Cytochalasin B
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| Category | Mycotoxins |
| Catalog number | BBF-01755 |
| CAS | 14930-96-2 |
| Molecular Weight | 479.61 |
| Molecular Formula | C29H37NO5 |
| Purity | >99% by HPLC |
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Description
It is produced by the strain of Helminthosporium dematioideum, Coriolus vernicipes. It has many biological activities, such as inhibiting cytokinesis reversibly, inhibiting megasophil endocytosis and exocytosis. Cytosine B has immunosuppressive effects.
Specification
| Synonyms | (7S,13E,16R,20R,21E)-7,20-Dihydroxy-16-methyl-10-phenyl-24-oxa[14]cytochalasa-6(12),13,21-triene-1,23-dione; (E,E)-(5R,9R,12aS,13S,15S,15aS,16S,18aS)-16-Benzyl-6,7,8,9,10,12a,13,14,15,15a,16,17-dodecahydro-5,13-dihydroxy-9,15-dimethyl-14-methylene-2H-Oxacyclotetradecino[2,3-d]isoindole-2,18(5H)-dione; NSC 107658; Phomin |
| Storage | -20 °C |
| IUPAC Name | (1S,4E,6R,10R,12E,14S,15S,17S,18S,19S)-19-benzyl-6,15-dihydroxy-10,17-dimethyl-16-methylidene-2-oxa-20-azatricyclo[12.7.0.01,18]henicosa-4,12-diene-3,21-dione |
| Canonical SMILES | CC1CCCC(C=CC(=O)OC23C(C=CC1)C(C(=C)C(C2C(NC3=O)CC4=CC=CC=C4)C)O)O |
| InChI | InChI=1S/C29H37NO5/c1-18-9-7-13-22(31)15-16-25(32)35-29-23(14-8-10-18)27(33)20(3)19(2)26(29)24(30-28(29)34)17-21-11-5-4-6-12-21/h4-6,8,11-12,14-16,18-19,22-24,26-27,31,33H,3,7,9-10,13,17H2,1-2H3,(H,30,34)/b14-8+,16-15+/t18-,19-,22-,23+,24+,26+,27-,29-/m1/s1 |
| InChI Key | GBOGMAARMMDZGR-TYHYBEHESA-N |
| Source | Cytochalasin B is isolated from a fungus, Helminthosporium dermatioideum, as well as hormiscium species and rhoma species. |
Properties
| Appearance | White to Off-White Solid |
| Boiling Point | 740.6 °C at 760 mmHg |
| Melting Point | 218-221 °C |
| Density | 1.20 g/cm3 |
| Solubility | Soluble in Acetone; Slightly soluble in DMSO, Methanol |
Toxicity
| Carcinogenicity | No indication of carcinogenicity to humans (not listed by IARC). |
| Mechanism Of Toxicity | Cytochalasins are known to bind to the barbed, fast growing plus ends of microfilaments, which then blocks both the assembly and disassembly of individual actin monomers from the bound end. Once bound, cytochalasin essentially caps the end of the new actin filament. One cytochalasin will bind to one actin filament. By blocking the polymerization and elongation of actin, cytochalasins can change cellular morphology, inhibit cellular processes such as cell division, and cause cells to undergo apoptosis. Cytochalasin B also inhibits glucose transport and platelet aggregation. It blocks adenosine-induced apoptotic body formation without affecting activation of endogenous ADP-ribosylation in leukemia HL-60 cells. |
| Toxicity | LD50: 11 mg/kg (Intraperitoneal, Rat). |
Reference Reading
1.Stability of the cytoskeleton of matured buffalo oocytes pretreated with cytochalasin B prior to vitrification.
Wang CL1, Xu HY1, Xie L1, Lu YQ1, Yang XG1, Lu SS1, Lu KH2. Cryobiology. 2016 Mar 18. pii: S0011-2240(16)30016-5. doi: 10.1016/j.cryobiol.2016.03.005. [Epub ahead of print]
Stabilizing the cytoskeleton system during vitrification can improve the post-thaw survival and development of vitrified oocytes. The cytoskeleton stabilizer cytochalasin B (CB) has been used in cryopreservation to improve the developmental competence of vitrified oocytes. To assess the effect of pretreating matured buffalo oocytes with CB before vitrification, we applied 0, 4, 8, or 12 μg/mL CB for 30 min. The optimum concentration of CB treatment (8 μg/mL for 30 min) was then used to evaluate the distribution of microtubules and microfilaments, the expression of the cytoskeleton proteins actin and tubulin, and the developmental potential of matured oocytes that were vitrified-warmed by the Cryotop method. Western blotting demonstrated that vitrification significantly decreased tubulin expression, but that the decrease was attenuated for oocytes pretreated with 8 μg/mL CB before vitrification. After warming and intracytoplasmic sperm injection, oocytes that were pretreated with 8 μg/mL CB before vitrification yielded significantly higher 8-cell and blastocyst rates than those that were vitrified without CB pretreatment.
