2. Cell Cycle/DNA Damage Cytoskeleton Apoptosis Autophagy Epigenetics Metabolic Enzyme/Protease Immunology/Inflammation NF-κB Anti-infection
  3. Microtubule/Tubulin Apoptosis Autophagy Caspase PARP Reactive Oxygen Species (ROS) Bacterial
  4. 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.

For research use only. We do not sell to patients.

Viriditoxin

Viriditoxin Chemical Structure

CAS No. : 1381782-08-6

Size Stock
50 mg   Get quote  
100 mg   Get quote  
250 mg   Get quote  

* Please select Quantity before adding items.

This product is a controlled substance and not for sale in your territory.

Viriditoxin Related Antibodies

Top Publications Citing Use of Products

View All Caspase Isoform Specific Products:

View All Isoforms
Caspase 1 Caspase 2 Caspase 3 Caspase 4 Caspase 5 Caspase 6 Caspase 7 Caspase 8 Caspase 9 Caspase 10 Caspase 12 Caspase Caspase 11 Caspase-13

View All PARP Isoform Specific Products:

View All Isoforms
PARP PARP1 PARP2 PARP3 PARP4 TNKS1/PARP5A TNKS2/PARP5B PARP7 PARP10 PARP14 PARP15 PARP12 PARP16

  • Biological Activity

  • Purity & Documentation

  • References

  • Customer Review

Description

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[1][2][3][4][5][6].

In Vitro

Viriditoxin (10-100 µM; 1 h) promotes the polymerization of purified porcine brain tubulin in vitro[1].
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].
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 (0-40 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].
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].
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].
Viriditoxin (0.0002-200 μg/mL; 15 min) potently inhibits the polymerization of fluorescein-labeled *E. coli* FtsZT65C protein, with a mean IC50 value of 8.2 μg/mL[3].
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].
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].
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].
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].
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].
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 (0.01-100 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].
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].
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].

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

Viriditoxin Related Antibodies

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.
Molecular Weight

662.60

Formula

C34H30O14
CAS No.
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
Structure Classification
Initial Source

Aspergillus viridinutans
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
  • No file chosen (Maximum size is: 1024 Kb)
  • If you have published this work, please enter the PubMed ID.
  • Your name will appear on the site.

Viriditoxin Related Classifications

  • Molarity Calculator

  • Dilution Calculator

The molarity calculator equation

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

Mass   Concentration   Volume   Molecular Weight *
= × ×

The dilution calculator equation

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
× = ×
C1   V1   C2   V2
Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Viriditoxin1381782-08-6(-)-ViriditoxinMicrotubule/TubulinApoptosisAutophagyCaspasePARPReactive Oxygen Species (ROS)Bacterialpoly ADP ribose polymeraseEscherichia colileukemia cellsFtsZtubulinmitochondrial electron transport chain complex ISK-OV-3 human ovarian cancer cellsCandida albicansGram-positive bacterialymphoma cellsLNCaP human prostate cancer cellsInhibitorinhibitorinhibit

Your Recently Viewed Products:

Inquiry Online

Your information is safe with us. * Required Fields.

Product Name

  

Requested Quantity *

Applicant Name *

 

Salutation

Email Address *

 

Phone Number *

Department

 

Organization Name *

City

State

Country or Region *

      

Remarks

Bulk Inquiry

Inquiry Information

Product Name:
Viriditoxin
Cat. No.:
HY-126051
Quantity:
MCE Japan Authorized Agent:

Customer Review

Thank You for Your Feedback!

Request for HNMR Report

Please fill out this form to request the QC report. We will send it to your Email address shortly.

Your information is safe with us. * Required Fields.

Product Name

  

Lot #

Applicant Name *

 

Email Address *

Phone Number

 

Department *

Organization Name *

 

Country or Region *

Remarks

SAFETY DATA SHEET (SDS)

Request for HNMR Report

We have received your request and will respond to you as soon as possible.