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autophagosome,

" in MedChemExpress (MCE) Product Catalog:

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-152100
    CUR5g

    		Autophagy Cancer
    CUR5g is a potent autophagy inhibitor. CUR5g selectively inhibits autophagosome degradation in cancer cells by blocking autophagosome-lysosome fusion. CUR5g blocks the recruitment of STX17 to autophagosomes via a UVRAG-dependent mechanism, resulting in the inability of autophagosomes to fuse with lysosomes. CUR5g improves the anticancer effect of Cisplatin (HY-17394) against A549 cells both in vitro and in vivo .
    CUR5g
  • HY-129111
    EACC
    3 Publications Verification

    		 Autophagy Infection Neurological Disease
    EACC is a reversible autophagy inhibitor, which can block autophagic flux. EACC selectively inhibits the translocation of autophagosome-specific SNARE Stx17 thereby blocking autophagosome-lysosome fusion .
    EACC
  • HY-B0795
    MHY1485
    135+ Cited Publications

    		 mTOR Autophagy Cancer
    MHY1485 is a potent cell-permeable mTOR activator that targets the ATP domain of mTOR. MHY1485 inhibits autophagy by suppression of fusion between autophagosomes and lysosomes .
    MHY1485
  • HY-103706
    ROC-325
    1 Publications Verification

    		 Autophagy Apoptosis Cancer
    ROC-325 is a potent and orally active autophagy inhibitor with a strong anticancer activity. ROC-325 induces the deacidification of lysosomes, accumulation of autophagosomes, and disrupted autophagic flux. ROC-325 also induces renal cell carcinoma apoptosis .
    ROC-325
  • HY-101535
    ARP101
    1 Publications Verification

    		 Atg8/LC3 MMP Cancer
    ARP101 is a potent and selective inhibitor matrix metalloproteinase-2 (MMP-2). ARP101 induces autophagy-associated cell death in cancer cells. ARP101 is effective in inducing the formation of autophagosome and conversion of LC3I into LC3II .
    ARP101
  • HY-110341
    MRT 68601 hydrochloride

    		IKK Cancer
    MRT 68601 hydrochloride is a TBK1 inhibitor with an IC50 value of 6 nM. MRT 68601 hydrochloride inhibits autophagosome formation in lung cancer cells .
    MRT 68601 hydrochloride
  • HY-N10365
    6-(1-Hydroxyethyl)-5,6-dihydrochelerythrine

    		Autophagy Neurological Disease
    6-(1-Hydroxyethyl)-5,6-dihydrochelerythrine, a alkaloid, significantly perturbates the features of cellular organelles including early endosomes, mitochondria and autophagosomes (Parkinson’s Disease patient-derived olfactory cells) .
    6-(1-Hydroxyethyl)-5,6-dihydrochelerythrine
  • HY-121546
    ALLO-1

    		Atg8/LC3 Autophagy Cancer
    ALLO-1, an autophagy receptor, is essential for autophagosome formation around paternal organelles and directly binds to the worm LC3 homologue LGG-1 through its LC3-interacting region (LIR) motif .
    ALLO-1
  • HY-P3990
    Coibamide A

    		VEGFR Autophagy Apoptosis Cancer
    Coibamide A, an N-methyl-stabilized cytotoxic depsipeptide, shows potent antiproliferative activity. Coibamide A induces autophagosome accumulation via an mTOR-independent mechanism. Coibamide A induces apoptosis. Coibamide A inhibits VEGFA/VEGFR2 expression and suppresses tumor growth in glioblastoma xenografts .
    Coibamide A
  • HY-147656
    NAMPT degrader-1

    		ATTECs NAMPT Autophagy Cancer
    NAMPT degrader-1 (Compound A3), an autophagosome-tethering compound (ATTEC), is an nicotinamide phosphoribosyltransferase (NAMPT) degrader with an IC50 of 0.023 μM. NAMPT degrader-1 significantly induces the degradation of NAMPT through the autophagy-lysosomal pathway and shows excellent cellular antitumor potency .
    NAMPT degrader-1
  • HY-N3831
    Epimedokoreanin B

