Phleomycin
Based on 3 publication(s) in Google Scholar
Phleomycin is a copper-dependent DNA damaging agent and antibiotic with antitumor activity. Phleomycin binds to DNA and produces ROS in the presence of reducing agents (such as dithiothreitol and glutathione), inducing single-strand and double-strand breaks in DNA. Phleomycin can induce cell apoptosis or mutation and is widely used in cancer inhibition, microbial genetic transformation (as a screening marker to improve fungal transformation efficiency) and DNA repair mechanism research.
For research use only. We do not sell to patients.
- Purity : 95.0%
- CAS No.: 11006-33-0
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Storage:
-20°C, stored under nitrogen
* In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)
Publications Citing Use of MedChemExpress (MCE) Phleomycin
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Biological Activity
Description
IC50 & Target
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Glycopeptide |
In Vitro
1. Phleomycin (1-25 μg/mL; overnight) can increase the transformation efficiency by more than 10 times in the protoplast transformation experiment of Schizophyllum commune, promote single copy integration, and upregulate the expression of DNA repair genes KU70 and RAD52[2].
2. Phleomycin (2 μg/mL, 10 μg/mL; 90 min-4 h) selectively inhibits DNA synthesis in Escherichia coli (E. coli) and HeLa cells and reduces 3H-thymidine incorporation into DNA. At 20 μg/mL, the DNA degradation activity is significantly lower than that of Mitomycin C (HY-13316)[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 11006-33-0
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Appearance Solid
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Color Light blue to blue
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SMILES
[Phleomycin]
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Structure Classification
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Initial Source
Streptoalloteichus hindustanus
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
-20°C, stored under nitrogen
* In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)
Publications (3)
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Journal Impact Factor
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Most Recent
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FEMS Yeast Res
Characterization of oncohistone H2B variants in Schizosaccharomyces pombe reveals a key role of H2B monoubiquitination deficiency in genomic instability by altering gene expression. [Abstract]2025 Jan 30:25:foaf027. PMID: 40402811 -
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Genes Cells
SRPKs Homolog Dsk1 Regulates Homologous Recombination Repair in Schizosaccharomyces pombe. [Abstract]2025 Jan;30(1):e13192. PMID: 39789818
Solvent & Solubility
In Vitro:
H2O : 100 mg/mL (Need ultrasonic)
Protocols
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Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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ROS/oxidative-stress fluorescent staining
ROS/oxidative-stress fluorescent staining uses cell-permeant fluorogenic probes that become fluorescent after oxidation inside cells or tissues; commonly used examples include DCFH-DA/DCFDA for broad cellular oxidant detection, DHE for superoxide-related signal detection, MitoSOX for mitochondrial superoxide-related signal detection, and CellROX probes for oxidative-stress-associated fluorescence readouts. The assay detects probe oxidation rather than a single ROS species unless the probe and analysis method have been chemically validated for that species. DCFH-DA enters cells, is deacetylated by intracellular esterases to DCFH, and produces fluorescent DCF after oxidation, so the readout is used as an operational measure of total cellular oxidative stress rather than a species-specific ROS measurement. DHE and MitoSOX can report superoxide-related oxidation, but red fluorescence alone can include non-specific ethidium-like oxidation products; HPLC or optimized spectral approaches are
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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Subcutaneous Cell-Line-Derived Xenograft
Subcutaneous cell-line-derived xenograft (CDX) models are established by implanting cultured human cancer cell lines into immunodeficient mice, where the injected cells form localized tumors that can be monitored in vivo as a measure of tumorigenic potential, growth kinetics, and treatment response. These models are widely used in oncology research because they allow reproducible tumor formation and enable comparative assessment of tumor growth between different cell lines or genetic manipulations in a controlled in vivo microenvironment. Subcutaneous implantation of cancer cells in immunodeficient mice is a standard approach for evaluating tumor growth behavior and therapeutic response across multiple cancer types, including prostate, esophageal, pancreatic, and colon cancer models.
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Genotoxicity/Mutagenicity Study
The bacterial reverse mutation assay detects point mutations that restore amino-acid prototrophy in auxotrophic Salmonella typhimurium or Escherichia coli tester strains; after exposure to a test article, mutagenic activity is read out as an increased number of revertant colonies on minimal agar compared with the vehicle control. The assay uses tester strains with different mutation targets so that base-substitution and frameshift mutagens can be detected, and testing is performed with and without exogenous mammalian metabolic activation because some chemicals require biotransformation to become mutagenic.
Purity & Documentation
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Data Sheet (270 KB)
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SDS (393 KB)
- English - EN (393 KB)
- Français - FR (393 KB)
- Deutsch - DE (393 KB)
- Norwegian - NO (393 KB)
- Español - ES (393 KB)
- Swedish - SV (393 KB)
- Italian - IT (393 KB)
- Korean - KR (393 KB)
- Portuguese - PT (393 KB)
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Handling Instructions (2659 KB)
References
[1]. Kamila Stokowa-Sołtys, et al. Phleomycin complex-Coordination mode and in vitro cleavage of DNA. J Inorg Biochem. 2019 Jun;195:71-82. [Content Brief]
[2]. van Peer AF, et al. Phleomycin increases transformation efficiency and promotes single integrations in Schizophyllum commune. Appl Environ Microbiol. 2009 Mar;75(5):1243-7. [Content Brief]
[3]. TANAKA N, et al. Mechanism of action of phleomycin, a tumor-inhibitory antibiotic. Biochem Biophys Res Commun. 1963 Jan 31;10:171-4. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)