| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 5mg | 电议 |
| 10mg | 电议 |
| 50mg | 电议 |
| 500mg | 电议 |
| 1g | 电议 |
Actinomycin D (dactinomycin)是一种从链霉菌属中分离出来的天然色肽，具有一个杂环发色团和两个环状五肽内酯环。
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 |
Applications | 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 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. |
Applications | 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. |
| 文献引用 |
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| 产品描述 | 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] Reference: |
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