beclin 1

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 polyglutamine expansion protein aggregates and inhibits various pathogens, such as HIV-1, in laboratory experiments. Additionally, it decreases mortality in mice infected with chikungunya (CHIKV) or West Nile virus (WNV).

Tat-beclin 1 acetate is a potent inducer of autophagy and interacts with the negative regulator of autophagy, GAPR-1. Tat-beclin 1 acetate decreases the accumulation of polyglutamine expansion protein aggregates and the replication of several pathogens (including HIV-1).

Tat-beclin 1 TFA, a peptide derived from a segment of the autophagy protein beclin 1, effectively induces autophagy and interacts with the autophagy negative regulator GAPR-1 (GLIPR2). It reduces the accumulation of polyglutamine expansion protein aggregates and limits the in vitro replication of various pathogens, including HIV-1. Additionally, Tat-beclin 1 TFA has been shown to decrease mortality rates in mice infected with chikungunya (CHIKV) or West Nile virus (WNV) [1].

D-CopA3 is an inhibitor of MDM2 and an activator of the p53 signaling pathway. It exhibits cytotoxicity in colorectal cancer cells HCT-116, LoVo, and RKO with IC50 values of 15-18 μM and induces JNK Beclin-1 mediated autophagy. D-CopA3 downregulates the expression of the cell cycle inhibitor protein p21Cip1 Waf1, enhances mucosal barrier function, and reduces infiltration of inflammatory mediators. It shows anti-inflammatory properties in mouse models of acute enteritis induced by C. difficile toxin A and chronic colitis induced by DSS. Additionally, D-CopA3 demonstrates antitumor activity in a mouse HCT-116 xenograft model.