目录号 | 产品详情 | 靶点 | |
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T3230 | NOD-like Receptor (NLR) NOD | ||
NLRP3-IN-2 (5-Chloro-N-(p-sulfamoylphenethyl)-o-anisamide) 是一种能够合成格列本脲的中间物,对心肌细胞中NLRP3炎症小体的形成具有抑制作用,在小鼠心肌缺血/再灌注后限制梗死面积,且对代谢无影响。 | |||
T61392 | NOD | ||
NLRP3-IN-10 (ZVN26391) 是强效的 NLRP3 抑制剂,抑制 IL-1β 释放的 IC50 为 251.1 nM。NLRP3-IN-10 通过减弱 ASC 斑点形成来抑制 NLRP3炎症小体激活。 | |||
T28178 | NOD | ||
NLRP3-IN-9 (INF-4E) 是 NLRP3 ATPase 和 caspase-1 的抑制剂。 NLRP3-IN-9 通过不可逆地捕获硫醇亲核体发挥作用,以时间和浓度依赖性方式防止 ATP 和尼日利亚菌素触发的人 THP-1 细胞焦亡。 | |||
T39607 | |||
NLRP3 modulators 1 (WO2017184746A1, compound 107) is a potent modulator of NLRP3, capable of agonizing or partially agonizing the activity of NLRP3. This compound proves valuable in investigating conditions, diseases, or disorders where a reduction in LRP3 activity plays a role in the pathology. | |||
T61132 | NOD | ||
NLRP3-IN-11 是一种NLRP3蛋白抑制剂,具有潜在的抗炎活性。NLRP3-IN-11 可用于研究 动脉粥样硬化、阿尔茨海默病和帕金森病类自身炎症性疾病炎症和退行性疾病。 | |||
T39552 | |||
NLRP3-IN-5, a compound disclosed in WO2016131098, is an inhibitor of NLRP3 inflammasome. It consists of the chemical structure N-((4-chloro-2,6-dimethylphenyl)carbamoyl)-4-(2-hydroxypropan-2-l)furan-2-sulfonamide. | |||
T79695 | NOD-like Receptor (NLR) | ||
NLRP3-IN-19(JT001)是一种高效、特异性且具有口服活性的NLRP3抑制剂,能够阻断NLRP3炎症小体的组装,抑制细胞因子释放,并预防细胞焦亡。该化合物适用于非酒精性脂肪性肝炎和肝纤维化研究。 | |||
T60442 | NOD AIM2 | ||
NLRP3/AIM2-IN-3 是一种独特的分子,能以物种特异性的方式抑制 NLRP3 和 AIM2 炎性体的激活。它对细胞裂解的 IC50 值为 0.077 ± 0.008 μ M。NLRP3/AIM2-IN-3是一种 NLRP3 和 AIM2 炎症体依赖性细胞裂解的强效抑制剂,对细胞裂解的 IC50 值为 0.077 ± 0.008 μ M。NLRP3/AIM2-IN-3 可抑制 LPS/nigericin 刺激的 THP-1 巨噬细胞的细胞裂解,其 IC50 值为 0.077 ± 0.008 μM。NLRP3/AIM2-IN-3 干扰了 NLRP3 或 AIM2 与桥接蛋白 ASC 的相互作用,抑制了 ASC 的寡聚。 | |||
T60404 | AIM2 | ||
NLRP3/AIM2-IN-2是一种新型强效抑制剂,对依赖于 NLRP3和 AIM2炎症体的热扩散具有不同物种特异性影响,IC50为0.2392 ± 0.0233 μ M。 | |||
T15052 | NOD-like Receptor (NLR) NOD | ||
Dapansutrile 是一种口服有活性的 NLRP3 炎性小体选择性抑制剂。它具有抗炎特性,可用于研究缓解疼痛。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPH-01739 | NLRP3 Protein, Human, Recombinant (His) | Human | E. coli | ||
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TMPH-02796 | NLRP3 Protein, Mouse, Recombinant (His & SUMO) | Mouse | E. coli | ||
May constitute a glutathione peroxidase-like protective system against peroxide damage in sperm membrane lipids. Since the purified porcine enzyme has very little activity towards hydrogen peroxide or organic hydroperoxides the protective effect is not likely to be exerted by its enzymatic activity. Instead, may protect sperm from premature acrosome reaction in the epididymis by binding to lipid peroxides, which might otherwise interact with phospholipase A2 and induce the acrosome reaction.
