317 Results for "

Nrf2 inducer

" in MedChemExpress (MCE) Product Catalog:
Products (317)

317 Results for "Nrf2 inducer" in MCE Product Catalog:

Cat. No.: HY-N0259R
CAS No.: 110623-73-9
Synonyms: Epmedin B (Standard)
Epimedin B (Standard) (Epmedin B (Standard)) is the analytical standard of Epimedin B (HY-N0259). This product is intended for research and analytical applications. Epimedin B (Epmedin B) is a flavonoid active component found in Epimedium, with oral activity, and exhibits anti-osteoporotic and neuroprotective effects. Epimedin B inhibits RANKL-induced osteoclast differentiation, F-actin ring formation, and mature osteoclast bone resorption, inhibits the phosphorylation of JNK, p38 MAPK, PI3K, and AKT, activates the AMPK-Nrf2 antioxidant pathway, and reduces cellular and mitochondrial ROS. Epimedin B acts on ESR1 and exerts its effects via GPER. Epimedin B alleviates bone loss and improves bone microstructure in vivo, and in Parkinson's models protects dopaminergic neurons and maintains striatal dopamine levels through anti-apoptotic and anti-endoplasmic reticulum stress effects. Epimedin B can be used for research related to osteoporosis, diabetic osteoporosis, and Parkinson's disease .
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Cat. No.: HY-13689G
CAS No.: 133053-19-7
Go 6983 GMP is Go 6983 (HY-13689) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. Go 6983 is a dual inhibitor targeting Suv39h1/2 (KMT1A/KMT1B) and PKC, as well as a transcriptional activator capable of inducing DNA hypomethylation. Go 6983 stimulates the transcription of Prdm14 by reducing Suv39h1/2 protein levels, decreasing histone modifications in the Prdm14 promoter region, and increasing the recruitment of RNA polymerase II. Go 6983 induces genome-wide DNA hypomethylation by inhibiting de novo methyltransferase expression and increasing Tet1/Tet2 levels, thereby promoting self-renewal and pluripotency maintenance of stem cells. Meanwhile, Go 6983 can block PKC-mediated signaling pathways to reduce the expression of EMT-related genes and eliminate the upregulation of antioxidant genes downstream of NRF2. Go 6983 is mainly used in mechanism studies related to myocardial ischemia/reperfusion injury .
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Cat. No.: HY-N2593R
CAS No.: 32507-66-7
Isorhapontigenin (Standard) is the analytical standard of Isorhapontigenin (HY-N2593). This product is intended for research and analytical applications. Isorhapontigenin is an orally active dietary polyphenol. Isorhapontigenin acts as a potent antioxidant that reduces the production of reactive oxygen species (ROS). Isorhapontigenin promotes the binding of JUN to the AP-1 site on the SESN2 promoter, induces SESN2 transcription, triggers MAPK8-dependent JUN activation, and upregulates the expression of PPAR-α, PGC-1α and CPT-1A to facilitate fatty acid oxidation. Isorhapontigenin induces autophagy, apoptosis and preadipocyte differentiation; it inhibits tumor growth, cell invasion, NF-κB transcriptional activity, the PI3K/Akt signaling pathway, STAT1 phosphorylation and MMP-2 expression. Isorhapontigenin alleviates oxidative stress, inflammatory cytokine release and triglyceride accumulation; it increases intracellular ATP levels and promotes Nrf2 nuclear translocation. Isorhapontigenin improves insulin sensitivity in adipose tissue and glucose tolerance, and reduces postprandial blood glucose, insulin and free fatty acid levels. Isorhapontigenin is applicable to research on bladder cancer, liver injury, chronic obstructive pulmonary disease, acute lung injury and type 2 diabetes.
