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Actinomycin D

(Synonyms: Cosmegen, Dactinomycin, Meractinomycin, NCI C04682, NSC 3053, Oncostatin K) Catalog No.: GC16866

A DNA-interacting transcription blocker with anti-cancer activity

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Actinomycin D Chemical Structure

Cas No.:50-76-0

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10mM (in 1mL DMSO)
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Sample solution is provided at 25 µL, 10mM.

Product has been cited by 32 publications

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Cell experiment [1]:

Cell lines

A10 cells (Vascular SMC)

Preparation Method

Dissolve actinomycin D in 0.1% DMSO and make 3 different concentration groups: 80 nM, 800 nM, 8 μM. Add various doses of actinomycin D to cultured SMC which have been starved for 24 h and incubate at 37 ℃. Drug treatment is carried out for 18-24 h. In the meantime, a vehicle control containing DMSO is also included.

Reaction Conditions

80 nM, 800 nM, 8 μM for 18-24h


Actinomycin D is a significant polypeptide antibiotic isolated from soil bacteria, Streptomyces. It inhibits DNA repair with IC50 of 0.42 μM and rests the cell cycle at G1 phase with IC50 of 0.4 nM.

Animal experiment [2]:

Animal models

C57BL/6 wild-type mice with Em-TCL-1 transgenic mice tumor cells

Preparation Method

The original Em-TCL1a transgenic mice have been backcrossed to C57BL/6 mice for 9 generations. Tumor cells from Em-TCL-1 transgenic mice were engrafted to C57BL/6 wild-type mice.

Dosage form

0.06 mg/kg, i.p.


Actinomycin D was chosen to further investigate as treatment option for CLL patients high-risk features, due to its activity in p53-aberrant CLL cells, known clinical properties, low IC50 and moderate toxicity. The presence of actinomycin D prevents the release of protective factors from the stroma cells. BCL2 mRNA downregulation in CLL is specific for actinomycin D treatment. Actinomycin D leads to tumor regression in this mouse model of CLL, and in two of four mice renewed lymphoma formation was prevented, strongly suggesting a potent role for actinomycin D in CLL treatment in humans.


[1]. Wu CH, et al. The molecular mechanism of actinomycin D in preventing neointimal formation in rat carotid arteries after balloon injury. J Biomed Sci. 2005;12(3):503-12.

[2]. Merkel O. et al. Actinomycin D induces p53-independent cell death and prolongs survival in high-risk chronic lymphocytic leukemia. Leukemia (2012) 26, 2508–2516.


Actinomycin D (dactinomycin) is a natural chromopeptide isolated from Streptomyces species, and has one heterocyclic chromophore and two cyclic pentapeptide lactone rings. [1] It is the first antibiotic showing anti-tumor activity, and has been implemented in the clinical practice for years to treat, such as testicular cancer, and choriocarcinoma.[2]

Actinomycin D intercalates into DNA to inhibit the transcription. It forms a very stable complex with DNA, preventing the unwinding of the DNA double-helix, so as to inhibit the DNA-dependent RNA polymerase activity. Actinomycin D is well implemented in mRNA stability assays to inhibit the synthesis of new mRNA, allowing the assessment of mRNA decay by measuring mRNA abundance following transcription inhibition. [3]

The in vitro experiment suggests that actinomycin D is an potent and effective agent to inhibit the proliferation of SMC by preventing cells from getting into S phase. The LD50 (260 lM) determined by measuring the remaining viable cells at various concentrations of actinomycin D was about five orders greater than that of IC50 (0.4 nM), which was calculated by measuring the percentage of cells in S phase following the treatment of actinomycin D. A dose-dependent inhibition by actinomycin D was found in PCNA, Raf and FAK. However, in contrast to those seen on PCNA, Raf and FAK expression, the phosphorylated Erk was significantly up-regulated by actinomycin D. An in vivo study using rat carotid artery as a model was conducted to evaluate if topically applied actinomycin D onto the arterial adventitia of the artery was effective in suppressing the formation of stenosis following a balloon angioplasty. Topical application of pluronic gel containing 80 nM and 80 μM actinomycin D to surround the adventitia of rat carotid arteries, the thickness of the neointima was significantly reduced (45% and 55%, respectively). [4]

[1]. Farber S. Chemotherapy in the treatment of leukemia and Wilms' tumor. JAMA. 1966 Nov 21;198(8):826-36. PMID: 4288581.
[2]. Lewis J.L., Jr. Chemotherapy of gestational choriocarcinoma. Obstet. Gynecol. Surv. 1973;28:7478–7480. doi: 10.1097/00006254-197307000-00006.
[3]. Shyu A. B., Greenberg M. E. and Belasco J. G.(1989). The c-fos transcript is targeted for rapid decay by two distinct mRNA degradation pathways. Genes Dev 3(1): 60-72.
[4]. Wu, C. H., Pan, J. S., Chang, W. C., Hung, J. S., & Mao, S. J. T. (2005). The molecular mechanism of actinomycin D in preventing neointimal formation in rat carotid arteries after balloon injury. Journal of Biomedical Science, 12(3), 503–512. doi:10.1007/s11373-005-6900-5.

