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

Death receptor signaling

" in MedChemExpress (MCE) Product Catalog:

36

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4

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10

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3

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Isotope-Labeled Compounds

3

Oligonucleotides

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-P1363
    β-Amyloid (1-42), human TFA
    Maximum Cited Publications
    24 Publications Verification

    Amyloid β-peptide (1-42) (human) TFA

    Amyloid-β Neurological Disease
    β-Amyloid (1-42) (Amyloid β-peptide (1-42), human TFA, a 42-amino acid peptide that has not been treated with HFIP, is a brain-penetrant amyloid protein fragment, which can be used in research on Alzheimer's disease and Down’s syndrome. β-Amyloid (1-42), human TFA remaining as a monomer exhibits antioxidant and neuroprotective effects. β-Amyloid (1-42), human TFA, after being monomericized by HFIP and dissolved in DMSO to form the stock solution, on the one hand, can form soluble oligomers (AβOs) when incubated at 4 °C, which have synaptic toxicity and neurotoxicity; on the other hand, it can be incubated at 37 °C to form insoluble fibrils, with lower neurotoxicity, and participating in the oxidative damage process. Aβ42 oligomers bind to various neuronal surface receptors (such as PrPc, mGluR5, NMDA receptors, etc.), triggering oxidative stress, calcium homeostasis imbalance, and synaptic toxicity via activating downstream signaling pathways, leading to neuronal dysfunction and death .
    β-Amyloid (1-42), human TFA
  • HY-P1363A
    β-Amyloid (1-42), human
    Maximum Cited Publications
    24 Publications Verification

    Amyloid β-peptide (1-42) (human)

    Amyloid-β Neurological Disease
    β-Amyloid (1-42) (Amyloid β-peptide (1-42)), human, a 42-amino acid peptide that has not been treated with HFIP, is a brain-penetrant amyloid protein fragment, which can be used in research on Alzheimer's disease and Down’s syndrome. β-Amyloid (1-42), human remaining as a monomer exhibits antioxidant and neuroprotective effects. β-Amyloid (1-42), human, after being monomericized by HFIP and dissolved in DMSO to form the stock solution, on the one hand, can form soluble oligomers (AβOs) when incubated at 4 °C, which have synaptic toxicity and neurotoxicity; on the other hand, it can be incubated at 37 °C to form insoluble fibrils, with lower neurotoxicity, and participating in the oxidative damage process. Aβ42 oligomers bind to various neuronal surface receptors (such as PrPc, mGluR5, NMDA receptors, etc.), triggering oxidative stress, calcium homeostasis imbalance, and synaptic toxicity via activating downstream signaling pathways, leading to neuronal dysfunction and death .
    β-Amyloid (1-42), human
  • HY-P1363B
    β-Amyloid (1-42), human, HFIP-treated
    Maximum Cited Publications
    24 Publications Verification

    Amyloid-β Neurological Disease
    β-Amyloid (1-42), human, HFIP-treated, a 42-amino acid peptide that has been treated with HFIP from β-Amyloid (1-42), human (HY-P1363A), is a brain-penetrant amyloid protein fragment, which can be used in research on Alzheimer's disease and Down’s syndrome. β-Amyloid (1-42), human, HFIP-treated remaining as a monomer exhibits antioxidant and neuroprotective effects. β-Amyloid (1-42), human, HFIP-treated, after being dissolved in DMSO to form the stock solution, on the one hand, can form soluble oligomers (AβOs) when incubated at 4°C, which have synaptic toxicity and neurotoxicity; on the other hand, it can be incubated at 37°C to form insoluble fibrils, with lower neurotoxicity, and participating in the oxidative damage process. Aβ42 oligomers bind to various neuronal surface receptors (such as PrPc, mGluR5, NMDA receptors, etc.), triggering oxidative stress, calcium homeostasis imbalance, and synaptic toxicity via activating downstream signaling pathways, leading to neuronal dysfunction and death .
    β-Amyloid (1-42), human, HFIP-treated
  • HY-N5134
    5'-Guanylic acid
    2 Publications Verification

