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Results for "

beclin 1

" in MedChemExpress (MCE) Product Catalog:

16

Inhibitors & Agonists

5

Peptides

2

Natural
Products

1

Recombinant Proteins

1

Antibodies

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-156237
    Beclin1-ATG14L interaction inhibitor 1

    		Autophagy Others
    Beclin1-ATG14L interaction inhibitor 1 (com 19) is a selective Beclin1-ATG14L interaction inhibitor. This protein interaction mechanism specifically targets complex I of the lipid kinase VPS34 without affecting complex II. Because the integrity of VPS34 complex II depends on the Beclin 1-UVRAG interaction. Beclin1-ATG14L interaction inhibitor 1 can disrupt the formation of VPS34 complex I and inhibit autophagy, but does not affect complex II-related vesicle transport .
    Beclin1-ATG14L interaction inhibitor 1
  • HY-P2260B
    Tat-beclin 1 scrambled

    		HIV Infection
    Tat-beclin 1 scrambled is the scrambled part and a scrambled control of Tat-beclin 1 (HY-P2260), which is derived from a region of the autophagy protein, beclin 1. beclin 1 induces autophagy via binding human immunodeficiency virus, HIV-1 Nef and interacting with negative regulator GAPR-1 (GLIPR2). Tat-beclin 1 decreases the accumulation of polyglutamine expansion protein aggregates and the replication of several pathogens, such as HIV-1. Tat-beclin 1 also reduces mortality in mice infected with chikungunya or West Nile virus .
    Tat-beclin 1 scrambled
  • HY-P2260C
    Tat-beclin 1 scrambled TFA

    		HIV Infection
    Tat-beclin 1 scrambled TFA is the scrambled part and a scrambled control of Tat-beclin 1 (HY-P2260), which is derived from a region of the autophagy protein, beclin 1. beclin 1 induces autophagy via binding human immunodeficiency virus, HIV-1 Nef and interacting with negative regulator GAPR-1 (GLIPR2). Tat-beclin 1 decreases the accumulation of polyglutamine expansion protein aggregates and the replication of several pathogens, such as HIV-1. Tat-beclin 1 also reduces mortality in mice infected with chikungunya or West Nile virus .
    Tat-beclin 1 scrambled TFA
  • HY-P2260
    Tat-beclin 1
    1 Publications Verification

    		 Autophagy HIV Infection
    Tat-beclin 1, a peptide derived from a region of the autophagy protein (beclin 1), is a potent inducer of autophagy and interacts with negative regulator of autophagy, GAPR-1 (GLIPR2). Tat-beclin 1 decreases the accumulation of polyglutamine expansion protein aggregates and the replication of several pathogens (including HIV-1) in vitro, and reduces mortality in mice infected with chikungunya (CHIKV) or West Nile virus (WNV) .
    Tat-beclin 1
  • HY-N4180
    Pennogenin 3-O-beta-chacotrioside

    		Atg8/LC3 Autophagy Cancer
    Pennogenin 3-O-beta-chacotrioside is an active component isolated from Paris polyphylla, modulates autophagy via increasing the expressions of autophagy-related proteins LC3 and Beclin-1. Anti-colorectal cancer activity .
    Pennogenin 3-O-beta-chacotrioside
  • HY-149681
    Beclin1-Bcl-2 interaction inhibitor 1

    		Bcl-2 Family Beclin1 Cancer
    Beclin1-Bcl-2 interaction inhibitor 1 potently inhibits Beclin 1/Bcl-2 binding. Beclin1-Bcl-2 interaction inhibitor 1 can be used for the research of cancer and neurodegeneration .
    Beclin1-Bcl-2 interaction inhibitor 1
  • HY-P2260A
    Tat-beclin 1 TFA

    		Autophagy HIV Infection
    Tat-beclin 1 TFA, a peptide derived from a region of the autophagy protein (beclin 1), is a potent inducer of autophagy and interacts with negative regulator of autophagy, GAPR-1 (GLIPR2). Tat-beclin 1 TFA decreases the accumulation of polyglutamine expansion protein aggregates and the replication of several pathogens (including HIV-1) in vitro, and reduces mortality in mice infected with chikungunya (CHIKV) or West Nile virus (WNV) .
    Tat-beclin 1 TFA
  • HY-P10110
    retro-inverso TAT-Beclin 1 (D-amino acid)

    		Autophagy Neurological Disease
    retro-inverso TAT-Beclin 1 D-amino acid is has higher activity and resistance to proteolytic degradation in vivo compared to L-amino acids peptide. TAT-Beclin 1 can induce autophagy in peripheral tissues in adult mice as well as in the central nervous system of neonatal mice .
    retro-inverso TAT-Beclin 1 (D-amino acid)
  • HY-156182
    JNK-IN-14

