2-Methoxy-4-[(5,6,7,8-tetrahydro-benzo[4,5]thieno[2,3-d]pyrimidin-4-yl)-hydrazonomethyl]-phenol

Exo2 (304684-77-3) disrupts the Golgi apparatus and stimulates Golgi-ER fusion in mammalian cells.1 May be used to completely ablate the Golgi apparatus.1 Like brefeldin A (BFA), it inhibits anterograde transport and disrupts morphology of the trans-Golgi network (TGN) but unlike BFA, it does not induce tubulation and merging of the TGN and endosomal compartments.2 It perturbs trafficking of Shiga toxin between endosomes and the trans-Golgi network, in contrast to cholera toxin.1,2 Accelerates degradation of perilipin-2 proteins.3

Exo2 is a secretion inhibitor. Exo2 perturbs trafficking of Shiga toxin between endosomes and the trans-Golgi network. Exo2 blocks secretory cargo exit from the ER (endoplasmic reticulum) and disrupts the Golgi apparatus, but does not affect the morphology of the TGN (trans-Golgi network) Exo2 can stimulate calcium-dependent exocytosis in permeabilized adrenal chromaff in cells[1][2].

ChEBI: Exo2 is a member of phenols and a member of methoxybenzenes.

Exo2 is a small-molecule inhibitor of secretion and retrograde trafficking in cells. Exo2 stimulates morphological changes at the mammalian Golgi and trans-Golgi network, fusing the endoplasmic reticulum and Golgi apparatus. These morphological changes prevent the release of secretory cargo from the ER and disrupts the Golgi apparatus. Exo2 also perturbs the retrograde transport of Shiga toxin to the ER. Chemical modification of the secretion inhibitor Exo2 has produced a host of useful Exo2 analogs, capable of distinguishing differences in organelle morphology, target specificity, innate toxicity, and toxin protection. In a study of Arabidopsis root epidermal cells, Exo2 had no significant effect on organelle morphology, while an Exo2 derivative induced severe morphological alterations in both the Golgi and the ER.

[1] YAN FENG. Retrograde transport of cholera toxin from the plasma membrane to the endoplasmic reticulum requires the trans-Golgi network but not the Golgi apparatus in Exo2-treated cells.[J]. EMBO Reports, 2004, 5 6: 596-601. DOI:10.1038/sj.embor.7400152
[2] ROBERT A SPOONER. The secretion inhibitor Exo2 perturbs trafficking of Shiga toxin between endosomes and the trans-Golgi network.[J]. Biochemical Journal, 2008: 471-484. DOI:10.1042/bj20080149
[3] ALAIN PAULOIN. The perilipin-2 (adipophilin) coat of cytosolic lipid droplets is regulated by an Arf1-dependent mechanism in HC11 mouse mammary epithelial cells[J]. Cell Biology International, 2015, 40 2: 143-155. DOI:10.1002/cbin.10547