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extracellular trap formation

" in MedChemExpress (MCE) Product Catalog:

18

Inhibitors & Agonists

1

Biochemical Assay Reagents

3

Peptides

2

Inhibitory Antibodies

3

Natural
Products

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-100574A
    Cl-amidine hydrochloride
    20+ Cited Publications

    		 Protein Arginine Deiminase Apoptosis MicroRNA Inflammation/Immunology Cancer
    Cl-amidine hydrochloride is an orally active peptidylarginine deminase (PAD) inhibitor, with IC50 values of 0.8 μM, 6.2 μM and 5.9 μM for PAD1, PAD3, and PAD4, respectively. Cl-amidine hydrochloride induces apoptosis in cancer cells. Cl-amidine hydrochloride induces microRNA (miR)-16 (miRNA-16, microRNA-16) expression and causes cell cycle arrest. Cl-Amidine hydrochloride prevents histone 3 citrullination and neutrophil extracellular trap formation, and improves survival in a murine sepsis model .
    Cl-amidine hydrochloride
  • HY-P99444
    Astegolimab
    2 Publications Verification

    MSTT 1041A; RG 6149

    		 Interleukin Related MDM-2/p53 NF-κB Cardiovascular Disease Inflammation/Immunology
    Astegolimab (MSTT 1041A; RG 6149) is a human IgG2 monoclonal antibody. Astegolimab blocks IL-33 signaling by targeting the IL-33 receptor ST2. Astegolimab reduces p53 expression, mitigates IL33-upregulated SASP factors such as IL1α, IL6 and MCP1. Astegolimab mitigates IL33-increased p-p65/p65 ratio. Astegolimab blocks CM-induced neutrophil extracellular trap (NET) formation. Astegolimab is used in chronic obstructive pulmonary disease (COPD) and myocardial research .
    Astegolimab
  • HY-123606
    GSK484
    Maximum Cited Publications
    49 Publications Verification

    		 Protein Arginine Deiminase MHC Cardiovascular Disease Inflammation/Immunology
    GSK484 is a PAD4 inhibitor that effectively inhibits protein citrullination and the formation of neutrophil extracellular traps (NETs) by blocking the catalytic activity of PAD4. GSK484 suppresses the production of histone H3, MHC-I expression, CD8 + T cell activation, proliferation and inflammatory cytokine release. GSK484 reduces inflammation and bone destruction in collagen-induced rheumatoid arthritis, alleviates pain and mast cell activation in sickle cell disease, and improves myocardial ischemia-reperfusion injury and experimental colitis. In addition, GSK484 restores intestinal microbial homeostasis by reversing ferroptosis-induced dysbiosis. GSK484 can be used to study the disease mechanisms of rheumatoid arthritis, sickle cell disease, thrombosis, myocardial injury, colitis and other conditions .
    GSK484
  • HY-Y1325I
    Sodium acetate trihydrate, 99.5%

    		Environmental Pollutants Biochemical Assay Reagents Apoptosis NO Synthase p38 MAPK Heme Oxygenase (HO) Keap1-Nrf2 Wnt β-catenin Metabolic Disease Inflammation/Immunology Cancer
    Sodium acetate trihydrate, 99.5% is a short-chain fatty acid salt with multiple biological activities. Sodium acetate trihydrate, 99.5% serves as a direct precursor of acetyl-CoA, and it extensively affects gene expression by promoting histone acetylation. Sodium acetate trihydrate, 99.5% can activate the p38 MAPK pathway to induce cancer cell apoptosis. Sodium acetate trihydrate, 99.5% can activate the Wnt/β-catenin signaling pathway to stimulate the proliferation and migration of cecal epithelial cells, thereby improving intestinal health. Sodium acetate trihydrate, 99.5% alleviates lead accumulation and oxidative damage by upregulating the testosterone-dependent eNOS/NO/cGMP signaling pathway, as well as activating the Nrf2/HO-1 pathway and its downstream antioxidant enzymes .
    Sodium acetate trihydrate, 99.5%
  • HY-N0353
    Curdione
    2 Publications Verification

