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Pathways Recommended: Neuronal Signaling JAK/STAT Signaling
Results for "

HIF signaling

" in MedChemExpress (MCE) Product Catalog:

48

Inhibitors & Agonists

2

Screening Libraries

1

Fluorescent Dyes

1

Biochemical Assay Reagents

4

Peptides

18

Natural
Products

10

Isotope-Labeled Compounds

4

Oligonucleotides

1

GMP Molecules

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-15893
    DMOG
    Maximum Cited Publications
    76 Publications Verification

    Dimethyloxallyl Glycine

    		 HIF/HIF Prolyl-Hydroxylase Autophagy Cancer
    DMOG (Dimethyloxallyl Glycine) is a cell permeable and competitive inhibitor of HIF-PH, which results in HIF-1α stabilisation and accmulation?in vitro and in vivo . DMOG is an α-ketoglutarate analogue and inhibits α-KG-dependent hydroxylases. DMOG?acts as a pro-angiogenic agent and plays a protective role in experimental model of colitis and diarrhoea via HIF-1 related signal . DMOG induces cell autophagy .
    DMOG
  • HY-N0171A
    Beta-Sitosterol (purity>98%)
    15+ Cited Publications

    β-Sitosterol (purity>98%); 22,23-Dihydrostigmasterol (purity>98%)

    		 Bacterial Apoptosis Reactive Oxygen Species (ROS) MDM-2/p53 Caspase PARP MMP Bcl-2 Family HIF/HIF Prolyl-Hydroxylase TNF Receptor Interleukin Related NF-κB mTOR Lactate Dehydrogenase CDK Glutathione Peroxidase SOD Infection Cardiovascular Disease Inflammation/Immunology Cancer
    Beta-Sitosterol (purity>98%) is orally active. Beta-Sitosterol exhibits multiple activities, including anti-inflammatory, anticancer, antioxidant, antimicrobial, antidiabetic, antioxidant enzyme, and analgesic. Beta-Sitosterol inhibits inflammation and impaired adipogenesis in bovine mammary epithelial cells by reducing levels of ROS, TNF-α, IL-1β, and NF-κB p65 and restoring the activity of the HIF-1α/mTOR signaling pathway. Beta-Sitosterol induces apoptosis in cancer cells through ROS-mediated mitochondrial dysregulation and p53 activation. Beta-Sitosterol exerts its anticancer effects in cancer cells by activating caspase-3, caspase-8, and caspase-9, mediating PARP inactivation, MMP loss, altered Bcl-2-Bax ratio, and cytochrome c release. Beta-Sitosterol modulates macrophage polarization and reduces rheumatoid inflammation in mice. Beta-Sitosterol inhibits tumor growth in multiple mouse cancer models. Beta-Sitosterol can be used in the research of arthritis, lung cancer, breast cancer and other cancers, diabetes, etc .
    Beta-Sitosterol (purity>98%)
  • HY-N0390S1
    L-Glutamine-13C5
    Maximum Cited Publications
    9 Publications Verification

    L-Glutamic acid 5-amide-13C5

    		 Isotope-Labeled Compounds mGluR Ferroptosis Environmental Pollutants Endogenous Metabolite HIF/HIF Prolyl-Hydroxylase mTOR STAT NF-κB Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology
    L-Glutamine- 13C5 is the 13C-labeled L-Glutamine (HY-N0390). L-Glutamine is an orally active nutritional agent and cellular metabolism regulator. L-Glutamine is taken up in a Na +-dependent manner and targets multiple key molecules including glutaminase, mTORC1, NF-κB, STAT-3 and HIF-1α. L-Glutamine enhances glutaminolytic catabolism, drives the conversion of glutamate to α-ketoglutarate, thereby regulating gene expression, integrating metabolic signals, mediating glutamine flux and maintaining redox homeostasis. L-Glutamine also promotes cell proliferation, osteogenic differentiation and fracture healing, exerts neuroprotective and cardioprotective effects, and inhibits osteoarthritis. L-Glutamine can be applied to research related to osteoporosis, osteoarthritis, ischemic stroke and acute cantharidin-induced cardiotoxicity .
    L-Glutamine-13C5
  • HY-N0484
    Liensinine
    15+ Cited Publications

    		 Reactive Oxygen Species (ROS) Autophagy Apoptosis VEGFR JAK Amyloid-β p38 MAPK HIF/HIF Prolyl-Hydroxylase STAT PI3K JNK Akt Cardiovascular Disease Neurological Disease Inflammation/Immunology Cancer
    Liensinine is a bisbenzylisoquinoline alkaloid. By inhibiting the PI3K/AKT and JNK/p38-MAPK signaling pathways, Liensinine suppresses autophagy and apoptosis, clears Aβ, and exerts anti-inflammatory, antioxidant and neuroprotective effects. Liensinine activates AMPK and inhibits the expression of HIF-1α and VEGF, thereby suppressing angiogenesis. Liensinine exerts anti-tumor effects through ROS-mediated inhibition of the JAK2/STAT3 signaling pathway. Liensinine can be used for the research of diseases such as Alzheimer's disease, hepatocellular carcinoma, osteosarcoma, sepsis-induced organ injury and stroke .
    Liensinine
  • HY-N0171
    Beta-Sitosterol (purity>80%)
    20+ Cited Publications

