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LC3II

" in MedChemExpress (MCE) Product Catalog:

35

Inhibitors & Agonists

1

Biochemical Assay Reagents

3

Peptides

5

Natural
Products

7

Isotope-Labeled Compounds

2

Oligonucleotides

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-B0113
    Omeprazole
    Maximum Cited Publications
    8 Publications Verification

    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 [3] .
    Omeprazole
  • HY-W050044
    L-Azetidine-2-carboxylic acid
    1 Publications Verification

    		 Endogenous Metabolite PERK Atg8/LC3 Autophagy Bcl-2 Family Apoptosis Eukaryotic Initiation Factor (eIF) ATF6 Cardiovascular Disease Neurological Disease Metabolic Disease Endocrinology Cancer
    L-Azetidine-2-carboxylic acid is a proline analog. L-Azetidine-2-carboxylic acid upregulates the lipid autophagy marker LC3-II via activation of the PERK pathway. L-Azetidine-2-carboxylic acid increases pro-apoptotic BAX protein. L-Azetidine-2-carboxylic acid induces ATF6 cleavage and upregulates phosphorylated eIF2α levels. L-Azetidine-2-carboxylic acid induces ER stress, inducing protein misfolding and aggregation. L-Azetidine-2-carboxylic acid shows teratogenic, pro-inflammatory and pro-apoptotic effects [3] .
    L-Azetidine-2-carboxylic acid
  • HY-B0633C
    Hyaluronic acid (Mw:1000-2000Da)

    		Biochemical Assay Reagents Interleukin Related Atg8/LC3 Inflammation/Immunology
    Hyaluronic acid (Mw: 1000-2000 Da) is a long-chain unbranched polysaccharide with a molecular weight of 1000-2000 Da. Hyaluronic acid (Mw: 2000 Da) inhibits IL-1β expression and increases LC3-II. Hyaluronic acid (Mw: 1000-2000Da) can regulate tissue homeostasis and stress resistance, promote angiogenesis and tissue remodeling. Hyaluronic acid (Mw: 1000-2000 Da) has good biocompatibility and biodegradability, and can be used in drug delivery systems and tissue engineering. Hyaluronic acid (Mw: 2000 Da) can reduce facial skin blemishes and sagging .
    Hyaluronic acid (Mw:1000-2000Da)
  • HY-B0113A
    Omeprazole sodium
    Maximum Cited Publications
    8 Publications Verification

    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 [3] .
    Omeprazole sodium
  • HY-N0538
    Xylitol

    Xylite

    		 Environmental Pollutants Endogenous Metabolite Bacterial Autophagy Atg7 Atg8/LC3 Metabolic Disease Cancer
    Xylitol can be classified as a polyol and sugar alcohol, exhibiting inhibitory activity on cancer cell proliferation. It induces autophagy (Autophagy) and cell death in A549 cells by activating the autophagy signaling pathway, as evidenced by the increased expression of LC3-II and Atg5-Atg12 upon Xylitol treatment. Additionally, Xylitol inhibits acetaldehyde production by Candida species, thereby reducing their carcinogenic potential. In vivo, Xylitol induces alterations in the gut microbiota of mice, which may enhance cholesterol accumulation and upregulate hepatic ChREBP, while also slowing tumor growth in the B16F10 melanoma C57BL/6 mouse model [3] .
    Xylitol
  • 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-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 [3].
    Dextran T5 (MW 5,000)
  • HY-163001
    Microcolin H
    1 Publications Verification

    		 Autophagy p62 Atg8/LC3 Cancer
    Microcolin H is a marine lipopeptide and phosphatidylinositol transfer protein ligand that targets PITPα/β. Microcolin H increases the conversion of LC3I to LC3II and reduces p62 levels in cancer cells, leading to autophagy cell death (Autophagy). Microcolin H effectively inhibits tumor development and has anti-proliferative activity in nude mouse subcutaneous tumor models .
    Microcolin H
  • 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 [3] .
    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 [3] .
    Omeprazole-d3
  • 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-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 [3] .
    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 [3] .
    Omeprazole-13C,d3
  • HY-P4532
    Ac-Leu-Val-Lys-Aldehyde

