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Results for "

inflammasome

" in TargetMol Product Catalog
  • Inhibitors & Agonists
    107
    TargetMol | Inhibitors_Agonists
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    3
    TargetMol | Peptide_Products
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    1
    TargetMol | Inhibitory_Antibodies
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    TargetMol | Inhibitors_Agonists
BAY 11-7082
BAY 11-7821
T190219542-67-7
BAY 11-7082 (BAY 11-7821) is an NF-κB inhibitor that suppresses TNFα-induced IκBα phosphorylation (IC50=10 μM) and also inhibits the ubiquitin-specific proteases USP7 and USP21 (IC50=0.19 0.96 μM).
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Stavudine
Sanilvudine, NSC 163661, d4T, BMY-27857
T14043056-17-5
Stavudine (BMY-27857), a nucleoside reverse transcriptase inhibitor analog of thymidine, has activity against HIV.
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Muscone
Methylexaltone, 3-Methylcyclopentadecanone
T2893541-91-3
Muscone (3-Methylcyclopentadecanone) is an organic compound that is the primary contributor to the odor of musk.
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NLRP3-IN-9
INF-4E, INF4E, INF 4E
T2817888039-46-7
NLRP3-IN-9 (INF-4E) is an inhibitor of NLRP3 ATPase and caspase-1. NLRP3-IN-9 acts by irreversibly trapping thiol nucleophiles, which prevents both ATP- and nigericin-triggered pyroptosis of human THP-1 cells in a time- and concentration-dependent manner.
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6-8 weeks
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Carvedilol
SKF 105517, BM 14190
T044772956-09-3
Carvedilol (SKF 105517) Phosphate is the phosphate salt form of carvedilol, a racemic mixture and adrenergic blocking agent with antihypertensive activity and devoid of intrinsic sympathomimetic activity. The S enantiomer of carvedilol nonselectively binds to and blocks beta-adrenergic receptors, thereby exerting negative inotropic and chronotropic effects, and leading to a reduction in cardiac output. In addition, both enantiomers of carvedilol bind to and block alpha 1-adrenergic receptors, thereby causing vasodilation and reducing peripheral vascular resistance.
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Nigericin sodium salt
T309228643-80-3
Nigericin sodium salt is an antibiotic, an NLRP3 activator, and a cationic ion carrier. Nigericin sodium triggers the activation of the NALP3 inflammasome, which inhibits Golgi function and suppresses the growth of Gram-positive bacteria.
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NLRP3/AIM2-IN-3
T604421787787-60-3
NLRP3 AIM2-IN-3 is a unique molecule that inhibits NLRP3 and AIM2 inflammasome activation in a species-specific manner. It has an IC50 value for cell lysis of 0.077 ± 0.008 μ M. NLRP3 AIM2-IN-3 is a potent inhibitor of NLRP3 and AIM2 inflammasome-dependent cell lysis with an IC50 value for cell lysis of 0.077 ± 0.008 μ M. NLRP3 AIM2-IN-3 inhibits LPS nigericin NLRP3 AIM2-IN-3 inhibits LPS nigericin-stimulated cell lysis in THP-1 macrophages with an IC50 value of 0.077 ± 0.008 μM. NLRP3 AIM2-IN-3 interferes with the interaction of NLRP3 or AIM2 with the bridging protein ASC, inhibiting oligomerization of ASC.
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6-8 weeks
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INT-777
S-EMCA
T11662L1199796-29-6In house
INT-777 (S-EMCA) is a potent TGR5 agonist with an EC50 of 0.82 μM. INT-777 (S-EMCA) inhibits NLRP5-ASC inflammasome-mediated neuroinflammation via the TGR3 cAMP PKA signaling pathway after subarachnoid hemorrhage in rats.
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8-10 weeks
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NT-0796
NT0796, NT 0796
T816372272917-13-0In house
NT-0796 is a brain-permeable, potent, and selective inhibitor of the inflammasome NLRP3, inhibiting NLRP3 activation.NT-0796 is a potential NDT-19795 delivery vector.