    		 Apoptosis Endogenous Metabolite Cardiovascular Disease Inflammation/Immunology Cancer
    Beta-Sitosterol (purity≥80%) is orally active. Beta-Sitosterol exhibits multiple activities, including anti-inflammatory, anticancer, antioxidant, antimicrobial, antidiabetic, antioxidant enzyme, and analgesic. Beta-Sitosterol inhibits inflammation and impaired adipogenesis in bovine mammary epithelial cells by reducing levels of ROS, TNF-α, IL-1β, and NF-κB p65 and restoring the activity of the HIF-1α/mTOR signaling pathway. Beta-Sitosterol induces apoptosis in cancer cells through ROS-mediated mitochondrial dysregulation and p53 activation. Beta-Sitosterol exerts its anticancer effects in cancer cells by activating caspase-3, caspase-8, and caspase-9, mediating PARP inactivation, MMP loss, altered Bcl-2-Bax ratio, and cytochrome c release. Beta-Sitosterol modulates macrophage polarization and reduces rheumatoid inflammation in mice. Beta-Sitosterol inhibits tumor growth in multiple mouse cancer models. Beta-Sitosterol can be used in the research of arthritis, lung cancer, breast cancer and other cancers, diabetes, etc .
    Beta-Sitosterol (purity>80%)
  • HY-111431
    p-Cresyl sulfate
    5+ Cited Publications

    p-Tolyl sulfate

    		 JNK p38 MAPK Reactive Oxygen Species (ROS) Metabolic Disease
    p-Cresyl sulfate (p-Tolyl sulfate) is a uremic toxin, that can cause renal damage and dysfunction. p-Cresyl sulfate shows antiproliferation activity. p-Cresyl sulfate increases the protein expression of HIF-1α and VHL, decreases the protein expression of HIF-2α. p-Cresyl sulfate induces epithelial-mesenchymal transition (EMT). p-Cresyl sulfate activates the JNK and p38 MAPK signaling pathways .
    p-Cresyl sulfate
  • HY-100543
    Zenidolol
    40+ Cited Publications

    ICI-118551

    		 Adrenergic Receptor Apoptosis Caspase Bcl-2 Family HIF/HIF Prolyl-Hydroxylase Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Zenidolol (ICI-118551) is a selective β2-adrenergic receptor antagonist with Ki values of Zenidolol for β2, β1 and β3 adrenergic receptors of 0.7, 49.5 and 611 nM, respectively. Zenidolol exerts antitumor effects via inducing apoptosis, inhibiting tumor sphere formation, and downregulating the HIF pathway by blocking β2-AR on tumor cells. Zenidolol exhibits a unique pulmonary vessel-specific vasodilatory effect in mouse models. Zenidolol can be used as an intraocular pressure-lowering agent in ophthalmic disease research .
    Zenidolol
  • HY-N0787
    Cryptochlorogenic acid
    4 Publications Verification

    4-Caffeoylquinic acid; 4-O-Caffeoylquinic acid

    		 Endogenous Metabolite NF-κB Keap1-Nrf2 mTOR HIF/HIF Prolyl-Hydroxylase Inflammation/Immunology
    Cryptochlorogenic acid (4-Caffeoylquinic acid) is a naturally occurring phenolic acid compound with oral effectiveness, anti-inflammatory, antioxidant and anti-cardiac hypertrophy effects. Alleviating LPS (HY-D1056) and ISO (HY-B0468) by regulating proinflammatory factor expression, inhibiting NF-κB activity, promoting Nrf2 nuclear transfer, and regulating PI3Kα/Akt/ mTOR / HIF-1α signaling pathway Induced physiological stress response .
    Cryptochlorogenic acid
  • HY-130413
    Protectin D1

    Neuroprotectin D1; NPD1

    		 Endogenous Metabolite PI3K Akt HIF/HIF Prolyl-Hydroxylase Reactive Oxygen Species (ROS) Caspase Interleukin Related MicroRNA Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Protectin D1, a neuroprotectin D1 produced by neuronal cells, is a member of a newly discovered family of bioactive products derived from docosahexaenoic acid. Protectin D1 also serves as a specialized pro-resolving mediator, exhibiting effective in vivo pro-resolving activity in various human disease models. Additionally, Protectin D1 is an inhibitor of NALP3 inflammasomes and regulates the PI3K/AKT and HIF-1α signaling pathways. Protectin D1 exerts anti-inflammatory effects by reducing ROS levels, inhibiting the expression of NALP3, ASC, and Caspase-1, and consequently decreasing the release of pro-inflammatory cytokines IL-1β and IL-18. Furthermore, Protectin D1 enhances miRNA-210 expression, activates the PI3K/AKT signaling pathway, and exerts cardioprotective effects. Protectin D1 holds promise for research in cardiovascular diseases and inflammatory disorders .
    Protectin D1
  • HY-N0390S
    L-Glutamine-15N
    3 Publications Verification

    L-Glutamic acid 5-amide-15N

    		 Isotope-Labeled Compounds mGluR Ferroptosis Environmental Pollutants Endogenous Metabolite HIF/HIF Prolyl-Hydroxylase mTOR STAT NF-κB Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology
    L-Glutamine- 15N is the 15N-labeled L-Glutamine (HY-N0390). L-Glutamine is an orally active nutritional agent and cellular metabolism regulator. L-Glutamine is taken up in a Na +-dependent manner and targets multiple key molecules including glutaminase, mTORC1, NF-κB, STAT-3 and HIF-1α. L-Glutamine enhances glutaminolytic catabolism, drives the conversion of glutamate to α-ketoglutarate, thereby regulating gene expression, integrating metabolic signals, mediating glutamine flux and maintaining redox homeostasis. L-Glutamine also promotes cell proliferation, osteogenic differentiation and fracture healing, exerts neuroprotective and cardioprotective effects, and inhibits osteoarthritis. L-Glutamine can be applied to research related to osteoporosis, osteoarthritis, ischemic stroke and acute cantharidin-induced cardiotoxicity .
    L-Glutamine-15N
  • HY-N0390S8
    L-Glutamine-15N2
    1 Publications Verification

