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Pathways Recommended: MAPK/ERK Pathway
Results for "

macrophage MAPK pathway

" in MedChemExpress (MCE) Product Catalog:

35

Inhibitors & Agonists

4

Peptides

18

Natural
Products

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-113402
    Gamma-glutamylcysteine
    4 Publications Verification

    γ-Glu-Cys

    Endogenous Metabolite Interleukin Related TNF Receptor AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    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 .
    Gamma-glutamylcysteine
  • HY-123942
    Diprovocim
    Maximum Cited Publications
    14 Publications Verification

    Toll-like Receptor (TLR) TNF Receptor p38 MAPK NF-κB Inflammation/Immunology Cancer
    Diprovocim is a potent TLR1/TLR2 agonist. Diprovocim elicits full agonist activity in human THP-1 cells (EC50=110 pM). Diprovocim stimulates the release of TNF-α from mouse macrophages (EC50=1.3 nM). Diprovocim activates downstream MAPK and NF-κB signaling pathway. Diprovocim displays strong adjuvant activity in mice, particularly abetting cellular immune responses .
    Diprovocim
  • HY-N0481
    Roburic acid
    1 Publications Verification

    COX TNF Receptor NO Synthase Interleukin Related NF-κB Apoptosis p38 MAPK JNK ERK Keap1-Nrf2 RANKL/RANK Neurological Disease Inflammation/Immunology Cancer
    Roburic acid acts as an anti-inflammatory, anti-tumor and osteoclastogenesis inhibitor, with a Ki of 7.066 μM against human TNF, an IC50 of 9 μM against human COX-2, and an IC50 of 5 μM against ovine COX-1. Roburic acid reduces the production of inflammatory mediators such as NO and IL-6 in macrophages by inhibiting the NF-κB and MAPK (p38/JNK) pathways. By competitively inhibiting the TNF-TNF-R1 interaction, Roburic acid blocks the downstream NF-κB signaling pathway, thereby inducing cell cycle arrest and apoptosis in cancer cells. Roburic acid specifically inhibits osteoclastogenesis and bone resorption by suppressing the RANKL/TRAF6/NF-κB/NFATc1 axis. Roburic acid can be used in research related to osteolytic diseases such as osteoporosis, colorectal cancer and inflammatory diseases .
    Roburic acid
  • HY-113402A
    Gamma-glutamylcysteine TFA
    4 Publications Verification

    γ-Glu-Cys TFA

    Interleukin Related TNF Receptor Endogenous Metabolite AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    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 .
    Gamma-glutamylcysteine TFA
  • HY-12687
    Tizoxanide
    10+ Cited Publications

    TIZ

    Bacterial HIV Autophagy Parasite IKK Influenza Virus Infection Cancer
    Tizoxanide (TIZ) is the active metabolite of Nitazoxanide, which is a thiazolide anti-infective compound against anaerobic bacteria, protozoa, and a range of viruses. Tizoxanide (TIZ) has anti-HIV-1 activities and potent inhibition of both HBV and HCV replication with values EC50 of 0.46μM and 0.15 μM, respectively. Tizoxanide also exerts anti-inflammatory effects by inhibiting the production of pro-inflammatory cytokines and suppressing of the activation of the NF-κB and the MAPK signaling pathways in LPS-treated macrophage cells .
    Tizoxanide
  • HY-W923189

    Interleukin Related COX TNF Receptor NOD-like Receptor (NLR) NO Synthase PERK p38 MAPK Reactive Oxygen Species (ROS) Caspase Autophagy Herbicide Inflammation/Immunology Cancer
    Neral is a plant-derived anti-inflammatory, antioxidant and anticancer agent. Neral inhibits the phosphorylation of ERK1/2, p38 MAPK and IκB in macrophages induced by LPS (HY-D1056), suppresses the secretion of TNF-α and IL-6, as well as the expression of pro-IL-1β, iNOS and COX-2 in cells, and reduces the production of ROS in cells. Neral inhibits the activation of the NLRP3 inflammasome, and decreases the activation of caspase-1 and the secretion of IL-1β in mouse macrophages. Neral induces autophagy, and exhibits antiproliferative activity both in in vitro breast cancer cell models and mouse xenograft models. Neral regulates brassinosteroid, jasmonic acid and ethylene signaling pathways, and induces the expression of AP2/ERF-ERF and bHLH family genes in rice roots. Neral acts as a herbicide safener, alleviates the damage induced by Fenoxaprop-P-ethyl (HY-B2013), and promotes the elongation of rice roots. Neral can be used in research related to breast cancer, inflammatory and immune system diseases, and herbicide safeners .
    Neral
  • HY-N1966
    (E)-Osmundacetone
    2 Publications Verification

