目录号 | 产品详情 | 靶点 | |
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T73013 | |||
NLRP3-IN-14 是一种有效的、选择性的 NLRP3炎症小体抑制剂 (KD: 5.87 μM)。NLRP3-IN-14 抑制 IL-1β 释放,IC50为 0.131 μM。NLRP3-IN-14可用于炎症研究。 | |||
T81637 | NOD-like Receptor (NLR) | ||
NT-0796为一种选择性穿透中枢神经系统的NLRP3炎性体抑制剂,其PBMC方法中的IC50值为0.32 nM。该化合物为异丙酯类,能够在细胞内转化为NDT-197959(羧酸活性物)。NT-0796在神经炎症疾病研究中显示出潜力。 | |||
T78061 | Gap Junction Protein | ||
Peptide5 TFA,一种connexin 43模拟肽,能够降低动物脊髓损伤后的肿胀、抑制星形胶质细胞增生和神经元死亡。该化合物还可抑制NLRP3炎症小体,具有抗炎作用。 | |||
T81579 | |||
P2X7 receptor antagonist-4(Compound 14a)是一种选择性P2X7R拮抗剂,其对人类和小鼠P2X7R的IC50值分别为64.7 nM和10.1 nM。该化合物能有效抑制NLRP3炎性体的激活,并在脓毒症模型小鼠中减少肾损伤,降低caspase-1、gasdermin D、IL-1β和IL-18的表达。 | |||
T69745 | |||
GDC-2394 是一种口服有效、选择性的 NLRP3抑制剂,同时也抑制 IL-1β,IC50为 0.4 μM (human IL-1β) 和 0.1 μM (mouse IL-1β)。GDC-2394 抑制 NLRP3诱导的 caspase-1活性,但不抑制 NLRC4 依赖的炎症小体激活。 | |||
T62221 | |||
NLRP3-IN-8 (compound 27) 是具有口服活性的、与 NLRP3直接结合的 NLRP3炎性体抑制剂,对 IL-1β 的 IC50值为1.23 μM. NLRP3-IN-8 对肝微粒体具有良好的代谢稳定性 (t1/2= 138.63 min),几乎没有毒性 (against L02: IC50> 100 μM) 。 | |||
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。 | |||
T79733 | NOD-like Receptor (NLR) | ||
NLRP3-IN-20(compound 11)是一款口服活性的NLRP3炎症小体抑制剂,其抑制IL-1β分泌的IC50值为25 nM。该化合物展现出卓越的药代动力学性质,并在非酒精性脂肪性肝炎、致命性感染性休克以及结肠炎模型中证明了其显著疗效。 | |||
T82621 | NOD-like Receptor (NLR) | ||
D359-0396 是一种口服活性的 NLRP3 炎性体抑制剂,能有效抑制巨噬细胞焦亡(pyroptosis)以及 IL-1β 的释放,并阻止 NLRP3 和 ASC 的寡聚化,抑制 GSDMD 的裂解。该化合物在动物模型中能减轻小鼠的 EAE 症状,并提高感染性休克后的小鼠存活率。 | |||
T73337 | |||
Articaine (Hoe-045 free base) 是一种含酯基的酰胺类麻醉剂,可逆地与神经内腔内电压门控钠通道的α亚基结合,能有效缓解疼痛。Articaine 通过抑制NF-ĸB 的激活和NLRP3炎症小体通路改善脂多糖 (LPS) 诱导的急性肾损伤。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPK-01228 | MARCO Protein, Human, Recombinant (His) | Human | HEK293 Cells | ||
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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TMPK-00161 | IL-1 beta/IL-1F2 Protein, Human, Recombinant (His & Avi) | Human | E. coli | ||
Interleukin-1 beta (IL-1β) is induced by inflammatory signals in a broad number of immune cell types. IL-1β (and IL-18) are the only cytokines which are processed by caspase-1 after inflammasome-mediated activation. IL-1 signaling activates innate immune cells including antigen presenting cells, and drives polarization of CD4 T cells towards T helper type (Th) 1 and Th17 cells. IL-1 beta/IL-1F2 Protein, Human, Recombinant (His & Avi) is expressed in E. coli expression system with C-His-Avi tag. The predicted molecular weight is 20.1 kDa and the accession number is P01584.