    		Cathepsin Neurological Disease
    Ac-Leu-Val-Lys-Aldehyde is a potent cathepsin B inhibitor with IC50s of 4 nM. Ac-Leu-Val-Lys-Aldehyde significantly reduces quinolinic acid (HY-100807)-induced striatal cell death and causes accumulation of LC3-II .
    Ac-Leu-Val-Lys-Aldehyde
  • 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-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-168640
    RIP3 activator 1

    		Autophagy Necroptosis RIP kinase Cancer
    RIP3 activator 1 (compound C8) is a potent RIP3 activator. RIP3 activator 1 inhibits cell growth. RIP3 activator 1 induces necroptosis through the RIP3/p62/Keap1 signaling pathway. RIP3 activator 1 increases the protein expression of p-MLKL. RIP3 activator 1 induces autophagy. RIP3 activator 1 increases accumulation of LC3-II and p62 protein expression .
    RIP3 activator 1
  • HY-W050044R
    L-Azetidine-2-carboxylic acid (Standard)

    		Reference Standards Endogenous Metabolite PERK Atg8/LC3 Autophagy Bcl-2 Family Apoptosis Eukaryotic Initiation Factor (eIF) ATF6 Cardiovascular Disease Neurological Disease Metabolic Disease Endocrinology Cancer
    L-Azetidine-2-carboxylic acid is a proline analog. L-Azetidine-2-carboxylic acid upregulates the lipid autophagy marker LC3-II via activation of the PERK pathway. L-Azetidine-2-carboxylic acid increases pro-apoptotic BAX protein. L-Azetidine-2-carboxylic acid induces ATF6 cleavage and upregulates phosphorylated eIF2α levels. L-Azetidine-2-carboxylic acid induces ER stress, inducing protein misfolding and aggregation. L-Azetidine-2-carboxylic acid shows teratogenic, pro-inflammatory and pro-apoptotic effects [3] .
    L-Azetidine-2-carboxylic acid (Standard)
  • HY-168206
    Autophagy-IN-6

    		Autophagy Cancer
    Autophagy-IN-6 (compound 1u) is a lysosomotropic autophagy inhibitor and can induces LC3-II protein accumulation. Autophagy-IN-6 shows anti-proliferative activity .
    Autophagy-IN-6
  • 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-P3148
    Astin B

    		p62 Atg8/LC3 Apoptosis Autophagy Reactive Oxygen Species (ROS) JNK Bcl-2 Family Caspase Metabolic Disease
    Astin B is a orally active and potent cyclic pentapeptide, that can be isolated from Aster tataricus. Astin B has hepatotoxic effects in vitro and in vivo and that hepatic injury was primarily mediated by apoptosis in a mitochondria/caspase-dependent manner. Astin B induces autophagy in L-02 cells, increases LC3-II and decreases p62 expression .
    Astin B
  • HY-125535
    OSU-53

    		AMPK mTOR Autophagy Atg8/LC3 Cancer
    OSU-53 is an orally active AMPK activator (EC50: 0.3 μM) and a direct mTOR inhibitor. OSU-53 induces autophagy and increases conversion of LC3 I to LC3 II. OSU-53 also modulates energy homeostasis by suppressing fatty acid biosynthesis and shifting the metabolism to oxidation by up-regulating the expression of PGC1α and NRF-1. OSU-53 has antitumor activity in various tumor models, such as breast cancer and thyroid cancer .
    OSU-53
  • HY-B0113S4
    Omeprazole-d3 sodium

    H 16868-d3 sodium

    		 Isotope-Labeled Compounds Na+/K+ ATPase Interleukin Related Proton Pump Cytochrome P450 Bacterial Apoptosis Autophagy TNF Receptor Atg8/LC3 Infection Metabolic Disease Cancer
    Omeprazole-d3 sodium is deuterated labeled Omeprazole (HY-B0113). Omeprazole sodium (H 16868) 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 [3] .
    Omeprazole-d3 sodium
  • HY-B0113AR
    Omeprazole sodium (Standard)

    H 16868 sodium (Standard)