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8-10 weeks
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nbc 6
T96552068818-02-8In house
NLRP3-IN-NBC6 is a potent, selective NLRP3 inflammasome inhibitor with an IC50 of 574 nM. It acts independently of Ca 2+ and inhibits Nigericin-induced inflammasome activation in THP-1 cells, as well as Imiquimod-induced IL-1β release from LPS-primed bone marrow-derived macrophages (BMDMs) [1].
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6-8 weeks
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Adrenalone hydrochloride
Adrenalone HCl
T094862-13-5
Adrenalone hydrochloride (Adrenalone HCl) is a dopamine β-oxidase inhibitor with a similar structure to the norepinephrine transporter (NET) ligand, with an IC50 of 36.9 μM. It is an adrenergic agonist that acts as a local vasoconstrictor and hemostatic agent.
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ATP disodium salt
Disodium adenosine triphosphate, ATP disodium, ATP, Adetide, Adenosine-Triphosphate, Adenosine 5'-triphosphate disodium salt
T1352987-65-5
ATP disodium salt (Adenosine-Triphosphate) is a P2 purinoceptor agonist.
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Brilliant blue G-250
Brilliant Blue G, BBG, Acid blue 90, Coomassie Brilliant Blue G
T207316104-58-1
Brilliant blue G-250 (Acid blue 90, Coomassie Brilliant Blue G) is an antagonist of the P2X7 purinergic receptor.
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NLRP3-IN-2
5-Chloro-N-(p-sulfamoylphenethyl)-o-anisamide, NLRP3 Inflammasome Inhibitor I
T323016673-34-0
NLRP3-IN-2 (5-Chloro-N-(p-sulfamoylphenethyl)-o-anisamide), an intermediate capable of synthesizing glibenclamide, exerts an inhibitory effect on the formation of NLRP3 inflammatory vesicles in cardiomyocytes, limiting infarct size after myocardial ischemia reperfusion in mice and has no effect on metabolism.
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Dapansutrile
T1505254863-37-5
Dapansutrile is a potent, selective and orally active NLRP3 inflammasome inhibitor, with Anti-inflammatory and analgesic activity.
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MCC950
CP-456773
T3701210826-40-7
CP-456773 (MCC950 (CP-456773) and CRID3) is an effective and specific cytokine release inhibitor and NLRP3 inflammasome inhibitor. CP-456773 inhibits IL-1β secretion and caspase 1 processing. MCC950 blocked canonical and noncanonical NLRP3 activation at nanomolar concentrations. MCC950 specifically inhibited activation of NLRP3 but not the AIM2, NLRC4 or NLRP1 inflammasomes. MCC950 reduced IL-1β production in vivo and attenuated the severity of experimental autoimmune encephalomyelitis (EAE), a disease model of multiple sclerosis.
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Talabostat
T37861149682-77-9
Talabostat (PT100, Val-boroPro) is a potent, nonselective and orally available dipeptidyl peptidase IV (DPP-IV) inhibitor with a Ki of 0.18 nM. Talabostat is a nonselective DPP-IV inhibitor, inhibiting DPP8 9, FAP, DPP2 and some other DASH family enzymes essentially as potently as it inhibits DPP-IV[1]. Talabostat stimulates the immune system by triggering a proinflammatory form of cell death in monocytes and macrophages known as pyroptosis. The inhibition of two serine proteases, DPP8 and DPP9, activates the proprotein form of caspase-1 independent of the inflammasome adaptor ASC[2]. Talabostat competitively inhibits the dipeptidyl peptidase (DPP) activity of FAP and CD26 DPP-IV, and there is a high-affinity interaction with the catalytic site due to the formation of a complex between Ser630 624 and the boron of talabostat[3]. Talabostat can stimulate immune responses against tumors involving both the innate and adaptive branches of the immune system. In WEHI 164 fibrosarcoma and EL4 and A20 2J lymphoma models, PT-100 causes regression and rejection of tumors. The antitumor effect appears to involve tumor-specific CTL and protective immunological memory. Talabostat treatment of WEHI 164-inoculated mice increases mRNA expression of cytokines