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autophagosome formation

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-B0146
    Verteporfin
    Maximum Cited Publications
    266 Publications Verification

    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-N2334
    Glycochenodeoxycholic acid
    5 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-N2334A
    Glycochenodeoxycholic acid sodium salt
    5 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-W250118
    Cephalin form bovine brain
    2 Publications Verification

    		 Liposome Autophagy Neurological Disease Metabolic Disease
    Cephalin form bovine brain is an orally active phospholipid widely present in organisms.Cephalin form bovine brain participates in the formation of autophagosome membrane as a lipid anchor of autophagy-related protein Atg8/LC3. Cephalin form bovine brain enhances Autophagic flux, promotes cell differentiation, regulates lipid droplet fusion, delays aging, and also affects lipid metabolism and membrane integrity .
    Cephalin form bovine brain
  • HY-100932
    ML-9
    5 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-112624K
    Dextran T5 (MW 5,000)

    Dextran 5; Dextran D5; Dextran T5(MW 4500-5500)

    		 Apoptosis Autophagy Others
    Dextran T5 (MW 5,000) is a sulfated polysaccharide anti-apoptotic and autophagic agent. Dextran T5 (MW 5,000) has sulfated groups and interacts with cell membranes by mimicking endogenous glycosaminoglycans, inhibiting the mitochondrial apoptotic pathway and delaying DNA fragmentation to exert anti-apoptotic activity. Dextran T5 (MW 5,000) also promotes the conversion of LC3-I to LC3-II and the formation of autophagosomes to activate the autophagic pathway. Dextran T5 (MW 5,000) can prolong the survival cycle of CHO cells and increase the production of recombinant erythropoietin (EPO). The Dextran series of compounds are also natural polysaccharide drug carriers that can be connected to drugs through covalent bonding methods such as ester bonds, amide bonds or click chemistry, or self-assembled to form carriers such as nanoparticles and hydrogels. Dextran is biodegradable and biocompatible, and can achieve targeted delivery and controlled release of drugs. Dextran derivatives can prolong drug half-life, increase local concentration and reduce immune clearance activity. The Dextran series of compounds are also natural polysaccharide drug carriers that can be connected to drugs through covalent bonding methods such as ester bonds, amide bonds or click chemistry, or self-assembled to form carriers such as nanoparticles and hydrogels. Dextran is biodegradable and biocompatible, and can achieve targeted delivery and controlled release of drugs. Dextran derivatives can prolong the half-life of drugs, increase local concentrations, and reduce the activity of immune clearance .
    Dextran T5 (MW 5,000)
  • HY-134807
    Indophagolin

    		P2X Receptor 5-HT Receptor Autophagy Cancer
    Indophagolin is a potent, indoline-containing autophagy inhibitor (IC50=140 nM). Indophagolin antagonizes the purinergic receptor P2X4 as well as P2X1 and P2X3 with IC50s of 2.71, 2.40 and 3.49 μM, respectively. Indophagolin also antagonizes the Gq-protein-coupled P2Y4, P2Y6, and P2Y11 receptors (IC50s =3.4~15.4 μM). Indophagolin has a strong antagonistic effect on serotonin receptor 5-HT6 (IC50=1.0 μM) and a moderate effect on receptors 5-HT1B, 5-HT2B, 5-HT4e, and 5-HT7 .
    Indophagolin
  • HY-N0805A
    Alisol B
    1 Publications Verification

    		 Epoxide Hydrolase CaMK Autophagy Apoptosis Metabolic Disease Inflammation/Immunology Cancer
    Alisol B is a triterpene with diverse biological activities. Alisol B binds human soluble epoxide hydrolase (sEH) with a Ki of 5.97 μM and reduces sEH activity. Alisol B inhibits RANKL-induced JNK phosphorylation, NFATc1 and c-Fos expression, osteoclast formation, mature osteoclast pit-forming and actin ring activity, and SERCA pump activity. Alisol B induces calcium mobilization, CaMKK-AMPK-mTOR pathway activation, autophagic flux, autophagosome formation, G1 phase cell cycle arrest, endoplasmic reticulum stress, unfolded protein responses, and cancer cell apoptosis. Alisol B can be used for the research of hypercalcemia, osteoporosis, rheumatoid arthritis, periodontitis, acute kidney injury, and breast cancer .
    Alisol B
  • HY-161746
    Anle138b-F105

    		AUTOTACs Autophagy Neurological Disease
    Anle138b-F105 is an autophagy-targeting chimera (AUTOTAC) that targets p62/Sequestosome-1/SQSTM1. Anle138b-F105 binds to the ZZ domain of p62, induces conformational activation, self-oligomerization, interaction with LC3, and formation of autophagosomes. Anle138b-F105 induces autophagic flux of ubiquitin-conjugated aggregated proteins, leading to their lysosomal degradation. Anle138b-F105 is applicable for the research of neurodegenerative proteinopathies .
    Anle138b-F105
  • 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-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-N2334R
    Glycochenodeoxycholic acid (Standard)

    Chenodeoxycholylglycine (Standard)

    		 Reference Standards 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-N2334AR
    Glycochenodeoxycholic acid sodium salt (Standard)

    Chenodeoxycholylglycine sodium salt (Standard); Sodium glycochenodeoxycholate (Standard)

    		 Reference Standards 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-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-B0146R
    Verteporfin (Standard)

    CL 318952 (Standard)

    		 Reference Standards 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-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-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-W665208
    Zapotin