    		 Reference Standards Na+/K+ ATPase Interleukin Related Proton Pump Cytochrome P450 Bacterial Apoptosis Autophagy TNF Receptor Atg8/LC3 Infection Metabolic Disease Cancer
    Omeprazole (sodium) (Standard) is the analytical standard of Omeprazole (sodium). This product is intended for research and analytical applications. Omeprazole sodium (H 16868) 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 [3] .
    Omeprazole sodium (Standard)
  • HY-B0113S2
    Omeprazole sulfone (methoxy-d3)

    Omeprazole sulphone (methoxy-d3)

    		 Isotope-Labeled Compounds Na+/K+ ATPase Interleukin Related Proton Pump Cytochrome P450 Bacterial Apoptosis Autophagy TNF Receptor Atg8/LC3 Infection Cancer
    Omeprazole sulfone (methoxy-d3) is the deuterium labeled Omeprazole sulfone. Omeprazole sulfone (H 16868) is an orally active H +,K +-ATPase inhibitor and a proton pump inhibitor. Omeprazole sulfone competitively inhibits CYP2C19, CYP3A4, and CYP2C9 activity. Omeprazole sulfone inhibits gastric acid secretion and can be used for acid-related gastrointestinal disorders. Omeprazole sulfone 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 sulfone alters small intestinal morphology and magnesium absorption, and induces gastric mucosa morphologic changes. Omeprazole sulfone aslo has neuroprotective and antibacterial effects [3] .
    Omeprazole sulfone (methoxy-d3)
  • HY-B0113S5
    Omeprazole-d6

    H 16868-d6

    		 Isotope-Labeled Compounds Na+/K+ ATPase Interleukin Related Proton Pump Cytochrome P450 Bacterial Apoptosis Autophagy TNF Receptor Atg8/LC3 Infection Metabolic Disease Cancer
    Omeprazole-d6 (H 16868-d6) 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 [3] .
    Omeprazole-d6
  • HY-179052
    Apoptosis inducer 50

    		Apoptosis Autophagy Bcl-2 Family Caspase Atg8/LC3 Atg7 CDK Reactive Oxygen Species (ROS) Cancer
    Apoptosis inducer 50 (Compound 5e) is an apoptosis inducer as well as an autophagy inducer agent. Apoptosis inducer 50 exhibits potent and selective anti-cancer activity against triple-negative breast cancer cells and metastatic colon cancer cells. Apoptosis inducer 50 upregulates the expression of pro-apoptotic proteins (Bax, Bim, cleaved Caspase-9) and downregulates the expression of the anti-apoptotic protein (BCL-XL). Apoptosis inducer 50 upregulates key autophagy markers such as Beclin-1 and ATG5, and enhances the conversion of LC3-I to LC3-II., Apoptosis inducer 50 arrests cancer cells in the G1/S phase by upregulating the expression of p21 and p27 while downregulating Cyclin D1. Apoptosis inducer 50 increases the level of ROS .
    Apoptosis inducer 50
  • HY-W768347
    Xylitol-13C5

    Xylite-13C5

    		 Isotope-Labeled Compounds Bacterial Autophagy Endogenous Metabolite Atg8/LC3 Atg7 Cancer
    Xylitol- 13C5 (Xylite- 13C5) is the 13C-labeled Xylitol (HY-N0538). Xylitol can be classified as a polyol and sugar alcohol, exhibiting inhibitory activity on cancer cell proliferation. It induces autophagy (Autophagy) and cell death in A549 cells by activating the autophagy signaling pathway, as evidenced by the increased expression of LC3-II and Atg5-Atg12 upon Xylitol treatment. Additionally, Xylitol inhibits acetaldehyde production by Candida species, thereby reducing their carcinogenic potential. In vivo, Xylitol induces alterations in the gut microbiota of mice, which may enhance cholesterol accumulation and upregulate hepatic ChREBP, while also slowing tumor growth in the B16F10 melanoma C57BL/6 mouse model [3] .
    Xylitol-13C5
  • HY-B0113S1
    Omeprazole-d3-1

