Art. -Nr.: HY-126051

Viriditoxin

Name: Viriditoxin
Brand: MedChemExpress
SKU: HY-126051
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(Synonyms: (-)-Viriditoxin)

Viriditoxin ((-)-Viriditoxin) is a mycotoxin. Viriditoxin promotes tubulin polymerization, and inhibits FtsZ polymerization and GTPase activity. Viriditoxin exhibits cytotoxicity against cancer cells, induces apoptosis, inhibits cell migration and colony formation, induces G₂/M phase arrest, and triggers autophagic cell death. Viriditoxin activates caspase-3, cleaves PARP, promotes cytochrome c release, and induces ROS production. Viriditoxin possesses broad-spectrum antibacterial activity against Gram-positive pathogenic bacteria, fish pathogenic bacteria, and permeabilized Gram-negative bacteria. Viriditoxin can be used in research related to ovarian cancer, lung cancer, nasopharyngeal carcinoma, colon cancer, neuroblastoma, prostate cancer, leukemia, lymphoma, bacterial infections, and streptococcosis.

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CAS. Nr.: 1381782-08-6
Formel: C₃₄H₃₀O₁₄
Molecular Weight:662.60

Speicherung:

Please store the product under the recommended conditions in the Certificate of Analysis.

Viriditoxin Chemical Structure

CAS. Nr.: 1381782-08-6

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Biologische Aktivität
- Beschreibung
- In Vitro
Chemical Information
Reinheit & Dokumentation
Verweise
Calculators
Help & FAQs
Classifications
Bioz

Biologische Aktivität

Beschreibung

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In Vitro

Anti-cancerApoptosisAutophagyCell Cycle RegulationCell ViabilityMitochondrial FunctionEnergy MetabolismOxidative StressBacterial InfectionFungal InfectionMicrotubule RegulationOthers

Anti-cancer

Viriditoxin (0.048-30 µM; 24 h) inhibits the viability of SK-OV-3 cells with an IC₅₀ of 14.3 µM, and induces characteristic cytotoxic morphological changes^[1].
Viriditoxin (0.05-20 μM; 24-48 h) inhibits the proliferation of LNCaP, DU145 and PC3 cells, with the strongest inhibitory activity against LNCaP cells (48 h IC₅₀ = 0.63 μM)^[2].

Anti-cancer

Apoptosis

Viriditoxin (0.01-30 μM; 8-24 h) activates the mitochondrial apoptotic pathway independently of Bcl-2 overexpression and the presence of Bax/Bak, but its induction of apoptosis in leukemia/lymphoma cells requires the involvement of caspase-9^[5].
Viriditoxin (0.01-30 μM; 8-24 h) potently induces caspase-dependent apoptosis in Ramos and Jurkat cells with a rapid kinetic process: it activates caspase-3, cleaves PARP, and increases the number of apoptotic nuclei in a dose-dependent manner at 3-5 h^[5].

Anti-cancer

Apoptosis

Autophagy

Cell Cycle Regulation

Viriditoxin (0.1-1 μM; 48 h) induces G₂/M phase arrest in LNCaP cells, increases the proportion of cells in the sub-G₁ phase, and is accompanied by altered expression of key cell cycle regulatory proteins. It also mildly induces apoptosis, triggers autophagic cell death, and induces mitotic catastrophe^[2].

Anti-cancer

Apoptosis

Cell Cycle Regulation

Viriditoxin (0-40 µM; 24 h) induces concentration-dependent G2/M phase arrest, concentration-dependent apoptosis, and inhibits migration and colony formation in SK-OV-3 cells^[1].

Anti-cancer

Cell Viability

Viriditoxin (0.01-100 μM; 5 min-72 h) potently induces cytotoxicity in human leukemia and lymphoma cell lines, with IC₅₀ values ranging from 0.04 μM (72 h, Ramos) to 1.66 μM (24 h, K562), and even a short exposure of only 5 minutes causes irreversible cell death in Ramos cells^[5].

Anti-cancer

Mitochondrial Function

Energy Metabolism

Viriditoxin (0.01-10 μM; 15 min-24 h) impairs mitochondrial respiratory function in leukemia cells by inhibiting the activity of ETC complex I and reducing the expression of key ETC subunits, thereby leading to decreases in ATP levels and oxygen consumption^[5].

Anti-cancer

Mitochondrial Function

Oxidative Stress

Viriditoxin (0.01-100 μM; 5 min-24 h) impairs the structure and function of mitochondria in leukemia/lymphoma cells, triggering rapid collapse of membrane potential, cytochrome c release, OPA1 cleavage, mitochondrial fragmentation, and ROS production, with its cytotoxicity partially mediated by ROS^[5].

Bacterial Infection

Viriditoxin (0.16-0.21 mg/mL) potently inhibits the growth of Gram-positive fish pathogens Streptococcus iniae, Streptococcus parauberis, as well as the human pathogen Staphylococcus aureus, with MIC values ranging from 0.16 to 0.21 mg/mL, but shows no activity against the Gram-negative fish pathogen Vibrio ichthyoenteri strains^[6].
Viriditoxin (12.5-100 μg/mL; 75 min) induces filament formation in permeabilized, SulA-deficient E. coli MB5431 cells, indicating that it inhibits bacterial cell division^[3].

