2. Search Result
Search Result
Results for "

beclin1

" in MedChemExpress (MCE) Product Catalog:

22

Inhibitors & Agonists

8

Peptides

4

Natural
Products

1

Recombinant Proteins

2

Antibodies

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-156237
    Beclin1-ATG14L interaction inhibitor 1
    1 Publications Verification

    		 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 [1].
    Beclin1-ATG14L interaction inhibitor 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 [1].
    Pennogenin 3-O-beta-chacotrioside
  • 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 Halo-tagged 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-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 [1].
    Tat-beclin 1 scrambled
  • HY-N1399
    Androsin

    		AMPK PI3K Autophagy Metabolic Disease Inflammation/Immunology
    Androsin is an active compound isolated from Picrorhiza Kurroa Royle ex Benth. Androsin activates AMPKα/PI3K/Beclin1/LC3 signaling pathway, inhibits SREBP1c/FASN signaling pathway. Androsin can be used in research of asthma and non-alcoholic fatty liver disease (NAFLD). Androsin is orally active [1] .
    Androsin
  • 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 [1].
    Tat-beclin 1 scrambled TFA
  • HY-P2260
    Tat-beclin 1
    3 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) [1].
    Tat-beclin 1
  • 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 [1].
    Beclin1-Bcl-2 interaction inhibitor 1
  • 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. [1]
    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 [1].
    TrxR-IN-3
  • 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) [1].
    Tat-beclin 1 TFA
  • HY-N1399R
    Androsin (Standard)

    		AMPK PI3K Autophagy Metabolic Disease Inflammation/Immunology
    Androsin (Standard) is the analytical standard of Androsin. This product is intended for research and analytical applications. Androsin is an active compound isolated from Picrorhiza Kurroa Royle ex Benth. Androsin activates AMPKα/PI3K/Beclin1/LC3 signaling pathway, inhibits SREBP1c/FASN signaling pathway. Androsin can be used in research of asthma and non-alcoholic fatty liver disease (NAFLD). Androsin is orally active [1] .
    Androsin (Standard)
  • 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 [1] .
    retro-inverso TAT-Beclin 1 (D-amino acid)
  • 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 [1].
    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 [1] [2.
    Neriifolin
  • HY-138779
    ICCB-19 hydrochloride
    1 Publications Verification

    		 Autophagy RIP kinase Apoptosis Inflammation/Immunology
    ICCB-19 hydrochloride is a TRADD (TNFRSF1A associated via death domain) inhibitor. ICCB-19 hydrochloride binds with N-terminal domain of TRADD (TRADD-N), disrupting its binding to both TRADD-C and TRAF2. ICCB-19 hydrochloride is indirect inhibitor of RIPK1 kinase activity. ICCB-19 hydrochloride effectively induces autophagy and the degradation of long-lived proteins [1].
    ICCB-19 hydrochloride
  • 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 [1].
    Apostatin-1
  • HY-P1723
    Spexin
    1 Publications Verification

    Neuropeptide Q

    		 Neuropeptide Y Receptor Apoptosis Ferroptosis Autophagy Cardiovascular Disease Neurological Disease
    Spexin (Neuropeptide Q) is a selective agonist of galanin receptors GAL2 and GAL3, and is a conserved peptide that functions as a neurotransmitter/neuromodulator and endocrine factor. Spexin can function through both central and peripheral actions. Spexin upregulates Beclin 1 to inhibit ferroptosis induced by excessive autophagy, reduces the uptake of long-chain fatty acids by adipocytes, and regulates energy metabolism by increasing lipid oxidation (e.g., reducing the respiratory exchange ratio in rodents). Spexin improves cardiac function in the Doxorubicin hydrochloride (HY-15142)-induced cardiotoxicity model, protects mitochondrial membrane potential, and reduces iron accumulation and lipid peroxidation. Spexin can be used to study obesity and its related metabolic disorders, cardiovascular diseases (e.g., cardioprotection), and side effects of tumor chemotherapy [1] .
    Spexin
  • HY-P1723A
    Spexin TFA

    Neuropeptide Q TFA

    		 Neuropeptide Y Receptor Apoptosis Ferroptosis Autophagy Cardiovascular Disease Metabolic Disease
    Spexin (Neuropeptide Q) TFA is a selective agonist of galanin receptors GAL2 and GAL3, and is a conserved peptide that functions as a neurotransmitter/neuromodulator and endocrine factor. Spexin TFA can function through both central and peripheral actions. Spexin TFA upregulates Beclin 1 to inhibit ferroptosis induced by excessive autophagy, reduces the uptake of long-chain fatty acids by adipocytes, and regulates energy metabolism by increasing lipid oxidation (e.g., reducing the respiratory exchange ratio in rodents). Spexin TFA improves cardiac function in the Doxorubicin hydrochloride (HY-15142)-induced cardiotoxicity model, protects mitochondrial membrane potential, and reduces iron accumulation and lipid peroxidation. Spexin TFA can be used to study obesity and its related metabolic disorders, cardiovascular diseases (e.g., cardioprotection), and side effects of tumor chemotherapy [1] .
    Spexin TFA
  • HY-P10914
    D-CopA3

    		MDM-2/p53 Autophagy Inflammation/Immunology Cancer
    D-CopA3 is the inhibitor for MDM2 and the activator for p53 signaling pathway. D-CopA3 exhibits cytotoxicity in colorectal cancer cells HCT-116, LoVo, and RKO (IC50=15-18 μM), induces JNK/Beclin-1 mediated autophagy. D-CopA3 downregulates the expression of cell cycle inhibitory protein p21Cip1/Waf1, enhances the mucosal barrier function and reduces penetration of inflammatory mediators. D-CopA3 exhibits anti-inflammtory activity in mouse C. difficile toxin A-induced acute enteritis models and DSS (HY-116282)-induced chronic colitis models. D-CopA3 exhibits antitumor efficacy in mouse HCT-116 xenograft models [1] .
    D-CopA3
  • 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 [1].
    Puquitinib

Inquiry Online

Your information is safe with us. * Required Fields.

Salutation

  

Country or Region *

Applicant Name *

 

Organization Name *

Department *

     

Email Address *

 

Product Name *

Cat. No.

  

Requested quantity *

Phone Number *

     

Remarks

Inquiry Online

Inquiry Information

Product Name:
Cat. No.:
Quantity:
MCE Japan Authorized Agent: