Toggle Nav
  • Menu
  • Setting

Cytochalasin D

Catalog No.
inhibitor of actin polymerization, selective
Grouped product items
SizePriceStock Qty
Ship with 5-10 days
Ship with 5-10 days
Ship with 5-10 days

Tel: +1-832-696-8203

Email: [email protected]

Worldwide Distributors


Cytochalasin D is a selective inhibitor of actin polymerization with with IC50 value of 25 nM [1].
Actin is a globular multi-functional protein and found nearly in all eukaryotic cells. it has been shown that actin polymerization plays a pivotal role in chemotaxis and cytokinesis. Cytochalasin D is reported as an inhibitor in the process of actin polymerization via disrupting actin microfilaments and activating p53-dependent pathways which in turn causes the arrest of cell cycle at the G1-S transition [2].
Cytochalasin D is a potent actin polymerization inhibitor. When tested with differentiating neurons, Cytochalasin D slowed down protrusion/retraction cycles and decreased lamellipodia axial motion via inhibiting actin polymerization [1]. In epithelial cell line HEp-2 cells, Cytochalasin D treatment regulated late and very late phases of viral transcription and shut down host transcription through blocking actin polymerization [3]. In the model of IPEC-J2 cells infected with PCV2, Cytochalasin D treatment could suppress PCV2 invasion, replication and release thus inhibited virus invasion [4].
[1] Sayyad, W.A., et al., The role of myosin-II in force generation of DRG filopodia and lamellipodia. Sci Rep, 2015. 5: p. 7842.
[2] Montazeri, M., et al., Activation of Toll-like receptor 3 reduces actin polymerization and adhesion molecule expression in endometrial cells, a potential mechanism for viral-induced implantation failure. Hum Reprod, 2015.
[3] Volkman, L.E., Baculoviruses and nucleosome management. Virology, 2015. 476c: p. 257-263.
[4] Yan, M., L. Zhu, and Q. Yang, Infection of porcine circovirus 2 (PCV2) in intestinal porcine epithelial cell line (IPEC-J2) and interaction between PCV2 and IPEC-J2 microfilaments. Virol J, 2014. 11: p. 193.

Product Citation

Chemical Properties

Physical AppearanceA crystalline solid
StorageDesiccate at -20°C
Cas No.22144-77-0
SolubilitySoluble in DMSO
Chemical Name(3S,3aR,4R,6R,6aS,7E,10R,12S,13Z,15R,15aS)-3-benzyl-6,12-dihydroxy-4,10,12-trimethyl-5-methylene-1,11-dioxo-2,3,3a,4,5,6,6a,9,10,11,12,15-dodecahydro-1H-cycloundeca[d]isoindol-15-yl acetate
SDFDownload SDF
Canonical SMILESO[[email protected]@H]1[[email protected]@H](/C=C/C[[email protected]@H](C)C2=O)[[email protected]]3([[email protected]@H](C=C[[email protected]]2(C)O)OC(C)=O)[[email protected]@H]([[email protected]@H](C)C1=C)[[email protected]](CC4=CC=CC=C4)NC3=O
Shipping ConditionShip with blue ice, or upon other requests.
General tipsFor obtaining a higher solubility, please warm the tube at 37°C and shake it in the ultrasonic bath for a while.


Cell experiment [1-3]:

Cell lines

HeLa, Vero, L, HEp2, and MDBK cells, SC-1 cells, Murine CT26 colorectal carcinoma cells

Preparation method

The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37°C for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below -20°C for several months.

Reacting condition

0.2-0.5 μg/mL


In HeLa, Vero, L, HEp2, and MDBK cells, cytochalasin D (0.2-0.5 μg/mL) induced sustained contraction (contracture), loss of microvilli, expression of endoplasmic contents (zeiosis), nuclear protrusion, and extension of cytoplasmic processes. Cells in G1 were most sensitive to CD; responsiveness decreased progressively during early S and is least in mid S through G2. CD inhibited transport of [14C]deoxyglucose in HeLa. In SC-1 cells, Cytochalasin D treatment severely disrupted network organization, increased the number of actin filament ends, and led to the formation of filamentous aggregates or foci composed mainly of actin filaments. Cytochalasin D (0.24-15 μg/mL, 16 h) inhibited CT26 tumor cell proliferation in time and dose dependent manner and induced significant CT26 cell apoptosis.

Animal experiment [3,4]:

Animal models

Murine CT26 tumor model, porcine coronary model

Dosage form

Intravenous injection, 50 mg/kg, every 3 days for 21 days


Cytochalasin D (i.v., 50 mg/kg) in vivo treatment significantly inhibited tumor growth and prolonged the survival times in CT26 tumor-bearing mice. In porcine coronary model, Cytochalasin D (2 μg) resulted in less late lumen loss in low-dose. High-dose Cytochalasin D (20 μg) inhibited both late lumen loss and intimal area.

Other notes

Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.


[1] Miranda A F, Godman G C, Deitch A D, et al. Action of cytochalasin D on cells of established lines [J]. The Journal of cell biology, 1974, 61 (2): 481-500.

[2] Schliwa M. Action of cytochalasin D on cytoskeletal networks[J]. The Journal of cell biology, 1982, 92 (1): 79-91.

[3] Huang F Y, Li Y N, Mei W L, et al. Cytochalasin D, a tropical fungal metabolite, inhibits CT26 tumor growth and angiogenesis[J]. Asian Pacific journal of tropical medicine, 2012, 5 (3): 169-174.

[4].Salu K J, Bosmans J M, Huang Y, et al. Effects of cytochalasin D-eluting stents on intimal hyperplasia in a porcine coronary artery model [J]. Cardiovascular research, 2006, 69 (2): 536-544.

Quality Control

Quality Control & MSDS

View current batch:

Chemical structure

Cytochalasin D

Related Biological Data

Cytochalasin D

Related Biological Data

Cytochalasin D

Related Biological Data

Cytochalasin D