    L-Glutamic acid 5-amide-15N2

    		 Isotope-Labeled Compounds mGluR Ferroptosis Environmental Pollutants Endogenous Metabolite HIF/HIF Prolyl-Hydroxylase mTOR STAT NF-κB Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology
    L-Glutamine- 15N2 is the 15N-labeled L-Glutamine (HY-N0390). L-Glutamine is an orally active nutritional agent and cellular metabolism regulator. L-Glutamine is taken up in a Na +-dependent manner and targets multiple key molecules including glutaminase, mTORC1, NF-κB, STAT-3 and HIF-1α. L-Glutamine enhances glutaminolytic catabolism, drives the conversion of glutamate to α-ketoglutarate, thereby regulating gene expression, integrating metabolic signals, mediating glutamine flux and maintaining redox homeostasis. L-Glutamine also promotes cell proliferation, osteogenic differentiation and fracture healing, exerts neuroprotective and cardioprotective effects, and inhibits osteoarthritis. L-Glutamine can be applied to research related to osteoporosis, osteoarthritis, ischemic stroke and acute cantharidin-induced cardiotoxicity .
    L-Glutamine-15N2
  • HY-N0390S9
    L-Glutamine-15N-1
    3 Publications Verification

    L-Glutamic acid 5-amide-15N-1

    		 Isotope-Labeled Compounds mGluR Ferroptosis Environmental Pollutants Endogenous Metabolite HIF/HIF Prolyl-Hydroxylase mTOR STAT NF-κB Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology
    L-Glutamine- 15N-1 is the 15N-labeled L-Glutamine (HY-N0390). L-Glutamine is an orally active nutritional agent and cellular metabolism regulator. L-Glutamine is taken up in a Na +-dependent manner and targets multiple key molecules including glutaminase, mTORC1, NF-κB, STAT-3 and HIF-1α. L-Glutamine enhances glutaminolytic catabolism, drives the conversion of glutamate to α-ketoglutarate, thereby regulating gene expression, integrating metabolic signals, mediating glutamine flux and maintaining redox homeostasis. L-Glutamine also promotes cell proliferation, osteogenic differentiation and fracture healing, exerts neuroprotective and cardioprotective effects, and inhibits osteoarthritis. L-Glutamine can be applied to research related to osteoporosis, osteoarthritis, ischemic stroke and acute cantharidin-induced cardiotoxicity .
    L-Glutamine-15N-1
  • HY-N0493
    Pectolinarigenin
    2 Publications Verification

    		 COX Lipoxygenase NF-κB p38 MAPK ERK HIF/HIF Prolyl-Hydroxylase Keap1-Nrf2 PI3K Apoptosis Autophagy Neurological Disease Inflammation/Immunology Cancer
    Pectolinarigenin is an orally active dual inhibitor of COX-2/5-LOX with anti-inflammatory, antioxidant, antitumor and neuroprotective activities. Pectolinarigenin exerts neuroprotective and anti-inflammatory effects on astrocyte inflammation via the NFκB and MAPK pathways. Pectolinarigenin inhibits LPS-induced phosphorylation of ERK1/2, N-FκB and p38MAPK, directly inhibits the enzymatic activity or binding of COX-2, 5-LOX and HIF-1α, and reduces the level of XIAP. Pectolinarigenin modifies Keap1 to promote nuclear accumulation of Nrf2, induces ARE-mediated antioxidant enzyme expression, and possesses direct free radical scavenging activity. Pectolinarigenin reduces the release of NO, proinflammatory mediators and leukotrienes, and increases the level of IL-10. Pectolinarigenin induces G2/M cell cycle arrest, apoptosis (Apoptosis) and autophagy (Autophagy) via the PI3K/AKT/mTOR signaling pathway. Pectolinarigenin reduces renal crystal deposition and inhibits melanin synthesis. Pectolinarigenin inhibits inflammation and alleviates allergy in mouse models of inflammation. Pectolinarigenin alleviates renal injury, inflammation and oxidative stress in mice by inhibiting HIF-1α activity. Pectolinarigenin can be used for the research of neurodegenerative diseases, inflammatory/allergic diseases, calcium oxalate nephrocalcinosis, gastric cancer, melasma, post-inflammatory diseases and chloasma .
    Pectolinarigenin
  • HY-N0390S2
    L-Glutamine-d5
    1 Publications Verification

    L-Glutamic acid 5-amide-d5

    		 Isotope-Labeled Compounds mGluR Ferroptosis Environmental Pollutants Endogenous Metabolite HIF/HIF Prolyl-Hydroxylase mTOR STAT NF-κB Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology
    L-Glutamine-d5 is the deuterium labeled L-Glutamine (HY-N0390). L-Glutamine is an orally active nutritional agent and cellular metabolism regulator. L-Glutamine is taken up in a Na +-dependent manner and targets multiple key molecules including glutaminase, mTORC1, NF-κB, STAT-3 and HIF-1α. L-Glutamine enhances glutaminolytic catabolism, drives the conversion of glutamate to α-ketoglutarate, thereby regulating gene expression, integrating metabolic signals, mediating glutamine flux and maintaining redox homeostasis. L-Glutamine also promotes cell proliferation, osteogenic differentiation and fracture healing, exerts neuroprotective and cardioprotective effects, and inhibits osteoarthritis. L-Glutamine can be applied to research related to osteoporosis, osteoarthritis, ischemic stroke and acute cantharidin-induced cardiotoxicity .
    L-Glutamine-d5
  • HY-N0390S6
    L-Glutamine-13C5,15N2