    		Bacterial Apoptosis Infection Inflammation/Immunology Cancer
    Epimedokoreanin B is a natural flavonoid with anticancer, anti-inflammatory and antibacterial effects. Epimedokoreanin B inhibits the growth of lung cancer cells through endoplasmic reticulum stress-mediated apoptosis accompanied by autophagosome accumulation. Epimedokoreanin B is an anti-periodontitis agent that inhibits gingipains and Porphyromonas gingivalis growth and biofilm formation .
    Epimedokoreanin B
  • HY-B0146
    Verteporfin
    190+ Cited Publications

    CL 318952

    		 YAP Apoptosis Autophagy Photosensitizer Cancer
    Verteporfin (CL 318952) is a photosensitizer for photodynamic therapy to eliminate the abnormal blood vessels in the eye associated with conditions such as age-related macular degeneration. Verteporfin is a YAP inhibitor which disrupts YAP-TEAD interactions. Verteporfin induces cell apoptosis . Verteporfinis an autophagy inhibitor that blocks autophagy at an early stage by inhibiting autophagosome formation .
    Verteporfin
  • HY-112698
    CA-5f

    		p62 Atg8/LC3 Autophagy Apoptosis Cancer
    CA-5f is a potent late-stage macroautophagy/autophagy inhibitor via inhibiting autophagosome-lysosome fusion. CA-5f increases LC3B-II (a marker to monitor autophagy) and SQSTM1 protein, and also increases ROS production. Anti-tumor activity .
    CA-5f
  • HY-111287
    Autophagonizer

    DK-1-49

    		 Autophagy Cancer
    Autophagonizer (DK-1-49) is a small molecule autophagy inducer that results in an accumulation of autophagy-associated LC3-II and enhances levels of autophagosomes and acidic vacuoles. Autophagonizer inhibits cell viability and induces cell death in not only cancer cells but also Bax/Bak double-knockout cells with EC50 values of 3-4 μM .
    Autophagonizer
  • HY-100932
    ML-9
    4 Publications Verification

    		 Myosin Cancer
    ML-9 is a selective and potent inhibitor of Akt kinase, inhibits myosin light-chain kinase (MLCK) and stromal interaction molecule 1 (STIM1) activity . ML-9 inhibits inhibits MLCK, PKA and PKC activity with Ki values of 4, 32 and 54 μM, respectively . ML-9 induces autophagy by stimulating autophagosome formation and inhibiting their degradation .
    ML-9
  • HY-N0485
    Liensinine Diperchlorate
    5+ Cited Publications

    		 Autophagy Mitophagy Cardiovascular Disease
    Liensinine Diperchlor​ate is a major isoquinoline alkaloid, extracted from the seed embryo of Nelumbo nucifera Gaertn. Liensinine Diperchlor​ate inhibits late-stage autophagy/mitophagy through blocking autophagosome-lysosome fusion. Liensinine Diperchlor​ate has a wide range of biological activities, including anti-arrhythmias, anti-hypertension, anti-pulmonary fibrosis, relaxation on vascular smooth muscle, etc .
    Liensinine Diperchlorate
  • HY-16121
    CAA-0225

    		Cathepsin Others
    CAA-0225 is a tissue protease L inhibitor that inhibits rat liver tissue protease L with a IC50 value of 1.9 nM. CAA-0225 can participate in the degradation of autophagosome membrane markers LC3-II and GABARAP (HY-P72639), improve cardiac function in mice with reperfusion injury, and kill and eliminate Trypanosoma brucei parasites [1][2][3].
    CAA-0225
  • HY-157458
    PDEδ autophagic degrader 1

    		ATTECs Phosphodiesterase (PDE) Autophagy Cancer
    PDEδ autophagic degrader 1 (compound 12c), an autophagosome-tethering compound (ATTEC). is a potent PDEδ autophagic degrader. PDEδ autophagic degrader 1 reduces the PDEδ protein level through lysosome-mediated autophagy without affecting the PDEδ mRNA expression. PDEδ autophagic degrader 1 suppresses the growth in KRAS mutant pancreatic cancer cells .
    PDEδ autophagic degrader 1
  • HY-B0146R
    Verteporfin (Standard)

    CL 318952 (Standard)