    (+)-Curdione

    		 Ferroptosis Apoptosis Reactive Oxygen Species (ROS) Autophagy Glutathione Peroxidase Keap1-Nrf2 Heme Oxygenase (HO) TGF-β Receptor Indoleamine 2,3-Dioxygenase (IDO) Cardiovascular Disease Neurological Disease Cancer
    Curdione ((+)-Curdione) is an orally active sesquiterpenoid. Curdione inhibits platelet aggregation. Curdione induces ferroptosis in colorectal cancer via m6A methylation mediated by METTL14 and YTHDF2. Curdione inhibits ferroptosis in Isoproterenol (HY-B0468)-induced myocardial infarction by regulating the Keap1/Trx1/GPX4 signaling pathway, suppressing oxidative stress (ROS) and apoptosis. Curdione ameliorates Doxorubicin (HY-15142)-induced cardiotoxicity by inhibiting oxidative stress (ROS) and activating the Nrf2/HO-1 pathway. Curdione ameliorates sepsis-induced lung injury by inhibiting platelet-mediated neutrophil extracellular trap formation. Curdione ameliorates Bleomycin (HY-17565A)-induced pulmonary fibrosis by inhibiting TGF-β-induced fibroblast-to-myofibroblast differentiation. Curdione exhibits neuroprotective effects against focal cerebral ischemia-reperfusion injury in rats. Curdione exerts antiproliferative effects against human uterine leiomyosarcoma by targeting IDO1. Curdione protects vascular endothelial cells and atherosclerosis by regulating DNMT1-mediated ERBB4 promoter methylation. Curdione inhibits inducible prostaglandin E2 production (IC50 = 1.1 μM) and cyclooxygenase 2 expression .
    Curdione
  • HY-100574
    Cl-amidine

    		Protein Arginine Deiminase Apoptosis MicroRNA Inflammation/Immunology Cancer
    Cl-amidine is an orally active peptidylarginine deminase (PAD) inhibitor, with IC50 values of 0.8 μM, 6.2 μM and 5.9 μM for PAD1, PAD3, and PAD4, respectively. Cl-amidine induces apoptosis in cancer cells. Cl-amidine induces microRNA (miR)-16 (miRNA-16, microRNA-16) expression and causes cell cycle arrest. Cl-Amidine prevents histone 3 citrullination and neutrophil extracellular trap formation, and improves survival in a murine sepsis model .
    Cl-amidine
  • HY-P991401
    GSK2862277

    		TNF Receptor Inflammation/Immunology
    GSK2862277 is a human monoclonal antibody (mAb) targeting TNFRSF1A. GSK2862277 increases neutrophil extracellular trap formation and alveolar macrophage phagocytosis. GSK2862277 can be used in Acute lung injury and Acute Respiratory Distress Syndrome (ARDS) research. Recommended isotype control: VHH-hFc .
    GSK2862277
  • HY-137655
    BMS-P5

    		Protein Arginine Deiminase Cancer
    BMS-P5 is a selective and orally active peptidylarginine deiminase 4 (PAD4) inhibitor with an IC50 of 98 nM. BMS-P5 shows selective for PAD4 over PAD1, PAD2, and PAD3. BMS-P5 blocks multiple myeloma (MM)-induced neutrophil extracellular trap (NET) formation and delays progression of MM in a syngeneic mouse model .
    BMS-P5
  • HY-137655A
    BMS-P5 free base

    		Protein Arginine Deiminase Cancer
    BMS-P5 free base is a selective and orally active peptidylarginine deiminase 4 (PAD4) inhibitor with an IC50 of 98 nM. BMS-P5 free base shows selective for PAD4 over PAD1, PAD2, and PAD3. BMS-P5 free base blocks multiple myeloma (MM)-induced neutrophil extracellular trap (NET) formation and delays progression of MM in a syngeneic mouse model .
    BMS-P5 free base
  • HY-145237
    BM213
    3 Publications Verification

    		 Complement System Apoptosis Reactive Oxygen Species (ROS) Cancer
    BM213 is a selective C5aR agonist, with an EC50 of 59 nM. BM213 specifically activates the C5a-C5aR1 axis, which in turn promotes neutrophil extracellular trap (NET) formation and exacerbates inflammatory responses. BM213 significantly induces ventricular dilationin, promotes myocardial ROS production, and induces cardiomyocyte apoptosis in rats. BM213 can be used for the study of myocardial ischemia/reperfusion (I/R) injury .
    BM213
  • HY-W996116
    AZM198

    		Glutathione Peroxidase Cardiovascular Disease Neurological Disease Inflammation/Immunology
    AZM198 is an orally active myeloperoxidase (MPO) inhibitor. AZM198 irreversibly inactivates MPO (IC50=0.015 μM) via covalent binding to the heme prosthetic group, preferentially targets extracellular MPO activity, and reduces neutrophil extracellular trap formation, reactive oxygen species production and degranulation. AZM198 increases the fibrous cap thickness of atherosclerotic plaques, reduces lesion area, ameliorates hepatic steatosis and fibrosis in non-alcoholic steatohepatitis, and alleviates proteinuria and inflammatory infiltration associated with glomerulonephritis. AZM198 also decreases circulating levels of high-sensitivity Cardiac Troponin I and IL-1β, and mitigates endothelial cell injury. Therefore, AZM198 is suitable for research on various MPO-related diseases, including atherosclerotic cardiovascular disease, myocardial infarction, ischemic stroke, non-alcoholic steatohepatitis and crescentic glomerulonephritis .
    AZM198
  • HY-100574B
    Cl-amidine TFA
    20+ Cited Publications

