14930-96-2

white to off-white powder

A cell-permeable fungal toxin used in actin polymerization studies and cytological

Cytochalasin B is one of the most extensively studied members of a family of potent mycotoxins produced by several species of fungi. All members of the class exhibit profound effects on cytoskeletal proteins, giving rise to pronounced morphogenic activity in animals and plants. Like most cytochalasins, cytochalasin B exhibits potent inhibition of actin filament function leading to cell death by apoptosis, and displays a broad range of resultant cellular actions. Despite the common mode of action, there is evidence that individual members of this class display diverse selectivity. However, lack of comparative co-metabolite analysis has restricted a more complete understanding of their individual selectivity.

Cytochalasin B is one of the most extensively studied members of a family of potent mycotoxins produced by several species of fungi. All members of the class exhibit profound effects on cytoskeletal proteins, giving rise to pronounced morphogenic activity in animals and plants. Like most cytochalsins, cytochalasin B exhibits potent inhibition of actin filament function leading to cell death by apoptosis, and displays a broad range of resultant cellular actions. Despite the common mode of action, there is evidence that individual members of this class display diverse selectivity. However, lack of comparative co-metabolite analysis has restricted a more complete understanding of their individual selectivity.

ChEBI: An organic heterotricyclic compound, that is a mycotoxin which is cell permeable an an inhibitor of cytoplasmic division by blocking the formation of contractile microfilaments.

As tools in cytological research and in characterization of polymerization properties of actin, q.v.

Cytochalasin B (14930-96-2) is a cell permeable fungal toxin which binds to the barbed end of actin, inhibiting its polymerization.1 Inhibits cell division, migration and glucose transport.2 Causes cell cycle arrest at G2/M and induces apoptosis in HCT-116 colorectal carcinoma cells.3? Cytochalasin B-induced membrane vesicles (CIMVs) retain cell surface receptors of the parent cells and retain fusion specificity with target cells.4 CIMVs are a promising new vector system for drug and biomolecule delivery due to their natural origin and participation in intercellular communication.5

Cell permeable fungal toxin that disrupts contractile microfilaments by inhibiting actin polymerization. This, in turn, induces DNA fragmentation, inhibits cell division, and disrupts many cell processes. Inhibits glucose transport.

Store at -20°C

Purify it by MeOH extraction, reverse phase C18 silica gel batch extraction by selective elution with 1:1 v/v hexane/tetrahydrofuran, crystallisation, subjected to TLC and recrystallisation [Lipski et al. Anal Biochem 161 332 1987]. It is soluble in EtOH (3.6%), Me2CO (1%), Me2SO (37%) and Me2NCHO (49%) at 24o, and can be crystallised from the first two solvents. It interferes with cellular movement [Korm Physiol Reviews 62 672 1982].

Threadoropoulos et al. (1994), Cytochalasin B may shorten actin filaments by a mechanism independent of barbed end capping; Biochem. Pharmacol., 47 1875 Whitesell et al. (2005), Compartmentalization of transport and phosphorylation of glucose in a hepatoma cell line; Biochem. J., 386 245 Buldak et al. (2014), Changes in subcellular localization of visfatin in human colorectal HCT-116 carcinoma cell line after cytochalasin B treatment; Eur. J. Histochem., 58 2408 Gomzikova et al. (2018), Evaluation of cytochalasin B-Induced Membrane Vesicles Fusion specificity with Target Cells; Biomed. Res. Int., 2018 7053623 Gomzikova et al. (2017), Cytochalasin B-induced membrane vesicles convey angiogenic activity of parental cells; Oncotarget, 8 70496