸阿霉素；盐酸多柔比星
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
4°C, sealed storage, away from moisture and light
*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
溶解性数据
In Vitro:
DMSO : 35.71 mg/mL (61.57 mM; ultrasonic and warming and heat to 60°C)
H2O : 20 mg/mL (34.48 mM; Need ultrasonic)
配制储备液
浓度溶剂体积质量
1 mg
5 mg
10 mg
1 mM
1.7242 mL
8.6210 mL
17.2420 mL
5 mM
0.3448 mL
1.7242 mL
3.4484 mL
10 mM
0.1724 mL
0.8621 mL
1.7242 mL
*
请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。
In Vivo:
请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：
将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
*以上所有助溶剂都可在 上海金畔生物科技有限公司 网站选购。
参考文献
[1]. John L. Nitiss, et al. Targeting DNA topoisomerase II in cancer chemotherapy.Nat Rev Cancer. 2009 May;9(5):338-50.
[2]. Hee-KyungRhee,et al. Synthesis, cytotoxicity, and DNA topoisomerase II inhibitory activity of benzofuroquinolinediones. Bioorg Med Chem. 2007 Feb 15;15(4):1651-8.
[3]. P D Foglesong, et al. Doxorubicin inhibits human DNA topoisomerase I. Cancer Chemother Pharmacol. 1992;30(2):123-5.
[4]. Nesstor Pilco-Ferreto, et al. Influence of doxorubicin on apoptosis and oxidative stress in breast cancer cell lines. Int J Oncol. 2016 Aug;49(2):753-62.
[5]. Regine Lüpertz, et al. Dose- and time-dependent effects of doxorubicin on cytotoxicity, cell cycle and apoptotic cell death in human colon cancer cells. Toxicology. 2010 May 27;271(3):115-21.
[6]. Penelope D Ottewell, et al. Antitumor effects of doxorubicin followed by zoledronic acid in a mouse model of breast cancer. J Natl Cancer Inst. 2008 Aug 20;100(16):1167-78.
Doxorubicin (Hydroxydaunorubicin) 是一种有细胞毒性的蒽环类抗生素，常用作肿瘤化疗剂。Doxorubicin 抑制拓扑异构酶 II (topoisomerase-II)，IC50 为 2.67 μM，从而抑制 DNA 复制。Doxorubicin 下调 AMPK 的基础磷酸化以及下游 acetyl-CoA 羧化酶。Doxorubicin 诱导凋亡 (apoptosis) 和自噬 (autophagy)。Doxorubicin 抑制人 DNA 拓扑异构酶 I (topoisomerase I)，IC50 为 0.8 μM。
Doxorubicin Chemical Structure
CAS No. : 23214-92-8
规格
是否有货
5 mg
询价
10 mg
询价
25 mg
询价
* Please select Quantity before adding items.
生物活性
Doxorubicin (Hydroxydaunorubicin), a cytotoxic anthracycline antibiotic, is an anti-cancer chemotherapy agent. Doxorubicin inhibits topoisomerase II with an IC50 of 2.67 μM, thus stopping DNA replication. Doxorubicin reduces basal phosphorylation of AMPK and its downstream target acetyl-CoA carboxylase. Doxorubicin induces apoptosis and autophagy[1][2]. Doxorubicin inhibits human DNA topoisomerase I with an IC50 of 0.8 μM[3].
IC50 & Target[1][2][3][7]
Topoisomerase II
2.67 μM (IC50)
Daunorubicins/Doxorubicins
Topoisomerase I
0.8 μM (IC50)
HIV-1
体外研究 (In Vitro)
Combination of Doxorubicin (Hydroxydaunorubicin) and Simvastatin in the highest tested concentrations (2 μM and 10 μM, respec-tively) kills 97% of the Hela cells[4].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
Mice bearing PC3 xenografts are injected with 2, 4 or 8 mg/kg Doxorubicin (Hydroxydaunorubicin) and tumor volume is measured over time. A dose of 2 mg/kg does not affect tumor growth while higher dosages delay tumor growth initially (p<0.05 at days 18 and 22), 4 mg/kg or 8 mg/kg Doxorubicin significantly reduces levels of c-FLIP in PC3 xenografts[5]. A single intraperitoneal injection 10 mg/kg (Doxorubicin 1) is administered in rats, 10 daily intraperitoneal injections of 1 mg/kg (Doxorubicin 2), or in 5 weekly intraperitoneal injections of 2 mg/kg (Doxorubicin 3). An 80% mortality rate is observed at day 28 in Doxorubicin 1, whereas Doxorubicin 2 and Doxorubicin 3 reached 80% mortality at days 107 and 98, respectively. Fractional shortening decreased by 30% at week 2 in Doxorubicin DOX1, 55% at week 13 in Doxorubicin 2, and 42% at week 13 in Doxorubicin 3[6].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
543.52
Formula
C27H29NO11
CAS 号
23214-92-8
中文名称
阿霉素；多柔比星
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
溶解性数据
In Vivo:
1.
