NLRP3 inhib 
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  • ||||||||||  Journal:  MicroRNA-22-3p alleviates atherosclerosis by mediating macrophage M2 polarization as well as inhibiting NLRP3 activation. (Pubmed Central) -  Nov 3, 2023   
    These findings indicated that VEGFC inhibited NLRP3 inflammasome activation by promoting VEGFR3-AMPK-dependent autophagy pathway in high-salt-induced macrophages, which provided a mechanistic basis for the therapeutic target in SSHTN and hypertensive kidney injury. MiR-22-3p appears to reduce the inflammatory response in AS, which might be achieved by inducing the M2 macrophage phenotype and suppressing NLRP3 activation via JAK1.
  • ||||||||||  Preclinical, Journal:  Isodopharicin C inhibits NLRP3 inflammasome activation and alleviates septic shock in mice (Pubmed Central) -  Nov 3, 2023   
    MiR-22-3p appears to reduce the inflammatory response in AS, which might be achieved by inducing the M2 macrophage phenotype and suppressing NLRP3 activation via JAK1. Iso C specifically inhibits NLRP3 inflammasome activation and alleviates septic shock in mice, and can serve as a potential small molecule compound for treatment of inflammatory diseases.
  • ||||||||||  Inhibition of NLRP3 leads to reduced tau pathology and improved social behavior in mice. (WCC Halls A-C) -  Nov 3, 2023 - Abstract #Neuroscience2023NEUROSCIENCE_10055;    
    We found that NLRP3 inhibition with drug treatment or gene knock down significantly reduce AD-associated tau pathology, together with reduced anxiety like symptoms. In conclusion, our study further confirms the role of NLRP3 in AD and tau phosphorylation.
  • ||||||||||  nibrozetone (RRx-001) / EpicentRx
    Evaluation of the phase-3 clinical candidate RRx-001 as a novel therapeutic agent for Amyotrophic Lateral Sclerosis (WCC Halls A-C) -  Nov 3, 2023 - Abstract #Neuroscience2023NEUROSCIENCE_6063;    
    Our early suggest that RRx-001, could have therapeutic potential for ALS by targeting multiple pathological mechanisms linked to disease progression, including NLRP3 activation, motor neuron death, mitochondrial dysfunction, and muscle degeneration. Given that RRx-001 has been tested in over 200 patients to date, with no dose limiting toxicity, our early results highlight the prospect of RRx-001 as a new disease-modifying therapeutic for ALS with the potential for rapid clinical translation.
  • ||||||||||  Spleen Tyrosine Kinase (Syk) is a druggable therapeutic target for Parkinson (WCC 147A) -  Nov 3, 2023 - Abstract #Neuroscience2023NEUROSCIENCE_1679;    
    Our results uncover Syk as new druggable therapeutic target which is highly activated in PD patients. Inhibition of Syk in the CNS could be a novel therapeutic strategy for disease modification in PD by targeting inflammasome driven neuropathology and dopaminergic degeneration.
  • ||||||||||  nibrozetone (RRx-001) / EpicentRx
    The CNS-permeable NLRP3 inhibitor RRx-001 is neuroprotective in experimental models of Parkinson (WCC 147A) -  Nov 3, 2023 - Abstract #Neuroscience2023NEUROSCIENCE_1676;    
    Our results highlight the neuroprotective properties of RRx-001 as a novel and unique disease-modifying therapeutic agent which can target multiple pathological mechanisms. Given the clinical safety record of RRx-001 in human studies to date, our results suggest that RRx-001 could be an attractive neuroprotective strategy for disease modification of PD.
  • ||||||||||  NLRP3 inhibitor / Halia Therap, HT-6184 / Halia Therap
    HT-6184 Inhibits the Formation of the NLRP3 Inflammasome in Human Monocytic THP-1 Cells (SDCC - Halls G-H) -  Nov 3, 2023 - Abstract #ASH2023ASH_5330;    
    Since THP-1 cells are a monocytic cell line, this data suggests our ability to inhibit the NLRP3 pathway in hematological disorders effectively. By preventing inflammasome formation and activation, we expect to be able to reduce disease burden in hematological diseases.
  • ||||||||||  DFV890 / Novartis
    Safety and Preliminary Efficacy of DFV890 in Adult Patients with Myeloid Diseases: A Phase 1b Study (Halls G-H (San Diego Convention Center)) -  Nov 3, 2023 - Abstract #ASH2023ASH_4186;    
    P1
    By preventing inflammasome formation and activation, we expect to be able to reduce disease burden in hematological diseases. Eligible pts must be 18 years of age, with an Eastern Cooperative Oncology Group performance status ?2, candidates for serial bone marrow assessments who are willing to undergo a bone marrow aspirate/biopsy during the trial, and meet one of the following: (a) IPSS-R
  • ||||||||||  progesterone / Generic mfg.