and chemokines known to promote T-cell priming and chemoattraction of T cells and innate effector cells[3]. Talabostat treated mice show significant less fibrosis and FAP expression is reduced. Upon PT100 treatment, significant differences in the MMP-12, MIP-1α, and MCP-3 mRNA expression levels in the lungs are also observed. Treatment with PT100 in this murine model of pulmonary fibrosis has an anti-fibro-proliferative effect and increases macrophage activation[4]. [1]. Connolly BA, et al. Dipeptide boronic acid inhibitors of dipeptidyl peptidase IV: determinants of potencyand in vivo efficacy and safety. J Med Chem. 2008 Oct 9;51(19):6005-13. [2]. Okondo MC, et al. DPP8 and DPP9 inhibition induces pro-caspase-1-dependent monocyte and macrophage pyroptosis. Nat Chem Biol. 2017 Jan;13(1):46-53. [3]. Adams S, et al. PT-100, a small molecule dipeptidyl peptidase inhibitor, has potent antitumor effects and augments antibody-mediated cytotoxicity via a novel immune mechanism. Cancer Res. 2004 Aug 1;64(15):5471-80. [4]. Egger C, et al. Effects of the fibroblast activation protein inhibitor, PT100, in a murine model of pulmonary fibrosis. Eur J Pharmacol. 2017 Aug 15;809:64-72.
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TNKS-2-IN-1
T776754765-59-7
TNKS-2-IN-1 is a TNKS-2 inhibitor.TNKS-2-IN-1 inhibits TNKS-1 and TNKS-2 with IC50s of 259 nM and 1100 nM, respectively.TNKS-2-IN-1 has antimicrobial activity against E. coli and S. aureus.TNKS-2-IN-1 inhibits the release of IL-1β from the NLRP3 inflammasome (IC50: 5 μM) by inhibiting IL-1β release from ATP-stimulated J1A.774 cells.
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Carvedilol phosphate hemihydrate
Carvedilol phosphate, BM 14190 (phosphate hemihydrate)
T0342610309-89-2
Carvedilol phosphate hemihydrate (BM 14190 phosphate hemihydrate) is the phosphate salt form of carvedilol, a racemic mixture and adrenergic blocking agent with antihypertensive activity and no intrinsic sympathomimetic activity.
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BAA473
T10447
BAA473, a bile acid analog, is a potent activator of the pyrin inflammasome, inducing secretion of interleukin-18 (IL-18) through inflammasome activation in both myeloid and intestinal epithelial cells [1].
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3-6 months
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YQ128
T133752454246-18-3
YQ128 is a potent and selective second-generation NLRP3 (NOD-like receptor P3) inflammasome inhibitor with an IC50 of 0.30 µM and exhibits significant anti-inflammatory activity.
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NLRP3-IN-45
T200214
NLRP3-IN-45 (D6) serves as an inhibitor specifically targeting the NLRP3 inflammasome, demonstrated through its ability to curb the activity of IL-1β (IC 50 = 41.79 nM). It effectively prevents the activation of the NLRP3 inflammasome while sparing the initial stages of its activation process. Furthermore, NLRP3-IN-45 has been shown to selectively inhibit NLRP3 inflammasome activation in the LPS-induced acute lung injury (ALI) mouse model.
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CIB-1476
T200261
CIB-1476, a caspase-1 inhibitor, effectively reduces joint swelling in mouse models of arthritis and demonstrates lasting anti-inflammatory effects. This compound achieves its benefits by blocking IL-1β production, NF-κB activation, and GSDMD-mediated pyroptosis, all of which are triggered by the NLRP3 inflammasome.
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Oxidized low density lipoprotein (Human)
Human ox-LDL
T200276
Oxidized low density lipoprotein (Human) (Human ox-LDL) plays a crucial role in atherogenesis and contributes to endothelial dysfunction through the cytoplasmic adapter protein TRAF3IP2. This compound also promotes endothelial cell activation, leads to increased production of adhesion molecules, and reduces eNOS activity and NO production. Additionally, Human ox-LDL activates the NLRP3 inflammasome in macrophages.
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