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Pathways Recommended: NF-κB
Results for "

HIF-1α/NF-κB

" in MedChemExpress (MCE) Product Catalog:

29

Inhibitors & Agonists

1

Screening Libraries

1

Fluorescent Dyes

1

Biochemical Assay Reagents

1

Peptides

12

Natural
Products

11

Isotope-Labeled Compounds

2

Oligonucleotides

1

GMP Molecules

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • 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-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-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-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-19357
    Erenapurstat
    4 Publications Verification

    E3330; APX-3330

    		 DNA/RNA Synthesis NF-κB AP-1 HIF/HIF Prolyl-Hydroxylase VEGFR Reactive Oxygen Species (ROS) Cardiovascular Disease Neurological Disease Cancer
    Erenapursta (E3330) is a direct, orally active and selective inhibitor of Ape-1 (apurinic/apyrimidinic endonuclease 1)/Ref-1 (redox factor-1) redox. Erenapursta is able to impair tumor growth and blocks the activity of NF-κB, AP-1, and HIF-1α in pancreatic cancer. Erenapursta shows anticancer activities .
    Erenapurstat
  • 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-13425
    Deguelin
    10+ Cited Publications

    (-)-Deguelin; (-)-cis-Deguelin

    		 Akt Autophagy Apoptosis Cancer
    Deguelin, a naturally occurring rotenoid, acts as a chemopreventive agent by blocking multiple pathways like PI3K-Akt, IKK-NF-κB, and MAPK-mTOR-survivin-mediated apoptosis. Deguelin binding to Hsp90 leads to a decreased expression of numerous oncogenic proteins, including MEK1/2, Akt, HIF1α, COX-2, and NF-κB.
    Deguelin
  • 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-W016409
    Ethyl 3,4-dihydroxybenzoate
    1 Publications Verification

    Protocatechuic acid ethyl ester

    		 HIF/HIF Prolyl-Hydroxylase Reactive Oxygen Species (ROS) NO Synthase Autophagy Apoptosis Metabolic Disease Cancer
    Ethyl 3,4-dihydroxybenzoate (Protocatechuic acid ethyl ester) is an orally effective, blood-brain barrier-permeable, competitive prolyl hydroxylase (PHD) inhibitor that inhibits the hydroxylation modification of hypoxia-inducible factor (HIF) by PHD. Ethyl 3,4-dihydroxybenzoate stabilizes HIF-1α by inhibiting PHD, activates downstream pathways to induce autophagy and apoptosis of tumor cells, and regulates inflammatory responses, inhibits the NF-κB pathway, improves vascular permeability, and promotes osteoblast differentiation. Ethyl 3,4-dihydroxybenzoate has anti-tumor, anti-hypoxic injury, and bone metabolism regulation effects. It can also be used in the research of cardiovascular protection (such as reducing myocardial ischemic damage), bone tissue engineering (promoting osteogenesis/inhibiting osteoclast differentiation), and prevention and treatment of high-altitude cerebral edema .
    Ethyl 3,4-dihydroxybenzoate
  • 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-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-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-N11709
    Theasaponin E1

    		Apoptosis VEGFR ATM/ATR PTEN Akt mTOR HIF/HIF Prolyl-Hydroxylase NF-κB Notch Cholinesterase (ChE) Amyloid-β γ-secretase Ferroptosis Fungal Infection Neurological Disease Metabolic Disease Cancer
    Theasaponin E1 is an orally effective tea saponin. Theasaponin E1 inhibits the proliferation of cancer cells by activating apoptosis. Theasaponin E1 inhibits angiogenesis in ovarian cancer cells and HUVECs by reducing the expression of VEGF. Theasaponin E1 upregulates the phosphorylation level of ATM protein and the expression level of PTEN protein in cancer cells, decreases the phosphorylation levels of Akt, mTOR, p70S6K and 4E-BP1 proteins, downregulates the expression of HIF-1α and NF-κB, and reduces the protein expression of Notch ligands Dll4 and Jagged1. Theasaponin E1 exerts neuroprotective effects by inhibiting the activity of acetylcholinesterase, activating α-secretase and neprilysin, reducing the concentration of Aβ, and inhibiting the activities of β-secretase and γ-secretase. Theasaponin E1 exhibits toxic effects on cancer cells and quinone reductase-inducing activity, and inhibits tumor growth in vivo. Theasaponin E1 induces ferroptosis in Pomacea canaliculata by synergistically disrupting cholesterol homeostasis and sphingolipid metabolism. Theasaponin E1 possesses anti-biofilm activity against Candida albicans. Theasaponin E1 can be used in the research of ovarian cancer, obesity, Alzheimer's disease and fungal infections .
    Theasaponin E1
  • HY-173488
    NF-κB/HIF-1α-IN-1

