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Actin disruption is used to study cell functions in vitro (e.g., migration, endocytosis) and in vivo (e.g., tumor cell invasion). Latrunculin A is a bioactive 2-thiazolidinone macrolide derived from sponges that sequesters G-actin and prevents F-actin assembly. It binds monomeric actin with 1:1 stoichiometry and can be used to block actin polymerization both in vitro (Kd = 0.2 μM) and in cells (0.5 μM, 30 min).[1],[2],[3] Latrunculin A (1-10 μM) causes depolymerization of tumor cell cytoskeleton within ten minutes.[4] Overnight treatment of cells with latrunculin A (10 μM) strongly suppresses actin synthesis.[5] Prolonged cell treatment blocks dexamethasone-induced changes in actin cytoskeleton with no effect on cell viability.[6]

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