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Cat. No.: HY-154795
CAS No.: 658701-67-8
Purity:  99.81%
Synonyms: 18α-Glycyrrhizic acid Magnesium hydrate; 18α-GA Magnesium hydrate; 18α-Licorice-saponin H2 Magnesium hydrate
Magnesium isoglycyrrhizinate hydrate (18α-Glycyrrhizic acid Magnesium hydrate; 18α-GA Magnesium hydrate; 18α-Licorice-saponin H2 Magnesium hydrate) is a derivative of glycyrrhizic acid with oral activity. Magnesium isoglycyrrhizinate hydrate exhibits antioxidant, anti-inflammatory, hepatoprotective and cardioprotective activities. Magnesium isoglycyrrhizinate hydrate protects against ethanol-induced alcoholic liver disease in rats by upregulating the expression levels of SOD, GSH, PPAR-α and CPT-1 . Magnesium isoglycyrrhizinate hydrate shows cytotoxicity against T lymphocytes and inhibits HIV-1 replication in these cells . Magnesium isoglycyrrhizinate hydrate alleviates oxidative stress by reducing the levels of ROS, Nrf2, HO-1 and p-P65, and alleviates pyroptosis by downregulating the expression levels of NLRP3, GSDMD-N, P20 and c-IL-1β. Magnesium isoglycyrrhizinate hydrate inhibits autophagy, colonic fibrosis and myocardial fibrosis, and regulates intestinal barrier integrity. Magnesium isoglycyrrhizinate hydrate can be used in research related to alcoholic liver disease, HIV-1 infection, hepatotoxicity, acute liver failure, inflammatory bowel disease and myocardial fibrosis .
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Cat. No.: HY-N7695
CAS No.: 23133-56-4
Physalin B is an orally active anti-inflammatory and anticancer agent. Physalin B can be isolated from Physalis alkekengi L. var. Franchetii. Physalin B inhibits the activation of the NF-κB, NLRP3 inflammasome, STAT3, PI3K/Akt and Hedgehog signaling pathways, regulates the phosphorylation levels of GSK-3β, p38 MAPK, ERK1/2 and JNK, and promotes the nuclear translocation of NRF2. Physalin B reduces the levels of pro-inflammatory cytokines and factors, induces mitochondrial reactive oxygen species (mito-ROS) production, Apoptosis, G2/M cell cycle arrest and incomplete Autophagy, alters cytoskeleton structure and alleviates oxidative stress. Physalin B reduces cancer cell viability, ameliorates liver and lung tissue damage and alleviates liver fibrosis. Physalin B can be used in research related to ulcerative colitis, breast cancer, acute lung injury, colon cancer, non-alcoholic steatohepatitis, liver fibrosis, lung cancer, pancreatic cancer, lymphoma, ovarian cancer, sarcoma and leukemia .
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Cat. No.: HY-N0660
CAS No.: 55466-05-2
Jujuboside B is a bioactive saponin component isolated from Ziziphi Spinosae Semen (sour jujube seed), with oral efficacy and blood-brain barrier permeability. Jujuboside B induces acute leukemia cell death and drives necroptosis apoptosis by activating the RIPK1/RIPK3/MLKL pathway. Jujuboside B upregulates the expression of NOXA, PARP and caspase-3, activates AMPK, inhibits the proliferation of breast cancer cells, and induces cell apoptosis and autophagy. Jujuboside B inhibits angiogenesis and tumor growth by blocking the VEGFR-2 signaling pathway. Jujuboside B alleviates liver injury in mice by regulating the Nrf2-STING signaling pathway . Jujuboside B alleviates liver injury by regulating anti-inflammatory responses and downregulating the expression of 11β-HSD2. Jujuboside B induces ferroptosis and overcomes radioresistance in non-small cell lung cancer via the PPARγ-ATF3-Gpx4 signaling pathway. Jujuboside B exerts inhibitory effects on platelet aggregation. Jujuboside B inhibits febrile seizures by suppressing the activity of AMPA receptors. Jujuboside B reverses chronic unpredictable mild stress-promoted tumor progression by blocking the PI3K/Akt and MAPK/ERK pathways and dephosphorylating CREB signaling. Jujuboside B is applicable to related studies on acute leukemia, breast cancer, PM2.5-induced lung injury, hepatotoxicity, liver injury, colorectal cancer, non-small cell lung cancer, thromboembolic diseases, cardiovascular diseases associated with high platelet aggregation, febrile seizures, and depressive-like phenotypes .