    H 16868-d3-1

    		 Na+/K+ ATPase Interleukin Related Proton Pump Cytochrome P450 Bacterial Apoptosis Autophagy TNF Receptor Atg8/LC3 Infection Metabolic Disease Cancer
    Omeprazole-d3-1 is the deuterium labeled Omeprazole. Omeprazole-1 (H 16868) is an orally active H +,K +-ATPase inhibitor and a proton pump inhibitor. Omeprazole-1 competitively inhibits CYP2C19, CYP3A4, and CYP2C9 activity. Omeprazole-1 inhibits gastric acid secretion and can be used for acid-related gastrointestinal disorders. Omeprazole-1 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-1 alters small intestinal morphology and magnesium absorption, and induces gastric mucosa morphologic changes. Omeprazole-1 aslo has neuroprotective and antibacterial effects [3] .
    Omeprazole-d3-1
  • 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
  • HY-183870
    NCO-90

    		Sirtuin Apoptosis Caspase Atg8/LC3 Autophagy Mitochondrial Metabolism Cancer
    NCO-90 is a selective SIRT2 inhibitor with an IC50 of 1.0 μM. NCO-90 induces Apoptosis via Caspase activation and mitochondrial superoxide anion production, and also induces Autophagic cell death by increasing LC3-II levels and autophagosome accumulation. NCO-90 exhibits anticancer activity against leukemia. NCO-90 can be used in research related to acute lymphoblastic leukemia and acute myeloid leukemia .
    NCO-90
  • HY-165539
    SMER10

    		Autophagy Atg8/LC3 Huntingtin α-synuclein Neurological Disease
    SMER10 is a small-molecule enhancer that can induce autophagy. SMER10 can increase the number of EGFP-LC3 positive autophagosoms in COS-7 and HeLa cells, promoting the conversion of LC3-I to autophagosome-associated LC3-II. SMER10 can efficiently promote the degradation of autophagy substrates, including the mutant huntingtin protein (EGFP-HDQ74) associated with Huntington's disease and the A53T α-synuclein protein associated with Parkinson's disease. SMER10 exerts neuroprotective effect .
    SMER10
  • HY-182054
    Topoisomerase ll/ME-1-IN-1

    		Topoisomerase Beclin1 Autophagy Apoptosis Cancer
    Topoisomerase ll/ME-1-IN-1 (Compound 7a) is a Topoisomerase ll and ME-1 inhibitor with an IC50 of 5.03 μM against Topoisomerase ll. Topoisomerase ll/ME-1-IN-1 functionally inhibits the activity of Topoisomerase II and functionally blocks the activity of ME-1. Topoisomerase ll/ME-1-IN-1 induces Autophagy by upregulating the expression of Beclin-1 and LC3-II. Topoisomerase ll/ME-1-IN-1 promotes Apoptosis. Topoisomerase ll/ME-1-IN-1 exhibits antiproliferative activity against breast cancer cells and shows no toxicity to normal mammary epithelial cells. Topoisomerase ll/ME-1-IN-1 can be used in studies related to breast cancer (including triple-negative breast cancer) .
    Topoisomerase ll/ME-1-IN-1
  • HY-181062
    VWK147

    		HSP Apoptosis Autophagy ULK RIP kinase CDK Cancer
    VWK147 is a second-generation HSP90 C-terminal domain (CTD) inhibitor. VWK147 targets the CTD dimerization interface, prevents HSP90 CTD dimerization, disrupts co-chaperone PPID binding to HSP90 CTD, and inhibits HSP90 chaperone function dependent on dimerization. VWK147 reduces protein levels of HSP90 client proteins ULK1, RIPK1, and CDK4 without inducing a heat shock response. VWK147 induces cell death, including apoptosis, in Cisplatin (HY-17394)-sensitive and -resistant urothelial carcinoma cells. VWK147 induces LC3-II accumulation, inhibits autophagosome-lysosome fusion to block canonical autophagy, and induces non-canonical LC3 lipidation independent of ULK1 and PIK3C3 complexes. VWK147 can be used for the research of urothelial carcinoma .
    VWK147
  • HY-RS27792
    Map1lc3a Rat Pre-designed siRNA Set A

    		Small Interfering RNA (siRNA) Others
    Map1lc3a Rat Pre-designed siRNA Set A contains three designed siRNAs for Map1lc3a gene (Rat), as well as a negative control, a positive control, and a FAM-labeled negative control.
    Map1lc3a Rat Pre-designed siRNA Set A
    Map1lc3a Rat Pre-designed siRNA Set A

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