1. Cell Cycle/DNA Damage
  2. DNA/RNA Synthesis
  3. Actinomycin D

Actinomycin D (Synonyms: Dactinomycin; Actinomycin IV)

Cat. No.: HY-17559 Purity: 99.58%
Handling Instructions

Actinomycin D inhibits DNA repair with an IC50 of 0.42 μM.

For research use only. We do not sell to patients.

Actinomycin D Chemical Structure

Actinomycin D Chemical Structure

CAS No. : 50-76-0

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5 mg USD 50 In-stock
Estimated Time of Arrival: December 31
10 mg USD 80 In-stock
Estimated Time of Arrival: December 31
50 mg USD 280 In-stock
Estimated Time of Arrival: December 31

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Customer Review

Based on 38 publication(s) in Google Scholar

Top Publications Citing Use of Products

Publications Citing Use of MCE Actinomycin D

    Actinomycin D purchased from MCE. Usage Cited in: Cancer Lett. 2017 Oct 28;407:45-56.

    UM-SCC6 and UM-SCC6H cells are treated with Actinomycin D (ActD 5 μg/mL) for the indicated times. The IGF2 mRNA level is measured by RT-PCR.

    Actinomycin D purchased from MCE. Usage Cited in: Cell Death Dis. 2019 May 21;10(6):395.

    • Biological Activity

    • Protocol

    • Purity & Documentation

    • References

    • Customer Review


    Actinomycin D inhibits DNA repair with an IC50 of 0.42 μM.

    IC50 & Target

    IC50: 0.42 μM (DNA repair)[1]

    In Vitro

    Actinomycin D is an inhibitor of DNA transcription and replication[1]. Actinomycin D markedly reduces the vascular smooth muscle cells (SMC) proliferation via the inhibition of BrdU incorporation at 80 nM. This is further supported by the G1-phase arrest using a flowcytometric analysis. Actinomycin D is extremely potent with an inhibitory concentration IC50 at 0.4 nM, whereas the lethal dose LD50 is at 260 microM. The protein expression levels of proliferating cell nuclear antigen (PCNA), focal adhesion kinase (FAK), and Raf are all suppressed by Actinomycin D. Extracellular signal-regulated kinases (Erk) involved in cell-cycle arrest are found to increase by Actinomycin D[2].

    In Vivo

    The pluronic gel containing 80 nM and 80 μM Actinomycin D is applied topically to surround the rat carotid adventitia, the thickness of neointima is substantially reduced (45 and 55%, respectively)[2]. Mice in the Actinomycin D and fludarabine group lives significantly longer than the control group with P values of <0.001 and 0.007, respectively. Interestingly, single treatment with Actinomycin D is superior to fludarabine regarding overall survival (P=0.026)[3].

    Clinical Trial
    Molecular Weight




    CAS No.



    O=C(C1=C(N)C(C(C)=C2OC3=C(N=C21)C(C(N[[email protected]@H]4C(N[[email protected]@H](C(C)C)C(N5[[email protected]](CCC5)([H])C(N(C)CC(N(C)[[email protected]@H](C(C)C)C(O[[email protected]@H]4C)=O)=O)=O)=O)=O)=O)=CC=C3C)=O)N[[email protected]@H]6C(N[[email protected]@H](C(C)C)C(N7[[email protected]](CCC7)([H])C(N(C)CC(N(C)[[email protected]@H](C(C)C)C(O[[email protected]@H]6C)=O)=O)=O)=O)=O


    Room temperature in continental US; may vary elsewhere.


    4°C, stored under nitrogen

    *In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)

    Solvent & Solubility
    In Vitro: 

    DMSO : ≥ 27 mg/mL (21.51 mM)

    H2O : < 0.1 mg/mL (insoluble)

    *"≥" means soluble, but saturation unknown.

    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 0.7965 mL 3.9827 mL 7.9655 mL
    5 mM 0.1593 mL 0.7965 mL 1.5931 mL
    10 mM 0.0797 mL 0.3983 mL 0.7965 mL
    *Please refer to the solubility information to select the appropriate solvent.
    In Vivo:
    • 1.

      Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% saline

      Solubility: ≥ 2.08 mg/mL (1.66 mM); Clear solution

    • 2.

      Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in saline)

      Solubility: 2.08 mg/mL (1.66 mM); Suspended solution; Need ultrasonic

    *All of the co-solvents are provided by MCE.
    Kinase Assay

    Actinomycin D is co-incubated for 3 h at 30°C with a reaction mixture containing: 120 mg of a whole-cell extract of HeLa cells, 70 mM KCl, 0.4 mM each of dGTP, dCTP, dATP, and digoxygenylated-dUTP in reaction buffer containing 40mM Hepes-KOH (pH 7.6), 5 mM MgCl2, 0.5 mM Dithiotreitol, 2 mM EGTA, 10 mM phosphocreatine, 50 mg/mL creatine phosphate, and 360 mg/mL of bovine serum albumin. During this reaction, DNA damage is recognized and the excised patches are replaced by neosynthesized DNA fragments. Throughout this DNA synthesis, digoxygenylated-dUMPs are incorporated. The DNA repair reaction is stopped by three washes[1].

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

    Animal Administration

    The original Eμ-TCL1a transgenic mice have been backcrossed to C57BL/6 mice for >9 generations.The C57BL/6 wild-type mice are engrafted with tumor cells from Eμ-TCL-1 transgenic mice. The percentage of CD5+/CD19+ cells in the peripheral blood is routinely checked in mice by taking blood from the tail vein and analyzing it via flow cytometry. When the percentage of tumor cells in the peripheral blood reached 40-60%, treatment is started. Actinomycin D (0.06 mg/kg by 10 days) is applied daily via i.p. injections.

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


    Purity: 99.58%

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    Actinomycin DDactinomycinActinomycin IVDNA/RNA SynthesisAutophagyInhibitorinhibitorinhibit

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