    L-Glutamic acid 5-amide-13C5,15N2

    		 Isotope-Labeled Compounds mGluR Ferroptosis Environmental Pollutants Endogenous Metabolite HIF/HIF Prolyl-Hydroxylase mTOR STAT NF-κB Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology
    L-Glutamine- 13C5, 15N2 is the 13C- and 15N-labeled L-Glutamine (HY-N0390). L-Glutamine is an orally active nutritional agent and cellular metabolism regulator. L-Glutamine is taken up in a Na +-dependent manner and targets multiple key molecules including glutaminase, mTORC1, NF-κB, STAT-3 and HIF-1α. L-Glutamine enhances glutaminolytic catabolism, drives the conversion of glutamate to α-ketoglutarate, thereby regulating gene expression, integrating metabolic signals, mediating glutamine flux and maintaining redox homeostasis. L-Glutamine also promotes cell proliferation, osteogenic differentiation and fracture healing, exerts neuroprotective and cardioprotective effects, and inhibits osteoarthritis. L-Glutamine can be applied to research related to osteoporosis, osteoarthritis, ischemic stroke and acute cantharidin-induced cardiotoxicity .
    L-Glutamine-13C5,15N2
  • HY-N2425
    Rhodiosin

    		Cholinesterase (ChE) Metabolic Disease
    Rhodiosin is a double inhibitor of CYP2D6 and AChE, and can be isolated from Rhodiolis rhodiolis root. The IC50 for CYP2D6 is 0.761 μM, and the Ki is 0.769 μM. Rhodiosin has antioxidant and neuroprotective activity and can regulate HIF-1α signaling pathway to protect the central nervous system
    Rhodiosin
  • HY-N0171R
    Beta-Sitosterol (Standard)
    5+ Cited Publications

    β-Sitosterol (Standard); 22,23-Dihydrostigmasterol (Standard))

    		 Reference Standards Apoptosis Endogenous Metabolite Cardiovascular Disease Inflammation/Immunology Cancer
    Beta-Sitosterol (Standard) is the analytical standard of Beta-Sitosterol. This product is intended for research and analytical applications. Beta-Sitosterol (purity≥80%) is orally active. Beta-Sitosterol exhibits multiple activities, including anti-inflammatory, anticancer, antioxidant, antimicrobial, antidiabetic, antioxidant enzyme, and analgesic. Beta-Sitosterol inhibits inflammation and impaired adipogenesis in bovine mammary epithelial cells by reducing levels of ROS, TNF-α, IL-1β, and NF-κB p65 and restoring the activity of the HIF-1α/mTOR signaling pathway. Beta-Sitosterol induces apoptosis in cancer cells through ROS-mediated mitochondrial dysregulation and p53 activation. Beta-Sitosterol exerts its anticancer effects in cancer cells by activating caspase-3, caspase-8, and caspase-9, mediating PARP inactivation, MMP loss, altered Bcl-2-Bax ratio, and cytochrome c release. Beta-Sitosterol modulates macrophage polarization and reduces rheumatoid inflammation in mice. Beta-Sitosterol inhibits tumor growth in multiple mouse cancer models. Beta-Sitosterol can be used in the research of arthritis, lung cancer, breast cancer and other cancers, diabetes, etc.
    Beta-Sitosterol (Standard)
  • HY-N0390R
    L-Glutamine (Standard)
    Maximum Cited Publications
    27 Publications Verification

    L-Glutamic acid 5-amide (Standard)

    		 Reference Standards mGluR Ferroptosis Environmental Pollutants Endogenous Metabolite HIF/HIF Prolyl-Hydroxylase mTOR STAT NF-κB Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology
    L-Glutamine (Standard) is the analytical standard of L-Glutamine (HY-N0390). This product is intended for research and analytical applications. L-Glutamine is an orally active nutritional agent and cellular metabolism regulator. L-Glutamine is taken up in a Na +-dependent manner and targets multiple key molecules including glutaminase, mTORC1, NF-κB, STAT-3 and HIF-1α. L-Glutamine enhances glutaminolytic catabolism, drives the conversion of glutamate to α-ketoglutarate, thereby regulating gene expression, integrating metabolic signals, mediating glutamine flux and maintaining redox homeostasis. L-Glutamine also promotes cell proliferation, osteogenic differentiation and fracture healing, exerts neuroprotective and cardioprotective effects, and inhibits osteoarthritis. L-Glutamine can be applied to research related to osteoporosis, osteoarthritis, ischemic stroke and acute cantharidin-induced cardiotoxicity .
    L-Glutamine (Standard)
  • HY-P1420
    TAT-cyclo-CLLFVY
    2 Publications Verification

    		 HIF/HIF Prolyl-Hydroxylase Cancer
    TAT-cyclo-CLLFVY is a cyclic peptide inhibitor of HIF-1 heterodimerization that inhibits hypoxia signaling in cancer cells. TAT-cyclo-CLLFVY disrupts HIF-1α/HIF-1β protein-protein interaction with an IC50 of 1.3 μM .
    TAT-cyclo-CLLFVY
  • HY-15672
    FM19G11

    		HIF/HIF Prolyl-Hydroxylase Neurological Disease Cancer
    FM19G11 is a hypoxia-inducible factor-1-alpha (HIF-1α) inhibitor, and it inhibits hypoxia-induced luciferase activity with an IC50 of 80 nM in HeLa cells. FM19G11 modulates other signaling pathways, including mTOR and PI3K/Akt/eNOS, when the HIF-1α pathway is inactivated under normoxic conditions .
    FM19G11
  • HY-147426
    Zifcasiran

    ADS-007; ARO HIF2

    		 Small Interfering RNA (siRNA) HIF/HIF Prolyl-Hydroxylase Cancer
    Zifcasiran (ADS-007; ARO HIF2) is an siRNA synthetic double-stranded RNAi trigger. Zifcasiran sodium selectively target hypoxia-inducible factor-2α (HIF2α) interrupting downstream pro-oncogenic signaling in clear cell renal cell carcinoma (ccRCC). Zifcasiran sodium engages the cell's RNAi machinery to target HIF2α (EPAS1) mRNA for degradation, thereby reducing the amount of free HIF2α mRNA available for translation .
    Zifcasiran
  • HY-148877
    AT-533

