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Results for "

sepsis models

" in MedChemExpress (MCE) Product Catalog:

21

Inhibitors & Agonists

6

Peptides

2

Natural
Products

1

Click Chemistry

2

Oligonucleotides

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-156519
    ALPK1-IN-3

    		NF-κB Inflammation/Immunology
    ALPK1-IN-3 is an inhibitor of ALPK1 extracted from patent WO2022063153A1 compound T007. ALPK1-IN-3 inhibits kidney proinflammatory gene expression and improves the survival rate of the animals in sepsis induced acute kidney injury animal model . ALPK1-IN-3 is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
    ALPK1-IN-3
  • HY-P10368
    P110

    		Dynamin Infection Cardiovascular Disease Neurological Disease Inflammation/Immunology
    P110, a peptide inhibitor of Drp1-Fis1 interaction, reduces pathology in numerous models of neurodegeneration, ischemia, and sepsis without blocking the physiological functions of Drp1 .
    P110
  • HY-164036
    Lolamicin

    		Antibiotic Bacterial Infection
    Lolamicin is a Gram-negative specific antibiotic. Lolamicin is active against more than 130 multidrug-resistant clinical isolates, has shown efficacy in multiple mouse models of acute pneumonia and sepsis infection, and protects the gut microbiome of mice against secondary infection with Clostridium difficile. The selective killing of pathogenic gram-negative bacteria by Lolamicin is a result of the low sequence homology of pathogenic bacteria and symbiotic bacteria. Lolamicin can be used in the study of infection caused by Gram-negative pathogens .
    Lolamicin
  • HY-163478
    TNIK-IN-9

    		NF-κB Inflammation/Immunology
    TNIK-IN-9 (Compound 54) is a selective and potent NIK inhibitor, with an IC50 of 1.27 nM. TNIK-IN-9 can inhibit pro-inflammatory cytokines and nitric oxide production. TNIK-IN-9 exhibits significant anti-inflammatory effects, improved mortality, and hepatoprotective effects in sepsis models .
    TNIK-IN-9
  • HY-P5949
    AMPR-22

    		Bacterial Infection
    AMPR-22 is an antimicrobial peptide. AMPR-22 can bind to the bacterial membrane and induces membrane permeabilization. AMPR-22 is effective against murine model of sepsis induced by MDR strains
    AMPR-22
  • HY-P2280
    TAT-P110

    		Dynamin Neurological Disease Inflammation/Immunology
    TAT-P110, a peptide inhibitor of Drp1-Fis1 interaction, reduces pathology in numerous models of neurodegeneration, ischemia, and sepsis without blocking the physiological functions of Drp1 .
    TAT-P110
  • HY-155250
    Antibacterial agent 154

    		Bacterial Infection
    Antibacterial agent 154 (compound 7) is a derivative of Fluoroqinolones and is an orally effective antibacterial agent. Antibacterial agent 154 inhibits Gram-positive and Gram-negative bacteria. Antibacterial agent 154 demonstrated in vivo efficacy in a mouse model of staphylococcal sepsis .
    Antibacterial agent 154
  • HY-P10580
    Vasculotide

    		Tie Infection Metabolic Disease Inflammation/Immunology Cancer
    Vasculotide, an angiopoietin-1 mimetic, is a Tie-2 activator and induces Tie-2 phosphorylation. Vasculotide has anti-inflammatiory effect and anti-permeability. Vasculotide ameliorates endotoxin-induced endothelial barrier dysfunction. Vasculotide promotes angiogenesis in a mouse model of diabetic ulcer. Vasculotide protects mice from vascular leakage and reduces mortality in murine abdominal sepsis. Vasculotide decreases microvascular leakage and improves microcirculatory perfusion in a rat model of hemorrhagic shock .
    Vasculotide
  • HY-149426
    SIRT5 inhibitor 7

    		Sirtuin Inflammation/Immunology
    SIRT5 inhibitor 7 (compound 58) is a substrate-competitive and selective SIRT5 inhibitor with anti-inflammatory activity. SIRT5 inhibitor 7 has renal protective effects and regulates protein succinylation and the release of pro-inflammatory cytokines. SIRT5 inhibitor 7 has in vivo activity in AKI mouse models of lipopolysaccharide (LPS) and cecal ligation/perforation (CLP)-induced sepsis-related acute kidney injury .
    SIRT5 inhibitor 7
  • HY-146974
    PDE4-IN-9

    		Phosphodiesterase (PDE) Inflammation/Immunology
    PDE4-IN-9 (Compound 5j) is a potent inhibitor of PDE4. PDE4-IN-9 exhibits lower IC50 value (1.4 μM) against PDE4 than parent rolipram (2.0 μM) in in vitro enzyme assay. PDE4-IN-9 also displays good in vivo activity in animal models of asthma/COPD and sepsis induced by LPS .
    PDE4-IN-9
  • HY-161059
    ZB-R-55

    		RIP kinase Infection
    ZB-R-55 is an orally active RIPK1 inhibitor. ZB-R-55 can be used for sepsis study .
    ZB-R-55
  • HY-161520
    Glucocorticoid receptor/NF-κB modulator-1

    		Glucocorticoid Receptor NF-κB Inflammation/Immunology
    Glucocorticoid receptor/NF-κB modulator-1 (Compound 20) is a derivative of ocotillol. Glucocorticoid receptor/NF-κB modulator-1 suppresses the degradation of glucocorticoid receptor (GR) mRNA and GR protein, inhibits the activation of NF-κB signaling pathway. Glucocorticoid receptor/NF-κB modulator-1 downregulates levels of NO, interleukin-6 and tumor necrosis factor-alpha (TNF-α). Glucocorticoid receptor/NF-κB modulator-1 ameliorates sepsis in mouse model .
    Glucocorticoid receptor/NF-κB modulator-1
  • HY-161072
    CSC-6