Doxorubicin (dissolved with distilled water) is incorporated into 0.035% CaCl2 solution[5].
2.
Doxorubicin (Adriamycin) is prepared in vehicle (PBS)[6].
参考文献
[1]. Nitiss JL, et al. Targeting DNA topoisomerase II in cancer chemotherapy.Nat Rev Cancer. 2009 May;9(5):338-50.
[2]. Rhee HK, et al. Synthesis, cytotoxicity, and DNA topoisomerase II inhibitory activity of benzofuroquinolinediones. Bioorg Med Chem. 2007 Feb 15;15(4):1651-8.
[3]. Foglesong PD, et al. Doxorubicin inhibits human DNA topoisomerase I. Cancer Chemother Pharmacol. 1992;30(2):123-5.
[4]. Sadeghi-Aliabadi H, et al. Cytotoxic evaluation of doxorubicin in combination with simvastatin against human cancer cells. Res Pharm Sci. 2010 Jul;5(2):127-33.
[5]. El-Zawahry A, et al. Doxorubicin increases the effectiveness of Apo2L/TRAIL for tumor growth inhibition of prostate cancerxenografts. BMC Cancer. 2005 Jan 7;5:2.
[6]. Hayward R, et al. Doxorubicin cardiotoxicity in the rat: an in vivo characterization. J Am Assoc Lab Anim Sci. 2007 Jul;46(4):20-32.
[7]. Johansson S, et al. Elimination of HIV-1 infection by treatment with a doxorubicin-conjugated anti-envelope antibody. AIDS. 2006;20(15):1911-1915.
Cell Assay [4]
160 μL of Hela cells suspension (3×104 cell/mL) is dispensed into three 96-well U-bottom microplates and incubated for 24 h at 37°C in a fully humidified atmosphere of 5% CO2. In plate 1, serial dilutions of Doxorubicin (20 μL; final concentration, 0.1-2 μM) and Simvastatin (20 μL; final concentration, 0.25-2 μM) are added to a final volume of 200 μL and incubated for another 72 h. In plates 2 and 3 serial dilutions of each drug (Simvastatin or Doxorubicin, 40 μL) are added. After an incubation period of 24 h, the medium is aspirated and the cells are washed in PBS. Then, serial dilutions of other drug (40 μL) are added and supplemented with culture medium to a final volume of 200 μL, and incubated for 48 h. Doxorubicin and Simvastatin are used individually as positive controls (40 μL in each well), and the cells treated only with solvent are considered as negative controls. To evaluate cell survival, 20 μL of MTT solution (5 mg/mL in PBS) is added to each well and incubated for 3 h. Then the media is replaced with 150 μL of DMSO, and complete solubilization of formazan crystals is achieved by repeated pipetting of the solution. Absorbance is then determined at 540 nm by an ELISA plate reader. Each drug concentration is assayed in 4 or 8 wells and repeated 3 times. The cytotoxic/cytostatic effect of Doxorubicin is expressed as the relative viability (% control) and calculated. Percentage of cell survival in the negative control is assumed as 100. Relative viability=(experimental absorbance-background absorbance)/ (absorbance of untreated controls-background absorbance)×100 %[4].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration [5][6]
Mice[5] 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 initated 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 intra-tumorally or systemically. All treatments are given once. Mice are monitored daily for signs of adverse effects (listlessness and scruffy apparance). 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. Rats[6] Thirty male Sprague-Dawley rats weighing 250 to 300 g are randomly assigned to 1 of 3 experimental groups: Doxorubicin schedule 1 (Doxorubicin 1, n=10), Doxorubicin schedule 2 (Doxorubicin 2, n=10), or Doxorubicin schedule 3 (Doxorubicin 3, n=10). For all Doxorubicin treatment schedules, the cumulative dose of Doxorubicin is 10 mg/kg. Schedule 1 involves a single bolus intraperitoneal injection of Doxorubicin at 10 mg/kg. Schedule 2 involves 10 intraperitoneal injections of Doxorubicin at 1 mg/kg for 10 consecutive days. Schedule 3 involves 5 intraperitoneal injections of Doxorubicin at 2 mg/kg, once each week, for 5 wk. Immediately before the first Doxorubicin treatment and at weekly intervals after beginning Doxorubicin treatment, blood pressure and cardiac function are assessed in all surviving animals as long as there are at least 3 rats per group.
