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LC3I

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19

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1

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1

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6

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1

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Cat. No. Nombre del producto Target Áreas de investigación 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-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-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-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-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-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-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-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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