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TMPK-00162 | IL-1 beta/IL-1F2 Protein, Human, Recombinant (His & Avi), Biotinylated | Human | E. coli | ||
Interleukin-1 beta (IL-1β) is induced by inflammatory signals in a broad number of immune cell types. IL-1β (and IL-18) are the only cytokines which are processed by caspase-1 after inflammasome-mediated activation. IL-1 signaling activates innate immune cells including antigen presenting cells, and drives polarization of CD4 T cells towards T helper type (Th) 1 and Th17 cells. IL-1 beta/IL-1F2 Protein, Human, Recombinant (His & Avi), Biotinylated is expressed in E. coli expression system with C-His-Avi tag. The predicted molecular weight is 20.1 kDa and the accession number is P01584.
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TMPK-00515 | IL-1 beta/IL-1F2 Protein, Cynomolgus, Recombinant (His) | Cynomolgus | E. coli | ||
Interleukin-1 beta (IL-1β) is induced by inflammatory signals in a broad number of immune cell types. IL-1β (and IL-18) are the only cytokines which are processed by caspase-1 after inflammasome-mediated activation. IL-1 signaling activates innate immune cells including antigen presenting cells, and drives polarization of CD4 T cells towards T helper type (Th) 1 and Th17 cells. IL-1 beta/IL-1F2 Protein, Cynomolgus, Recombinant (His) is expressed in E. coli expression system with C-His tag. The predicted molecular weight is 18.33 kDa and the accession number is A0A2K5VDC7.
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TMPH-02521 | PYCARD Protein, Mouse, Recombinant (His & Myc) | Mouse | E. coli | ||
Functions as key mediator in apoptosis and inflammation. Promotes caspase-mediated apoptosis involving predominantly caspase-8 and also caspase-9 in a probable cell type-specific manner. Involved in activation of the mitochondrial apoptotic pathway, promotes caspase-8-dependent proteolytic maturation of BID independently of FADD in certain cell types and also mediates mitochondrial translocation of BAX and activates BAX-dependent apoptosis coupled to activation of caspase-9, -2 and -3. Involved in macrophage pyroptosis, a caspase-1-dependent inflammatory form of cell death and is the major constituent of the ASC pyroptosome which forms upon potassium depletion and rapidly recruits and activates caspase-1. In innate immune response believed to act as an integral adapter in the assembly of the inflammasome which activates caspase-1 leading to processing and secretion of proinflammatory cytokines. The function as activating adapter in different types of inflammasomes is mediated by the pyrin and CARD domains and their homotypic interactions. Required for recruitment of caspase-1 to inflammasomes containing certain pattern recognition receptors, such as NLRP2, NLRP3, AIM2 and probably IFI16. In the NLRP1 and NLRC4 inflammasomes seems not be required but facilitates the processing of procaspase-1. In cooperation with NOD2 involved in an inflammasome activated by bacterial muramyl dipeptide leading to caspase-1 activation. May be involved in DDX58-triggered proinflammatory responses and inflammasome activation. In collaboration with AIM2 which detects cytosolic double-stranded DNA may also be involved in a caspase-1-independent cell death that involves caspase-8. In adaptive immunity may be involved in maturation of dendritic cells to stimulate T-cell immunity and in cytoskeletal rearrangements coupled to chemotaxis and antigen uptake may be involved in post-transcriptional regulation of the guanine nucleotide exchange factor DOCK2; the latter function is proposed to involve the nuclear form. Also involved in transcriptional activation of cytokines and chemokines independent of the inflammasome; this function may involve AP-1, NF-kappa-B, MAPK and caspase-8 signaling pathways. For regulation of NF-kappa-B activating and inhibiting functions have been reported. Modulates NF-kappa-B induction at the level of the IKK complex by inhibiting kinase activity of CHUK and IKBK. Proposed to compete with RIPK2 for association with CASP1 thereby down-regulating CASP1-mediated RIPK2-dependent NF-kappa-B activation and activating interleukin-1 beta processing. Modulates host resistance to DNA virus infection, probably by inducing the cleavage of and inactivating CGAS in presence of cytoplasmic double-stranded DNA.
