NLRP3 inhib 
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  • ||||||||||  Ilaris (canakinumab) / Novartis
    Journal:  Interleukin-1β suppression dampens inflammatory leukocyte production and uptake in atherosclerosis. (Pubmed Central) -  Oct 26, 2022   
    Our murine and human data reveal that anti-IL-1β treatment and NLRP3-inflammasome inhibition dampened vascular inflammation and progression of atherosclerosis through reduced blood inflammatory leucocyte (i) supply and (ii) uptake into atherosclerotic aortas providing additional mechanistic insights into links between haematopoiesis and atherogenesis, and into the beneficial effects of NLRP3-inflammasome- and IL-1β-targeted therapies.
  • ||||||||||  Visudyne (verteporfin) / Novartis
    Preclinical, Journal:  IL-37 improves mice myocardial infarction via inhibiting YAP-NLRP3 signaling mediated macrophage programming. (Pubmed Central) -  Oct 21, 2022   
    In addition, we focus on some inhibitors of NLRP3 inflammatory pathways to alleviate the progression of PD. Our results demonstrated that IL-37 achieves a favorable therapeutical function on myocardial infarction by modulating YAP-NLRP3 mediated macrophage programming, providing a promising drug for the treatment of myocardial infarction.
  • ||||||||||  RRx-001 / EpicentRx
    Preclinical, Journal:  Superficial Venous-Associated Inflammation from Direct IV Administration of RRx-001 in Rats. (Pubmed Central) -  Oct 21, 2022   
    The main observed toxicity was a significant inflammatory response in the vein wall, consistent with superficial venous thrombosis observed in man. Due to this development, direct IV infusion of RRx-001 is relatively contraindicated in favor of co-administration with autologous blood.
  • ||||||||||  Journal:  Investigating the NLRP3 Inflammasome and its Regulator miR-223-3p in Multiple Sclerosis and Experimental Demyelination. (Pubmed Central) -  Oct 20, 2022   
    Finally, systemic delivery of MCC950 to mice following lysolecithin-induced demyelination resulted in a significant reduction in axonal injury within demyelinated lesions. In conclusion, we demonstrate that NLRP3 inflammasome activity by macrophages and microglia is a critical component of the inflammatory microenvironment following demyelination and represents a potential therapeutic target for inflammatory-mediated demyelinating diseases, including MS.
  • ||||||||||  Journal:  POP1 inhibits MSU-induced inflammasome activation and ameliorates gout. (Pubmed Central) -  Oct 20, 2022   
    Strikingly, administration of an engineered cell permeable version of POP1 was able to ameliorate MSU crystal-mediated inflammation in vivo, as measured by neutrophil infiltration. Overall, we demonstrate that POP1 may play a crucial role in regulating inflammatory responses in gout.
  • ||||||||||  GYY4137 / National University of Singapore
    Journal:  GYY4137 ameliorates sepsis-induced cardiomyopathy via NLRP3 pathway. (Pubmed Central) -  Oct 19, 2022   
    We further found that the protective effects of GYY4137 were absent in Nlrp3-knockout models. GYY4137 ameliorates myocardial injury in SICM via the NLRP3 pathway by inhibiting the inflammatory response and reducing the production of myocardial ROS.
  • ||||||||||  Journal:  Inhibition of CEBPB Attenuates Lupus Nephritis via Regulating Pim-1 Signaling. (Pubmed Central) -  Oct 18, 2022   
    Furthermore, the knockdown of CEBPB could inhibit NLRP3 inflammasome activation and pyroptosis via binding to Pim-1 promoter to downregulate its expression, and the overexpression of Pim-1 reversed the effects of CEBPB deficiency. The regulation of CEBPB on Pim-1 facilitated pyroptosis by activating NLRP3 inflammasome, thereby promoting the development of LN.
  • ||||||||||  Bay11-7082 / InvivoGen
    Preclinical, Journal:  BAY-117082-driven NLRP3 inflammasome inhibition resolves nitro-glycerine (NTG) neuronal damage in in vivo model of migraine. (Pubmed Central) -  Oct 18, 2022   
    Additionally, the treatment with BAY-117082 at both higher doses significantly modulated CREB/Erk/Akt pathways strictly correlated to the expression of neurotrophic factors. Taken together, obtained results confer new insight into the role of the NLRP3 inflammasome pathway in migraine pathogenesis, suggesting that BAY-117082 could be considered a novel strategy therapeutics for migraine treatment despite unconventional drug use.
