For research use only. Not for therapeutic Use.
Retro-2 is a selective inhibitor of retrograde protein trafficking at the endosome-trans-Golgi network interface. Retro-2 is an ebolavirus (EBOV) infection inhibitor with an EC50 of 12.2 µM in HeLa cells. Retro-2 induces cell autophagy[1][2][3].
Retro-2 (1 μM; 1-4 hours) induces autophagy in GFP-LC3-expressing HeLa cells and promoted the dramatic cytoplasmic accumulation of large autophagosomes[2].
Retro-2 (1 μM; 0.5-4 hours) treatment hows an increase over time of the abundance of LC3-II protein in cells[2].
Retro-2 impairs the trafficking between autophagosomes and lysosomes. Retro-2 abolishes autolysosomes formation[2].
Retro-2 (20 μM; pretreatment for 30 min) inhibits HeLa cell intoxication by ricin, Shiga-like toxins 1 (Stx1) and 2 (Stx2)[1].
Retro-2 blocked invasion of cells by the intracellular parasite Leishmania, as well as replication of non-enveloped viruses, including polyoma-, papilloma-, and adeno-associated viruses[3].
Retro-2 (2-200 mg/kg; i.p; daily; for 21 days) treatment clearly protects from lethal nasal exposure to ricin in mice. 200 mg/kg of Retro-2 fully protects mice against ricin challenge[1].
| Catalog Number | I045524 |
| CAS Number | 1201652-50-7 |
| Molecular Formula | C19H16N2OS |
| Purity | ≥95% |
| Reference | [1]. Bahne Stechmann, et al. Inhibition of retrograde transport protects mice from lethal ricin challenge. Cell. 2010 Apr 16;141(2):231-42. [2]. Valérie Nicolas, et al. Small Trafficking Inhibitor Retro-2 Disrupts the Microtubule-Dependent Trafficking of Autophagic Vacuoles. Front Cell Dev Biol. 2020 Jun 18;8:464. [3]. Olena Shtanko, et al. Retro-2 and its dihydroquinazolinone derivatives inhibit filovirus infection. Antiviral Res. 2018 Jan;149:154-163. |
