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autophagosome,

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Cat. No. Nombre del producto Target Áreas de investigación Chemical Structure
  • HY-100558
    Bafilomycin A1
    Maximum Cited Publications
    802 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-B0146
    Verteporfin
    265+ 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-B0795
    MHY1485
    200+ 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-B0113
    Omeprazole
    5+ Cited Publications

    H 16868

    		 Na+/K+ ATPase Proton Pump Bacterial Cytochrome P450 Apoptosis Autophagy Atg8/LC3 TNF Receptor Interleukin Related Infection Neurological Disease Inflammation/Immunology Cancer
    Omeprazole (H 16868) is an orally active H +,K +-ATPase inhibitor and a proton pump inhibitor. Omeprazole competitively inhibits CYP2C19, CYP3A4, and CYP2C9 activity. Omeprazole inhibits gastric acid secretion and can be used for acid-related gastrointestinal disorders. Omeprazole inhibits pancreatic cancer cell proliferation, induces apoptosis, autophagosome accumulation (elevated LC3-I and LC3-II levels), oxidative stress, and cytogenetic imbalance, modulates lysosomal transport, reduces inflammatory cytokines. Omeprazole alters small intestinal morphology and magnesium absorption, and induces gastric mucosa morphologic changes. Omeprazole aslo has neuroprotective and antibacterial effects .
    Omeprazole
  • 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-B0113A
    Omeprazole sodium
    5+ Cited Publications

    H 16868 sodium

    		 Na+/K+ ATPase Interleukin Related Proton Pump Cytochrome P450 Bacterial Apoptosis Autophagy TNF Receptor Atg8/LC3 Infection Inflammation/Immunology
    Omeprazole (H 16868) sodium is an orally active H +,K +-ATPase inhibitor and a proton pump inhibitor. Omeprazole sodium competitively inhibits CYP2C19, CYP3A4, and CYP2C9 activity. Omeprazole sodium inhibits gastric acid secretion and can be used for acid-related gastrointestinal disorders. Omeprazole sodium inhibits pancreatic cancer cell proliferation, induces apoptosis, autophagosome accumulation (elevated LC3-I and LC3-II levels), oxidative stress, and cytogenetic imbalance, modulates lysosomal transport, reduces inflammatory cytokines. Omeprazole sodium alters small intestinal morphology and magnesium absorption, and induces gastric mucosa morphologic changes. Omeprazole sodium aslo has neuroprotective and antibacterial effects .
    Omeprazole sodium
  • 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-129111
    EACC
    4 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-103706
    ROC-325
    3 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-N0485
    Liensinine Diperchlorate
    15+ 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-N3415
    Kumatakenin
    1 Publications Verification

    		 Apoptosis Autophagy Caspase Ferroptosis SARS-CoV Neurological Disease Inflammation/Immunology Cancer
    Kumatakenin is an orally active apoptosis inducer and autophagy inhibitor, with a Kd value of 2.94 μM for mouse ATG5. Kumatakenin increases the activities of caspase-3, caspase-8 and caspase-9, thereby inducing caspase-dependent apoptosis in ovarian cancer cells. Kumatakenin reduces the expression of chemokines and pro-oncogenic factors in ovarian cancer cells, and inhibits M2 macrophage polarization. Kumatakenin inactivates TRIM65 function, reduces the expression and stability of FASN, and thus inhibits the proliferation, migration, invasion and tumor progression of esophageal cancer cells. Kumatakenin interacts with ATG5 to reduce its protein level, decrease LC3 level, and reduce the number of autophagosomes in the hippocampus. Kumatakenin binds to Eno3 to upregulate its expression, reduce the stability and expression level of IRP1 mRNA, inhibit ferroptosis, alleviate intestinal inflammation, and restore epithelial barrier function. Kumatakenin enhances the efficacy of antibiotics against pathogenic bacteria, inhibits SARS-CoV-2 replication, and reduces cytokine production. Kumatakenin is applicable to research related to ovarian cancer, esophageal cancer, depression and colitis .
    Kumatakenin
  • HY-174806
    Y040-7904