    p38 MAPK PPAR Cancer
    (E)-Osmundacetone is an inhibitor of the MAPK pathway. (E)-Osmundacetone inhibits the activation of the MAPK signaling pathway and restores the expression of PPARα/ACOX1. (E)-Osmundacetone abrogates abnormal cell proliferation, migration and liver metastasis induced by PTPRO silencing in colorectal cancer cells. (E)-Osmundacetone blocks OA-RD17-mediated activation of the MAPK signaling pathway, thereby reducing macrophage proliferation and migration. (E)-Osmundacetone is applicable to relevant research on colorectal cancer .
    (E)-Osmundacetone
  • HY-N2963
    Broussonin E
    2 Publications Verification

    ERK p38 MAPK JAK STAT TNF Receptor Interleukin Related COX Arginase Inflammation/Immunology
    Broussonin E is a phenolic compound and shows anti-inflammatory activity. Broussonin E can suppress inflammation by modulating macrophages activation statevia inhibiting the ERK and p38 MAPK and enhancing JAK2-STAT3 signaling pathway. Broussonin E can be used for the research of inflammation-related diseases such as atherosclerosis .
    Broussonin E
  • HY-N2217

    Akt mTOR p38 MAPK Apoptosis Phosphatase Interleukin Related NF-κB PI3K Keap1-Nrf2 Heme Oxygenase (HO) Toll-like Receptor (TLR) Reactive Oxygen Species (ROS) Metabolic Disease Inflammation/Immunology Cancer
    Rotundic acid is an orally effective triterpenoid with a Kd value of 51.3 µM for PTP1B. Rotundic acid downregulates the AKT/mTOR pro-survival pathway and modulates the MAPK pathway. Rotundic acid induces cell cycle S-phase arrest, DNA damage and apoptosis; it inhibits migration, invasion, angiogenesis and proliferation of cancer cells. Rotundic acid improves leptin sensitivity, regulates gut microbiota and reduces cellular senescence. Rotundic acid can be used in research related to hepatocellular carcinoma, obesity, aging, acute lung injury and type 2 diabetes .
    Rotundic acid
  • HY-N0566

    Anemosapogenin

    Apoptosis Autophagy Bcl-2 Family Caspase Survivin p38 MAPK MMP Cancer
    23-Hydroxybetulinic acid (Anemosapogenin) is an orally active triterpenoid with broad-spectrum anticancer activity. 23-Hydroxybetulinic acid reduces the levels of Bcl-2 and survivin, elevates the level of Bax, promotes the cleavage/activation of caspase-3 and caspase-9, and induces apoptosis via the endogenous mitochondrial pathway involving cytochrome C release and mitochondrial membrane potential disruption. 23-Hydroxybetulinic acid arrests the cell cycle at S and G1 phases, inhibits cancer cell proliferation, blocks the MAPK signaling pathway, regulates MMP2, and induces autophagic apoptosis by upregulating beclin-1. 23-Hydroxybetulinic acid inhibits the activity and efflux function of P-gp, increases the intracellular accumulation of chemotherapeutic drugs, and synergistically enhances cytotoxicity with Doxorubicin (HY-15142). 23-Hydroxybetulinic acid inhibits the phosphorylation and nuclear translocation of STAT6, blocks M2 macrophage polarization, and reduces M2 macrophage-mediated apoptosis resistance of colon cancer cells. 23-Hydroxybetulinic acid can be used in related studies on chronic myeloid leukemia, hepatocellular carcinoma, sarcoma 180, multidrug-resistant breast cancer, leukemia, Doxorubicin-induced cardiotoxicity, and colorectal cancer .
    23-Hydroxybetulinic acid
  • HY-147972

    NF-κB p38 MAPK NO Synthase COX Inflammation/Immunology
    NF-κB/MAPK-IN-1 (compound 11a) is a potent inhibitor of NF-κB and MAPK pathway. NF-κB/MAPK-IN-1 shows inhibitory activity against NO production, with an IC50 of 6.96 µM. NF-κB/MAPK-IN-1 suppresses LPS-induced iNOS, COX-2, ERΚ and P38 signaling activation. NF-κB/MAPK-IN-1 can prevent LPS induced inflammatory response in macrophages. NF-κB/MAPK-IN-1 can be used for rheumatoid arthritis (RA) research .
    NF-κB/MAPK-IN-1
  • HY-160851