    5'-GMP; 5'-guanosine monophosphate

    Endogenous Metabolite iGluR Neurological Disease Metabolic Disease
    5'-Guanylic acid is a purine nucleotide that participates in physiological processes such as energy metabolism, signal transduction, and gene expression regulation. 5'-Guanylic acid regulates the expression of genes related to fatty acid metabolism. 5'-Guanylic acid is the weak agonist for ionotropic glutamate receptors (iGluR), reduces the activity of the glutamatergic system and exhibits neuroprotective effect. 5'-Guanylic acid also causes neuronal cell death at high concentrations .
    5'-Guanylic acid
  • HY-126741
    Azadirachtin
    2 Publications Verification

    Environmental Pollutants Parasite Caspase NF-κB Apoptosis Bcl-2 Family Infection Inflammation/Immunology Cancer
    Azadirachtin is an oral active triterpenoid compound with anticancer, antimalarial, anti-inflammatory, and insecticidal activities. Azadirachtin induces cell apoptosis through the mitochondrial pathway (by inhibiting Bcl-2/Bax ratio or activating Apaf-1 and caspase-3) or through death receptors (by inhibiting TNFR activation). Additionally, Azadirachtin exerts its anti-inflammatory effects by inhibiting NF-кB signaling pathway activation, and it exhibits insecticidal activity by inducing apoptosis in insect cells .
    Azadirachtin
  • HY-108610A
    Edelfosine
    1 Publications Verification

    ET-18-OCH3

    Apoptosis Parasite Bcl-2 Family Cytochrome P450 Infection Inflammation/Immunology Cancer
    Edelfosine (ET-18-OCH3) is an orally active lipid raft modulator and apoptosis inducer that alters membrane fluidity and preferentially inserts into tumor cell membranes. Edelfosine recruits death receptor ligands (FasL/CD95L, TRAIL) and Bid to lipid rafts to form death-inducing signaling complexes, thereby initiating mitochondria-dependent apoptosis and inducing cytochrome c release. Edelfosine also exerts anti-inflammatory effects, promotes L-Selectin shedding, and causes no gastrointestinal or organ toxicity. In addition, Edelfosine inhibits nucleic acid and protein synthesis in Leishmania donovani and exhibits antiproliferative activity. Edelfosine can be used in research on multiple myeloma, inflammatory bowel diseases (such as ulcerative colitis and Crohn's disease), and visceral leishmaniasis .
    Edelfosine
  • HY-W010970
    5'-Guanylic acid disodium salt
    2 Publications Verification

    5'-GMP disodium salt; 5'-guanosine monophosphate disodium salt

    Endogenous Metabolite iGluR Neurological Disease Metabolic Disease
    5'-Guanylic acid disodium salt is the disodium salt form of 5'-Guanylic acid (HY-N5134). 5'-Guanylic acid disodium salt is a purine nucleotide that participates in physiological processes such as energy metabolism, signal transduction, and gene expression regulation. 5'-Guanylic acid disodium salt regulates the expression of genes related to fatty acid metabolism. 5'-Guanylic acid disodium salt is the weak agonist for ionotropic glutamate receptors (iGluR), reduces the activity of the glutamatergic system and exhibits neuroprotective effect. 5'-Guanylic acid disodium salt also causes neuronal cell death at high concentrations .
    5'-Guanylic acid disodium salt
  • HY-157562

    Phospholipase Apoptosis Cancer
    DS68591889 is a selective and orally active phosphatidylserine synthase 1 (PTDSS1) inhibitor. DS68591889 has no inhibitory activity against PTDSS2. DS68591889 induces the phospholipid imbalance in a wide range of cancer cells. DS68591889 negatively regulates B cell receptor (BCR)-induced Ca 2+ signaling and subsequent apoptotic cell death. DS68591889 can be used for the cancer research, such as B cell lymphoma .
    DS68591889
  • HY-P1137
    10Panx
    1 Publications Verification

    Gap Junction Protein Others
    10Panx is a competitive inhibitor of selective Pannexin 1 (PANX1) channels. 10Panx blocks the opening of PANX1 channels, inhibits ATP release and downstream P2X7 receptor-mediated signaling pathways, thereby reducing cell death and inflammatory responses. 10Panx can be used in the study of diseases such as neuropathic pain, inflammatory bowel disease, and Clostridioides difficile infection. 10Panx can effectively reduce mechanical hyperalgesia and enhanced C-reflexes, and inhibit the expression of pro-inflammatory factors such as IL-6[1][2][3].
    10Panx
  • HY-N1431
    Tabersonine
    3 Publications Verification

