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tissue necrosis

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Isotope-Labeled Compounds

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-107910
    Hyaluronidase, Bovine testes
    5+ Cited Publications

    Hyaluronate 4-glycanohydrolase, Bovine testes; Hyaluronoglucosaminidase, Bovine testes

    NF-κB Inflammation/Immunology Cancer
    Hyaluronidase, Bovine testes (Hyaluronate 4-glycanohydrolase; Hyaluronoglucosaminidase) is an endoglycosidase that depolymerizes Hyaluronic acid (HA) (HY-B0633A) by cleavage of glycosidic bonds. Hyaluronidase degrades HA and activates membrane receptors that trigger pathways converging in NF-κB activation. Hyaluronidase is employed in the research of granulomatous foreign body reactions, soft-tissue necrosis caused by vascular compromise and uncomplicated nodules, overcorrection, inflamed nodules or tissue ischemia associated with HA filler injection .
    Hyaluronidase, Bovine testes
  • HY-109540

    AF-0150

    Heme Oxygenase (HO) Interleukin Related Inflammation/Immunology
    Perfluorohexane (AF-0150) is a perfluorocarbon. Perfluorohexane is also an enhancer of high-intensity focused ultrasound (HIFU) therapy. Perfluorohexane increases HO-1 and IL-10. Perfluorohexane exerts an antioxidant effect. Perfluorohexane alleviates lung injury induced by LPS (HY-D1056A1). Perfluorohexane improves the efficiency and precision of treatment and reduces damage to surrounding normal tissues. Perfluorohexane can be used in the study of acute lung injury .
    Perfluorohexane
  • HY-105017

    ATL 313; DE 112

    Adenosine Receptor Infection Inflammation/Immunology
    Evodenoson is a selective agonist of the A2A adenosine receptor. Evodenoson’s primary actions include reducing inflammatory responses, decreasing intestinal fluid secretion, edema, tissue damage, and neutrophil infiltration induced by Clostridium difficile toxin A. Evodenoson’s protective effect is achieved by reducing myeloperoxidase (MPO) and adenosine deaminase (ADA) activities, and by lowering the production of tumor necrosis factor-alpha (TNF-α) .
    Evodenoson
  • HY-N2909

    NF-κB RIP kinase Mixed Lineage Kinase Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Aurantiamide is a non-covalent, orally active, blood-brain-permeable GRPR selective antagonist with anti-inflammatory and neuroprotective effects. Aurantiamide reduces inflammation and oxidative stress in renal tissue by inhibiting GRPR-mediated renal necrosis pathways (such as RIPK3/MLKL signaling) and NF-κB inflammatory pathways, exerting anti-acute kidney injury and endothelial function activities. Aurantiamide also inhibits the M1 polarization of microglia and inhibits NLRP3 activation, thereby improving AD mouse models. Aurantiamide has in vivo inhibitory efficacy in acute kidney injury models such as ischemia/reperfusion, sepsis, and hypertension models .
    Aurantiamide
  • HY-100573
    Necrosulfonamide
    Maximum Cited Publications
    122 Publications Verification

    Mixed Lineage Kinase Necroptosis Pyroptosis Caspase NOD-like Receptor (NLR) Keap1-Nrf2 TNF Receptor Interleukin Related NO Synthase Heme Oxygenase (HO) Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Endocrinology
    Necrosulfonamide is a MLKL and Gasdermin D (GSDMD) inhibitor, capable of separately inhibiting necroptosis and pyroptosis of cells. Necrosulfonamide does not affect the activation of upstream signals, but specifically inhibits the downstream executor oligomerization step. Necrosulfonamide reduces the expression of the key kinases NLRP3 and caspase-1 involved in necroptosis and pyroptosis, activate the Nrf2 pathway and the downstream antioxidant enzymes, and also downregulates a variety of inflammatory factors. Necrosulfonamide plays significant roles in various diseases such as neurodegenerative diseases (such as Parkinson’s disease), tissue damage and ischemia-reperfusion injury, inflammatory bowel disease, osteoarthritis and fracture repair, and hair loss by regulating two important programmed necrosis pathways .
    Necrosulfonamide
  • HY-100573S