    AK3287; AKEX0011

    ASK1 p38 MAPK Inflammation/Immunology
    GDC-3280 (AK3287; AKEX0011) is an orally active compound based on Pirfenidone (HY-B0673)'s phenyl pyridone scaffold. GDC-3280 alleviates the inflammatory and fibrotic reaction of silicosis by inhibiting the ASK1-p38 MAPK pathway and regulating macrophage polarization. GDC-3280 exhibits anti-inflammatory and anti-fibrotic effects .
    GDC-3280
  • HY-P6084

    NOD-like Receptor (NLR) p38 MAPK Apoptosis Inflammation/Immunology
    RP-220 is a renalase peptide targeting NLRP3. RP220 has anti-inflammatory and anti-apoptotic activities. RP220 inhibits renal tubular epithelial cells apoptosis with alkaline insult by activating MAPK signaling pathway. RP220 significantly inhibits NLRP3 expression and reduces macrophage infiltration and kidney tissue damage in acute kidney injury (AKI) mice model. RP-220 can be uses for systemic lupus erythematosus (SLE) and its complication lupus nephritis (LN) research .
    RP-220
  • HY-117548
    UNC1062
    2 Publications Verification

    TAM Receptor Apoptosis p38 MAPK ERK PI3K Akt JAK STAT Cardiovascular Disease Cancer
    UNC1062 is a highly selective tyrosine kinase (MERTK) inhibitor with an IC50 of 1.1 nM (Morrison Ki = 0.33 nM). UNC1062 exhibits good selectivity for the TAM family (TYRO3 IC50 = 60 nM, AXL IC50 = 85 nM). UNC1062 exhibits significant anti-proliferative effects and induces apoptosis in various cancer models (such as melanoma, gastric cancer, and acute myeloid leukemia). UNC1062 inhibits multiple pathways, including MAPK/ERK, PI3K/AKT and JAK/STAT and affects the motility of head and neck squamous cell carcinoma (HNSCC) cells through the RhoA signaling pathway. UNC1062 inhibits macrophage efferocytosis, and it suitable for research on atherosclerosis .
    UNC1062
  • HY-177106

    Drug Intermediate Ras Cancer
    ADT-1004 is an orally active prodrug of ADT-007 (HY-157887). ADT-007 is a reversible, highly potent and selective pan-RAS inhibitor that binds to the nucleotide-free conformation of RAS proteins and blocks their GTP activation, thereby inhibiting the downstream MAPK and AKT signaling pathways. ADT-1004 can be used for the research of pancreatic ductal adenocarcinoma .
    ADT-1004
  • HY-N4233

    p38 MAPK Inflammation/Immunology
    Bisabolangelone, a sesquiterpene derivative, is isolated from the roots of Osterici Radix. Bisabolangelone possesses anti-inflammatory properties, which inhibits LPS-stimulated inflammation through the blocking of NF-kappaB and MAPK pathways in macrophages. Bisabolangelone has anti-ulcer activities .
    Bisabolangelone
  • HY-176192

    Toll-like Receptor (TLR) NF-κB p38 MAPK ERK IKK TNF Receptor Interleukin Related Inflammation/Immunology
    SMU-14a is a selective Toll-like receptor 3 (TLR3) inhibitor wirh an IC50 of 0.18 μM. SMU-14a reduces phosphorylation of p65, ERK, and TBK1 via NF-κB, MAPK, and IRF3 signaling pathways. SMU-14a inhibits IL-6 secretion in mouse peritoneal macrophages, downregulates TNF-α in human peripheral blood monocytes and decreases serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. SMU-14a can be used for the research of acute hepatitis .
    SMU-14a
  • HY-113402R

    γ-Glu-Cys (Standard)

    Reference Standards Endogenous Metabolite Interleukin Related TNF Receptor AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Inflammation/Immunology
    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.
    Gamma-glutamylcysteine (Standard)
  • HY-179047