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TMPH-01565 | IARS Protein, Human, Recombinant (His & Myc) | Human | E. coli | ||
As the sensor component of the NLRP3 inflammasome, plays a crucial role in innate immunity and inflammation. In response to pathogens and other damage-associated signals, initiates the formation of the inflammasome polymeric complex, made of NLRP3, PYCARD and CASP1 (and possibly CASP4 and CASP5). Recruitment of proCASP1 to the inflammasome promotes its activation and CASP1-catalyzed IL1B and IL18 maturation and secretion in the extracellular milieu. Activation of NLRP3 inflammasome is also required for HMGB1 secretion. The active cytokines and HMGB1 stimulate inflammatory responses. Inflammasomes can also induce pyroptosis, an inflammatory form of programmed cell death. Under resting conditions, NLRP3 is autoinhibited. NLRP3 activation stimuli include extracellular ATP, reactive oxygen species, K(+) efflux, crystals of monosodium urate or cholesterol, amyloid-beta fibers, environmental or industrial particles and nanoparticles, cytosolic dsRNA, etc. However, it is unclear what constitutes the direct NLRP3 activator. Activation in presence of cytosolic dsRNA is mediated by DHX33. Independently of inflammasome activation, regulates the differentiation of T helper 2 (Th2) cells and has a role in Th2 cell-dependent asthma and tumor growth. During Th2 differentiation, required for optimal IRF4 binding to IL4 promoter and for IRF4-dependent IL4 transcription. Binds to the consensus DNA sequence 5'-GRRGGNRGAG-3'. May also participate in the transcription of IL5, IL13, GATA3, CCR3, CCR4 and MAF.
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TMPH-02512 | TEM8/ANTXR1 Protein, Mouse, Recombinant (His) | Mouse | E. coli | ||
As the sensor component of the NLRP3 inflammasome, plays a crucial role in innate immunity and inflammation. In response to pathogens and other damage-associated signals, initiates the formation of the inflammasome polymeric complex, made of NLRP3, PYCARD and CASP1 (or possibly CASP4/CASP11). Recruitment of proCASP1 to the inflammasome promotes its activation and CASP1-catalyzed IL1B and IL18 maturation and secretion in the extracellular milieu. Activation of NLRP3 inflammasome is also required for HMGB1 secretion. The active cytokines and HMGB1 stimulate inflammatory responses. Inflammasomes can also induce pyroptosis, an inflammatory form of programmed cell death. Under resting conditions, NLRP3 is autoinhibited. NLRP3 activation stimuli include extracellular ATP, reactive oxygen species, K(+) efflux, crystals of monosodium urate or cholesterol, amyloid-beta fibers, environmental or industrial particles and nanoparticles, cytosolic dsRNA, etc. However, it is unclear what constitutes the direct NLRP3 activator. Activation in presence of cytosolic dsRNA is mediated by DHX33. Independently of inflammasome activation, regulates the differentiation of T helper 2 (Th2) cells and has a role in Th2 cell-dependent asthma and tumor growth. During Th2 differentiation, required for optimal IRF4 binding to IL4 promoter and for IRF4-dependent IL4 transcription. Binds to the consensus DNA sequence 5'-GRRGGNRGAG-3'. May also participate in the transcription of IL5, IL13, GATA3, CCR3, CCR4 and MAF.
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TMPK-01228 | MARCO Protein, Human, Recombinant (His) | Human | HEK293 | ||
Macrophage receptor with collagenous structure (MARCO) is the predominant scavenger receptor for recognition and binding of silica particles by alveolar macrophages (AM). MARCO contributes to normal cholesterol uptake in macrophages; therefore, in the absence of MARCO, macrophages are more susceptible to a greater inflammatory response by particulates known to cause NLRP3 inflammasome activation and the effect is due to increased LMP.