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Nitiss JL, et al. Targeting DNA topoisomerase II in cancer chemotherapy.Nat Rev Cancer. 2009 May;9(5):338-50.
[2]. Rhee HK, et al. Synthesis, cytotoxicity, and DNA topoisomerase II inhibitory activity of benzofuroquinolinediones. Bioorg Med Chem. 2007 Feb 15;15(4):1651-8.
[3]. Foglesong PD, et al. Doxorubicin inhibits human DNA topoisomerase I. Cancer Chemother Pharmacol. 1992;30(2):123-5.
[4]. Sadeghi-Aliabadi H, et al. Cytotoxic evaluation of doxorubicin in combination with simvastatin against human cancer cells. Res Pharm Sci. 2010 Jul;5(2):127-33.
[5]. El-Zawahry A, et al. Doxorubicin increases the effectiveness of Apo2L/TRAIL for tumor growth inhibition of prostate cancerxenografts. BMC Cancer. 2005 Jan 7;5:2.
[6]. Hayward R, et al. Doxorubicin cardiotoxicity in the rat: an in vivo characterization. J Am Assoc Lab Anim Sci. 2007 Jul;46(4):20-32.
[7]. Johansson S, et al. Elimination of HIV-1 infection by treatment with a doxorubicin-conjugated anti-envelope antibody. AIDS. 2006;20(15):1911-1915.
Nemorubicin (Methoxymorpholinyl doxorubicin) is a Doxorubicin derivative with potent antitumor activity. Nemorubicin is highly cytotoxic to a variety of tumor cell lines presenting a multidrug-resistant phenotype. Nemorubicin requirs an intact nucleotide excision repair (NER) system to exert its activity[1][2][3][4].
体外研究 (In Vitro)
Nemorubicin has antitumor activity, with IC70s of 578 nM, 468 nM, 193 nM, 191 nM, 68 nM, and 131 ± 9 nM for HT-29, A2780, DU145, EM-2, Jurkat and CEM cell lines, respectively[1]. Nemorubicin is CYP3A-activated anticancer prodrug, which can produce a more cytotoxic metabolite, PNU-159682[1][2]. Nemorubicin acts through nucleotide excision repair (NER) system to exert its activity. Nemorubicin (0-0.3 μM) is more active in the L1210/DDP cells with intact NER than in the XPG-deficient L1210/0 cells. Cells resistant to nemorubicin show increased sensitivity to UV damage[3]. Nemorubicin is cytotoxic to 9L/3A4 cells, with an IC50 of 0.2 nM, 120-fold lower than that of P450-deficient 9L cells (IC50, 23.9 nM). Nemorubicin also potently inhibits Adeno-3A4 infected U251 cells with IC50 of 1.4 nM. P450 reductase overexpression enhances cytotoxicity of Nemorubicin[4].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
Nemorubicin is converted to PNU-159682 by human liver cytochrome P450 (CYP) 3A4 in rat, mouse, and dog liver microsomes[2]. Nemorubicin (60 µg/kg) induces sifnificant tumor growth delay in scid mice bearing 9L/3A4 tumors, but shows no obvious effect on the tumor growth delay of 9L tumors in mice by i.v. or intratumoral injection (i.t.). Nemorubicin (40 µg/kg, i.p.) exhibits no antitumor activity and no host toxicity in mice bearing 9L/3A4 tumors[4].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
643.64
Formula
C32H37NO13
CAS 号
108852-90-0
中文名称
奈莫柔比星
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Quintieri L, et al. Formation and antitumor activity of PNU-159682, a major metabolite of nemorubicin in human liver microsomes. Clin Cancer Res. 2005 Feb 15;11(4):1608-17.