    		NF-κB HIF/HIF Prolyl-Hydroxylase Keap1-Nrf2 Cancer
    NF-κB/HIF-1α-IN-1 (compound 9c) is a potent blocker of the NF-κB activation pathway and demonstrates selective anti-fibrotic activity. NF-κB/HIF-1α-IN-1 shows no significant cytotoxicity in NCI tumor cell lines. In rat models. NF-κB/HIF-1α-IN-1 has been shown to effectively ameliorate liver fibrosis by inhibiting the expression levels of NF-κB and HIF-1α, while simultaneously inducing the activation of Nrf2 .
    NF-κB/HIF-1α-IN-1
  • HY-13425R
    Deguelin (Standard)

    (-)-Deguelin (Standard); (-)-cis-Deguelin (Standard)

    		 Akt Autophagy Apoptosis Reference Standards Cancer
    Deguelin (Standard) is the analytical standard of Deguelin. This product is intended for research and analytical applications. Deguelin, a naturally occurring rotenoid, acts as a chemopreventive agent by blocking multiple pathways like PI3K-Akt, IKK-NF-κB, and MAPK-mTOR-survivin-mediated apoptosis. Deguelin binding to Hsp90 leads to a decreased expression of numerous oncogenic proteins, including MEK1/2, Akt, HIF1α, COX-2, and NF-κB.
    Deguelin (Standard)
  • 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-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-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-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-W778057
    Ethyl 3,4-Dihydroxybenzoate-13C3

    Protocatechuic acid ethyl ester-13C3

    		 Reactive Oxygen Species (ROS) Cancer
    Ethyl 3,4-Dihydroxybenzoate- 13C3 (Protocatechuic acid ethyl ester- 13C3) is the 13C-labeled Ethyl 3,4-dihydroxybenzoate (HY-W016409). Ethyl 3,4-dihydroxybenzoate (Protocatechuic acid ethyl ester) is an orally effective, blood-brain barrier-permeable, competitive prolyl hydroxylase (PHD) inhibitor that inhibits the hydroxylation modification of hypoxia-inducible factor (HIF) by PHD. Ethyl 3,4-dihydroxybenzoate stabilizes HIF-1α by inhibiting PHD, activates downstream pathways to induce autophagy and apoptosis of tumor cells, and regulates inflammatory responses, inhibits the NF-κB pathway, improves vascular permeability, and promotes osteoblast differentiation. Ethyl 3,4-dihydroxybenzoate has anti-tumor, anti-hypoxic injury, and bone metabolism regulation effects. It can also be used in the research of cardiovascular protection (such as reducing myocardial ischemic damage), bone tissue engineering (promoting osteogenesis/inhibiting osteoclast differentiation), and prevention and treatment of high-altitude cerebral edema .
    Ethyl 3,4-Dihydroxybenzoate-13C3
  • HY-W016409R
    Ethyl 3,4-dihydroxybenzoate (Standard)

    Protocatechuic acid ethyl ester (Standard)

    		 Reference Standards HIF/HIF Prolyl-Hydroxylase Reactive Oxygen Species (ROS) NO Synthase Autophagy Apoptosis Metabolic Disease Cancer
    Ethyl 3,4-dihydroxybenzoate (Standard) (Protocatechuic acid ethyl ester (Standard)) is the analytical standard of Ethyl 3,4-dihydroxybenzoate (HY-W016409). This product is intended for research and analytical applications. Ethyl 3,4-dihydroxybenzoate (Protocatechuic acid ethyl ester) is an orally effective, blood-brain barrier-permeable, competitive prolyl hydroxylase (PHD) inhibitor that inhibits the hydroxylation modification of hypoxia-inducible factor (HIF) by PHD. Ethyl 3,4-dihydroxybenzoate stabilizes HIF-1α by inhibiting PHD, activates downstream pathways to induce autophagy and apoptosis of tumor cells, and regulates inflammatory responses, inhibits the NF-κB pathway, improves vascular permeability, and promotes osteoblast differentiation. Ethyl 3,4-dihydroxybenzoate has anti-tumor, anti-hypoxic injury, and bone metabolism regulation effects. It can also be used in the research of cardiovascular protection (such as reducing myocardial ischemic damage), bone tissue engineering (promoting osteogenesis/inhibiting osteoclast differentiation), and prevention and treatment of high-altitude cerebral edema .
    Ethyl 3,4-dihydroxybenzoate (Standard)
  • 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-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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