Actinomycin D - CAS50-76-0 Catalog number: BADC-00798

Actinomycin D - CAS50-76-0 Catalog number: BADC-00798

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Actinomycin D is a chromopeptide antineoplastic antibiotic that exhibits high antibacterial and antitumor activity. Actinomycin D binds to single- and double-stranded DNA and subsequent inhibition of RNA and protein synthesis.

ADCs Cytotoxin
Product Name
Actinomycin D
Catalog Number
Molecular Formula
Molecular Weight
Actinomycin D

Ordering Information

Catalog Number Size Price Quantity
BADC-00798 50 mg $298
BADC-00798 100 mg $629
Actinomycin D is a chromopeptide antineoplastic antibiotic that exhibits high antibacterial and antitumor activity. Actinomycin D binds to single- and double-stranded DNA and subsequent inhibition of RNA and protein synthesis.
Actinomycin; Cosmegen; Cosmegen Lyovac; Dactinomycin; Lyovac Cosmegen
Canonical SMILES
1.42 g/cm3
Soluble in water
Melting Point
3.21 at pH 7.4
Vapor Pressure
0 mm Hg at 25 °C (est)
Mechanism Of Action
Good evidence exists that this drug bind strongly, but reversibly, to DNA, interfering with synthesis of RNA (prevention of RNA polymerase elongation) and, consequently, with protein synthesis.
Generally, the actinomycins exert an inhibitory effect on gram-positive and gram-negative bacteria and on some fungi. However, the toxic properties of the actinomycins (including dactinomycin) in relation to antibacterial activity are such as to preclude their use as antibiotics in the treatment of infectious diseases. Because the actinomycins are cytotoxic, they have an antineoplastic effect which has been demonstrated in experimental animals with various types of tumor implant. This cytotoxic action is the basis for their use in the treatment of certain types of cancer. Dactinomycin is believed to produce its cytotoxic effects by binding DNA and inhibiting RNA synthesis.
Toxicity (LD50)
In Vitro
A dramatic decrease in anti-apoptotic myeloid leukemia cell differentiation protein (Mcl-1) mRNA and protein expression was detected upon actinomycin D treatment. Further, Mcl-l over-expression caused resistance to cell death upon treatment with actinomycin D, implicating a role for the down-regulation of Mcl-1 in actinomycin D-induced apoptosis. Actinomycin D sensitized cells to ABT-737 treatment in a Bak- or Bax-dependent manner. Importantly, low concentrations of actinomycin D and ABT-737 were more effective in inducing cell death in transformed cells than their untransformed counterparts. A synergistic effect of actinomycin D and ABT-737 on cell death was observed in several human tumor cell lines. Like actinomycin D treatment, knocking down Mcl-1 expression greatly sensitized tumor cells to ABT-737, and Mcl-1 over-expression abrogated the cytotoxic effect induced by ABT-737 and actinomycin D. These results suggest that the down-regulation of Mcl-1 by actinomycin D is likely responsible for the observed synergistic effect between the two drugs.
In Vivo
In an in vivo study, the pluronic gel containing 80 nM and 80 microM actinomycin D was applied topically to surround the rat carotid adventitia; the thickness of neointima was substantially reduced (45 and 55%, respectively). The protein expression levels of proliferating cell nuclear antigen (PCNA), focal adhesion kinase (FAK), and Raf were all suppressed by actinomycin D. Extracellular signal-regulated kinases (Erk) involved in cell-cycle arrest were found to increase by actinomycin D.
Clinical Trial Information
NCT NumberCondition Or DiseasePhaseStart DateSponsorStatus
NCT00003688Gestational Trophoblastic TumorPhase 22013-06-10Gynecologic Oncology GroupCompleted
NCT01823315Gestational Trophoblastic DiseasePhase 32019-12-24Ding MaActive, not recruiting
NCT00075582Adult RhabdomyosarcomaPhase 32021-11-19Children's Oncology GroupCompleted
NCT04562558Gestational Trophoblastic TumorNot Applicable2021-11-16xiang yangRecruiting
NCT00900354Unspecified Childhood Solid Tumor, Protocol Specific2013-08-12Children's Cancer and Leukaemia GroupUnknown Verified June 2009 by National Cancer Institute (NCI). Recruitment status was Recruiting
Red Crystalline Powder
Shelf Life
Dilute soln are very sensitive to light /Trihydrate/;Soln should not be exposed to direct sunlight
Room temperature
Store at -20°C
Acute Toxic; Health Hazard
Signal Word
Boiling Point
1386°C at 760 mmHg
1. Actinomycin D: a novel Pseudomonas aeruginosa quorum sensing inhibitor from the endophyte Streptomyces cyaneochromogenes RC1
Shi Tang, Ying-Jie Wang, Yue-Xiang Zeng, Da-Yong Wang, Jun-Sheng Liu, Ai-Qun Jia, Shi-Ming Deng World J Microbiol Biotechnol . 2022 Jul 29;38(10):170. doi: 10.1007/s11274-022-03360-y.
The infections caused by Pseudomonas aeruginosa are difficult to treat due to its multidrug resistance. A promising strategy for controlling P. aeruginosa infection is targeting the quorum sensing (QS) system. Actinomycin D isolated from the metabolite of endophyte Streptomyces cyaneochromogenes RC1 exhibited good anti-QS activity against P. aeruginosa PAO1. Actinomycin D (50, 100, and 200 μg/mL) significantly inhibited the motility as well as reduced the production of multiple virulence factors including pyocyanin, protease, rhamnolipid, and siderophores. The images of confocal laser scanning microscopy and scanning electron microscopy revealed that the treatment of actinomycin D resulted in a looser and flatter biofilm structure. Real-time quantitative PCR analysis showed that the expression of QS-related genes lasI, rhlI, rhlR, pqsR, pslA, and pilA were downregulated dramatically. The production of QS signaling molecules N-(3-oxododecanoyl)-L-homoserine lactone and N-butanoyl-L-homoserine lactone were also decreased by actinomycin D. These findings suggest that actinomycin D, a potent in vitro anti-virulence agent, is a promising candidate to treat P. aeruginosa infection by interfering with the QS systems.
2. [Modifications of actinomycin D structure as example of actinomycins structure-activity relationship]
Marcin Koba Postepy Hig Med Dosw (Online) . 2005;59:276-82.
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.
3. Antifungal effects of actinomycin D on Verticillium dahliae via a membrane-splitting mechanism
Chuan-Xing Wan, Hong Zeng, Pei-Xian Feng Nat Prod Res . 2019 Jun;33(12):1751-1755. doi: 10.1080/14786419.2018.1431630.
Antifungal bioassays led to the isolation of actinomycins D and A1fromStreptomyces luteusTRM45540 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 ofVerticillium dahliaein 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 ofV. dahliaevia a membrane-splitting mechanism, which provided new insights into the functional mechanism of actinomycin D.
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