    7-(β-D-Galactopyranosyloxy)-4-phenylchromen-2-one

    		 Mitophagy PINK1/Parkin Amyloid-β Neurological Disease
    Y040-7904 is a mitophagy activator. Y040-7904 enhances mitophagy by promoting mitochondria transport to autophagosomes and the fusion of autophagosomes with autolysosomes. Y040-7904 induces mitophagy through the SIRT1/FoxO3 pathway. Y040-7904 upregulates the levels of Parkin, PINK1, and LC3II/I. Y040-7904 reduces amyloid-β (Aβ) accumulation in both in vitro and in vivo models of Alzheimer’s disease.
    Y040-7904
  • HY-112698
    CA-5f
    4 Publications Verification

    		 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-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-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-119357
    TN-16

    		Microtubule/Tubulin Apoptosis Autophagy Neurological Disease Cancer
    TN-16 is a Microtubule polymerization inhibitor. TN-16 induces G2/M cell cycle arrest, metaphase mitotic arrest and Apoptotic cell death in cells, and blocks late Autophagic flux by inhibiting autophagosome-lysosome fusion. TN-16 suppresses tumor growth in syngeneic mouse breast cancer models. TN-16 can be used in research related to neuroblastoma, cervical cancer, breast cancer and other tumors .
    TN-16
  • 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-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-148114
    MOPIPP

    		Autophagy Neurological Disease 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 can be used for the study of glioblastoma cells .
    MOPIPP
  • 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-B0113R
    Omeprazole (Standard)

    H 16868 (Standard)

    		 Reference Standards Na+/K+ ATPase Interleukin Related Proton Pump Cytochrome P450 Bacterial Apoptosis Autophagy TNF Receptor Atg8/LC3 Infection Metabolic Disease Cancer
    Omeprazole (Standard) is the analytical standard of Omeprazole. This product is intended for research and analytical applications. Omeprazole (H 16868) is an orally active H +,K +-ATPase inhibitor and a proton pump inhibitor. Omeprazole competitively inhibits CYP2C19, CYP3A4, and CYP2C9 activity. Omeprazole inhibits gastric acid secretion and can be used for acid-related gastrointestinal disorders. Omeprazole inhibits pancreatic cancer cell proliferation, induces apoptosis, autophagosome accumulation (elevated LC3-I and LC3-II levels), oxidative stress, and cytogenetic imbalance, modulates lysosomal transport, reduces inflammatory cytokines. Omeprazole alters small intestinal morphology and magnesium absorption, and induces gastric mucosa morphologic changes. Omeprazole aslo has neuroprotective and antibacterial effects .
    Omeprazole (Standard)
  • HY-B0113S
    Omeprazole-d3
    1 Publications Verification

    H 16868-d3

    		 Na+/K+ ATPase Interleukin Related Proton Pump Cytochrome P450 Bacterial Apoptosis Autophagy TNF Receptor Atg8/LC3 Infection Metabolic Disease Cancer
    Omeprazole-d3 (H 16868-d3) is deuterium labeled Omeprazole. Omeprazole (H 16868) is an orally active H +,K +-ATPase inhibitor and a proton pump inhibitor. Omeprazole competitively inhibits CYP2C19, CYP3A4, and CYP2C9 activity. Omeprazole inhibits gastric acid secretion and can be used for acid-related gastrointestinal disorders. Omeprazole inhibits pancreatic cancer cell proliferation, induces apoptosis, autophagosome accumulation (elevated LC3-I and LC3-II levels), oxidative stress, and cytogenetic imbalance, modulates lysosomal transport, reduces inflammatory cytokines. Omeprazole alters small intestinal morphology and magnesium absorption, and induces gastric mucosa morphologic changes. Omeprazole aslo has neuroprotective and antibacterial effects .
    Omeprazole-d3
  • HY-177120
    DMBP

    		Autophagy Cancer
    DMBP is a VPS41 inhibitor. DMBP induces methuosis and inhibits autophagy in cancer cells. DMBP inhibits the fusion of late endosomes and autophagosomes with lysosomes. DMBP effectively inhibits metastasis in a mouse metastatic melanoma model. DMBP can be used for the study of melanoma .
    DMBP
  • 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-122232
    SW083688