Chemical Properties

Cas No. 50-76-0 SDF
Synonyms Cosmegen, Dactinomycin, Meractinomycin, NCI C04682, NSC 3053, Oncostatin K
Chemical Name 2-amino-4,6-dimethyl-3-oxo-1-N,9-N-bis[7,11,14-trimethyl-2,5,9,12,15-pentaoxo-3,10-di(propan-2-yl)-8-oxa-1,4,11,14-tetrazabicyclo[14.3.0]nonadecan-6-yl]phenoxazine-1,9-dicarboxamide
Canonical SMILES CC1C(C(=O)NC(C(=O)N2CCCC2C(=O)N(CC(=O)N(C(C(=O)O1)C(C)C)C)C)C(C)C)NC(=O)C3=C4C(=C(C=C3)C)OC5=C(C(=O)C(=C(C5=N4)C(=O)NC6C(OC(=O)C(N(C(=O)CN(C(=O)C7CCCN7C(=O)C(NC6=O)C(C)C)C)C)C(C)C)C)N)C
Formula C62H86N12O16 M.Wt 1255.43
Solubility ≥ 62.75 mg/mL in DMSO Storage Store at -20℃; protected from light
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
Shipping Condition Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request

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Research Update

[Actinomycin D and its mechanisms of action]

Postepy Hig Med Dosw (Online)2005;59:290-8.PMID: 15995596DOI: 10.1080/14786419.2018.1431630

Actinomycin D is a well-known antibiotic of the actinomycin group that exhibits high antibacterial and antitumor activity. Actinomycin D has been widely used in clinical practice since 1954 as an anticancer drug for treating many tumors and it is also a useful tool in biochemistry and molecular biology. According to the Internet bibliographic database -- MEDLINE, actinomycins, and mainly actinomycin D, have been the subject of about 3300 science papers so far, and this paper is a review of the information concerning the mechanisms of action of actinomycin D. There are several mechanisms of its action that are responsible for its cytotoxic and antitumor action, these being associated with DNA functionality, leading to RNA and, consequently, protein synthesis inhibition. The two main mechanisms are intercalation to DNA and the stabilization of cleavable complexes of topoisomerases I and II with DNA, in which a phenoxazone ring localizes between GpC base pair sequence in DNA and polypeptide lactones rings occupy a position in the minor groove of the DNA helix or the drug penetrates to a place in the DNA structure where topoisomerase binds with DNA, respectively. Moreover, the slow dissociation of actinomycin D from DNA complexes, its photodynamic activity and free radical formation, as well as other biochemical effects of activity of actinomycin D may be, as suggested, important factors that influence the biological activity of this drug. In the literature not enough convincing evidence has been proposed that could indicate one particular mechanism of action as responsible for the biological activity of actinomycin D.

Antifungal effects of actinomycin D on Verticillium dahliae via a membrane-splitting mechanism

Nat Prod Res2019 Jun;33(12):1751-1755.PMID: 29382222DOI: 10.1080/14786419.2018.1431630

Antifungal bioassays led to the isolation of actinomycins D and A1 from Streptomyces luteus TRM45540 collected from Norpo in Xinjiang, and these compounds were identified by nuclear magnetic resonance spectroscopy. The antifungal activity of actinomycin D was higher than that of actinomycin A1. Actinomycin D clearly inhibited the spore germination, hyphal growth and biomass accumulation of Verticillium dahliae in a dose-dependent manner. Flow cytometric analysis with propidium iodide, total ergosterol measurement, cell leakage and scanning electron microscopy experiments demonstrated that the plasma membrane of this fungus was damaged by actinomycin D, resulting in swollen cells and cellular content leakage. Transmission electron microscopy revealed that parts of the plasma membrane infolded after being treated with actinomycin D. The antifungal activity of actinomycin D damaged the fungal plasma membrane of V. dahliae via a membrane-splitting mechanism, which provided new insights into the functional mechanism of actinomycin D.