    		JNK Cytochrome P450 Cancer
    JNK-IN-14 is a potent JNK inhibitor with IC50 values of 1.81, 12.7 and 10.5 nM for JNK1, JNK2 and JNK3, respectively. JNK-IN-14 induces early-stage apoptosis. JNK-IN-14 shows cell population arrest at the G2/M phase and slightly inhibits beclin-1 production at K562 leukemia cells relative to SP600125 (HY-12041), showing higher inhibitory ability.
    JNK-IN-14
  • HY-146307
    TrxR-IN-3

    		TrxR Cancer
    TrxR-IN-3 (Compound 2c) is a potent inhibitor of TrxR. TrxR-IN-3 exhibits potent antiproliferative activities against five human cancer cell lines, especially against breast tumor cells. TrxR-IN-3 increases ROS levels and resulted in marked apoptosis by regulating apoptosis-related proteins expressed in the breast cancer cells. TrxR-IN-3 also triggers the formation of autophagosomes and autolysosomes by promoting the expression of LC3-II and Beclin-1 and diminishing the expression of LC3-I and p62 proteins .
    TrxR-IN-3
  • HY-145752
    HaloPROTAC-E
    1 Publications Verification

    		 PROTACs SGK Autophagy Cancer
    HaloPROTAC-E is a potent Halo PROTAC degrader that reversibly induces degradation of two endoplasmic reticulum-localized proteins, SGK3 and VPS34, with a DC50 of 3-10 nM. HaloPROTAC-E significantly and selectively induces degradation of endogenous VPS34 complexes (VPS34, VPS15, Beclin1, and ATG14) labeled with Halo and inhibits autophagy.
    HaloPROTAC-E
  • HY-122047
    SW063058

    		Autophagy Cancer
    SW063058 is an autophagy inducer that specifically disrupts the binding of Beclin 1 to Bcl-2 while leaving the interaction between Bcl-2 and pro-apoptotic members like Bax and BIM unaffected. By inhibiting the negative regulatory effects of Bcl-2 on Beclin 1, which is crucial for the initiation of autophagy, SW063058 promotes autophagic activity without triggering cytotoxicity, apoptosis, or other forms of cell death in vitro.
    SW063058
  • HY-125191
    BRD1991

    		Bcl-2 Family Beclin1 Cancer
    BRD1991 selectively disrupts Beclin 1/Bcl-2 binding and induces autophagy without triggering apoptosis or other forms of cell death .
    BRD1991
  • HY-N8441
    Neriifolin

    17β-Neriifolin

    		 Atg8/LC3 Na+/K+ ATPase Apoptosis Beclin1 Cardiovascular Disease Inflammation/Immunology Cancer
    Neriifolin, a CNS-penetrating cardiac glycoside, is an inhibitor of the Na +, K +-ATPase. Neriifolin can target beclin 1, inhibits the formation of LC3-associated phagosomes and ameliorates experimental autoimmune encephalomyelitis (EAE) development. Neriifolin induces cell cycle arrest and apoptosis in human hepatocellular carcinoma HepG2 cells [2.
    Neriifolin
  • HY-134050
    Apostatin-1

    Apt-1

    		 RIP kinase Autophagy Apoptosis Beclin1 Necroptosis Inflammation/Immunology
    Apostatin-1 (Apt-1) is a potent TRADD inhibitor. Apostatin-1 can bind with TRADD-N (KD=2.17 μM), disrupting its binding to both TRADD-C and TRAF2. Apostatin-1 modulates the ubiquitination of RIPK1 and beclin 1. Apostatin-1 blocks apoptosis and restores cellular homeostasis by activating autophagy in cells with accumulated mutant tau, α-synuclein, or huntingtin .
    Apostatin-1
  • HY-111137
    Puquitinib

    XC-302 free base

    		 Akt Cancer
    Puquitinib (XC-302 free base) is a multi-target inhibitor with the activity of inducing autophagy in nasopharyngeal carcinoma cells by inhibiting the PI3K/AKT/mTOR signaling pathway. Puquitinib was able to inhibit the proliferation of CNE-2 cells, showing a dose-dependent antiproliferative effect. Puquitinib induced the formation of autophagosomes and autolysosomes in CNE-2 cells, which were observed by fluorescence microscopy and electron microscopy. Puquitinib promoted the formation of LC3-II and increased the expression of beclin 1, while reducing the level of p62. Puquitinib inhibited the PI3K/AKT/mTOR pathway by reducing the expression of p-AKT and p-mTOR. Puquitinib also induced apoptosis in CNE-2 cells, and when autophagy was inhibited, the apoptosis rate was reduced, which means that autophagy may interact with apoptosis to induce cell death .
    Puquitinib

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