Cytochalasin D (22144-77-0) is a potent inhibitor of actin polymerization which also causes the disruption of actin filaments. More potent that cytochalasin B (10-fold) and does not inhibit monosaccharide transport across cell membranes. Disruption of actin microfilaments leads to activation of p53. Cell permeable
A cell cycle arresting compound used in actin polymerization studies and cytological research
Cytochalasin D is the most studied of the cytochalasins. Like most of the members of this mycotoxin class, cytochalasin D exhibits potent inhibition of actin filament function leading to cell death by apoptosis. This led to early investigation of the metabolite as an antitumour agent. Cytochalasin D has become one of the standard cellular probes for investigating the role of actin in cell biology.
Cytochalasin D acts as an anti-hypertensive drug acting on human intestinal epithelial caco-2 cells. Also has activity in HMG-CoA reductase inhibitors used in the lowering of cholesterol. Actin inhib
itor, actin polymerization inhibitor affecting cell movement, growth, phagocytosis and even secretion.
ChEBI: An organic heterotricyclic compound that is a mycotoxin produced by Helminthosporium and other moulds which is cell permeable and a potent inhibitor of actin polymerisation and DNA synthesis.
Needles or fluffy white powder.
CYTOCHALASIN D may be sensitive to exposure to heat. CYTOCHALASIN D can react with strong oxidizing agents, strong acids and strong bases. .
Flash point data for CYTOCHALASIN D are not available; however, CYTOCHALASIN D is probably combustible.
Potent disruptor of actin filament function. Alters tight junction permeability. Unlike cytochalasin B, does not inhibit monosaccharide transport across the plasma membrane.
Cell permeable fungal toxin; potent inhibitor of actin polymerization. Disrupts actin microfilaments and activates the p53-dependent pathways causing arrest of the cell cycle at the G1-S transition. Inhibits smooth muscle contraction. Inhibits insulin-stimulated, but not basal, transport of glucose.
Poison by ingestion,
subcutaneous, and intraperitoneal routes. An
experimental teratogen. Experimental
reproductive effects. Human mutation data
reported. When heated to decomposition it
emits toxic fumes of NOx.
p38MAPK | PI3K | Akt | Calcium Channel | ATPase
The fungal-derived toxin Cytochalasin D is a potent inhibitor of actin polymerization, limiting elongation at both the barbed and pointed ends of the actin filament. While several related Cytochalasin toxins bind actin and alter polymerization, Cytochalasin D is the most specific inhibitor of actin microfilaments. The cytoskeleton takes part in signal transduction, protein transport, signal compartmentalization, and cell mobility. Depolymerization of the actin cytoskeleton by Cytochalasin D in mesenchymal stem cells results in localization of G-actin to the nucleus, which leads to mesenchymal stem cell differentiation and bone formation. Treatment of a pair of cancer cell lines with Cytochalasin D results in the inhibition of actin polymerization and decreased cell motility. Treatment of murine CT26 colorectal carcinoma cells with Cytochalasin D inhibited tumor growth through reduced cell proliferation, induction of cell apoptosis, and suppression of tumor angiogenesis.
[1] D. GODDETTE C F. Actin polymerization. The mechanism of action of cytochalasin D.[J]. The Journal of Biological Chemistry, 1986, 1 1: 15974-15980. DOI:
10.1016/s0021-9258(18)66662-1[2] S.N RUBTSOVA . Disruption of actin microfilaments by cytochalasin D leads to activation of p53[J]. FEBS Letters, 1998, 430 3: Pages 353-357. DOI:
10.1016/s0014-5793(98)00692-9