    		HSP HSV HIF/HIF Prolyl-Hydroxylase VEGFR NF-κB ERK Akt FAK Infection Inflammation/Immunology Cancer
    AT-533 is a potent Hsp90 and HSV inhibitor. AT-533 suppresses tumor growth and angiogenesis by blocking the HIF-1α/VEGF/VEGFR-2 signaling pathway. AT-533 also inhibits the activation of the downstream pathways, including Akt/mTOR/p70S6K, Erk1/2 and FAK. AT-533 inhibits the tube formation, cell migration, and invasion of human umbilical vein endothelial cells (HUVECs) .
    AT-533
  • HY-N0390S5
    L-Glutamine-1-13C
    1 Publications Verification

    L-Glutamic acid 5-amide-1-13C

    		 Isotope-Labeled Compounds mGluR Ferroptosis Environmental Pollutants Endogenous Metabolite HIF/HIF Prolyl-Hydroxylase mTOR STAT NF-κB Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology
    L-Glutamine-1- 13C is the 13C-labeled L-Glutamine (HY-N0390). L-Glutamine is an orally active nutritional agent and cellular metabolism regulator. L-Glutamine is taken up in a Na +-dependent manner and targets multiple key molecules including glutaminase, mTORC1, NF-κB, STAT-3 and HIF-1α. L-Glutamine enhances glutaminolytic catabolism, drives the conversion of glutamate to α-ketoglutarate, thereby regulating gene expression, integrating metabolic signals, mediating glutamine flux and maintaining redox homeostasis. L-Glutamine also promotes cell proliferation, osteogenic differentiation and fracture healing, exerts neuroprotective and cardioprotective effects, and inhibits osteoarthritis. L-Glutamine can be applied to research related to osteoporosis, osteoarthritis, ischemic stroke and acute cantharidin-induced cardiotoxicity .
    L-Glutamine-1-13C
  • HY-N0390S4
    L-Glutamine-5-13C

    L-Glutamic acid 5-amide-5-13C

    		 Isotope-Labeled Compounds mGluR Ferroptosis Environmental Pollutants Endogenous Metabolite HIF/HIF Prolyl-Hydroxylase mTOR STAT NF-κB Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology
    L-Glutamine-5- 13C is the 13C-labeled L-Glutamine (HY-N0390). L-Glutamine is an orally active nutritional agent and cellular metabolism regulator. L-Glutamine is taken up in a Na +-dependent manner and targets multiple key molecules including glutaminase, mTORC1, NF-κB, STAT-3 and HIF-1α. L-Glutamine enhances glutaminolytic catabolism, drives the conversion of glutamate to α-ketoglutarate, thereby regulating gene expression, integrating metabolic signals, mediating glutamine flux and maintaining redox homeostasis. L-Glutamine also promotes cell proliferation, osteogenic differentiation and fracture healing, exerts neuroprotective and cardioprotective effects, and inhibits osteoarthritis. L-Glutamine can be applied to research related to osteoporosis, osteoarthritis, ischemic stroke and acute cantharidin-induced cardiotoxicity .
    L-Glutamine-5-13C
  • HY-15893R
    DMOG (Standard)

    Dimethyloxallyl Glycine (Standard)

    		 HIF/HIF Prolyl-Hydroxylase Autophagy Reference Standards Cancer
    DMOG (Standard) is the analytical standard of DMOG. This product is intended for research and analytical applications. DMOG (Dimethyloxallyl Glycine) is a cell permeable and competitive inhibitor of HIF-PH, which results in HIF-1α stabilisation and accmulation in vitro and in vivo . DMOG is an α-ketoglutarate analogue and inhibits α-KG-dependent hydroxylases. DMOG acts as a pro-angiogenic agent and plays a protective role in experimental model of colitis and diarrhoea via HIF-1 related signal . DMOG induces cell autophagy .
    DMOG (Standard)
  • HY-N13009
    MO-2097

    		Raf HIF/HIF Prolyl-Hydroxylase ERK MEK Reactive Oxygen Species (ROS) Apoptosis Caspase Cancer
    MO-2097 is a RAF-1/HIF-1α inhibitor. MO-2097 induces RAF-1 destabilization, leading to a reduction in EMT-associated transcription factors and mesenchymal markers. MO-2097 inhibits HIF-1a protein expression mediated by hnRNPA2B1 under hypoxic and mimetic hypoxia. MO-2097 induces mitochondrial ROS, which leads to apoptosis in cells. MO-2097 effectively suppresses colorectal cancer metastasis by inhibiting the RAF/MEK/ERK signaling pathway. MO-2097 attenuates tumor growth in a xenograft HCT116 cell mouse model. MO-2097 can be used for the study of colorectal cancer .
    MO-2097
  • HY-N0390S3
    L-Glutamine-13C5,15N2,d5

    L-Glutamic acid 5-amide-13C5,15N2,d5

    		 Isotope-Labeled Compounds mGluR Ferroptosis Environmental Pollutants Endogenous Metabolite HIF/HIF Prolyl-Hydroxylase mTOR STAT NF-κB Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology
    L-Glutamine- 13C5, 15N2,d5 is the deuterium, 13C-, and 15N-labeled L-Glutamine (HY-N0390). L-Glutamine is an orally active nutritional agent and cellular metabolism regulator. L-Glutamine is taken up in a Na +-dependent manner and targets multiple key molecules including glutaminase, mTORC1, NF-κB, STAT-3 and HIF-1α. L-Glutamine enhances glutaminolytic catabolism, drives the conversion of glutamate to α-ketoglutarate, thereby regulating gene expression, integrating metabolic signals, mediating glutamine flux and maintaining redox homeostasis. L-Glutamine also promotes cell proliferation, osteogenic differentiation and fracture healing, exerts neuroprotective and cardioprotective effects, and inhibits osteoarthritis. L-Glutamine can be applied to research related to osteoporosis, osteoarthritis, ischemic stroke and acute cantharidin-induced cardiotoxicity .
    L-Glutamine-13C5,15N2,d5
  • HY-170027
    LW1564