    		 Protein Arginine Deiminase Apoptosis MicroRNA Inflammation/Immunology Cancer
    Cl-amidine TFA is an orally active peptidylarginine deminase (PAD) inhibitor, with IC50 values of 0.8 μM, 6.2 μM and 5.9 μM for PAD1, PAD3, and PAD4, respectively. Cl-amidine TFA induces apoptosis in cancer cells. Cl-amidine TFA induces microRNA (miR)-16 (miRNA-16, microRNA-16) expression and causes cell cycle arrest. Cl-Amidine TFA prevents histone 3 citrullination and neutrophil extracellular trap formation, and improves survival in a murine sepsis model .
    Cl-amidine TFA
  • HY-N7314
    Asebogenin

    		Syk Inflammation/Immunology
    Asebogenin has antimalarial activity in vitro . Asebogenin can inhibit the phosphorylation of Syk, thereby effectively suppressing platelet activation and the formation of neutrophil extracellular traps .
    Asebogenin
  • HY-157157
    PAD4-IN-3

    		Protein Arginine Deiminase Cancer
    PAD4-IN-3 (compound 4B) is a PAD4 inhibitor with antitumor activity in vitro and in vivo. PAD4-IN-3 was covalently linked to RGD sequence peptide-modified chitosan (K-CRGDV), resulting in an enhanced oxidative stress-responsive nanoagent. K-CRGDV-PAD4-IN-3 can actively target tumors, inhibit PAD4 activity, block the formation of neutrophil extracellular traps (NETs), and improve the tumor immune microenvironment in response to the tumor microenvironment .
    PAD4-IN-3
  • HY-181449
    CAY10729

    		Protein Arginine Deiminase Inflammation/Immunology
    CAY10729 (Compound 21) is a selective PAD2 inhibitor. CAY10729 inhibits neutrophil extracellular trap formation .
    CAY10729
  • HY-N0353R
    Curdione (Standard)

    (+)-Curdione (Standard)

    		 Reference Standards Ferroptosis Apoptosis Reactive Oxygen Species (ROS) Autophagy Glutathione Peroxidase Keap1-Nrf2 Heme Oxygenase (HO) TGF-β Receptor Indoleamine 2,3-Dioxygenase (IDO) Others
    Curdione (Standard) is the analytical standard of Curdione. This product is intended for research and analytical applications. Curdione ((+)-Curdione) is an orally active sesquiterpenoid. Curdione inhibits platelet aggregation. Curdione induces ferroptosis in colorectal cancer via m6A methylation mediated by METTL14 and YTHDF2. Curdione inhibits ferroptosis in Isoproterenol (HY-B0468)-induced myocardial infarction by regulating the Keap1/Trx1/GPX4 signaling pathway, suppressing oxidative stress (ROS) and apoptosis. Curdione ameliorates Doxorubicin (HY-15142)-induced cardiotoxicity by inhibiting oxidative stress (ROS) and activating the Nrf2/HO-1 pathway. Curdione ameliorates sepsis-induced lung injury by inhibiting platelet-mediated neutrophil extracellular trap formation. Curdione ameliorates Bleomycin (HY-17565A)-induced pulmonary fibrosis by inhibiting TGF-β-induced fibroblast-to-myofibroblast differentiation. Curdione exhibits neuroprotective effects against focal cerebral ischemia-reperfusion injury in rats. Curdione exerts antiproliferative effects against human uterine leiomyosarcoma by targeting IDO1. Curdione protects vascular endothelial cells and atherosclerosis by regulating DNMT1-mediated ERBB4 promoter methylation. Curdione inhibits inducible prostaglandin E2 production (IC50 = 1.1 μM) and cyclooxygenase 2 expression .
    Curdione (Standard)
  • HY-P11868
    PADI4_3

    		Protein Arginine Deiminase Inflammation/Immunology Cancer
    PADI4_3 is a substrate-competitive and selective PADI4 inhibitor with an IC50 of 56 nM. PADI4_3 blocks citrullination of histone H3 and reduces the formation of neutrophil extracellular traps. PADI4_3 can be used in research related to autoimmune diseases and cancers .
    PADI4_3
  • HY-P11791
    nNIF peptide

    		Endogenous Metabolite Infection
    nNIF peptide is an endogenous polypeptide detectable in human umbilical cords and neonatal blood. nNIF peptide specifically inhibits neutrophil extracellular trap (NETs) formation by neutrophils without interfering with other key immune functions of neutrophils. nNIF peptide can be used in studies related to COVID-19 acute respiratory distress syndrome, polymicrobial sepsis, and neonatal infectious peritonitis .
    nNIF peptide

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