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TMPH-01551 | IFNLR1 Protein, Human, Recombinant (His & SUMO) | Human | E. coli | ||
Adapter protein involved in the Toll-like receptor and IL-1 receptor signaling pathway in the innate immune response. Acts via IRAK1, IRAK2, IRF7 and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response. Increases IL-8 transcription. Involved in IL-18-mediated signaling pathway. Activates IRF1 resulting in its rapid migration into the nucleus to mediate an efficient induction of IFN-beta, NOS2/INOS, and IL12A genes. Upon TLR8 activation by GU-rich single-stranded RNA (GU-rich RNA) derived from viruses such as SARS-CoV-2, SARS-CoV and HIV-1, induces IL1B release through NLRP3 inflammasome activation. MyD88-mediated signaling in intestinal epithelial cells is crucial for maintenance of gut homeostasis and controls the expression of the antimicrobial lectin REG3G in the small intestine.
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TMPH-00939 | Anoctamin-5/ANO5 Protein, Human, Recombinant (His) | Human | HEK293 | ||
G-protein coupled receptor for endogenous cannabinoids (eCBs), including N-arachidonoylethanolamide (also called anandamide or AEA) and 2-arachidonoylglycerol (2-AG), as well as phytocannabinoids, such as delta(9)-tetrahydrocannabinol (THC). Mediates many cannabinoid-induced effects, acting, among others, on food intake, memory loss, gastrointestinal motility, catalepsy, ambulatory activity, anxiety, chronic pain. Signaling typically involves reduction in cyclic AMP. In the hypothalamus, may have a dual effect on mitochondrial respiration depending upon the agonist dose and possibly upon the cell type. Increases respiration at low doses, while decreases respiration at high doses. At high doses, CNR1 signal transduction involves G-protein alpha-i protein activation and subsequent inhibition of mitochondrial soluble adenylate cyclase, decrease in cyclic AMP concentration, inhibition of protein kinase A (PKA)-dependent phosphorylation of specific subunits of the mitochondrial electron transport system, including NDUFS2. In the hypothalamus, inhibits leptin-induced reactive oxygen species (ROS) formation and mediates cannabinoid-induced increase in SREBF1 and FASN gene expression. In response to cannabinoids, drives the release of orexigenic beta-endorphin, but not that of melanocyte-stimulating hormone alpha/alpha-MSH, from hypothalamic POMC neurons, hence promoting food intake. In the hippocampus, regulates cellular respiration and energy production in response to cannabinoids. Involved in cannabinoid-dependent depolarization-induced suppression of inhibition (DSI), a process in which depolarization of CA1 postsynaptic pyramidal neurons mobilizes eCBs, which retrogradely activate presynaptic CB1 receptors, transiently decreasing GABAergic inhibitory neurotransmission. Also reduces excitatory synaptic transmission. In superior cervical ganglions and cerebral vascular smooth muscle cells, inhibits voltage-gated Ca(2+) channels in a constitutive, as well as agonist-dependent manner. In cerebral vascular smooth muscle cells, cannabinoid-induced inhibition of voltage-gated Ca(2+) channels leads to vasodilation and decreased vascular tone. Induces leptin production in adipocytes and reduces LRP2-mediated leptin clearance in the kidney, hence participating in hyperleptinemia. In adipose tissue, CNR1 signaling leads to increased expression of SREBF1, ACACA and FASN genes. In the liver, activation by endocannabinoids leads to increased de novo lipogenesis and reduced fatty acid catabolism, associated with increased expression of SREBF1/SREBP-1, GCK, ACACA, ACACB and FASN genes. May also affect de novo cholesterol synthesis and HDL-cholesteryl ether uptake. Peripherally modulates energy metabolism. In high carbohydrate diet-induced obesity, may decrease the expression of mitochondrial dihydrolipoyl dehydrogenase/DLD in striated muscles, as well as that of selected glucose/ pyruvate metabolic enzymes, hence affecting energy expenditure through mitochondrial metabolism. In response to cannabinoid anandamide, elicits a proinflammatory response in macrophages, which involves NLRP3 inflammasome activation and IL1B and IL18 secretion. In macrophages infiltrating pancreatic islets, this process may participate in the progression of type-2 diabetes and associated loss of pancreatic beta-cells.; Binds both 2-AG and anandamide.; Only binds 2-AG with high affinity. Contrary to its effect on isoform 1, 2-AG behaves as an inverse agonist on isoform 2 in assays measuring GTP binding to membranes.; Only binds 2-AG with high affinity. Contrary to its effect on isoform 1, 2-AG behaves as an inverse agonist on isoform 3 in assays measuring GTP binding to membranes.
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