    Toll-like Receptor (TLR) MyD88 IKK p38 MAPK ERK TNF Receptor Interleukin Related Inflammation/Immunology Cancer
    SMU-L11-R is a selective TLR7 agonist with an EC50 of 0.012 μM for human TLR7. SMU-L11-R specifically activates TLR7, recruits  MyD88, and triggers MAPK/NF-κB pathways, leading to TNF-α/IL-1β/IL-6 secretion in both mouse and human peripheral blood mononuclear cells. SMU-L11-R promotes M1-like macrophage polarization. SMU-L11-R exhibits excellent synergistic anti-tumor effects with PD-L1 inhibitors by upregulating CD8 +T cells. SMU-L11-R shows potential in colorectal cancer studies .
    SMU-L11-R
  • HY-169703
    SPA0355
    1 Publications Verification

    RANKL/RANK p38 MAPK Akt NF-κB Inflammation/Immunology
    SPA0355 is a thiourea derivative that has antioxidant and anti-inflammatory properties. SPA0355 inhibits the RANKL (receptor activator of nuclear factor κB ligand) induced osteoclast formation in primary bone marrow-derived macrophages. SPA0355 also suppresses the activation of the MAPKs, Akt, and NF-κB pathways. Additionally, SPA0355 promotes osteoblast differentiation, increases alkaline phosphatase activity, and enhances mineral nodule formation. SPA0355 can protect ovariectomized mice from bone loss by stimulating osteoblast differentiation and inhibiting osteoclast resorption, making it useful for studying postmenopausal osteoporosis .
    SPA0355
  • HY-12687R

    TIZ (Standard)

    Reference Standards Bacterial HIV Autophagy Parasite IKK Influenza Virus Infection Cancer
    Tizoxanide (Standard) is the analytical standard of Tizoxanide. This product is intended for research and analytical applications. Tizoxanide (TIZ) is the active metabolite of Nitazoxanide, which is a thiazolide anti-infective compound against anaerobic bacteria, protozoa, and a range of viruses. Tizoxanide (TIZ) has anti-HIV-1 activities and potent inhibition of both HBV and HCV replication with values EC50 of 0.46μM and 0.15 μM, respectively. Tizoxanide also exerts anti-inflammatory effects by inhibiting the production of pro-inflammatory cytokines and suppressing of the activation of the NF-κB and the MAPK signaling pathways in LPS-treated macrophage cells .
    Tizoxanide (Standard)
  • HY-N10009

    NF-κB TNF Receptor COX ERK p38 MAPK Sirtuin Inflammation/Immunology
    Cudraflavone B is a prenylated flavonoid with anti-inflammatory and anti-tumor properties. Cudraflavone B is also a dual inhibitor of COX-1 and COX-2. Cudraflavone B blocks the translocation of nuclear factor κB (NF-κB) from the cytoplasm to the nucleus in macrophages. Thus, Cudraflavone B inhibits tumor necrosis factor α (TNFα) gene expression and secretion. Cudraflavone B also triggers the mitochondrial apoptotic pathway, activates NF-κB, the MAPK p38, and ERK, and induced the expression of SIRT1. Thus Cudraflavone B inhibits the growth of human oral squamous cell carcinoma cells .
    Cudraflavone B
  • HY-113402AR

    γ-Glu-Cys TFA (Standard)

    Interleukin Related TNF Receptor Endogenous Metabolite Reference Standards AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    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.
    Gamma-glutamylcysteine TFA (Standard)
  • HY-N1966R

    Reference Standards p38 MAPK PPAR Cancer
    (E)-Osmundacetone (Standard) is the analytical standard of (E)-Osmundacetone (HY-N1966). This product is intended for research and analytical applications. (E)-Osmundacetone is an inhibitor of the MAPK pathway. (E)-Osmundacetone inhibits the activation of the MAPK signaling pathway and restores the expression of PPARα/ACOX1. (E)-Osmundacetone abrogates abnormal cell proliferation, migration and liver metastasis induced by PTPRO silencing in colorectal cancer cells. (E)-Osmundacetone blocks OA-RD17-mediated activation of the MAPK signaling pathway, thereby reducing macrophage proliferation and migration. (E)-Osmundacetone is applicable to relevant research on colorectal cancer .
    (E)-Osmundacetone (Standard)
  • HY-124508

    Antibiotic Bacterial Fungal p38 MAPK NF-κB Infection Inflammation/Immunology
    Lambertellin is an effective antibiotic that can be used as a bactericide and as a fungicide. Lambertellin exerts its anti-inflammatory effect in LPS (HY-D1056)-stimulated RAW 264.7 macrophage cells by modulating the activation of the MAPK and NF-κB signaling pathways .
    Lambertellin
  • HY-162641