    Isotope-Labeled Compounds Mixed Lineage Kinase Necroptosis Pyroptosis Caspase NOD-like Receptor (NLR) Keap1-Nrf2 TNF Receptor Integrin NO Synthase Heme Oxygenase (HO) Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Endocrinology
    Necrosulfonamide-d4 is the deuterium labeled Necrosulfonamide (HY-100573). Necrosulfonamide is a MLKL and Gasdermin D (GSDMD) inhibitor, capable of separately inhibiting necroptosis and pyroptosis of cells. Necrosulfonamide does not affect the activation of upstream signals, but specifically inhibits the downstream executor oligomerization step. Necrosulfonamide reduces the expression of the key kinases NLRP3 and caspase-1 involved in necroptosis and pyroptosis, activate the Nrf2 pathway and the downstream antioxidant enzymes, and also downregulates a variety of inflammatory factors. Necrosulfonamide plays significant roles in various diseases such as neurodegenerative diseases (such as Parkinson’s disease), tissue damage and ischemia-reperfusion injury, inflammatory bowel disease, osteoarthritis and fracture repair, and hair loss by regulating two important programmed necrosis pathways.
    Necrosulfonamide-d4
  • HY-100573A
    (E/Z)-Necrosulfonamide
    1 Publications Verification

    Mixed Lineage Kinase Necroptosis Pyroptosis Caspase NOD-like Receptor (NLR) Keap1-Nrf2 TNF Receptor Interleukin Related NO Synthase Heme Oxygenase (HO) Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Endocrinology
    (E/Z)-Necrosulfonamide is a racemic compound of Necrosulfonamide (HY-100573). Necrosulfonamide is a MLKL and Gasdermin D (GSDMD) inhibitor, capable of separately inhibiting necroptosis and pyroptosis of cells. Necrosulfonamide does not affect the activation of upstream signals, but specifically inhibits the downstream executor oligomerization step. Necrosulfonamide reduces the expression of the key kinases NLRP3 and caspase-1 involved in necroptosis and pyroptosis, activate the Nrf2 pathway and the downstream antioxidant enzymes, and also downregulates a variety of inflammatory factors. Necrosulfonamide plays significant roles in various diseases such as neurodegenerative diseases (such as Parkinson’s disease), tissue damage and ischemia-reperfusion injury, inflammatory bowel disease, osteoarthritis and fracture repair, and hair loss by regulating two important programmed necrosis pathways.
    (E/Z)-Necrosulfonamide
  • HY-126758

    Apoptosis Glutathione Peroxidase Inflammation/Immunology
    Ludartin a sesquiterpene lactone, which can be isolated from the plant Artemisia carruthii Wood. Ludartin reduces the expression of myeloperoxidase and malondialdehyde, enhances the expression of glutathione and superoxide dismutase in spinal cord tissue. Ludartin inhibits neuronal apoptosis. Ludartin inhibits the upregulation of tumor necrosis factor-α, interleukin-1β, and interleukin-6. Ludartin improves the motor function of rats with spinal cord injury .
    Ludartin
  • HY-109076

    EBC-46

    PKC Caspase Cancer
    Tigilanol tiglate (EBC-46) is a protein kinase C (PKC)/C1 domain activator. Tigilanol tiglate is associated with mitochondrial/endoplasmic reticulum (ER) dysfunction, leading to activation of the unfolded protein response (UPRmt/ER) and subsequent induction of ATP depletion, organelles expansion, Caspase activation, gasdermin E cleavage, and terminal necrosis. Tigilanol tiglate, as a small anti-tumor molecule with immunomodulatory effects, can be used in the study of head and neck squamous cell carcinoma and soft tissue sarcoma .
    Tigilanol tiglate
  • HY-N8501

    Bacterial Infection
    Emestrin is a mycotoxin originally isolated from E. striata that has antimicrobial, immunomodulatory, and cytotoxic activities. It is active against the fungi C. albicans and C. neoformans, as well as the bacteria E. coli, S. aureus, and methicillin-resistant S. aureus (MRSA; IC50s=3.94, 0.6, 2.21, 4.55, and 2.21 μg/mL, respectively).2 Emestrin is a chemokine (C-C motif) receptor 2 (CCR2) antagonist (IC50=5.4 μM in a radioligand binding assay using isolated human monocytes).3 Emestrin (0.1 μg/mL) induces apoptosis in HL-60 cells. It induces heart, thymus, and liver tissue necrosis in mice when administered at doses ranging from 18 to 30 mg/kg.
    Emestrin

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