beclin 1

Apostatin-1 (Apt-1) is a novel TRADD inhibitor that binds to a pocket on the N-terminal TRAF2 binding domain of TRADD.

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].

The compound retro-inverso TAT-Beclin 1 D-amino acid demonstrates superior activity and resistance to proteolytic degradation compared to the L-amino acid peptide when used in vivo. TAT-Beclin 1 is capable of inducing autophagy in peripheral tissues of adult mice and in the central nervous system of newborn mice.

Tat-beclin 1scrambled is the disordered segment and control of Tat-beclin 1, derived from a region of the autophagy protein beclin 1. Beclin 1 induces autophagy by interacting with HIV-1Nef and the autophagy inhibitory factor GAPR-1 (GLIPR2). Tat-beclin 1 decreases both the accumulation of polyglutamine-expanded protein aggregates and the replication of several pathogens, such as HIV. Additionally, Tat-beclin 1 reduces mortality rates in mice infected with chikungunya or West Nile virus.

Chloramphenicol (Chloromycetin) is a broad-spectrum antibiotic that inhibits the biosynthesis of bacterial proteins. Chloramphenicol acts primarily on the 50S subunit of the bacterial 70S ribosome and is active against peptidyltransferases, inhibiting the formation of peptide bonds.

ICCB-19 hydrochloride (ICCB-19 HCl) is an inhibitor of TRADD (TNFRSF1A Associated Via Death Domain). It binds to a pocket on the N-terminal TRAF2-binding domain of TRADD (TRADD-N), which interacts with the C-terminal domain (TRADD-C) and TRAF2 to modulate the ubiquitination of RIPK1 and beclin 1.

Corynoxine B (Cory B), a natural alkaloid isolated from Uncaria rhynchophylla (Miq. ), is an autophagy inducer that enhances the activity of Beclin 1/VPS34 complex and increases autophagy by facilitating the interaction between Beclin 1 and HMGB1/2, which may ameliorate Alzheimer's disease. NVP-BAG956 (NVP-BAG956)

Inflachromene (ICM) is an inhibitor of HMGB1 and HMGB expression with anti-inflammatory activity.Inflachromene reduces seizure severity in a mouse model of epilepsy by inhibiting HMGB1 translocation, inhibits endothelial proliferation through the HMGB1/2-regulated TLR4-NF-κB pathway, and inhibits autophagy by regulating Beclin 1 activity. Inflachromene can be used to study epilepsy.

SW063058 is an autophagy inducer that specifically disrupts the interaction between Beclin 1 and Bcl-2 without affecting the interactions of Bcl-2 with pro-apoptotic members (such as Bax and BIM). By inhibiting the negative regulation of Beclin 1 (key to autophagy initiation) by Bcl-2, SW063058 enhances autophagic activity without inducing cytotoxicity, apoptosis, or other forms of cell death in vitro.

TrxR-IN-3 (Compound 2c) is an effective TrxR inhibitor that exhibits strong antiproliferative activities against five human cancer cell lines, particularly breast tumor cells. It increases ROS levels, induces apoptosis by regulating apoptosis-related protein expression in breast cancer cells, and promotes autophagosome and autolysosome formation by enhancing LC3-II and Beclin-1 expression and reducing LC3-I and p62 protein expression [1].

Autophagy Inducer 3 is a chemical compound that exhibits autophagy-induced activity, specifically inducing robust autophagic cell death in various cancer cells while sparing normal cells. This compound induces lethal autophagy through the formation of distinct autophagic vacuoles, LC3 puncta formation, and upregulation of signature autophagy markers such as Beclin and Atg family proteins [1].

BRD1991 is a chemical compound that specifically disrupts the interaction between Beclin 1 and Bcl-2, thereby inducing autophagy. It accomplishes this without initiating apoptosis or other forms of cell death.

JNK-IN-14 is a potent inhibitor of JNK with IC50 values of 1.81 nM for JNK1, 12.7 nM for JNK2, and 10.5 nM for JNK3. It induces early-stage apoptosis, arrests cell population at the G2/M phase, and moderately inhibits beclin-1 production in K562 leukemia cells, demonstrating greater inhibitory efficacy than SP600125. [1]

Beclin1-ATG14L Interaction Inhibitor 1 (COM 19) is a selective inhibitor targeting the specific interaction between Beclin1 and ATG14L. It impedes the formation of complex I in the lipid kinase VPS34, thus inhibiting autophagy, while leaving complex II intact, which relies on the Beclin 1-UVRAG interaction for its integrity and is essential for vesicle transport [1].

Pennogenin 3-O-beta-chacotrioside, isolated from *Paris polyphylla*, exhibits anti-colorectal cancer activity by modulating autophagy through increased expression of autophagy-related proteins LC3 and Beclin-1.

Beclin1-Bcl-2 Interaction Inhibitor 1 effectively disrupts the binding of Beclin 1 to Bcl-2, and is utilized in cancer and neurodegeneration research [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.