regenerating sites. Sequestering by nudibranchs Sea slugs of the genus Chromodoris sequester different toxics from the sponges that they eat as defensive metabolites, including latrunculin. They selectively transfer and store latrunculin in the sites of the mantle that are most exposed to potential predators. It is thought that the digestive system of the nudibranchs plays an important role in the detoxification. In 2015, the discovery that five closely related sea slugs of the genus Chromodoris all use latrunculin as defense, indicates that the toxic might be used via Müllerian mimicry. Research Latrunculins are used for fundamental research like cytoskeleton studies. Many functions of actin have been determined by using latrunculins to block actin polymerization followed by examining the effects on the cell. Using this method, the importance of actin for the polarized localization of proteins, polarized exocytosis and the maintenance of cell polarity have been shown. In the field of Neuroscience, latrunculin has been used to demonstrate the role of actin in regulating voltage-gated ion channels in different nerve cells, showing that latrunculin treatment can alter the electrical activity of nerve cells. Latrunculin shows a dose-dependent inhibition of K+ currents and acute application can induce the firing of multiple action potentials , which could underlie a mechanism of defense via nociceptors. In addition, latrunculin-A was used to demonstrate the role of dentritic spine neck shrinkage for the induction of synaptic plasticity. Medical applications Latrunculin A and B and derivatives have potential as novel chemotherapeutic agents. The potential use of latrunculin as growth inhibitors of tumor cells has already been investigated for certain forms of gastric cancer, metastatic breast cancer and prostate tumors. In lower doses, latrunculin can be used to decrease disaggregation and cell migration, thereby preventing invasive activities of tumor cells. In higher doses, latrunculin can induce acute cell injury and programmed cell death through activating the caspase-3/7 pathway, and thus be used to kill tumor cells. Latrunculin A and its 17-O-[N-(benzyl)carbamate ( suppress hypoxia-induced HIF-1 activation in T47D breast tumor cells. Latrunculin also is a potential therapeutic for ocular hypertension and glaucoma. Latrunculin A and B are shown to disrupt the actin cytoskeleton of the trabecular meshwork that is important for regulating humor outflow resistance and thereby intraocular pressure. By cellular relaxation and loosened cell-cell junctions, latrunculin can increase humor outflow facility. The first human trial of lantruculin B as treatment of ocular hypertension and glaucoma showed significantly