    NOD-like Receptor (NLR) Apoptosis Cytochrome P450 NF-κB PI3K Akt CDK Caspase Interleukin Related p38 MAPK Inflammation/Immunology Cancer
    Tabersonine is a selective, orally active NLRP3 inhibitor. Tabersonine directly binds to the NACHT domain of NLRP3, inhibiting its ATPase activity and oligomerization, thereby blocking ASC spot formation and caspase-1 activation, and reducing the release of pro-inflammatory cytokines such as IL-1β. Tabersonine also inhibits K63-linked ubiquitination of TRAF6, blocking NF-κB, PI3K/Akt, and p38 MAPK signaling pathways. Tabersonine can inhibit inflammatory responses, induce apoptosis of liver cancer cells through mitochondrial pathways and death receptor pathways, reduce mitochondrial membrane potential, promote cytochrome c release, and activate caspase proteins. Tabersonine is mainly used in the study of NLRP3-driven inflammatory diseases (such as acute lung injury, sepsis, peritonitis) and tumors such as liver cancer .
    Tabersonine
  • HY-N0660

    Apoptosis PARP Caspase AMPK Autophagy VEGFR Keap1-Nrf2 STING 11β-HSD Ferroptosis PI3K Akt p38 MAPK ERK Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    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 .
    Jujuboside B
  • HY-168438
    ERBB agonist-1
    1 Publications Verification

    EGFR Akt ERK Cardiovascular Disease
    ERBB agonist-1 (Compound EF-1) is an agonist for ERBB4, that activates the ERBB4 signaling pathway by inducing dimerization of the ERBB4 receptor with an EC50 of 10.5 μM. ERBB agonist-1 induces phosphorylation of Akt and ERK1/2, reduces the collagen expression in cardiac fibroblasts, inhibits H2O2-induced cardiomyocyte death and Ang II (HY-13948)-induced cardiomyocyte hypertrophy. ERBB agonist-1 prevents fibrosis and exhibits cardioprotective efficacy in mouse models .
    ERBB agonist-1
  • HY-P99031

    CAM 3001

    c-Fms Cardiovascular Disease Inflammation/Immunology
    Mavrilimumab (CAM 3001) is a monoclonal antibody that binds to the α subunit of the granulocyte-macrophage colony stimulating factor (GM-CSF) receptor and blocks intracellular signalling downstream of GM-CSF. GM-CSF might be a mediator of the hyperactive inflammatory response associated with respiratory failure and death .
    Mavrilimumab
  • HY-P11108

    NF-κB Apoptosis TNF Receptor Caspase Inflammation/Immunology Cancer
    RP-182 is a synthetic immunomodulatory peptide that exerts anti-tumor effects by targeting the mannose receptor CD206 (Kd = 8 μM) on the surface of tumor-associated macrophages (TAMs). RP-182 induces a conformational switch of the CD206 receptor, which activates NF-κB signaling and phagocytosis in CD206 high TAMs. RP-182 has dual function: activation of canonical NF-κB signaling, triggering TNFα secretion and autocrine activation of the TNF receptor 1 (TNFR1), leading to activation of caspase 8, apoptosis, and cell death. RP-182 is used in pancreatic cancer and melanoma research .
    RP-182
  • HY-N5134R

    5'-GMP (Standard); 5'-guanosine monophosphate (Standard)

    Reference Standards Endogenous Metabolite
    5'-Guanylic acid is a purine nucleotide that participates in physiological processes such as energy metabolism, signal transduction, and gene expression regulation. 5'-Guanylic acid regulates the expression of genes related to fatty acid metabolism. 5'-Guanylic acid is the weak agonist for ionotropic glutamate receptors (iGluR), reduces the activity of the glutamatergic system and exhibits neuroprotective effect. 5'-Guanylic acid also causes neuronal cell death at high concentrations .
    5'-Guanylic acid (Standard)
  • HY-N0910
    Notoginsenoside Ft1
    1 Publications Verification