Multi-Omics Analysis Reveals Anti- Staphylococcus aureus Activity of Actinomycin D Originating from Streptomyces parvulus

Int J Mol Sci2021 Nov 12;22(22):12231.PMID: 34830114DOI: 10.3390/ijms222212231

Staphylococcus aureus (S. aureus) is a common pathogen that causes various serious diseases, including chronic infections. Discovering new antibacterial agents is an important aspect of the pharmaceutical field because of the lack of effective antibacterial drugs. In our research, we found that one anti-S. aureus substance is actinomycin D, originating from Streptomyces parvulus (S. parvulus); then, we further focused on the anti-S. aureus ability and the omics profile of S. aureus in response to actinomycin D. The results revealed that actinomycin D had a significant inhibitory activity on S. aureus with a minimum inhibitory concentration (MIC) of 2 μg/mL and a minimum bactericidal concentration (MBC) of 64 μg/mL. Bacterial reactive oxygen species (ROS) increased 3.5-fold upon treatment with actinomycin D, as was measured with the oxidation-sensitive fluorescent probe DCFH-DA, and H2O2 increased 3.5 times with treatment by actinomycin D. Proteomics and metabolomics, respectively, identified differentially expressed proteins in control and treatment groups, and the co-mapped correlation network of proteomics and metabolomics annotated five major pathways that were potentially related to disrupting the energy metabolism and oxidative stress of S. aureus. All findings contributed to providing new insight into the mechanisms of the anti-S. aureus effects of actinomycin D originating from S. parvulus.

[Modifications of actinomycin D structure as example of actinomycins structure-activity relationship]

Postepy Hig Med Dosw (Online)2005;59:276-82.PMID: 15995594DOI: 10.3802/jgo.2019.30.e87

For over 60 years, actinomycins, well-known antibacterial and anticancer antibiotics, have been the subject of the scientific research. These compounds exhibit high toxicity and therefore are not widely used in the chemotherapeutic treatment of antibacterial and antifungal diseases. However, actinomycin D, the best-known compound from the actinomycin group, has been introduced into clinical practice as an anticancer drug. Actinomycin D, together with 7-amino-actinomycin D, also became a useful tool in biochemistry and molecular biology. The isolation, production, chemistry, and biological and clinical use of the actinomycins have been thoroughly investigated. Many derivatives of actinomycins, differing in chemical structure as well as biological activity, have been isolated and synthesized and their modifications involved not only the chromphoric phenoxazone ring, but also two cyclic pentapeptide lacton rings. Modifications of the actinomycins' chromophore mainly concerned introducing an amino group in position 2 and a carbon atom in position 7, but also modifications in positions 4, 6, and 8 of the phenoxazone ring. The actinomycin peptide moiety was mainly modified by replacement of amino acids in the pentapeptide rings and also by the synthesis of actinomycin derivatives with open peptide lacton rings. These modifications enabled separating the elements in the actinomycin structure which are responsible for the biological activity of these compounds. That was key information for recognizing the performance of these compounds, and an important way of planning effective new chemotherapeutics.

Actinomycin D shortage in the Brazilian market: new challenges for successful treatment of gestational trophoblastic neoplasia

J Gynecol Oncol2019 Jul;30(4):e87.PMID: 31074249DOI: 10.3802/jgo.2019.30.e87

Objective: To compare the treatment outcome and cost-effectiveness of pulsed actinomycin D (Act-D) and 5-day Act-D in patients with low-risk gestational trophoblastic neoplasia (GTN).
Method: The present retrospective study included patients with low-risk GTN who received pulsed Act-D or 5-day Act-D as first-line chemotherapy at West China Second Hospital, Chengdu, China, between January 1, 2016, and December 31, 2017. Complete remission rates, mean number of treatment courses, and adverse events were compared, and a cost-effectiveness analysis was performed.
Results: The study included 34 patients treated with pulsed Act-D and 26 patients treated with 5-day Act-D. Overall complete remission was observed in 21 (62%) patients in the pulsed Act-D group and 19 (73%) patients in the 5-day Act-D group (P=0.355); the mean number of treatment courses were 5.1 and 5.3, respectively (P=0.686). When Act-D failed, patients in each group required 4.9 and 4.6 courses, respectively, of a multi-agent regimen (P=0.545). No major adverse events were observed but moderate adverse events were more frequent in the pulsed Act-D group (P=0.011). The 5-day Act-D regimen was more expensive compared with pulsed Act-D regimen (US$7504.33 vs $5541.79), with an incremental cost-effectiveness ratio of $64 557.08 per avoidance of treatment failure.
Conclusion: Pulsed Act-D was more cost-effective than 5-day Act-D and could be preferred when considering Act-D as chemotherapy for low-risk GTN.


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