    		 YAP Apoptosis Autophagy Cancer
    Verteporfin (Standard) is the analytical standard of Verteporfin. This product is intended for research and analytical applications. Verteporfin (CL 318952) is a photosensitizer for photodynamic therapy to eliminate the abnormal blood vessels in the eye associated with conditions such as age-related macular degeneration. Verteporfin is a YAP inhibitor which disrupts YAP-TEAD interactions. Verteporfin induces cell apoptosis . Verteporfinis an autophagy inhibitor that blocks autophagy at an early stage by inhibiting autophagosome formation .
    Verteporfin (Standard)
  • HY-150636
    Autophagy-IN-1

    		Autophagy Apoptosis Cancer
    Autophagy-IN-1 is a potent autophagy/mitophagy inhibitor, acts by selectively increasing the autophagic flux while blocking the autophagosome-lysosome fusion in cancer cells. Autophagy-IN-1 can induce apoptosis and cell cycle arrest. Autophagy-IN-1 significantly inhibits tumor growth in an HCT116 xenograft mouse model and with low toxicity. Autophagy-IN-1 can be used for researching colorectal cancer .
    Autophagy-IN-1
  • HY-148114
    MOPIPP

    		Autophagy Cancer
    MOPIPP is a novel indolebased chalcone, and vacuolin-1, is a non-lethal vacuoleinducing 2-propyl analog of MOMIPP (HY-119624). MOPIPP induces cellular vacuolization and increases autophagosomes numbers. MOPIPP also triggers methuosis, and interrupts glucose uptake and glycolytic metabolism. MOPIPP can cross the blood-brain barrier and shows efficacy in suppressing tumor progression agaisnt glioblastoma cells .
    MOPIPP
  • HY-W250118
    Phosphatidylethanolamine

    		Liposome Autophagy Neurological Disease Metabolic Disease
    Phosphatidylethanolamine is an orally active phospholipid widely present in organisms. Phosphatidylethanolamine participates in the formation of autophagosome membrane as a lipid anchor of autophagy-related protein Atg8/LC3. Phosphatidylethanolamine enhances Autophagic flux, promotes cell differentiation, regulates lipid droplet fusion, delays aging, and also affects lipid metabolism and membrane integrity .
    Phosphatidylethanolamine
  • HY-100558
    Bafilomycin A1
    Maximum Cited Publications
    537 Publications Verification

    BafA1

    		 Proton Pump Autophagy Antibiotic Bacterial Apoptosis Infection Cancer
    Bafilomycin A1 (BafA1) is a specific and reversible inhibitor of vacuolar H +-ATPase (V-ATPase) with IC50 values of 4-400 nmol/mg. Bafilomycin A1, a macrolide antibiotic, is also used as an autophagy inhibitor at the late stage. Bafilomycin A1 blocks autophagosome-lysosome fusion and inhibits acidification and protein degradation in lysosomes of cultured cells. Bafilomycin A1 induces apoptosis .
    Bafilomycin A1
  • HY-118326
    MRT 68601

    		Autophagy Cancer
    MRT 68601 is a potent TBK1 inhibitor with the activity of inhibiting autophagosome formation in lung cancer cells. MRT 68601 may have potential effects against targets associated with host-dependent factors identified in SARS-CoV-2 infection. The drug targets involved in MRT 68601 are related to existing FDA-approved drugs and compounds in clinical trials, which can provide support for the development of broad-spectrum antiviral therapies .
    MRT 68601
  • HY-100932A
    ML-9 Free Base

    		Myosin Cancer
    ML-9 (Free Base) is a selective and potent inhibitor of Akt kinase, inhibits myosin light-chain kinase (MLCK) and stromal interaction molecule 1 (STIM1) activity . ML-9 (Free Base) inhibits inhibits MLCK, PKA and PKC activity with Ki values of 4, 32 and 54 μM, respectively . ML-9 (Free Base) induces autophagy by stimulating autophagosome formation and inhibiting their degradation .
    ML-9 Free Base
  • HY-176043
    PCSK9 autophagic degrader 2

    		ATTECs PCSK9 Cancer
    PCSK9 autophagic degrader 2 (W6) is a PCSK9 targeted autophagosome, with an DC50 of 20.6 nM. PCSK9 autophagic degrader 2 (W6) demonstrates comparable antiatherosclerosis effect and exhibits a KD of 2.5 μM for LC3B (Pink: PCSK9 ligand HY-176044; Blue: LC3B ligand HY-176045; Black: linker HY-141373) .
    PCSK9 autophagic degrader 2
  • HY-N2334A
    Glycochenodeoxycholic acid sodium salt
    4 Publications Verification