    PI3K mTOR Akt Apoptosis p38 MAPK ERK Transmembrane Glycoprotein Glutathione Reductase (GR) Estrogen Receptor/ERR Calcium Channel Ferroptosis G protein-coupled Bile Acid Receptor 1 FXR Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Notoginsenoside Ft1 is an orally active bioactive saponin. Notoginsenoside Ft1 inhibits the PI3K/AKT/mTOR signaling pathway, activates the p38 MAPK and ERK1/2 signaling pathways, and increases the proportion of CD8 + T cells, thereby inducing apoptosis and lysosomal cell death in various cancer cells, and promoting angiogenesis. Notoginsenoside Ft1 causes vasodilation by activating glucocorticoid receptors (GR) and estrogen receptor beta (ERβ) in endothelial cells. Notoginsenoside Ft1 increases intracellular Ca 2+ accumulation, reduces cAMP levels by activating a signaling network mediated through P2Y12 receptors, and promotes platelet aggregation, thereby exerting a procoagulant effect. Notoginsenoside Ft1 inhibits ferroptosis (ferroptosis) in renal tubular epithelial cells by activating the TGR5 receptor, thereby demonstrating a renal protective effect. Notoginsenoside Ft1 acts as a TGR5 agonist and an FXR antagonist to combat obesity and insulin resistance .
    Notoginsenoside Ft1
  • HY-121833

    Trk Receptor Akt ERK Neurological Disease Cancer
    Gambogic amide is a potent and selective agonist of TrkA and also induces its tyrosine phosphorylation and activation of downstream signaling, including Akt and MAPK. Gambogic amide specifically interacts with the cytoplasmic juxtamembrane domain of the TrkA receptor and triggers its dimerization, leading to activation. Gambogic amide has neuroprotective activity preventing glutamate-induced neuronal cell death. Gambogic amide has improved efficacy in a transient middle cerebral artery occlusion model of stroke and could be used to study neurodegenerative diseases and stroke .
    Gambogic amide
  • HY-160167

    DZD8586

    Src Btk Inflammation/Immunology Cancer
    Birelentinib (DZD8586) is an orally effective, selective, non-covalent inhibitor targeting LYN tyrosine kinase and BTK tyrosine kinase, capable of penetrating the blood-brain barrier. Birelentinib exhibits concentration-dependent antiproliferative effects in RI-1 cells and diffuse large B-cell lymphoma (DLBCL) cell lines carrying BTK resistance mutations (such as C481X, V416L, etc.). Birelentinib blocks both BTK-dependent and independent signaling of the B-cell receptor (BCR), thereby inhibiting tumor cell proliferation and inducing cell death. Birelentinib can be used in research to overcome resistance to existing covalent and non-covalent BTK inhibitors in B-cell non-Hodgkin lymphoma (B-NHL) .
    Birelentinib
  • HY-156871

    CaMK Cancer
    CAMK1D-IN-1 (compound I) is an inhibitor of CAMK1D, targeting cytotoxic T lymphocyte (CTL)-resistant tumor cells. CAMK1D impairs CTL-induced death receptor signaling and apoptosis by inhibiting caspases, making it a key and effective target for PD-L1-refractory tumors .
    CAMK1D-IN-1
  • HY-P10208A
    RKH acetate
    1 Publications Verification

    Toll-like Receptor (TLR) Infection Inflammation/Immunology
    RKH acetate exerts protective effects against sepsis-induced death and organ damage. RKH acetate can directly bind to Toll-like receptor 4 (TLR4) and block TLR4 signal transduction in immune cells .
    RKH acetate
  • HY-176236

    LXR Autophagy Metabolic Disease
    Lipophagy inducer 1 is a lipophagy inducer. Lipophagy inducer 1 has activity of reducing lipid droplet accumulation and rescuing cell death. Lipophagy inducer 1 exerts its effects by activating lipophagy, increasing steady-state autophagosome and regulating the LXR signaling pathway. Lipophagy inducer 1 can be used in the study of diabetic nephropathy (DKD) and other diseases related to lipid metabolism disorders .
    Lipophagy inducer 1
  • HY-N1431A
    Tabersonine hydrochloride
    3 Publications Verification

