22144-77-0 Usage
Description
Cytochalasin D is a potent inhibitor of actin polymerization, which also causes the disruption of actin filaments. It is a mycotoxin produced by Helminthosporium and other molds, and is cell permeable. It is available as needles or a fluffy white powder.
Uses
Used in Pharmaceutical Industry:
Cytochalasin D is used as an anti-hypertensive drug, acting on human intestinal epithelial caco-2 cells. It also has activity in HMG-CoA reductase inhibitors, which are used in the lowering of cholesterol.
Used in Cancer Research:
Cytochalasin D exhibits potent inhibition of actin filament function, leading to cell death by apoptosis. This has led to its investigation as an antitumor agent.
Used in Cell Biology Research:
Cytochalasin D is a standard cellular probe for investigating the role of actin in cell biology. It is used as a cell cycle arresting compound in actin polymerization studies and cytological research.
Used in Actin Polymerization Inhibition:
Cytochalasin D is used as an actin polymerization inhibitor, affecting cell movement, growth, phagocytosis, and even secretion. It is more potent than cytochalasin B (10-fold) and does not inhibit monosaccharide transport across cell membranes. Disruption of actin microfilaments leads to activation of p53.
Reactivity Profile
CYTOCHALASIN D may be sensitive to exposure to heat. CYTOCHALASIN D can react with strong oxidizing agents, strong acids and strong bases. .
Fire Hazard
Flash point data for CYTOCHALASIN D are not available; however, CYTOCHALASIN D is probably combustible.
Biological Activity
Potent disruptor of actin filament function. Alters tight junction permeability. Unlike cytochalasin B, does not inhibit monosaccharide transport across the plasma membrane.
Biochem/physiol Actions
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.
Safety Profile
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.
References
1)) Goddetteand et al. (1986), Actin polymerization. The mechanism of action of cytochalasin D; J. Biol. Chem., 261 15974
2) Rubtsova et al. (1998), Disruption of actin microfilaments by cytochalasin D leads to activation of p53; FEBS Lett., 430 353
Check Digit Verification of cas no
The CAS Registry Mumber 22144-77-0 includes 8 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 5 digits, 2,2,1,4 and 4 respectively; the second part has 2 digits, 7 and 7 respectively.
Calculate Digit Verification of CAS Registry Number 22144-77:
(7*2)+(6*2)+(5*1)+(4*4)+(3*4)+(2*7)+(1*7)=80
80 % 10 = 0
So 22144-77-0 is a valid CAS Registry Number.
InChI:InChI=1/C30H37NO6/c1-17-10-9-13-22-26(33)19(3)18(2)25-23(16-21-11-7-6-8-12-21)31-28(35)30(22,25)24(37-20(4)32)14-15-29(5,36)27(17)34/h6-9,11-15,17-18,22-26,33,36H,3,10,16H2,1-2,4-5H3,(H,31,35)/b13-9-,15-14-/t17-,18+,22-,23-,24+,25-,26+,29+,30?/m1/s1
22144-77-0Relevant articles and documents
Total synthesis of cytochalasin D: Total synthesis and full structural assignment of cytochalasin O
Merifield, Eric,Thomas, Eric J.
, p. 3269 - 3283 (2007/10/03)
A total synthesis of cytochalasin D 3 is reported in which the key step is an intramolecular Diels-Alder reaction used to close the 11-membered ring simultaneously introducing the required stereochemistry at four of the stereogenic centres, C(4), C(5), C(8) and C(9). The precursor 21 for the Diels-Alder reaction was prepared from the aldehyde 13 by condensation with the dienyl phosphonate 14 to give the triene 15 which, after conversion into the acyl imidazole 17, was used to acylate the pyrrolidinone 18. The unstable pyrrolinone 21 was then generated from the pyrrolidinone by phenylselenation-oxidative elimination and was cyclised by heating in toluene under high dilution conditions to give the macrocyclic triene 22 (25-30%). Selective functionalisation of the double-bonds in this triene was investigated with epoxidation being selective for the 17,18-double-bond and hydroxylation using osmium tetroxide taking place selectively at the 6,7-double-bond. For completion of the synthesis of cytochalasin D 3, the 6,7-diol 26 was converted into the exocyclic alkene 30 by protection and dehydration. Further hydroxylation using osmium tetroxide gave the diol 31 which was taken through to the enone 36 by protection followed by phenylselenation, N-debenzoylation and oxidative elimination. Reduction under Luche's conditions gave the alcohol 37 which was converted into the acetate 41 by acetylation followed by protecting group exchange. Selective deprotection of the vicinal diol and mild oxidation then gave the ketone 43. Final deprotection gave cytochalasin D 3 so completing the first total synthesis of this natural product. During the course of this work, the Diels-Alder adduct 22 was oxidised using an excess of osmium tetroxide to give the tetraol 28. After protection as its bis-acetonide 46, this was converted into the allylic acetate 51 using the chemistry developed during the synthesis of cytochalasin D 3. Selective hydrolysis of the 17,18-acetonide and oxidation under Swern conditions gave the hydroxyketone 53 which on deprotection gave cytochalasin O 54 so confirming the structure of this natural product. The Royal Society of Chemistry 1999.