2.Application of cell sorting for enhancing the performance of the cytokinesis-block micronucleus assay.
Nakamura A1, Monzen S1, Takasugi Y1, Wojcik A2, Mariya Y3. J Radiat Res. 2016 Mar;57(2):121-6. doi: 10.1093/jrr/rrv103. Epub 2016 Jan 28.
Among the numerous methods available to assess genotoxicity, the cytokinesis-block micronucleus (CBMN) assay is very popular due its relative simplicity and power to detect both clastogenic and aneugenic compounds. A problem with the CBMN assay is that all DNA damaging agents also inhibit the ability of cells to progress through mitosis, leading to a low number of binucleated cells (BNCs). One method to resolve this issue is to ensure a sufficient proportion of BNCs in the samples. In the current study, the applicability of a cell sorting system capable of isolating cell fractions containing abundant BNCs was investigated. Furthermore, to investigate the relationship between the cell division delay due to radiation exposure and the generation of BNCs and micronuclei (MN), we assessed a series of lag times between radiation exposure and addition of cytochalasin-B (Cyt-B). Cells from the human chronic myelogenous leukemia cell line K562 were exposed to X-rays (2 Gy and 4 Gy), and Cyt-B was subsequently added at 0, 6 and 12 h following irradiation.
3.Mechanism of inhibition of human glucose transporter GLUT1 is conserved between cytochalasin B and phenylalanine amides.
Kapoor K1, Finer-Moore JS1, Pedersen BP2, Caboni L1, Waight A1, Hillig RC3, Bringmann P4, Heisler I5, Müller T5, Siebeneicher H3, Stroud RM6. Proc Natl Acad Sci U S A. 2016 Apr 12. pii: 201603735. [Epub ahead of print]
Cancerous cells have an acutely increased demand for energy, leading to increased levels of human glucose transporter 1 (hGLUT1). This up-regulation suggests hGLUT1 as a target for therapeutic inhibitors addressing a multitude of cancer types. Here, we present three inhibitor-bound, inward-open structures of WT-hGLUT1 crystallized with three different inhibitors: cytochalasin B, a nine-membered bicyclic ring fused to a 14-membered macrocycle, which has been described extensively in the literature of hGLUTs, and two previously undescribed Phe amide-derived inhibitors. Despite very different chemical backbones, all three compounds bind in the central cavity of the inward-open state of hGLUT1, and all binding sites overlap the glucose-binding site. The inhibitory action of the compounds was determined for hGLUT family members, hGLUT1-4, using cell-based assays, and compared with homology models for these hGLUT members. This comparison uncovered a probable basis for the observed differences in inhibition between family members.
4.Fibroblast growth factor (Fgf) 23 gene transcription depends on actin cytoskeleton reorganization.
Fajol A1, Honisch S1, Zhang B1, Schmidt S1, Alkahtani S2,3, Alarifi S2,3, Lang F1, Stournaras C1,3, Föller M4. FEBS Lett. 2016 Mar;590(6):705-15. doi: 10.1002/1873-3468.12096. Epub 2016 Feb 27.
FGF23 regulates renal phosphate and vitamin D metabolism. Loss of FGF23 results in massive calcification and rapid aging. FGF23 production is stimulated by 1,25(OH)2 D3 and NFκB signaling. Here, we report that treatment of UMR106 osteoblast-like cells with 1,25(OH)2 D3 , inducing Fgf23 transcription, resulted in actin polymerization which was blocked by NFκB inhibitor wogonin. Interestingly, 1,25(OH)2 D3 -induced Fgf23 gene transcription was abolished by the actin microfilament-disrupting agent cytochalasin B, as well as by the inhibition of actin-regulating Rac1/PAK1 signaling. Our results provide strong evidence that actin redistribution regulated by the Rac1/PAK1 pathway participates in 1,25(OH)2 D3 -induced Fgf23 gene transcription.
Spectrum
Predicted LC-MS/MS Spectrum - 10V, Positive
Experimental Conditions
Ionization Mode: Positive
Collision Energy: 10 eV
Instrument Type: QTOF (generic), spectrum predicted by CFM-ID
Mass Resolution: 0.0001 Da
Molecular Formula: C29H37NO5
Molecular Weight (Monoisotopic Mass): 479.2672 Da
Molecular Weight (Avergae Mass): 479.6078 Da
Collision Energy: 10 eV
Instrument Type: QTOF (generic), spectrum predicted by CFM-ID
Mass Resolution: 0.0001 Da
Molecular Formula: C29H37NO5
Molecular Weight (Monoisotopic Mass): 479.2672 Da
Molecular Weight (Avergae Mass): 479.6078 Da
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Bio Calculators
* Our calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
It is commonly abbreviated as: C1V1 = C2V2
* Total Molecular Weight:
g/mol
Tip: Chemical formula is case sensitive. C22H30N4O √ c22h30n40 ╳