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Cat. No.: HY-N0660R
CAS No.: 55466-05-2
Jujuboside B (Standard) is the analytical standard of Jujuboside B. This product is intended for research and analytical applications. Jujuboside B is a bioactive saponin component isolated from Ziziphi Spinosae Semen (sour jujube seed), with oral efficacy and blood-brain barrier permeability. Jujuboside B induces acute leukemia cell death and drives necroptosis apoptosis by activating the RIPK1/RIPK3/MLKL pathway. Jujuboside B upregulates the expression of NOXA, PARP and caspase-3, activates AMPK, inhibits the proliferation of breast cancer cells, and induces cell apoptosis and autophagy. Jujuboside B inhibits angiogenesis and tumor growth by blocking the VEGFR-2 signaling pathway. Jujuboside B alleviates liver injury in mice by regulating the Nrf2-STING signaling pathway . Jujuboside B alleviates liver injury by regulating anti-inflammatory responses and downregulating the expression of 11β-HSD2. Jujuboside B induces ferroptosis and overcomes radioresistance in non-small cell lung cancer via the PPARγ-ATF3-Gpx4 signaling pathway. Jujuboside B exerts inhibitory effects on platelet aggregation. Jujuboside B inhibits febrile seizures by suppressing the activity of AMPA receptors. Jujuboside B reverses chronic unpredictable mild stress-promoted tumor progression by blocking the PI3K/Akt and MAPK/ERK pathways and dephosphorylating CREB signaling. Jujuboside B is applicable to related studies on acute leukemia, breast cancer, PM2.5-induced lung injury, hepatotoxicity, liver injury, colorectal cancer, non-small cell lung cancer, thromboembolic diseases, cardiovascular diseases associated with high platelet aggregation, febrile seizures, and depressive-like phenotypes.
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Cat. No.: HY-N6911A
CAS No.: 83896-44-0
Synonyms: 18α-GA; Isoglycyrrhizinic acid; 18α-Glycyrrhizic acid
18α-Glycyrrhizic acid (18α-GA; Isoglycyrrhizinic acid; 18α-Glycyrrhizic acid) is a derivative of glycyrrhizic acid with oral activity. 18α-Glycyrrhizic acid exhibits antioxidant, anti-inflammatory, hepatoprotective and cardioprotective activities. 18α-Glycyrrhizic acid protects against ethanol-induced alcoholic liver disease in rats by upregulating the expression levels of SOD, GSH, PPAR-α and CPT-1 . 18α-Glycyrrhizic acid shows cytotoxicity against T lymphocytes and inhibits HIV-1 replication in these cells . 18α-Glycyrrhizic acid alleviates oxidative stress by reducing the levels of ROS, Nrf2, HO-1 and p-P65, and alleviates pyroptosis by downregulating the expression levels of NLRP3, GSDMD-N, P20 and c-IL-1β. 18α-Glycyrrhizic acid inhibits autophagy, colonic fibrosis and myocardial fibrosis, and regulates intestinal barrier integrity. 18α-Glycyrrhizic acid can be used in research related to alcoholic liver disease, HIV-1 infection, hepatotoxicity, acute liver failure, inflammatory bowel disease and myocardial fibrosis .
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Cat. No.: HY-113402AR
CAS No.: 283159-88-6
Synonyms: γ-Glu-Cys TFA (Standard)
Gamma-glutamylcysteine (TFA) (Standard) is the analytical standard of Gamma-glutamylcysteine (TFA). This product is intended for research and analytical applications. Gamma-glutamylcysteine TFA (γ-Glu-Cys TFA) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine TFA activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine TFA regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine TFA is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease.
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Cat. No.: HY-113402B
Synonyms: γ-Glu-Cys ammonium
Gamma-glutamylcysteine ammonium (γ-Glu-Cys ammonium) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine ammonium activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine ammonium regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine ammonium is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease .
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Cat. No.: HY-113402R
CAS No.: 636-58-8
Synonyms: γ-Glu-Cys (Standard)
Gamma-glutamylcysteine (Standard) is the analytical standard of Gamma-glutamylcysteine. This product is intended for research and analytical applications. Gamma-glutamylcysteine (γ-Glu-Cys) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease.