    		Autophagy p62 Cancer
    SW083688 is a selective TAOK2 inhibitor with an IC50 of 1.3 μM. SW083688 increases the abundance of p62 protein, inhibits autophagosome maturation, and blocks Autophagic flux. SW083688 is applicable for the research of non-small cell lung cancer and pancreatic cancer .
    SW083688
  • 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-176236
    Lipophagy inducer 1

    		LXR Autophagy Metabolic Disease
    Lipophagy inducer 1 is a lipophagy inducer. Lipophagy inducer 1 has activity of reducing lipid droplet accumulation and rescuing cell death. Lipophagy inducer 1 exerts its effects by activating lipophagy, increasing steady-state autophagosome and regulating the LXR signaling pathway. Lipophagy inducer 1 can be used in the study of diabetic nephropathy (DKD) and other diseases related to lipid metabolism disorders .
    Lipophagy inducer 1
  • 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-109546
    Omeprazole magnesium

    		Na+/K+ ATPase Interleukin Related Proton Pump Cytochrome P450 Bacterial Apoptosis Autophagy TNF Receptor Atg8/LC3 Infection Metabolic Disease Cancer
    Omeprazole (H 16868) magnesium is an orally active H +,K +-ATPase inhibitor and a proton pump inhibitor. Omeprazole magnesium competitively inhibits CYP2C19, CYP3A4, and CYP2C9 activity. Omeprazole magnesium inhibits gastric acid secretion and can be used for acid-related gastrointestinal disorders. Omeprazole magnesium inhibits pancreatic cancer cell proliferation, induces apoptosis, autophagosome accumulation (elevated LC3-I and LC3-II levels), oxidative stress, and cytogenetic imbalance, modulates lysosomal transport, reduces inflammatory cytokines. Omeprazole magnesium alters small intestinal morphology and magnesium absorption, and induces gastric mucosa morphologic changes. Omeprazole magnesium aslo has neuroprotective and antibacterial effects .
    Omeprazole magnesium
  • HY-B0113S3
    Omeprazole-13C,d3

    H 16868-13C,d3

    		 Isotope-Labeled Compounds Na+/K+ ATPase Interleukin Related Proton Pump Cytochrome P450 Bacterial Apoptosis Autophagy TNF Receptor Atg8/LC3 Infection Metabolic Disease Cancer
    Omeprazole- 13C,d3 is a 13C-labeled and deuterium labeled Omeprazole. Omeprazole (H 16868) is an orally active H +,K +-ATPase inhibitor and a proton pump inhibitor. Omeprazole competitively inhibits CYP2C19, CYP3A4, and CYP2C9 activity. Omeprazole inhibits gastric acid secretion and can be used for acid-related gastrointestinal disorders. Omeprazole inhibits pancreatic cancer cell proliferation, induces apoptosis, autophagosome accumulation (elevated LC3-I and LC3-II levels), oxidative stress, and cytogenetic imbalance, modulates lysosomal transport, reduces inflammatory cytokines. Omeprazole alters small intestinal morphology and magnesium absorption, and induces gastric mucosa morphologic changes. Omeprazole aslo has neuroprotective and antibacterial effects .
    Omeprazole-13C,d3
  • HY-123056
    EAD1

    		p62 Autophagy Apoptosis Cancer
    EAD1 is a Chloroquine (HY-17589A) analog with anticancer activity. EAD1 blocks autophagy, leading to the intracellular accumulation of autophagosome-related proteins LC3-II and p62. EAD1 induces cancer cell apoptosis and inhibits cancer cell proliferation. EAD1 can be used in the research of lung cancer and pancreatic cancer .
    EAD1
  • 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-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-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-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-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-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-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-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-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-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-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-176451
    CDK9 degrader-1

    		CDK Cancer
    CDK9 degrader-1 (Compound AZ-9) is a selective CDK9 degrader (DC50: 0.4073 µM). CDK9 degrader-1 recruits ATG101 to initiate the autophagy-lysosome pathway and forms autophagosomes by recruiting LC3, which then fuses with lysosomes to degrade CDK9 and its partner protein Cyclin T1 (DC50: 1.215 µM). CDK9 degrader-1 induces caspase 3-mediated apoptosis. CDK9 degrader-1 has antitumor activity in a mouse HCT116 xenograft model .
    CDK9 degrader-1
  • 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-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

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