    IRAK NF-κB p38 MAPK TNF Receptor Inflammation/Immunology
    AF-45 inhibits IRAK4 and IRAK1, with IC50s of 128 nM and 1765 nM. AF-45 inhibits the release of IL-6 and TNF-α in macrophages, with IC50s of 0.53-1.54 μM and 0.6-2.75 μM. AF-45 is also an inhibitor for NF-κB/MAPK signaling pathway. AF-45 exhibits anti-inflammatory activities against DSS-induced ulcerative colitis and Lipopolysaccharide (HY-D1056)-induced acute lung injury in mouse model. AF-45 exhibits good pharmacokinetic characteristics in rat models .
    AF-45
  • HY-N0481R

    Reference Standards COX TNF Receptor NO Synthase Interleukin Related NF-κB Apoptosis p38 MAPK JNK ERK Keap1-Nrf2 RANKL/RANK Inflammation/Immunology
    Roburic acid (Standard) is the analytical standard of Roburic acid. This product is intended for research and analytical applications. Roburic acid acts as an anti-inflammatory, anti-tumor and osteoclastogenesis inhibitor, with a Ki of 7.066 μM against human TNF, an IC50 of 9 μM against human COX-2, and an IC50 of 5 μM against ovine COX-1. Roburic acid reduces the production of inflammatory mediators such as NO and IL-6 in macrophages by inhibiting the NF-κB and MAPK (p38/JNK) pathways. By competitively inhibiting the TNF-TNF-R1 interaction, Roburic acid blocks the downstream NF-κB signaling pathway, thereby inducing cell cycle arrest and apoptosis in cancer cells. Roburic acid specifically inhibits osteoclastogenesis and bone resorption by suppressing the RANKL/TRAF6/NF-κB/NFATc1 axis. Roburic acid can be used in research related to osteolytic diseases such as osteoporosis, colorectal cancer and inflammatory diseases.
    Roburic acid (Standard)
  • HY-N0566R

    Anemosapogenin (Standard)

    Reference Standards Apoptosis Autophagy Bcl-2 Family Caspase Survivin p38 MAPK MMP Cancer
    23-Hydroxybetulinic acid (Standard) is the analytical standard of 23-Hydroxybetulinic acid (HY-N0566). This product is intended for research and analytical applications. 23-Hydroxybetulinic acid (Anemosapogenin) is an orally active triterpenoid with broad-spectrum anticancer activity. 23-Hydroxybetulinic acid reduces the levels of Bcl-2 and survivin, elevates the level of Bax, promotes the cleavage/activation of caspase-3 and caspase-9, and induces apoptosis via the endogenous mitochondrial pathway involving cytochrome C release and mitochondrial membrane potential disruption. 23-Hydroxybetulinic acid arrests the cell cycle at S and G1 phases, inhibits cancer cell proliferation, blocks the MAPK signaling pathway, regulates MMP2, and induces autophagic apoptosis by upregulating beclin-1. 23-Hydroxybetulinic acid inhibits the activity and efflux function of P-gp, increases the intracellular accumulation of chemotherapeutic drugs, and synergistically enhances cytotoxicity with Doxorubicin (HY-15142). 23-Hydroxybetulinic acid inhibits the phosphorylation and nuclear translocation of STAT6, blocks M2 macrophage polarization, and reduces M2 macrophage-mediated apoptosis resistance of colon cancer cells. 23-Hydroxybetulinic acid can be used in related studies on chronic myeloid leukemia, hepatocellular carcinoma, sarcoma 180, multidrug-resistant breast cancer, leukemia, Doxorubicin-induced cardiotoxicity, and colorectal cancer.
    23-Hydroxybetulinic acid (Standard)
  • HY-113402B

    γ-Glu-Cys ammonium

    Interleukin Related TNF Receptor Endogenous Metabolite AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    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 .
    Gamma-glutamylcysteine ammonium
  • HY-P11242