    Chenodeoxycholylglycine sodium salt; Sodium glycochenodeoxycholate

    		 Endogenous Metabolite Apoptosis STAT BCL6 Interleukin Related Caspase Metabolic Disease Cancer
    Glycochenodeoxycholic acid sodium salt (Sodium glycochenodeoxycholate) is a relatively toxic bile salt generated in the liver from chenodeoxycholic acid and glycine. Glycochenodeoxycholic acid sodium salt inhibits Autophagosome formation and impairs lysosomal function by inhibiting lysosomal proteolysis and increasing lysosomal pH in human normal liver cells, leading to the Apoptosis of human hepatocyte cells. Glycochenodeoxycholic acid sodium salt induces stemness and chemoresistance via activating STAT3 signaling pathway in hepatocellular carcinoma cells (HCC). Glycochenodeoxycholic acid sodium salt is promising for research in the field of cholestasis desease, hepatocellular carcinoma and primary sclerosing cholangitis (PSC) .
    Glycochenodeoxycholic acid sodium salt
  • HY-N2334
    Glycochenodeoxycholic acid
    4 Publications Verification

    Chenodeoxycholylglycine

    		 Endogenous Metabolite Apoptosis STAT BCL6 Interleukin Related Caspase Metabolic Disease Cancer
    Glycochenodeoxycholic acid (Chenodeoxycholylglycine) is a relatively toxic bile salt generated in the liver from chenodeoxycholic acid and glycine. Glycochenodeoxycholic acid inhibits Autophagosome formation and impairs lysosomal function by inhibiting lysosomal proteolysis and increasing lysosomal pH in human normal liver cells, leading to the Apoptosis of human hepatocyte cells. Glycochenodeoxycholic acid induces stemness and chemoresistance via activating STAT3 signaling pathway in hepatocellular carcinoma cells (HCC). Glycochenodeoxycholic acid is promising for research in the field of cholestasis desease, hepatocellular carcinoma and primary sclerosing cholangitis (PSC) .
    Glycochenodeoxycholic acid
  • HY-173150
    YAP-IN-1

    		YAP Cancer
    YAP-IN-1 (Compound (+)-1) is an autophagy (Autophagy) inhibitor targeting YAP1. YAP-IN-1 binds to the Hippo pathway transcription factor YAP1 with a Kd of 9.13 μM and induces its degradation via the chaperone-mediated autophagy (CMA) pathway. This process inhibits Rab7-mediated fusion of autophagosomes and lysosomes, thereby reducing overall autophagy levels without affecting lysosomal function. YAP-IN-1 holds promise for research in cancer (e.g., liver cancer, breast cancer, etc.) .
    YAP-IN-1
  • HY-N2334R
    Glycochenodeoxycholic acid (Standard)

    Chenodeoxycholylglycine (Standard)

    		 Endogenous Metabolite Apoptosis STAT BCL6 Interleukin Related Caspase Metabolic Disease Cancer
    Glycochenodeoxycholic acid (Standard) is the analytical standard of Glycochenodeoxycholic acid. This product is intended for research and analytical applications. Glycochenodeoxycholic acid (Chenodeoxycholylglycine) is a relatively toxic bile salt generated in the liver from chenodeoxycholic acid and glycine. Glycochenodeoxycholic acid inhibits Autophagosome formation and impairs lysosomal function by inhibiting lysosomal proteolysis and increasing lysosomal pH in human normal liver cells, leading to the Apoptosis of human hepatocyte cells. Glycochenodeoxycholic acid induces stemness and chemoresistance via activating STAT3 signaling pathway in hepatocellular carcinoma cells (HCC). Glycochenodeoxycholic acid is promising for research in the field of cholestasis desease, hepatocellular carcinoma and primary sclerosing cholangitis (PSC)[1][2][3][4].
    Glycochenodeoxycholic acid (Standard)
  • 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-170992
    Autophagy agonist-1