    		Biochemical Assay Reagents Fungal Reactive Oxygen Species (ROS) Infection Neurological Disease Metabolic Disease Cancer
    Zapotin is a member of the polymethoxyflavones, which are natural polyphenols from the group of flavonoid. Zapotin exhibits antidepressant, anticancer, antifungal, and antioxidant activity. Zapotin is a chemopreventive and chemotherapeutic agent. Zapotin can result in a reduction of large aberrant crypt foci in CF-1 mouse model. Zapotin inhibits autophagosome formation. Zapotin has inhibitory activity in mouse mammary organ culture with an IC50 of 50 µg/mL .
    Zapotin
  • 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-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-179003
    mTOR/GLS1-IN-1

    		mTOR Glutaminase Reactive Oxygen Species (ROS) Autophagy Apoptosis Ferroptosis Glutathione Peroxidase Cancer
    mTOR/GLS1-IN-1 (Compoud 9d) is a potent dual targeted mTOR/GLS1 inhibitor. Has anti proliferative activity against various tumor cells. mTOR/GLS1-IN-1 dose dependently induces ROS accumulation, induces autophagosome formation, and induces apoptosis. mTOR/GLS1-IN-1 can increase Fe 2+, decrease GPX4, and induce ferroptosis. mTOR/GLS1-IN-1 can inhibit cell migration, invasion, and angiogenesis. mTOR/GLS1-IN-1 can be used in the research of cancer, such as breast cancer .
    mTOR/GLS1-IN-1
  • 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-138813R
    N-Desethyl Sunitinib hydrochloride (Standard)

    SU-12662 hydrochloride (Standard)

    		 Reference Standards 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-N0805AR
    Alisol B (Standard)

    		Reference Standards Epoxide Hydrolase CaMK Autophagy Apoptosis Metabolic Disease Inflammation/Immunology Cancer
    Alisol B (Standard) is the analytical standard of Alisol B (HY-N0805A). This product is intended for research and analytical applications. Alisol B is a triterpene with diverse biological activities. Alisol B binds human soluble epoxide hydrolase (sEH) with a Ki of 5.97 μM and reduces sEH activity. Alisol B inhibits RANKL-induced JNK phosphorylation, NFATc1 and c-Fos expression, osteoclast formation, mature osteoclast pit-forming and actin ring activity, and SERCA pump activity. Alisol B induces calcium mobilization, CaMKK-AMPK-mTOR pathway activation, autophagic flux, autophagosome formation, G1 phase cell cycle arrest, endoplasmic reticulum stress, unfolded protein responses, and cancer cell apoptosis. Alisol B can be used for the research of hypercalcemia, osteoporosis, rheumatoid arthritis, periodontitis, acute kidney injury, and breast cancer.
    Alisol B (Standard)
  • 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
  • HY-183835
    Autophagy-IN-10

    		Autophagy Others
    Autophagy-IN-10 (Compound 12a) is an Autophagy inhibitor and an inhibitor of ATG5 interaction with other proteins, with an IC50 value of 2.29 μM against ATG5-ATG16L1 and an IC50 value of 3.68 μM against ATG5-TECAIR .
    Autophagy-IN-10
  • HY-183807
    T1742

    		Autophagy Cancer
    T1742 is an autophagy inhibitor targeting ATG5. T1742 blocks and disrupts protein-protein interactions between ATG5 and ATG16L1, and between ATG5 and TECAIR.T 1742 inhibits autophagy in living cells via reduced autophagosome formation and downregulated ATG8-PE conjugation. T1742 can be used to study autophagy mechanisms .
    T1742
  • HY-183737
    ATG5/TECAIR-IN-1

    		Autophagy Infection Cancer
    ATG5/TECAIR-IN-1 is a ATG5-TECAIR interaction inhibitor with an IC50 of 20.79 μM. ATG5/TECAIR-IN-1 inhibits autophagy. TG5/TECAIR-IN-1 is applicable to research on modulating protein-protein interactions to intervene in autophagy-related diseases, such as infectious diseases and cancers .
    ATG5/TECAIR-IN-1
  • HY-183833
    Autophagy-IN-9

    		Autophagy Infection
    Autophagy-IN-9 is a ATG5 inhibitor with an IC50 of 21.29 μM against ATG5-TECAIR. Autophagy-IN-9 blocks the binding of ATG5 to the hot-spot amino acid residues of TECAIR protein, disrupts the assembly of ATG5-related ternary complexes, inhibits autophagosome formation, and thereby downregulates cellular autophagy levels. Autophagy-IN-9 can be used in autophagy-related research, such as studies on infection .
    Autophagy-IN-9
  • HY-100932R
    ML-9 (Standard)

    		Myosin Reference Standards Cancer
    ML-9 (Standard) is the analytical standard of ML-9 (HY-100932). This product is intended for research and analytical applications. 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 (Standard)
  • HY-183257
    ATI-1

    		Autophagy Beclin1 Reactive Oxygen Species (ROS) p97 Cancer
    ATI-1 is an autophagy initiation inhibitor. ATI-1 targets valosin-containing protein (VCP/p97, disrupts its interaction with UFL1, impairs UFMylation homeostasis associated with VCP, promotes polyubiquitination and degradation of Beclin1, and blocks the formation of early autophagosomes. ATI-1 induces synergistic death of autophagy-dependent malignant tumor cells under nutrient deprivation conditions, accompanied by decreased mitochondrial membrane potential, reduced ROS levels and lysosomal stress. ATI-1 exhibits anti-tumor efficacy in a pancreatic adenocarcinoma xenograft mouse model. ATI-1 can be used for the research of pancreatic adenocarcinoma and lung cancer .
    ATI-1

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