[2]. Quintieri L, et al. In vitro hepatic conversion of the anticancer agent nemorubicin to its active metabolite PNU-159682 in mice, rats and dogs: a comparison with human liver microsomes. Biochem Pharmacol. 2008 Sep 15;76(6):784-95.
[3]. Sabatino MA, et al. Down-regulation of the nucleotide excision repair gene XPG as a new mechanism of drug resistance in human and murine cancer cells. Mol Cancer. 2010 Sep 24;9:259.
[4]. Lu H, et al. Potentiation of methoxymorpholinyl doxorubicin antitumor activity by P450 3A4 gene transfer. Cancer Gene Ther. 2009 May;16(5):393-404.
Cell Assay [4]
9L and CHO cells are plated in triplicate wells of a 96-well plate at 3000 cells per well 24 hr prior to drug treatment. Cells are treated with various concentrations of Nemorubicin or IFA for 4d. Cells are then stained with crystal violet (A595) and relative cell survival is calculated. IC50 values are determined from a semi-logarithmic graph of the data points using Prism 4[4].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration [4]
9L and 9L/3A4 cells are grown as solid tumors in male ICR/Fox Chase SCID mice. Cells cultured in DMEM medium to 75% confluence are trypsinized and washed in PBS and then adjusted to 2 × 107 cells/mL of FBS-free DMEM. Four-week-old SCID mice (18-20 g) are implanted with either 9L or 9L/3A4 tumor cells by injection of 4 × 106 cells/0.2 mL of cell suspension, s.c. on each hind flank. Tumor sizes (length and width) are measured twice a week using Vernier calipers beginning 7d after tumor implantation. When the average tumor size reach 300 to 400 mm3, Nemorubicin dissolved in PBS is administered by tail vein injection (i.v.) or by direct intratumoral (i.t.) injection (three injections spaced 7 d apart, each at 60 µg Nemorubicin per kg body weight). Intratumoral injections are performed using a syringe pump set a 1 µL/s with a 30-gauge needle. Each i.t. treatment dose is divided into three injections per tumor, with the injected volume set at 50 µL per tumor per 25 g mouse. Thus, for a 30 g mouse, a total of 120 µL of 15 µg/mL of Nemorubicin solution is administered: 20 µL per site × 3 sites per tumor × 2 tumors/mouse. Drug-free controls are injected i.t. with the same vol of PBS. In some experiments, Nemorubicin is administered by i.p. injection at 40 or 60 µg/kg body weight. Tumor sizes and body weights are measured twice/wk for the duration of the study. Tumor volumes are calculated using the formula: V = π/6 (L × W)3/2. Percent tumor regression is calculated as 100 × (V1-V2)/V1, where V1 is the tumor vol on the day of drug treatment and V2 is the vol on the day when the largest the decrease in tumor size is seen following drug treatment. Tumor doubling time is calculated as the time required for tumors to double in vol after drug treatment[4].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Quintieri L, et al. Formation and antitumor activity of PNU-159682, a major metabolite of nemorubicin in human liver microsomes. Clin Cancer Res. 2005 Feb 15;11(4):1608-17.
[2]. Quintieri L, et al. In vitro hepatic conversion of the anticancer agent nemorubicin to its active metabolite PNU-159682 in mice, rats and dogs: a comparison with human liver microsomes. Biochem Pharmacol. 2008 Sep 15;76(6):784-95.
[3]. Sabatino MA, et al. Down-regulation of the nucleotide excision repair gene XPG as a new mechanism of drug resistance in human and murine cancer cells. Mol Cancer. 2010 Sep 24;9:259.
[4]. Lu H, et al. Potentiation of methoxymorpholinyl doxorubicin antitumor activity by P450 3A4 gene transfer. Cancer Gene Ther. 2009 May;16(5):393-404.
Doxorubicin PEG DSPE is one of Nanocs' bioactive phospholipid conjugates that can be used to make bioactive liposomes. Doxorubicin is a water soluble anthracyclin antibiotic used in the treatment of a wide range of cancers. Doxorubicin inhibits DNA and RNA but not protein synthesis in intact cells. DSPE PEG conjugated Doxorubicin can be used to make pegylated liposome that prolongs the circulation time of doxorubicin in blood.