    Bacterial NF-κB p38 MAPK JNK ERK TNF Receptor Interleukin Related Infection
    Cm-CATH2 is an antimicrobial peptide discovered from Chelonia mydas. Cm-CATH2 has a potent, broad-spectrum and rapid bactericidal ability by rapidly destroying the integrity of bacterial cell membranes. It shows strong activity against Gram-positive bacteria (such as VREF, Staphylococcus aureus), Gram-negative bacteria (such as Escherichia coli, Klebsiella pneumoniae), and fungi (such as Candida albicans) with MICs ranges from 1.17 to 18.75 μg/mL. Cm-CATH2 is also effective against various aquatic pathogenic bacteria. Cm-CATH2 not only inhibits biofilm formation but can also remove the formed biofilms. Cm-CATH2 has immunomodulatory functions and chemotactic effects on immune cells, and can inhibit the production of pro-inflammatory cytokines by macrophages stimulated by LPS (HY-D1056). Cm-CATH2 prevents the activation of NF-κB by inhibiting the degradation of IκBα, and also inhibits the phosphorylation of MAPK signaling pathways (p38, JNK, ERK). Cm-CATH2 demonstrates strong anti-infective ability in mouse peritonitis models and pneumonia models .
    Cm-CATH2
  • HY-183688

    Bacterial Phosphatase p38 MAPK ERK Infection
    MptpB-IN-3 is a selective inhibitor of Mycobacterium tuberculosis protein tyrosine phosphatase B (MptpB) with an IC50 of 0.19 μM. MptpB-IN-3 blocks MptpB-mediated inhibition of the macrophage MAPK pathway and restores the phosphorylation levels of Erk1/2 and p38. MptpB-IN-3 exhibits direct anti-tuberculosis activity against Mycobacterium tuberculosis and reduces the Mycobacterium tuberculosis load in mouse macrophages. MptpB-IN-3 can be used for tuberculosis research .
    MptpB-IN-3
  • HY-N17888

    NF-κB p38 MAPK FAK Akt Apoptosis NO Synthase COX TNF Receptor Interleukin Related Inflammation/Immunology Cancer
    Ephemeranthol A is a phenanthrene compound with anticancer and anti-inflammatory activities. Ephemeranthol A exerts significant anti-inflammatory effects in macrophages by inhibiting the NF-κB and MAPK signaling pathways. Ephemeranthol A induces apoptosis and inhibits metastasis of lung cancer cells by suppressing the FAK/Akt signaling and EMT processes. Ephemeranthol A can be used for the research of acute and chronic inflammatory diseases and non-small cell lung cancer .
    Ephemeranthol A
  • HY-N19215

    p38 MAPK ERK JNK NO Synthase PGE synthase Interleukin Related COX Inflammation/Immunology
    Arnicolide B is a sesquiterpene lactone. Arnicolide B is isolated from Centipeda minima. Arnicolide B inhibits the phosphorylation of ERK, JNK and p38 proteins in the MAPK signaling pathway. Arnicolide B reduces the production of inflammatory mediators NO, PGE2 and IL-6. Arnicolide B downregulates the overexpression of inflammatory proteins iNOS and COX-2. Arnicolide B has no effect on IκB-α degradation or NF-κB pathway activation. Arnicolide B is applicable to inflammation-related research .
    Arnicolide B
  • HY-P11467

    Bacterial p38 MAPK NF-κB PERK JNK Cardiovascular Disease Infection
    Gy-CATH is an anionic antimicrobial peptide. Gy-CATH activates MAPK and NF-κB signaling pathways (elevated levels of phospho-ERK, -p38, -JNK, -p65, and -IκBα). Gy-CATH upregulates the expression levels of three physiological anticoagulant pathways. Gy-CATH inhibits ADP-, Collagen-, and PMA-induced platelet aggregation. Gy-CATH has no direct antimicrobial activity, but shows significant preventive abilities against mice infected with Staphylococcus aureus, Escherichia coli, and Methicillin (HY-121544)-resistant Staphylococcus aureus. Gy-CATH exhibits potent immunomodulatory activity, enhancing macrophage-and neutrophil-mediated bactericidal functions. Gy-CATH significantly reduces the extent of pulmonary fibrin deposition and prevents thrombosis in mice .
    Gy-CATH
  • HY-N18025

    NF-κB p38 MAPK Akt Prostaglandin Receptor TNF Receptor Interleukin Related NO Synthase COX Inflammation/Immunology
    Kaempferol 3-O-(2G-glucosylrutinoside)-7-O-glucoside is an anti-inflammatory agent. Kaempferol 3-O-(2G-glucosylrutinoside)-7-O-glucoside exerts significant anti-inflammatory effects in LPS (HY-D1056)-induced RAW 264.7 macrophages by inhibiting the NF-κB, MAPK and Akt signaling pathways, thereby reducing the production of inflammatory mediators (NO, PGE2) and pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) .
    Kaempferol 3-O-(2G-glucosylrutinoside)-7-O-glucoside

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