    		Autophagy CDK Atg8/LC3 PINK1/Parkin Cancer
    Autophagy agonist-1 (compound 22) is an Autophagy agonist. Autophagy agonist-1 exhibits significant anticancer activity against HepG2 cells and normal cells with IC50s of 8.8 μM and > 50 μM. Autophagy agonist-1 induces G1/S phase cell cycle arrest and inhibits CDK4 and CyclinD1 expression while upregulating P21. Autophagy agonist-1 promotes the accumulation of autophagosomes and the proteins LC3 and PINK1, enhancing autophagy and mitophagy in HepG2 cells .
    Autophagy agonist-1
  • HY-138813R
    N-Desethyl Sunitinib (hydrochloride) (Standard)

    		Drug Metabolite Cancer
    Glycochenodeoxycholic acid sodium salt (Standard) is the analytical standard of Glycochenodeoxycholic acid sodium salt. This product is intended for research and analytical applications. Glycochenodeoxycholic acid sodium salt (Sodium glycochenodeoxycholate) is a relatively toxic bile salt generated in the liver from chenodeoxycholic acid and glycine. Glycochenodeoxycholic acid sodium salt inhibits Autophagosome formation and impairs lysosomal function by inhibiting lysosomal proteolysis and increasing lysosomal pH in human normal liver cells, leading to the Apoptosis of human hepatocyte cells. Glycochenodeoxycholic acid sodium salt induces stemness and chemoresistance via activating STAT3 signaling pathway in hepatocellular carcinoma cells (HCC). Glycochenodeoxycholic acid sodium salt is promising for research in the field of cholestasis desease, hepatocellular carcinoma and primary sclerosing cholangitis (PSC) .
    N-Desethyl Sunitinib (hydrochloride) (Standard)
  • HY-N2334AR
    Glycochenodeoxycholic acid sodium salt (Standard)

    		Endogenous Metabolite Apoptosis STAT BCL6 Interleukin Related Caspase Metabolic Disease Cancer
    Glycochenodeoxycholic acid sodium salt (Standard) is the analytical standard of Glycochenodeoxycholic acid sodium salt. This product is intended for research and analytical applications. Glycochenodeoxycholic acid sodium salt (Sodium glycochenodeoxycholate) is a relatively toxic bile salt generated in the liver from chenodeoxycholic acid and glycine. Glycochenodeoxycholic acid sodium salt inhibits Autophagosome formation and impairs lysosomal function by inhibiting lysosomal proteolysis and increasing lysosomal pH in human normal liver cells, leading to the Apoptosis of human hepatocyte cells. Glycochenodeoxycholic acid sodium salt induces stemness and chemoresistance via activating STAT3 signaling pathway in hepatocellular carcinoma cells (HCC). Glycochenodeoxycholic acid sodium salt is promising for research in the field of cholestasis desease, hepatocellular carcinoma and primary sclerosing cholangitis (PSC) .
    Glycochenodeoxycholic acid sodium salt (Standard)
  • HY-P10416
    Q14

    Q14 peptide

    		 Deubiquitinase Mitophagy Others Neurological Disease
    Q14 is a polypeptide derived from the USP30 (ubiquitin specific peptidase 30) transmembrane (TM) domain with the ability to inhibit the deubiquitination activity of USP30 (IC50=57.2 nM). Q14 reduces USP30 activity by inhibiting the interaction between the USP30 transmembrane domain and its catalytic domain. Q14 peptide contains the LC3 interaction region (LIR) motif, which enables it to bind to the LC3 and accelerate the formation of autophagosomes, thereby promoting mitophagy. Q14 can be used in the study of neurodegenerative diseases as well as mitochondrial quality control and cell metabolism .
    Q14
  • HY-N8380
    (-)-Latifolin

    		Apoptosis Autophagy PI3K Necroptosis Cardiovascular Disease Inflammation/Immunology Cancer
    (-)-Latifolin, a flavonoid, induces apoptotic cell death by targeting PI3K/AKT/mTOR/p70S6K signaling. (-)-Latifolin significantly inhibits the cell proliferation of oral squamous cell carcinoma (OSCC), and causes the anti-metastatic activities by effectively blocking cell migration, invasion, and adhesion via the inactivation of FAK/Src. (-)-Latifolin suppresses autophagic-related proteins and autophagosome formation. (-)-Latifolin inhibits necroptosis by dephosphorylating necroptosis-regulatory proteins (RIP1, RIP3, and MLKL). (-)-Latifolin has beneficial effects on anti-aging, anti-carcinogenic, anti-inflammatory, and cardio-protective activities .
    (-)-Latifolin
  • 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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