    		HIF/HIF Prolyl-Hydroxylase AMPK Cancer
    LW1564 is an inhibitor for HIF-1α with an IC50 of 1.2 µM in HepG2. LW1564 inhibits mitochondrial respiration, reduces ATP production, stimulates HIF-1α degradation, and inhibits proliferation of various cancer cells with GI50 of 0.4-4.6 μM. LW1564 activates AMPK signaling pathway and inhibits lipid synthesis. LW1564 exhibits antitumor in HepG2 xenograft mouse model .
    LW1564
  • HY-N5136
    25(R,S)-Ruscogenin

    		Apoptosis PI3K Akt mTOR Cancer
    Ruscogenin suppresses HCC metastasis by reducing the expression of MMP-2, MMP-9, uPA, VEGF and HIF-1α via regulating the PI3K/Akt/mTOR signaling pathway . And Ruscogenin alleviates LPS-induced pulmonary endothelial cell apoptosis by su
    25(R,S)-Ruscogenin
  • HY-147426A
    Zifcasiran sodium

    ADS-007 sodium; ARO HIF2 sodium

    		 Small Interfering RNA (siRNA) HIF/HIF Prolyl-Hydroxylase Cancer
    Zifcasiran (ADS-007) sodium is an siRNA synthetic double-stranded RNAi trigger. Zifcasiran sodium selectively target hypoxia-inducible factor-2α (HIF2α) interrupting downstream pro-oncogenic signaling in clear cell renal cell carcinoma (ccRCC). Zifcasiran sodium engages the cell's RNAi machinery to target HIF2α (EPAS1) mRNA for degradation, thereby reducing the amount of free HIF2α mRNA available for translation .
    Zifcasiran sodium
  • HY-111431AR
    p-Cresyl sulfate potassium (Standard)

    p-Tolyl sulfate potassium (Standard)

    		 JNK p38 MAPK Reactive Oxygen Species (ROS) Reference Standards Metabolic Disease
    p-Cresyl sulfate (potassium) (Standard) is the analytical standard of p-Cresyl sulfate (potassium). This product is intended for research and analytical applications. p-Cresyl sulfate (p-Tolyl sulfate) potassium is a uremic toxin, that can cause renal damage and dysfunction. p-Cresyl sulfate potassium shows antiproliferation activity. p-Cresyl sulfate potassium increases the protein expression of HIF-1α and VHL, decreases the protein expression of HIF-2α. p-Cresyl sulfate potassium induces epithelial-mesenchymal transition (EMT). p-Cresyl sulfate potassium activates the JNK and p38 MAPK signaling pathways .
    p-Cresyl sulfate potassium (Standard)
  • HY-15476
    VU 0364439

    		mGluR HIF/HIF Prolyl-Hydroxylase PDK-1 VEGFR Neurological Disease
    VU 0364439 is a mGlu4 positive allosteric modulator with an EC50 of 19.8 nM. VU 0364439 modulates the GRM4/CBX4/HIF-1α signaling pathway by enhancing GRM4-CBX4 interaction. VU 0364439 can be used for the research of parkinson’s disease .
    VU 0364439
  • HY-N5014
    Liensinine perchlorate
    15+ Cited Publications

    		 Reactive Oxygen Species (ROS) Autophagy Apoptosis VEGFR JAK Amyloid-β p38 MAPK HIF/HIF Prolyl-Hydroxylase STAT PI3K JNK Akt Cardiovascular Disease Neurological Disease Inflammation/Immunology Cancer
    Liensinine perchlorate is a bisbenzylisoquinoline alkaloid. By inhibiting the PI3K/AKT and JNK/p38-MAPK signaling pathways, Liensinine perchlorate suppresses autophagy and apoptosis, clears Aβ, and exerts anti-inflammatory, antioxidant and neuroprotective effects. Liensinine perchlorate activates AMPK and inhibits the expression of HIF-1α and VEGF, thereby suppressing angiogenesis. Liensinine perchlorate exerts anti-tumor effects through ROS-mediated inhibition of the JAK2/STAT3 signaling pathway. Liensinine perchlorate can be used for the research of diseases such as Alzheimer's disease, hepatocellular carcinoma, osteosarcoma, sepsis-induced organ injury and stroke .
    Liensinine perchlorate
  • HY-P1420A
    TAT-cyclo-CLLFVY TFA

    		HIF/HIF Prolyl-Hydroxylase Cancer
    TAT-cyclo-CLLFVY TFA is a cyclic peptide inhibitor of HIF-1 heterodimerization that inhibits hypoxia signaling in cancer cells. TAT-cyclo-CLLFVY TFA disrupts HIF-1α/HIF-1β protein-protein interaction with an IC50 of 1.3 μM .
    TAT-cyclo-CLLFVY TFA
  • HY-175521
    HIF-1α-IN-8

    		HIF/HIF Prolyl-Hydroxylase IKK NF-κB Apoptosis Reactive Oxygen Species (ROS) Inflammation/Immunology
    HIF-1α-IN-8 is an orally active HIF-1α inhibitor, with an IC50 of 2.02 μM. HIF-1α-IN-8 significantly suppresses the expression of inflammation factors of IL-6 and NO, reduces hypoxia-induced ROS production and apoptosis in C8-D1A cells. HIF-1α-IN-8 inhibits HIF-1α/IKKα/NF-κB signaling pathway and reduces the expression of blood-brain barrier permeability-related proteins. HIF-1α-IN-8 reduces brain water content and oxidative stress level in mice with high altitude cerebral edema (HACE) model. HIF-1α-IN-8 can be used for the study of high altitude cerebral edema (HACE) .
    HIF-1α-IN-8
  • HY-163512
    Anti-inflammatory agent 79