Bacterial Infection

Fungal Infection

Viriditoxin (2-32 μg/mL; 20-24 h) exhibits broad-spectrum antibacterial activity against Gram-positive pathogens (including drug-resistant strains), inhibits permeabilized E. coli MB5431 at a concentration of 25 μg/mL, and shows no cytotoxicity against Candida albicans or HeLa cells at concentrations >64 μg/mL and >66.7 μg/mL, respectively^[3].

Microtubule Regulation

Anti-cancer

Viriditoxin (0-100 µM; 24 h) converts soluble tubulin into polymerized particulate fractions in SK-OV-3 cells in a concentration-dependent manner, enhances tubulin polymerization and stabilizes microtubules in SK-OV-3 cells, leading to the formation of dense pericytoplasmic microtubule structures and disorganized perinuclear microtubule bundles^[1].

Others

Viriditoxin (0.0002-200 μg/mL; 15 min) potently inhibits the polymerization of fluorescein-labeled *E. coli* FtsZ^T65C protein, with a mean IC₅₀ value of 8.2 μg/mL^[3].
Viriditoxin (10-100 µM; 1 h) promotes the polymerization of purified porcine brain tubulin in vitro^[1].
Viriditoxin (200 μg/mL; 120 min) inhibits the GTPase activity of wild-type and luciferase-labeled *Escherichia coli* FtsZ protein, with an average IC₅₀ of 7.0 μg/mL^[3].

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

Western Blot Analysis^[1]

Cell Line:

SK-OV-3 human ovarian cancer cells
Concentration:

10, 25, 50 µM
Incubation Time:

24 h
Result:

Induced a concentration-dependent shift of soluble tubulin to the particulate (polymerized) fraction, similar to the microtubule-stabilizing effect of paclitaxel.

Immunofluorescence^[1]

Cell Line:

SK-OV-3 human ovarian cancer cells
Concentration:

15 µM (24 h incubation); 100 µM (1 h and 4 h incubation)
Incubation Time:

1 h, 4 h, 24 h
Result:

Increased microtubule density and formed long, thick, disarrayed microtubule bundles surrounding the nucleus after treatment with 100 µM for 4 h.
Enhanced tubulin polymerization with highly dense microtubule linings close to the cell membrane after 24 h at 15 µM, distinct from the multipolar spindles induced by paclitaxel.

Cell Viability Assay^[1]

Cell Line:

SK-OV-3 human ovarian cancer cells
Concentration:

0.048, 0.24, 1.2, 6, 30 µM
Incubation Time:

24 h
Result:

Inhibited SK-OV-3 cell viability in a dose-dependent manner, with an IC50 value of 14.3 µM.
Induced morphological changes including cytoplasmic shrinkage, cellular flattening, and rugged cell peripheries with fragments.

Cell Cycle Analysis^[1]

Cell Line:

SK-OV-3 human ovarian cancer cells
Concentration:

5, 10, 20, 40 µM
Incubation Time:

24 h
Result:

Increased the population of SK-OV-3 cells in the G2/M phase in a concentration-dependent manner (from 17.6% at 5 µM to 27.2% at 40 µM).
Decreased the G0/G1 population (from 70.7% at 5 µM to 52.0% at 40 µM).
Increased the S phase population (from 7.6% at 5 µM to 12.0% at 40 µM).

Apoptosis Analysis^[1]

Cell Line:

SK-OV-3 human ovarian cancer cells
Concentration:

5, 10, 20, 40 µM
Incubation Time:

24 h
Result:

Induced a concentration-dependent increase in early and late apoptotic cell death: at 40 µM, live cells decreased to 76.0%, early apoptosis increased to 10.9%, and late apoptosis increased to 11.0%.

Cell Migration Assay ^[1]

Cell Line:

SK-OV-3 human ovarian cancer cells
Concentration:

2.5, 5, 10 µM
Incubation Time:

24 h
Result:

Inhibited SK-OV-3 cell migration in a concentration-dependent manner; at 10 µM, migration was significantly reduced relative to controls.

Cell Viability Assay^[2]

Cell Line:

human prostate cancer LNCaP, DU145, and PC3 cell lines
Concentration:

0.05, 0.1, 0.5, 1, 5, 10, 20 μM
Incubation Time:

24 h; 48 h
Result:

Inhibited the growth of all three prostate cancer cell lines in a concentration- and time-dependent manner.
Exhibited IC₅₀ values of 14.84 μM for LNCaP cells, 18.47 μM for DU145 cells, and 18.72 μM for PC3 cells after 24 h treatment.
Showed decreased IC₅₀ values of 0.63 μM for LNCaP cells, 5.36 μM for DU145 cells, and 7.60 μM for PC3 cells after 48 h treatment.
Induced morphological changes including cytoplasmic shrinkage and cellular flattening in LNCaP cells after 48 h.

