Tat-beclin 1, a peptide derived from the autophagy protein beclin 1, is a powerful inducer of autophagy. It interacts with GAPR-1 (GLIPR2), a negative regulator of autophagy. Tat-beclin 1 effectively reduces the buildup of polyglutamine expansion protein aggregates and inhibits the replication of various pathogens, such as HIV-1, in laboratory experiments. In addition, it has demonstrated the ability to decrease mortality in mice infected with chikungunya (CHIKV) or West Nile virus (WNV).

Tat-beclin 1, at concentrations of 10, 30, and 50 μM administered for 24 hours, promotes autophagy, leading to a dose-dependent reduction in p62 levels—a selective autophagy marker—and facilitates the transformation of LC3-I into its autophagosome-associated, lipidated counterpart, LC3-II, across various cell lines and in primary murine embryonic fibroblasts (MEFs). Additionally, at a concentration of 10 μM and applied 2-4 hours after infection, Tat-beclin 1 significantly reduces the intracellular survival rate of L. monocytogenes within primary murine bone-marrow-derived macrophages (BMDMs).

Tat-beclin 1, administered intraperitoneally at a dosage of 15 mg/kg daily starting one day after infection and continuing for 20 days, induces autophagy in the peripheral tissues of adult mice and in the central nervous system of neonatal mice (6-week-old GFP-LC3 mice)[1].