    		HIF/HIF Prolyl-Hydroxylase Inflammation/Immunology
    Anti-inflammatory agent 79 (compound 17q) is an isoquinolinone derivative-based HIF-1 inhibitor (IC50: 0.55 μM), which can effectively block HIF-1 signals and increase HIF- Degradation of 1α. Anti-inflammatory agent 79 inhibits synovial invasion and migration and inhibits angiogenesis. Anti-inflammatory agent 79 also effectively reduced foot swelling and arthritis in a mouse inflammation model, and down-regulated the levels of inflammatory factors and blood vessel proliferation in the body .
    Anti-inflammatory agent 79
  • HY-169100
    Antiproliferative agent-57

    		VEGFR PI3K Akt mTOR p38 MAPK HIF/HIF Prolyl-Hydroxylase Cancer
    Antiproliferative agent-57 (compound M2) is a tumor angiogenesis inhibitor. Antiproliferative agent-57 inhibits the secretion of VEGF in SiHa cells under hypoxic conditions (IC50=0.68 μM) without inducing cytotoxicity. Antiproliferative agent-57 can modulate the PI3K/AKT/mTOR and MAPK signaling pathways in tumor cells to inhibit the expression of HIF-1α and VEGF in tumor tissues .
    Antiproliferative agent-57
  • HY-P10797
    TAT-N24

    		NF-κB HIF/HIF Prolyl-Hydroxylase VEGFR TNF Receptor Interleukin Related Cardiovascular Disease Inflammation/Immunology
    TAT-N24 is a cell-permeable TAT peptide as a p55PIK signaling inhibitor. TAT-N24 is effective for corneal neovascularization (CNV) and ocular inflammation by inhibiting the HIF-1α/NF-κB signaling pathway in corneal suture (CS). TAT-N24 also inhibits corneal neovascularization .
    TAT-N24
  • HY-P10869
    dCNP
    1 Publications Verification

    		 Natriuretic Peptide Receptor (NPR) Inflammation/Immunology Cancer
    dCNP binds to NPR-B/C receptor, activates cGMP signaling pathway, and regulates vascular function. dCNP exhibits anti-hypoxia property through downregulation of hypoxia-related genes expressions like HIF1α and HIF2α. dCNP inhibits the induction of tumor stroma and exhibits anti-fibrosis activity. dCNP upregulates CTLs, NK cells, and conventional type 1 dendritic cells in tumors, and activates immune responses .
    dCNP
  • HY-164483
    HS-345

    		Akt Trk Receptor Cancer
    HS-345 is a TrkA/Ak inhibitor with significant anti-pancreatic cancer effects. HS-345 inhibits the growth and proliferation of pancreatic cancer cells by targeting the TrkA/Akt signaling pathway, while also inducing apoptosis. Additionally, HS-345 suppresses blood vessel formation by decreasing the expression of HIF-1α and VEGF. HS-345 holds promise for research in pancreatic cancer .
    HS-345
  • HY-N2425R
    Rhodiosin (Standard)

    		Reference Standards Cholinesterase (ChE) Metabolic Disease
    Rhodiosin (Standard) is the analytical standard of Rhodiosin. This product is intended for research and analytical applications. Rhodiosin is a double inhibitor of CYP2D6 and AChE, and can be isolated from Rhodiolis rhodiolis root. The IC50 for CYP2D6 is 0.761 μM, and the Ki is 0.769 μM. Rhodiosin has antioxidant and neuroprotective activity and can regulate HIF-1α signaling pathway to protect the central nervous system
    Rhodiosin (Standard)
  • HY-N0484R
    Liensinine (Standard)

    		Reference Standards Reactive Oxygen Species (ROS) Autophagy Apoptosis VEGFR JAK Amyloid-β p38 MAPK HIF/HIF Prolyl-Hydroxylase STAT PI3K JNK Akt Cardiovascular Disease Neurological Disease Cancer
    Liensinine (Standard) is the analytical standard of Liensinine (HY-N0484). This product is intended for research and analytical applications. Liensinine is a bisbenzylisoquinoline alkaloid. By inhibiting the PI3K/AKT and JNK/p38-MAPK signaling pathways, Liensinine suppresses autophagy and apoptosis, clears Aβ, and exerts anti-inflammatory, antioxidant and neuroprotective effects. Liensinine activates AMPK and inhibits the expression of HIF-1α and VEGF, thereby suppressing angiogenesis. Liensinine exerts anti-tumor effects through ROS-mediated inhibition of the JAK2/STAT3 signaling pathway. Liensinine can be used for the research of diseases such as Alzheimer's disease, hepatocellular carcinoma, osteosarcoma, sepsis-induced organ injury and stroke .
    Liensinine (Standard)
  • HY-172201
    NF-κB-IN-19

    		NF-κB Reactive Oxygen Species (ROS) Autophagy Apoptosis HIF/HIF Prolyl-Hydroxylase Akt STAT PI3K Inflammation/Immunology Cancer
    NF-κB-IN-19 (Compound 8) is an NF-κB inhibitor. NF-κB-IN-19 effectively induces DNA damage, promotes the generation of ROS, and induces autophagy and apoptosis through the NF-κB signaling pathway in tumor cells. In addition, NF-κB-IN-19 can inhibit the levels of VEGF and HIF-1α, and exert antiproliferative activity in tumor cells through the PI3K/AKT and STAT-3 pathways. NF-κB-IN-19 can effectively overcome cisplatin resistance and has anti-tumor activity .
    NF-κB-IN-19
  • HY-155721
    22-(4′-py)-JA