Cell Cycle Analysis^[2]

Cell Line:

human prostate cancer LNCaP cells
Concentration:

0.1, 0.5, 1 μM
Incubation Time:

48 h
Result:

Significantly increased the percentage of LNCaP cells in the G2/M phase and decreased the percentage of cells in the S phase in a concentration-dependent manner.
Increased the proportion of cells in the sub-G1 phase, an indicator of apoptosis.
Decreased expression levels of cyclin A, cyclin B1, and Cdc2, while increasing expression of cyclin E, Cdk2, p27, p53, and p21 in a concentration-dependent manner.

Apoptosis Analysis^[2]

Cell Line:

human prostate cancer LNCaP cells
Concentration:

0.1, 0.5, 1 μM
Incubation Time:

48 h
Result:

Caused only a slight concentration-dependent increase in apoptotic cell death, most noticeable at the highest viriditoxin concentration.
Revealed an increase in apoptotic nuclei with condensed or fragmented chromatin compared to untreated controls via DAPI staining.
Increased expression levels of cleaved PARP, Bax, cytochrome c, and cleaved caspase-3, while decreasing Bcl-2 expression in LNCaP cells at high concentrations.

Cell Autophagy Assay^[2]

Cell Line:

human prostate cancer LNCaP cells
Concentration:

0.1, 0.5, 1 μM
Incubation Time:

48 h
Result:

Significantly increased the level of LC3-II and increased expression of autophagy initiation proteins beclin-1, Atg5, and Atg7 in a concentration-dependent manner via western blot analysis.
Induced a concentration-dependent increase in red fluorescent acidic vesicular organelles, confirmed by flow cytometric analysis showing increased red fluorescence intensity.

Related Protocols :

Chemical Information

CAS. Nr. 1381782-08-6
Molecular Weight 662.60
Formel C₃₄H₃₀O₁₄
SMILES

O=C1OC(CC(=O)OC)CC2=CC3=C(C(O)=CC(OC)=C3C4=C(OC)C=C(O)C=5C(O)=C6C(=O)OC(CC(=O)OC)CC6=CC54)C(O)=C12
Synonyms

(-)-Viriditoxin
Structure Classification
- Phenols
- Polyphenols
Initial Source
- Microorganism
Aspergillus viridinutans
Versand

Room temperature in continental US; may vary elsewhere.
Speicherung

Please store the product under the recommended conditions in the Certificate of Analysis.

Reinheit & Dokumentation

Handling Instructions (2659 KB)

Verweise

[1]. Su M, et al. Viriditoxin Stabilizes Microtubule Polymers in SK-OV-3 Cells and Exhibits Antimitotic and Antimetastatic Potential. Marine drugs. 2020 Aug 27;18(9):445. [Content Brief]

[2]. Kundu S, et al. Viriditoxin regulates apoptosis and autophagy via mitotic catastrophe and microtubule formation in human prostate cancer cells. International journal of oncology. 2014 Dec;45(6):2331-40. [Content Brief]

[3]. Wang J, et al. Discovery of a small molecule that inhibits cell division by blocking FtsZ, a novel therapeutic target of antibiotics. The Journal of biological chemistry. 2003 Nov 07;278(45):44424-8. [Content Brief]

[4]. Grove CI, et al. Second-Generation Synthesis of (-)-Viriditoxin. Synthesis. 2012;2012(3):362-371. [Content Brief]

[5]. Stuhldreier F, et al. The mycotoxin viriditoxin induces leukemia- and lymphoma-specific apoptosis by targeting mitochondrial metabolism. Cell death & disease. 2022 Nov 08;13(11):938. [Content Brief]

[6]. Noh TH, et al. Antibacterial activities of viriditoxin congeners and synthetic analogues against fish pathogens. Bioorganic & medicinal chemistry letters. 2017 Nov 15;27(22):4970-4974. [Content Brief]

Calculators

Molaritätsrechner

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Konzentration Konzentration

Volumen Volumen

Molecular Weight Molecular Weight

Verdünnungsrechner

Konzentration _{(Stammlösung)} × Volumen _{(Stammlösung)} = Konzentration _{(Ziellösung)} × Volumen _{(Ziellösung)}

Konzentration _{(Stammlösung)} Konzentration _{(Stammlösung)}

Volumen _{(Stammlösung)} Volumen _{(Stammlösung)}

Konzentration _{(Ziellösung)} Konzentration _{(Ziellösung)}

Volumen _{(Ziellösung)} Volumen _{(Ziellösung)}

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

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Viriditoxin

Alle Caspase Isoform-spezifische Produkte anzeigen

Alle PARP Isoform-spezifische Produkte anzeigen

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Chemical Information

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Verweise

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Viriditoxin

Alle Caspase Isoform-spezifische Produkte anzeigen

Alle PARP Isoform-spezifische Produkte anzeigen

Biologische Aktivität

Beschreibung

In Vitro

Chemical Information

Reinheit & Dokumentation

Verweise

Calculators

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Viriditoxin Related Classifications

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