    NOD-like Receptor (NLR) Apoptosis Cytochrome P450 NF-κB PI3K Akt CDK Caspase Interleukin Related p38 MAPK Neurological Disease Inflammation/Immunology
    Tabersonine hydrochloride is a selective, orally active NLRP3 inhibitor. Tabersonine hydrochloride directly binds to the NACHT domain of NLRP3, inhibiting its ATPase activity and oligomerization, thereby blocking ASC spot formation and caspase-1 activation, and reducing the release of pro-inflammatory cytokines such as IL-1β. Tabersonine hydrochloride also inhibits K63-linked ubiquitination of TRAF6, blocking NF-κB, PI3K/Akt, and p38 MAPK signaling pathways. Tabersonine hydrochloride can inhibit inflammatory responses, induce apoptosis of liver cancer cells through mitochondrial pathways and death receptor pathways, reduce mitochondrial membrane potential, promote cytochrome c release, and activate caspase proteins. Tabersonine hydrochloride is mainly used in the study of NLRP3-driven inflammatory diseases (such as acute lung injury, sepsis, peritonitis) and tumors such as liver cancer .
    Tabersonine hydrochloride
  • HY-171450

    Trk Receptor Cancer
    VMD-928 is an orally active, allosteric, irreversible and selective tropomyosin receptor kinase A (TrkA) inhibitor. VMD-928 blocks the downstream signaling pathways triggered by the binding of nerve growth factor (NGF) to TrkA, thereby inhibiting cell proliferation, invasion, and promoting cancer cell death. VMD-928 is promising for research of various cancers, including prostate cancer, thymic carcinoma, mesothelioma, squamous cell carcinoma of the head and neck, squamous cell carcinoma of the lung, ovarian cancer, hepatocellular carcinoma .
    VMD-928
  • HY-P11108A

    NF-κB Apoptosis TNF Receptor Caspase Inflammation/Immunology Cancer
    RP-182 acetate is a synthetic immunomodulatory peptide that exerts anti-tumor effects by targeting the mannose receptor CD206 (Kd = 8 μM) on the surface of tumor-associated macrophages (TAMs). RP-182 acetate induces a conformational switch of the CD206 receptor, which activates NF-κB signaling and phagocytosis in CD206 high TAMs. RP-182 acetate has dual function: activation of canonical NF-κB signaling, triggering TNFα secretion and autocrine activation of the TNF receptor 1 (TNFR1), leading to activation of caspase 8, apoptosis, and cell death. RP-182 acetate is used in pancreatic cancer and melanoma research .
    RP-182 acetate
  • HY-P10992

    PI3K Akt mTOR Caspase Apoptosis Bcl-2 Family Cancer
    YVPGP is an oligopeptide exacted from Anthopleura anjunae. YVPGP has a significant antitumor activity by mediating PI3K/AKT/mTOR signaling pathway. YVPGP arrests DU-145 cells in the S phase and induces apoptosis via mitochondrial and death receptor pathways (caspase3, 7, 8, 9). YVPGP effectively inhibits tumor growth in DU-145 xenografts mice model, promising for prostate cancer research .
    YVPGP
  • HY-P10833

    VEGFR PI3K Akt mTOR ERK Apoptosis Cardiovascular Disease Cancer
    C-VGB3 is a selective vascular endothelial growth factor receptor 2 (VEGFR2) antagonist, which inhibits VEGFR2-mediated PI3K/AKT/mTOR and PLCγ/ERK1/2 signaling pathways. C-VGB3 binds to the extracellular domain of VEGFR2, blocking ligand-receptor interaction and inducing apoptosis in endothelial and tumor cells through both intrinsic (involving Bcl2 family and caspases) and extrinsic (death receptor-mediated) pathways. C-VGB3 is promising for research of angiogenesis-related cancers, such as breast cancer .
    C-VGB3
  • HY-P1363S1

    Isotope-Labeled Compounds Amyloid-β Neurological Disease
    β-Amyloid (1-42), human, Ala( 13C3, 15N) TFA is the 13C and 15N-labeled β-Amyloid (1-42), human (HY-P1363A). β-Amyloid (1-42) (Amyloid β-peptide (1-42)), human, a 42-amino acid peptide that has not been treated with HFIP, is a brain-penetrant amyloid protein fragment, which can be used in research on Alzheimer's disease and Down’s syndrome. β-Amyloid (1-42), human remaining as a monomer exhibits antioxidant and neuroprotective effects. β-Amyloid (1-42), human, after being monomericized by HFIP and dissolved in DMSO to form the stock solution, on the one hand, can form soluble oligomers (AβOs) when incubated at 4 °C, which have synaptic toxicity and neurotoxicity; on the other hand, it can be incubated at 37 °C to form insoluble fibrils, with lower neurotoxicity, and participating in the oxidative damage process. Aβ42 oligomers bind to various neuronal surface receptors (such as PrPc, mGluR5, NMDA receptors, etc.), triggering oxidative stress, calcium homeostasis imbalance, and synaptic toxicity via activating downstream signaling pathways, leading to neuronal dysfunction and death .
    β-Amyloid (1-42), human, Ala(13C3,15N) TFA
  • HY-W750355