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Cat. No.: HY-N0493R
CAS No.: 520-12-7
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.
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Cat. No.: HY-110067
CAS No.: 675848-25-6
VO-OHPic is a reversible, noncompetitive PTEN inhibitor with an human IC50 value of 46 nM. VO-OHPic inhibits PTEN signaling, activates Akt-GSK3β and Nrf-2/HO-1 pathways, induces apoptosis resistance and elevates IL-10 levels. VO-OHPic inhibits autophagy, ferroptosis and oxidative stress. VO-OHPic can be used for the research of acute myocardial infarction, intervertebral disc degeneration, cardiomyopathy and cancer .
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Cat. No.: HY-183905
CAS No.: 1401564-00-8
KR-67607 is a selective 11β-HSD1 inhibitor, with an IC50 value of 4.8 nM against h11β-HSD1 and 7.1 nM against mouse 11β-HSD1. KR-67607 inhibits stress-induced Glucocorticoid receptor nuclear translocation, reduces cortisol levels, suppresses the expression of ROS and proinflammatory cytokines, and enhances Nrf-2-mediated antioxidant gene transcription. KR-67607 maintains trabecular meshwork structure and reverses elevated intraocular pressure. KR-67607 improves ocular antioxidant activity and mucus secretion, reverses ocular surface damage, and prevents ischemia-reperfusion induced ocular injury. KR-67607 can be used in research related to glaucoma and dry eye disease .
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Cat. No.: HY-N2535R
CAS No.: 458-36-6
Synonyms: 4-Hydroxy-3-methoxycinnamaldehyde (Standard)
Coniferaldehyde (Standard) is the analytical standard of Coniferaldehyde. This product is intended for research and analytical applications. Coniferaldehyde (4-Hydroxy-3-methoxycinnamaldehyde) is an effective inducer of heme oxygenase-1 (HO-1). Coniferaldehyde inhibits LPS-induced apoptosis through the PKCα/β II/Nrf-2/HO-1 dependent pathway in RAW264.7 macrophage cells. Coniferaldehyde has antioxidant and anti-inflammatory activities .
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Cat. No.: HY-W017982
CAS No.: 55965-84-9
Synonyms: CMI/MI
CMIT/MIT (14.5% in water) (CMI/MI) is a mixture of CMIT and MIT, and is also a preservative and skin sensitizer. CMIT/MIT (14.5% in water) increases the levels of phosphorylated ERK1/2, p38, JNK1/2, p53, p21 and Bax, decreases the level of Bcl-2, and activates the Nrf-2/HO-1 signaling pathway. CMIT/MIT (14.5% in water) increases LDH release and lipid peroxidation levels, impairs antioxidant defense capacity, promotes pro-inflammatory cytokine release, induces apoptosis, triggers cell cycle arrest, exhibits neurotoxicity in neuroblastoma cells, and causes dysregulation of Th2/Th17 immune responses. CMIT/MIT (14.5% in water) can be used in studies related to allergy, atopic dermatitis and lung injury .
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Cat. No.: HY-W017982A
CAS No.: 55965-84-9
Synonyms: CMI/MI (2.0-2.5% in water)
CMIT/MIT (2.0-2.5% in water) (CMI/MI (2.0-2.5% in water)) is a mixture of CMIT and MIT, and is also a preservative and skin sensitizer. CMIT/MIT (2.0-2.5% in water) increases the levels of phosphorylated ERK1/2, p38, JNK1/2, p53, p21 and Bax, decreases the level of Bcl-2, and activates the Nrf-2/HO-1 signaling pathway. CMIT/MIT (2.0-2.5% in water) increases LDH release and lipid peroxidation levels, impairs antioxidant defense capacity, promotes pro-inflammatory cytokine release, induces apoptosis, triggers cell cycle arrest, exhibits neurotoxicity in neuroblastoma cells, and causes dysregulation of Th2/Th17 immune responses. CMIT/MIT (2.0-2.5% in water) can be used in studies related to allergy, atopic dermatitis and lung injury .
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