  • ||||||||||  Review, Journal:  The NLRP3 inflammasome as a new target in respiratory disorders treatment. (Pubmed Central) -  Oct 14, 2022   
    The review presented, discusses the contribution of NLRP3 inflammasome to the development of allergic rhinitis, allergic asthma, and COPD. Moreover, the modulatory properties of probiotics as potential inhibitors of NLRP3 inflammasome are emphasised.
  • ||||||||||  Intra-Organ Cross-Talk via YB1 in the Kidney (Exhibit Hall, Orange County Convention Center, West Building) -  Oct 13, 2022 - Abstract #KIDNEYWEEK2022KIDNEY_WEEK_2868;    
    Conclusion YB1 secreted from podocytes suppresses TLR-4- and NLRP3-mediated sterile inflammation in the tubular compartment, thus maintaining tubular physiology and kidney function. This uncovers a molecular mechanism of glomerular-tubular cross-talk required for normal renal physiology.
  • ||||||||||  NLRP3 Inflammasome Inhibition Decreases NETosis in AKI (Exhibit Hall, Orange County Convention Center, West Building) -  Oct 13, 2022 - Abstract #KIDNEYWEEK2022KIDNEY_WEEK_1039;    
    In conclusion, we have demonstrated that NLRP3 inflammasome inhibition reduces kidney inflammation and inhibits NETosis-mediated kidney injury. The role of neutrophils as key effector cells and NLRP3 inflammasome pathway in kidney diseases warrants further investigation.
  • ||||||||||  Review, Journal:  Targeting autophagy regulation in NLRP3 inflammasome-mediated lung inflammation in COVID-19. (Pubmed Central) -  Oct 13, 2022   
    Specifically, we highlighted the therapeutic potential of autophagy activators in COVID-19 by inhibiting the NLRP3 inflammasome, thereby avoiding the cytokine storm. We hope this review provides enlightenment for the use of autophagy activators targeting the inhibition of the NLRP3 inflammasome, specifically the combinational therapy of autophagy modulators with the inhibitors of the NLRP3 inflammasome, antiviral drugs, or anti-inflammatory drugs in the fight against COVID-19.
  • ||||||||||  Journal:  Schisandrol B protects against cholestatic liver injury by inhibiting pyroptosis through pregnane X receptor. (Pubmed Central) -  Oct 12, 2022   
    The results illustrated that SolB could significantly inhibit NLRP3 inflammasome-induced canonical pyroptosis through the PXR/NF-κB/NLRP3 axis and inhibit Apaf-1 pyroptosome-induced noncanonical pyroptosis through the PXR/FoxO1/Apaf-1 axis. Collectively, this study revealed that SolB protected against CLI by inhibiting pyroptosis through PXR, providing new insights for understanding the molecular mechanism of SolB as a promising anti-cholestatic agent.
  • ||||||||||  Development and characterization of a microglia-restricted mouse model of NLRP3 driven neuroinflammation (SDCC Halls B-H) -  Oct 10, 2022 - Abstract #Neuroscience2022NEUROSCIENCE_11241;    
    Ongoing characterization of this and similar model systems will allow for determination of cell-type specific activities of the NLRP3 inflammasome. Such insight into neuroinflammatory mechanisms will improve our understanding of NLRP3 biology, impacting the detection and treatment of the many diseases in which NLRP3 has been identified to play a role while providing a platform for testing novel drugs targeting the NLRP3 inflammasome.
  • ||||||||||  Withdrawn (SDCC Halls B-H) -  Oct 10, 2022 - Abstract #Neuroscience2022NEUROSCIENCE_11159;    
    Such insight into neuroinflammatory mechanisms will improve our understanding of NLRP3 biology, impacting the detection and treatment of the many diseases in which NLRP3 has been identified to play a role while providing a platform for testing novel drugs targeting the NLRP3 inflammasome. Grant Support: NIH grant AG058673
  • ||||||||||  Bay-117082-driven nlrp3 inflammasome inhibition resolves nitro-glycerine neuronal damage in in vivo model of migraine (SDCC Halls B-H) -  Oct 10, 2022 - Abstract #Neuroscience2022NEUROSCIENCE_11157;    
    Additionally, the treatment with BAY-117082 at both higher doses significantly modulated CREB/Erk/Akt pathways strictly correlated to the modulation of neurotrophic factors. Taken together, obtained results confer new insight into the role of the NLRP3 inflammasome pathway in migraine pathogenesis, suggesting that BAY-117082 could be considered a novel strategy therapeutics for migraine treatment despite unconventional drug use.