    Insecticide Infection
    Azadirachtin D is an insect growth regulator targeting ecdysone receptor (EcR) in insects. Azadirachtin D blocks the 20-hydroxyecdysone signaling pathway, leading to developmental arrest or death in insects. Azadirachtin D is promising for research of agricultural pests .
    Azadirachtin D
  • HY-168770

    RIP kinase TNF Receptor Apoptosis Cardiovascular Disease
    Cl-Necrostatin-1 is a RIPK1 inhibitor. Cl-Necrostatin-1 can also inhibit TNF-α-induced necroptosis in Jurkat cells deficient in Fas-associated death domain protein (FADD; EC50 = 180 nM), a modification that prevents caspase activation in response to death-domain receptor signaling. Cl-Necrostatin-1 can also reduce infarct size in a mouse model of middle cerebral artery occlusion (MCAO). Cl-Necrostatin-1 is used for research in cardiovascular and cerebrovascular diseases .
    Cl-Necrostatin-1
  • HY-E70851

    AMPK Cancer
    NUAK2 is a member of the SNF1/AMP kinase (AMPK) family (serine/threonine kinases) that is regulated by the putative tumor suppressor LKB1 (20-23) and also by death receptor signaling through NF-κB. Nuak2 Recombinant Human Active Protein Kinase is a recombinant Nuak2 protein that can be used to study Nuak2-related functions .
    Nuak2 Recombinant Human Active Protein Kinase
  • HY-174586

    mRNA Inflammation/Immunology
    Human LTBR mRNA encodes the human lymphotoxin beta receptor (LTBR) protein, a member of the tumor necrosis factor receptor superfamily. LTBR plays a role in signalling during the development of lymphoid and other organs, lipid metabolism, immune response, and programmed cell death.
    Human LTBR mRNA
  • HY-E70802

    AMPK Cancer
    NUAK2 is a member of the SNF1/AMP kinase (AMPK) family (serine/threonine kinases) that is regulated by the putative tumor suppressor LKB1 (20-23) and also by death receptor signaling through NF-κB. Biotin-Nuak2 Recombinant Human Active Protein Kinase is a recombinant Nuak2 protein that can be used to study Nuak2-related functions, and is biotinylated .
    Biotin-Nuak2 Recombinant Human Active Protein Kinase
  • HY-P992473

    TNF Receptor Inflammation/Immunology Cancer
    TAS266 is a tetrameric nanobody agonist targeting DR5. TAS266 selectively induces cancer cell death. TAS266 triggers sustained tumor regression in xenograft models and also elicits immunogenic responses including antibody binding. TAS266 exhibits superior anti-tumor efficacy compared with traditional DR5-targeting strategies. TAS266 can be used in research related to pancreatic cancer and advanced solid tumors .
    TAS266
  • HY-W017180

    α-(Bromomethyl)acrylic acid; α-Methylated acrylamide; α-MAA

    Drug Intermediate Cancer
    2-(Bromomethyl) acrylic acid (α-MAA) is a component of Ibt-DOX (HY-181546) .
    2-(Bromomethyl)acrylic acid
  • HY-P992448

    PD-1/PD-L1 Cancer
    RC98 is a monoclonal antibody targeting programmed cell death ligand 1 (PD-L1) and acts as a selective PD-L1 inhibitor. RC98 binds specifically to human and cynomolgus monkey PD-L1. RC98 blocks the interaction between PD-L1 and its receptor PD-1 to reverse T-cell inactivation mediated by PD-1/PD-L1 signaling. RC98 enhances the cytotoxic T-lymphocyte-mediated anti-tumor immune response against PD-L1-expressing tumor cells. RC98 can be used for the research of tumor immunity and solid tumors .
    RC98
  • HY-N0660R

    Reference Standards ERK p38 MAPK Akt PI3K 11β-HSD STING VEGFR Ferroptosis Autophagy Apoptosis Keap1-Nrf2 Caspase PARP AMPK Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    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.
    Jujuboside B (Standard)

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