Cytochalasin B

Cytochalasin B
Product Name Cytochalasin B
CAS No.: 14930-96-2
Catalog No.: CFN96781
Molecular Formula: C29H37NO5
Molecular Weight: 479.61 g/mol
Purity: >=98%
Type of Compound: Alkaloids
Physical Desc.: Powder
Targets: VEGFR | DNA/RNA Synthesis | TNF-α
Source: The seed culture of solid wheat.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Price:
Cytochalasin B is a phytotoxin, it induces membrane vesicles convey angiogenic activity of parental cells, and triggers a novel pertussis toxin sensitive pathway in TNF-alpha primed neutrophils. Cytochalasin B can exert its inhibitory effect on DNA synthesis by inhibiting glucose transport.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

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The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    CAS No: 14930-96-2
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    Oncotarget. 2017 Jul 31;8(41):70496-70507.
    Cytochalasin B-induced membrane vesicles convey angiogenic activity of parental cells.[Pubmed: 29050297 ]
    Naturally occurring extracellular vesicles (EVs) play essential roles in intracellular communication and delivery of bioactive molecules. Therefore it has been suggested that EVs could be used for delivery of therapeutics. However, to date the therapeutic application of EVs has been limited by number of factors, including limited yield and full understanding of their biological activities.
    METHODS AND RESULTS:
    To address these issues, we analyzed the morphology, molecular composition, fusion capacity and biological activity of Cytochalasin B-induced membrane vesicles (CIMVs). The size of these vesicles was comparable to that of naturally occurring EVs. In addition, we have shown that CIMVs from human SH-SY5Y cells contain elevated levels of VEGF as compared to the parental cells, and stimulate angiogenesis in vitro and in vivo.
    Biocontrol Science & Technology, 2014, 24(1):53-64.
    Effect of strain and cultural conditions on the production of cytochalasin B by the potential mycoherbicide Pyrenophora semeniperda (Pleosporaceae, Pleosporales).[Reference: WebLink]
    The seed pathogen Pyrenophora semeniperda has demonstrated potential as a mycoherbicidal biocontrol for eliminating persistent seed banks of annual bromes on western North American rangelands. This pathogen exhibits variation in virulence that is related to mycelial growth rate, but direct laboratory tests of virulence on seeds often have low repeatability.
    METHODS AND RESULTS:
    We developed a rapid and sensitive high pressure liquid chromatography method for quantification of the phytotoxin Cytochalasin B in complex mixtures in order to evaluate its use in virulence screening. All 10 strains tested produced large quantities of this metabolite in solid wheat seed culture, with production varying over a fourfold range (535–2256 mg kg−1). No Cytochalasin B was produced in liquid potato dextrose broth culture, showing that its synthesis is strongly dependent on cultural conditions. In a Bromus tectorum coleoptile bioassay, solid culture extracts showed mild toxicity similar to the Cytochalasin B standard at a concentration equivalent to 10−4 M Cytochalasin B (72–95% of control), whereas at 10−3 M equivalent, the extracts exhibited significantly higher toxicity (8–18% of control) than the Cytochalasin B standard (34% of control).
    CONCLUSIONS:
    This suggests the possible presence of other phytotoxic metabolites. Cytochalasin B production in solid wheat seed culture exhibited the predicted significant negative correlation with mycelial growth rate on potato dextrose agar, but the correlation was not very strong, possibly because Cytochalasin B production and growth rate were measured under different cultural conditions.
    Nature, 1978, 272(5651):359-359.
    Cytochalasin B inhibits lymphocyte transformation through its effects on glucose transport[Reference: WebLink]
    The effects of the fungal metabolite, Cytochalasin B, on lymphocyte transformation induced by mitogenic plant Jectins have been much studied1–7. Results have generally been interpreted in terms of the known effects of Cytochalasin B on the microfilaments of the cellular cytoskeleton. A potential site of action which has been largely ignored lies in the inhibitory effects of Cytochalasin B on metabolite transport.
    METHODS AND RESULTS:
    Cytochalasin B is a potent, competitive inhibitor of erythrocyte glucose transport8, and we have shown that it also inhibits thymocyte glucose transport, and that concanavalin A-stimulated glucose transport is more sensitive to this inhibition9. Glucose transport has been shown to be rate-limiting for thymocyte glycolysis10. Also, glucose has been found to be essential for mitogen-stimulated DNA synthesis in lymphocytes11, and we show here that Cytochalasin B can exert its inhibitory effect on DNA synthesis by inhibiting glucose transport.
    BMC Cell Biol. 2004; 5: 21.
    Cytochalasin B triggers a novel pertussis toxin sensitive pathway in TNF-alpha primed neutrophils[Pubmed: 15157285]

    METHODS AND RESULTS:
    Tumor necrosis factor alpha (TNF-alpha) primes neutrophils for subsequent activation by Cytochalasin B. Pretreatment with TNF-alpha induced mobilization of receptor-storing neutrophil organelles, suggesting that receptor up-regulation significantly contributes to the response, but the receptor mobilization was not sufficient for induction of the Cytochalasin B sensitive state. The TNF-alpha primed state resembled that of the desensitized non-signaling state of agonist-occupied neutrophil formyl peptide receptors. The fact that the TNF-alpha primed, Cytochalasin B-triggered activation process was pertussis toxin sensitive suggests that the activation process involves a GPCR.
    CONCLUSIONS:
    Based on desensitization experiments the unidentified receptor was found to be distinct from the C5a receptor as well as the formyl peptide receptor family members FPR and FPRL1. Based on the fact the occupied and desensitized receptors for interleukin-8 and platelet activating factor could not be reactivated by Cytochalasin B, also these could be excluded as receptor candidates involved in the TNF-alpha primed state.
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