    22-4′-Pyridinecarbonyl jorunnamycin A

    		 Akt mTOR Cancer
    22-(4′-py)-JA is a semisynthetic derivative of junamycin A (JA) that can be isolated from the Thai blue sponge (Xestospongia sp.). 22-(4′-py)-JA has antimetastatic activity and can inhibit AKT/mTOR/p70S6K signaling. 22-(4′-py)-JA inhibits tumor cell invasion and tube formation in human umbilical vein endothelial cells (HUVEC), downregulates metalloproteinases (MMP-2 and MMP-9), hypoxia-inducible factor 1α (HIF-1α) and vascular endothelial growth factor (VEGF). 22-(4′-py)-JA has potent anticancer activity against non-small cell lung cancer (NSCLC) .
    22-(4′-py)-JA
  • HY-N0493R
    Pectolinarigenin (Standard)

    		Reference Standards COX Lipoxygenase NF-κB p38 MAPK ERK HIF/HIF Prolyl-Hydroxylase Keap1-Nrf2 PI3K Apoptosis Autophagy Inflammation/Immunology
    Pectolinarigenin (Standard) is the analytical standard of Pectolinarigenin. This product is intended for research and analytical applications. Pectolinarigenin is an orally active dual inhibitor of COX-2/5-LOX with anti-inflammatory, antioxidant, antitumor and neuroprotective activities. Pectolinarigenin exerts neuroprotective and anti-inflammatory effects on astrocyte inflammation via the NFκB and MAPK pathways. Pectolinarigenin inhibits LPS-induced phosphorylation of ERK1/2, N-FκB and p38MAPK, directly inhibits the enzymatic activity or binding of COX-2, 5-LOX and HIF-1α, and reduces the level of XIAP. Pectolinarigenin modifies Keap1 to promote nuclear accumulation of Nrf2, induces ARE-mediated antioxidant enzyme expression, and possesses direct free radical scavenging activity. Pectolinarigenin reduces the release of NO, proinflammatory mediators and leukotrienes, and increases the level of IL-10. Pectolinarigenin induces G2/M cell cycle arrest, apoptosis (Apoptosis) and autophagy (Autophagy) via the PI3K/AKT/mTOR signaling pathway. Pectolinarigenin reduces renal crystal deposition and inhibits melanin synthesis. Pectolinarigenin inhibits inflammation and alleviates allergy in mouse models of inflammation. Pectolinarigenin alleviates renal injury, inflammation and oxidative stress in mice by inhibiting HIF-1α activity. Pectolinarigenin can be used for the research of neurodegenerative diseases, inflammatory/allergic diseases, calcium oxalate nephrocalcinosis, gastric cancer, melasma, post-inflammatory diseases and chloasma.
    Pectolinarigenin (Standard)
  • HY-N15353
    1-Palmitoyl-2-linoleoyl-sn-glycerol

    		Bacterial Infection
    1-Palmitoyl-2-linoleoyl-sn-glycerol is a diacylglycerol (DAG)-type lipid signaling molecule found in the coralloid roots of Cycas revoluta, and serves as a major active component of the plant-secreted hormogonium-inducing factor (HIF). At a concentration of 1 nmol/disc (approximately 0.6 µg), 1-palmitoyl-2-linoleoyl-sn-glycerol can significantly induce the differentiation of filamentous aggregates of Nostoc into motile hormogonia, thereby promoting chemotaxis toward host roots and the establishment of symbiosis. This compound holds significant research and application potential in areas such as plant–microbe interactions, rhizosphere signaling pathways, and nitrogen-fixing symbiosis .
    1-Palmitoyl-2-linoleoyl-sn-glycerol
  • HY-N0390S7
    L-Glutamine-15N2,d5

    L-Glutamic acid 5-amide-15N2,d5

    		 Isotope-Labeled Compounds mGluR Ferroptosis Environmental Pollutants Endogenous Metabolite HIF/HIF Prolyl-Hydroxylase mTOR STAT NF-κB Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology
    L-Glutamine- 15N2,d5 is the deuterium and 15N-labeled L-Glutamine (HY-N0390). L-Glutamine is an orally active nutritional agent and cellular metabolism regulator. L-Glutamine is taken up in a Na +-dependent manner and targets multiple key molecules including glutaminase, mTORC1, NF-κB, STAT-3 and HIF-1α. L-Glutamine enhances glutaminolytic catabolism, drives the conversion of glutamate to α-ketoglutarate, thereby regulating gene expression, integrating metabolic signals, mediating glutamine flux and maintaining redox homeostasis. L-Glutamine also promotes cell proliferation, osteogenic differentiation and fracture healing, exerts neuroprotective and cardioprotective effects, and inhibits osteoarthritis. L-Glutamine can be applied to research related to osteoporosis, osteoarthritis, ischemic stroke and acute cantharidin-induced cardiotoxicity .
    L-Glutamine-15N2,d5
  • HY-N0390G
    L-Glutamine

    		mTOR NF-κB STAT HIF/HIF Prolyl-Hydroxylase Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology
    L-Glutamine GMP is L-Glutamine (HY-N0390) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. L-Glutamine is an orally active nutritional agent and cellular metabolism regulator. L-Glutamine is taken up in a Na +-dependent manner and targets multiple key molecules including glutaminase, mTORC1, NF-κB, STAT-3 and HIF-1α. L-Glutamine enhances glutaminolytic catabolism, drives the conversion of glutamate to α-ketoglutarate, thereby regulating gene expression, integrating metabolic signals, mediating glutamine flux and maintaining redox homeostasis. L-Glutamine also promotes cell proliferation, osteogenic differentiation and fracture healing, exerts neuroprotective and cardioprotective effects, and inhibits osteoarthritis. L-Glutamine can be applied to research related to osteoporosis, osteoarthritis, ischemic stroke and acute cantharidin-induced cardiotoxicity .
    L-Glutamine

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