Tat-beclin 1 (Tat-BECN1), a peptide known to stimulate autophagy through mobilization of endogenous Beclin 1, induces autophagy in vitro and in vivo and improves clinical outcomes.
Tat-beclin 1 is a cell-permeable peptide that induces autophagy. Treatment with Tat-beclin 1, but not Tat-scrambled, results in a dose-dependent decrease in amounts of p62, a selective autophagy substrate, and a dose-dependent conversion of the non-lipidated form of LC3, LC3-I, to the lipidated, autophagosome-associated form of LC3, LC3-II, in multiple cell lines and primary murine embryonic fibroblasts (MEFs). Tat-beclin 1 markedly inhibits HIV-1 replication in primary human monocyte-derived macrophages[1].
Tat-beclin 1 can induce autophagy in peripheral tissues in adult mice as well as in the central nervous system of neonatal mice. Daily Tat-beclin 1 peptide treatment is well-tolerated in both neonatal and adult mice. Tat-beclin 1 peptide improves the clinical outcome of mice with CNS WNV(West Nile virus) infection[1].
[1] Shoji-Kawata S, et al. Nature. 2013, 494(7436):201-6.