1. Cell Cycle/DNA Damage
    Antibody-drug Conjugate/ADC Related
    PI3K/Akt/mTOR
    Epigenetics
    Autophagy
    Apoptosis
    Anti-infection
  2. Topoisomerase
    ADC Cytotoxin
    AMPK
    Autophagy
    Apoptosis
    HIV
    HBV
    Mitophagy
    Bacterial
    Antibiotic
  3. Doxorubicin hydrochloride

Doxorubicin hydrochloride (Synonyms: Hydroxydaunorubicin hydrochloride)

目录号: HY-15142 纯度: 99.47%
产品使用指南

Doxorubicin hydrochloride (Hydroxydaunorubicin hydrochloride) 是一种有细胞毒性的蒽环类抗生素,常用作肿瘤化疗剂。Doxorubicin hydrochloride 抑制拓扑异构酶 II (topoisomerase-II),IC50 为 2.67 μM,从而抑制 DNA 复制。Doxorubicin hydrochloride 下调 AMPK 的基础磷酸化以及下游 acetyl-CoA 羧化酶。Doxorubicin hydrochloride 诱导凋亡 (apoptosis) 和自噬 (autophagy)。Doxorubicin hydrochloride 抑制人 DNA 拓扑异构酶 I (topoisomerase I),IC50 为 0.8 μM。

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Doxorubicin hydrochloride Chemical Structure

Doxorubicin hydrochloride Chemical Structure

CAS No. : 25316-40-9

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Free Sample (0.1-0.5 mg)   Apply now  
10 mM * 1  mL in DMSO ¥990 In-stock
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Customer Review

Top Publications Citing Use of Products

MCE 顾客使用本产品发表的科研文献

    Doxorubicin hydrochloride purchased from MCE. Usage Cited in: Nat Med. 2016 May;22(5):547-56.

    Immunofluorescent staining for α-actinin (ACTN2) and cardiac troponin T (TNNT2) to demonstrate sarcomeric organization in hiPSC–CMs derived from patients who do not experience Doxorubicin–induced cardiotoxicity (DOX) versus those who do experience Doxorubicin-induced cardiotoxicity (DOXTOX) after 24 h treatment with Doxorubicin. Scale bar, 20 µm.

    Doxorubicin hydrochloride purchased from MCE. Usage Cited in: Nat Commun. 2018 Oct 8;9(1):4139.

    One hour after treated with UV or 2 h after treated with MMS, Camptothecin (CPT) (10 μM), or Doxorubicin (DOX; 0.5 μM), HEK293T cells expressing HA-SUMO2 and His-RhoB are subjected to sumoylation assay to detect the SUMO2 conjugation of RhoB.

    Doxorubicin hydrochloride purchased from MCE. Usage Cited in: Nanoscale Res Lett. 2018 Nov 3;13(1):350.

    HY-15142

    Doxorubicin hydrochloride purchased from MCE. Usage Cited in: Free Radic Biol Med. 2019 Jan;130:557-567.

    Representative pictures of Live/Dead staining of effects of 7,8-DHF on high dose of Dox-induced cell death and MMP reduction of H9c2 cells.
    • 生物活性

    • 实验参考方法

    • 纯度 & 产品资料

    • 参考文献

    Description

    Doxorubicin hydrochloride (Hydroxydaunorubicin hydrochloride), a cytotoxic anthracycline antibiotic, is an anti-cancer chemotherapy agent. Doxorubicin hydrochloride inhibits topoisomerase II with an IC50 of 2.67 μM, thus stopping DNA replication. Doxorubicin hydrochloride reduces basal phosphorylation of AMPK and its downstream target acetyl-CoA carboxylase. Doxorubicin hydrochloride induces apoptosis and autophagy[1][2]. Doxorubicin hydrochloride inhibits human DNA topoisomerase I with an IC50 of 0.8 μM[3].

    IC50 & Target[1][2][3][7]

    Topoisomerase I

    0.8 μM (IC50)

    Topoisomerase II

    2.67 μM (IC50)

    Daunorubicins/Doxorubicins

     

    HIV-1

     

    In Vitro

    Combination of Doxorubicin hydrochloride (Hydroxydaunorubicin hydrochloride) and MK 733 in the highest tested concentrations (2 μM and 10 μM, respectively) kills 97% of the Hela cells[4].
    Doxorubicin hydrochloride also increases exosome release[8].

    In Vivo

    Mice bearing PC3 xenografts are injected with 2, 4 or 8 mg/kg Doxorubicin hydrochloride (Hydroxydaunorubicin hydrochloride) 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].

    Clinical Trial
    Molecular Weight

    579.98

    Formula

    C₂₇H₃₀ClNO₁₁

    CAS No.

    25316-40-9

    SMILES

    COC1=C2C(C(C(C(O)=C(C[C@](C(CO)=O)(O)C[C@@H]3O[C@@]4([H])C[C@H](N)[C@H](O)[C@H](C)O4)C3=C5O)=C5C2=O)=O)=CC=C1.[H]Cl

    Shipping

    Room temperature in continental US; may vary elsewhere.

    Storage

    4°C, protect from light

    *In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

    Solvent & Solubility
    In Vitro: 

    DMSO : 50 mg/mL (86.21 mM; Need ultrasonic)

    H2O : 33.33 mg/mL (57.47 mM; Need ultrasonic)

    Preparing
    Stock Solutions
    Concentration Solvent Mass 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 (protect from 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:

    ——为保证实验结果的可靠性,澄清的储备液可以根据储存条件,适当保存;体内实验的工作液,建议您现用现配,当天使用; 以下溶剂前显示的百
    分比是指该溶剂在您配制终溶液中的体积占比;如在配制过程中出现沉淀、析出现象,可以通过加热和/或超声的方式助溶

    • 1.

      请依序添加每种溶剂: 10% DMSO    40% PEG300    5% Tween-80    45% saline

      Solubility: ≥ 2.5 mg/mL (4.31 mM); Clear solution

      此方案可获得 ≥ 2.5 mg/mL (4.31 mM,饱和度未知) 的澄清溶液。

      以 1 mL 工作液为例,取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中,混合均匀;向上述体系中加入50 μL Tween-80,混合均匀;然后继续加入 450 μL生理盐水定容至 1 mL。

      将 0.9 g 氯化钠,完全溶解于 100 mL ddH₂O 中,得到澄清透明的生理盐水溶液
    • 2.

      请依序添加每种溶剂: 10% DMSO    90% (20% SBE-β-CD in saline)

      Solubility: ≥ 2.5 mg/mL (4.31 mM); Clear solution

      此方案可获得 ≥ 2.5 mg/mL (4.31 mM,饱和度未知) 的澄清溶液。

      以 1 mL 工作液为例,取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中,混合均匀。

      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 MCE 网站选购。
    References
    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 MK 733 (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 (MK 733 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 MK 733 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].

    MCE 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.

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    References

    Purity: 99.47%

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    × = ×
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    Keywords:

    DoxorubicinHydroxydaunorubicinTopoisomeraseADC CytotoxinAMPKAutophagyApoptosisHIVHBVMitophagyBacterialAntibioticAMP-activated protein kinaseHuman immunodeficiency virusHepatitis B virusMitochondrial AutophagyInhibitorinhibitorinhibit

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