    		NOD-like Receptor (NLR) Inflammation/Immunology
    CSC-6 is a NLRP3 inhibitor. CSC-6 can significantly inhibit IL-1β secreted by PMATHP-1 cells with an IC50 value of 2.3 μM. CSC-6 specifically binds NLRP3 and inhibits NLRP3 activation by blocking ASC oligomerization during NLRP3 assembly. CSC-6 effectively reduces the symptoms of NLRP3 overactivation-mediated sepsis and gout in mouse models .
    CSC-6
  • HY-164102
    TNF-α-IN-18

    		TNF Receptor NF-κB Inflammation/Immunology
    TNF-α-IN-18 (Compound 61) is an inhibitor for TNF-α (IC50 of 1.8 μM), that inhibits TNF signaling pathway through block of NF-kB migration from cytoplasm to nucleus. TNF-α-IN-18 exhibits slight cytotoxicity to mouse fibroblast LM cell, with a CC50 >50 μM. TNF-α-IN-18 ameliorates the TNF- or Lipopolysaccharide (HY-D1056)-induced sepsis in mouse models. TNF-α-IN-18 protects mice from rheumatoid arthritis .
    TNF-α-IN-18
  • HY-100574A
    Cl-amidine hydrochloride
    Maximum Cited Publications
    10 Publications Verification

    		 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-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-100574B
    Cl-amidine TFA

    		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-P3496
    Pep19-2.5

    		Pyroptosis Inflammation/Immunology
    Pep19-2.5 is an synthetic and antitoxin peptide, blocks the intracellular endotoxin signaling cascade. Pep19-2.5 inhibits signaling of lipopeptides (LP) and lipopolysaccharides (LPS) mediated by transmembrane and cytosolic pattern recognition receptors (PRRs). The signaling cascades lead to inflammation and cell pyroptosis .
    Pep19-2.5
  • HY-161988
    Antimicrobial agent-34

    		Bacterial Infection Inflammation/Immunology
    Antimicrobial agent-34 (compound 4h) is an antibacterial agent (MIC = 1–4 μg/mL), with a clogP value of 9.14. Antimicrobial agent-34 has good plasma stability (HC50 of 131.1 μg/mL) and good membrane selectivity (HC50/MIC is 65.6), with rapid sterilization capability. Antimicrobial agent-34 destroys the integrity of bacterial cell membranes, induces an increase in intracellular reactive oxygen species, and leaks protein and DNA, ultimately leading to bacterial death. Antimicrobial agent-34 demonstrates significant in vivo antibacterial potency in a mouse sepsis model infected with Staphylococcus aureus ATCC43300 .
    Antimicrobial agent-34
  • HY-N0469R
    L-Lysine (Standard)

    		Endogenous Metabolite Virus Protease HSV Infection Metabolic Disease Inflammation/Immunology
    L-Lysine (Standard) is the analytical standard of L-Lysine. This product is intended for research and analytical applications. L-lysine is an essential amino acid for humans with orally activity. L-lysine can inhibit the occurrence of HSV infections and is used in herpes research. L-lysine increases calcium absorption, reduces diabetes-related diseases, improves gut health, and alleviates pancreatic inflammation. L-lysine can be used in research on metabolism, infection, and inflammation . IC50 & Target:L-lysine (150 mg/kg) promotes, but not initiates, bladder cancer. The administration of L-lysine to rats submitted to colovesical cystoplasty accelerates the development of transitional metaplasia of the intestinal epithelium .
    L-lysine (10 mg/kg) treatment attenuates pancreatic tissue injury induced by L-arginine by inhibiting the release of the inflammatory cytokine IL-6 and enhance antioxidant activity . In Vivo:L-lysine (10?mg/kg, p.o., pre-treated or post-treated, administration duration 15 days) treatment attenuates pancreatic tissue injury induced by L-arginine by inhibiting the release of the inflammatory cytokine IL-6 and enhance antioxidant activity in acute pancreatitis mice model . L-lysine (5 or 10?mg/kg, p.o., 45 days) ameliorates sepsis-induced acute lung injury in a lipopolysaccharide (HY-D1056)-induced mouse model .
    L-Lysine (Standard)
  • HY-N6871
    Abietic acid

    		Bacterial IKK Ferroptosis Infection Metabolic Disease Inflammation/Immunology Cancer
    Abietic acid, an orally active diterpene isolated from Colophony, displays significant anti-proliferative, anti-inflammatory, anti-obesity effect, bacteriostatic, cell cycle arresting and pro-apoptotic activities. Abietic acid inhibits lipoxygenase activity for allergy. Abietic acid enhances cell migration and tube formation in HUVECs. Abietic acid induces significant angiogenic potential, which is associated with upregulation of extracellular signal-regulated kinase (ERK) and p38 expression. Abietic acid attenuates sepsis-induced lung injury by inhibiting nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway to inhibit M1 macrophage polarization. Abietic acid exhibits a positive effect against liver injury by attenuating inflammation and ferroptosis. Abietic acid shows accelerated wound closure in a mouse model of cutaneous wounds. Abietic acid significantly reduces the proliferation and growth of NSCLC cells by IKKβ inhibition.Additionally, Abietic acid ameliorates psoriasis-like inflammation and modulates gut microbiota in mice. Abietic acid is promising for research in non-small-cell lung cancer (NSCLC), liver injury-related deseases and psoriasis .
    Abietic acid

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