    Journal, Machine learning:  Network Pharmacology Analysis and Machine-Learning Models Confirmed the Ability of YiShen HuoXue Decoction to Alleviate Renal Fibrosis by Inhibiting Pyroptosis. (Pubmed Central) -  Oct 30, 2023   
    Quercetin, kaempferol, luteolin, beta-sitosterol, wogonin, stigmasterol, isorhamnetin, baicalein, and dihydrotanshinlactone progesterone were identified as the main active components of YSHXD in the treatment of unilateral ureteral ligation-induced RF, with IL-6, IL1?, TNF, AR, and PTGS2 as core target proteins...YSHXD downregulated NLRP3, ASC, NF-?Bp65, Caspase-1, GSDMD, PTGS2, IL-1?, IL-6, IL-18, TNF-?, ?-SMA and upregulated HGF, effectively alleviating the RF process. YSHXD exerts important anti-inflammatory and anti-cellular inflammatory necrosis effects by inhibiting the NLRP3/caspase-1/GSDMD-mediated pyroptosis pathway, indicating that YSHXD represents a new strategy and complementary approach to RF therapy.
  • ||||||||||  Journal:  Oridonin supplementation attenuates atherosclerosis via NLRP-3 inflammasome pathway suppression. (Pubmed Central) -  Oct 30, 2023   
    Finally, Ori treated group had significantly (p?0.001) lower IL-1B immunostaining intensity than the atherogenic group (mean rank 14.5,25 respectively). The study concluded that Oridonin supplementation resulted in less severe initial atherosclerotic lesions, likely due to the suppression of NLRP3 inflammasome and the anti-inflammatory effect through the downregulation of IL1B expression.
  • ||||||||||  belnacasan (VX-765) / Vertex
    Journal:  Sorcin regulate pyroptosis by interacting with NLRP3 inflammasomes to facilitate the progression of hepatocellular carcinoma. (Pubmed Central) -  Oct 14, 2023   
    Similarly, suppression of Caspase-1 reversed the inhibitory effect of Sorcin knockdown on the malignant progression of HCC via knockdown of Caspase-1 or the inhibitor VX765...Collectively, high Sorcin expression in HCC negatively regulates pyroptosis by interacting with the NLRP3 inflammasome to promote HCC proliferation, migration, and invasion. The results of this study provide a scientific basis for Sorcin as a new biomarker and potential therapeutic target for HCC.
  • ||||||||||  NLRP3 Inflammasome Mediates Aortic Valve Calcification Through the Loss of Lysosomal Function in Osteoclasts (126A) -  Oct 12, 2023 - Abstract #AHA2023AHA_8675;    
    Three of which, Berbamine dihydrochloride, Praeruptorin A, and EVP4593 posed significant elevations on cathepsin K levels and mature lysosome percentages in mouse BMDM-derived osteoclasts, exhibiting enhanced bone resorption.Conclusions NLRP3 inflammasome mediated aortic valve calcification by activating inflammation and impairing local bone resorption function of osteoclasts. Berbamine dihydrochloride intervention effectively inhibited NLRP3 and restores osteoclasts function, contributing to reversing the progression of valve calcification.
  • ||||||||||  Immunomodulatory Effect of Human Heart-Derived Extracellular Vesicles on Atrial Inflammation and the NLRP3 Inflammasome (Zone 1, Science and Technology Hall, Level 2) -  Oct 12, 2023 - Abstract #AHA2023AHA_8482;    
    EVs suppressed the NLRP3 inflammasome in atrial fibroblasts and macrophages, potentially exerting their influence through the cargo miRs on NLRP3 expression within atrial tissue. Our results propose that the immunomodulatory impact of EVs in postoperative AF might be linked to their ability to hinder the NLRP3 inflammasome through the transmission of miRNA cargo.
  • ||||||||||  Journal, IO biomarker:  Rutin alleviates ventilator-induced lung injury by inhibiting NLRP3 inflammasome activation. (Pubmed Central) -  Oct 11, 2023   
    Mechanistically, rutin suppressed the TLR4/NF-?B-P65 pathway, which promoted the M1 to M2 macrophage transition and alleviated inflammation in mice with VILI. Rutin relieved NLRP3 inflammasome activation by regulating M1/M2 macrophage polarization and inhibiting the activation of the TLR4/NF-?B-P65 pathway, resulting in the amelioration of VILI in mice.
  • ||||||||||  Ilaris (canakinumab) / Novartis
    Review, Journal:  Inflammasome Signaling, Thromboinflammation, and Venous (Pubmed Central) -  Oct 4, 2023   
    Rosuvastatin reduces primary venous thrombotic events at least in part through lipid-lowering independent mechanisms, paving the way to targeted anti-inflammatory strategies in VTE. This review outlines recent preclinical and clinical evidence supporting a role for inflammasome pathway activation in venous thrombosis, and discusses
  • ||||||||||  Journal, IO biomarker:  Glomerular-tubular crosstalk via cold shock Y-box binding protein-1 in the kidney. (Pubmed Central) -  Sep 30, 2023   
    Thus, our data show that YBX1 is physiologically secreted from podocytes, thereby negatively modulating sterile inflammation in the tubular compartment, apparently by binding to and inhibiting tubular TLR4 signaling. Hence, we have uncovered an YBX1-dependent molecular mechanism of glomerular-tubular crosstalk.