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TMPY-01775 | AIM2 Protein, Human, Recombinant (GST) | Human | Baculovirus Insect Cells | ||
AIM2, Absent In Melanoma 2 is a member of the interferon-inducible HIN-200 protein family that contains an amino-terminal pyrin domain and a carboxy-terminal oligonucleotide/oligosaccharide-binding domain, senses cytoplasmic DNA by means of its oligonucleotide/oligosaccharide-binding domain and interacts with ASC (apoptosis-associated speck-like protein containing a CARD) through its pyrin domain to activate caspase-1. In response to foreign cytoplasmic DNA, AIM2 forms an inflammasome, resulting in caspase activation in inflammatory cells. It had been pointed to a role of AIM2 function in both inflammation and cancer. AIM-2 antigen is expressed in a wide variety of tumor types, including neuroectodermal tumors, as well as breast, ovarian and colon carcinomas. AIM-2 could be used as a tumor antigen target for monitoring vaccine trials or to develop antigen specific active immunotherapy for glioma patients.
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TMPJ-00789 | Flagellin Protein, Salmonella Typhimurium, Recombinant | Salmonella typhimurium | E. coli | ||
Flagellin is the major structural protein monomer of bacterial flagella. Flagellin through binding to its receptor and activation of antigen presenting cells stimulates the innate and adaptive immune responses. Flagellin is used as an effective systemic or mucosal adjuvant to stimulate the immune system. Flagellin is an agonist of Toll-like receptor 5 (TLR5), a pattern recognition receptor (PRR) of the innate immune system expressed on the basolateral surface of intestinal epithelial cells and on the surface of a subset of intestinal dendritic cells. Flagellin is delivered into the cytosol of macrophages by the T3SS-1 of serotype Typhimurium, where it activates the cytosolic interleukin-1 (IL-1) converting enzyme-protease activating factor (IPAF), a nucleotide-binding and oligomerization domain-like receptor (NLR) of the innate immunesystem. Recognition of flagellin by IPAF leads to activation of the inflammasome, followed by proteolytic activation of IL-1 and IL-18.
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TMPH-02671 | Gasdermin-D Protein, Mouse, Recombinant (His & Myc) | Mouse | E. coli | ||
Precursor of a pore-forming protein that plays a key role in host defense against pathogen infection and danger signals. This form constitutes the precursor of the pore-forming protein: upon cleavage, the released N-terminal moiety (Gasdermin-D, N-terminal) binds to membranes and forms pores, triggering pyroptosis.; Promotes pyroptosis in response to microbial infection and danger signals. Produced by the cleavage of gasdermin-D by inflammatory caspases CASP1 or CASP4/CASP11 in response to canonical, as well as non-canonical (such as cytosolic LPS) inflammasome activators. After cleavage, moves to the plasma membrane where it strongly binds to inner leaflet lipids, including monophosphorylated phosphatidylinositols, such as phosphatidylinositol 4-phosphate, bisphosphorylated phosphatidylinositols, such as phosphatidylinositol (4,5)-bisphosphate, as well as phosphatidylinositol (3,4,5)-bisphosphate, and more weakly to phosphatidic acid and phosphatidylserine. Homooligomerizes within the membrane and forms pores of 10-15 nanometers (nm) of inner diameter, allowing the release of mature IL1B and triggering pyroptosis. Exhibits bactericidal activity. Gasdermin-D, N-terminal released from pyroptotic cells into the extracellular milieu rapidly binds to and kills both Gram-negative and Gram-positive bacteria, without harming neighboring mammalian cells, as it does not disrupt the plasma membrane from the outside due to lipid-binding specificity. Under cell culture conditions, also active against intracellular bacteria, such as Listeria monocytogenes. Also active in response to MAP3K7/TAK1 inactivation by Yersinia toxin YopJ, which triggers cleavage by CASP8 and subsequent activation. Strongly binds to bacterial and mitochondrial lipids, including cardiolipin. Does not bind to unphosphorylated phosphatidylinositol, phosphatidylethanolamine nor phosphatidylcholine.
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TMPH-01502 | Humanin Protein, Human, Recombinant (GST) | Human | E. coli | ||
Plays a role as a neuroprotective factor. Protects against neuronal cell death induced by multiple different familial Alzheimer disease genes and amyloid-beta proteins in Alzheimer disease. Mediates its neuroprotective effect by interacting with a receptor complex composed of IL6ST/GP130, IL27RA/WSX1 and CNTFR. Also acts as a ligand for G-protein coupled receptors FPR2/FPRL1 and FPR3/FPRL2. Inhibits amyloid-beta protein 40 fibril formation. Also inhibits amyloid-beta protein 42 fibril formation. Suppresses apoptosis by binding to BAX and preventing the translocation of BAX from the cytosol to mitochondria. Also suppresses apoptosis by binding to BID and inhibiting the interaction of BID with BAX and BAK which prevents oligomerization of BAX and BAK and suppresses release of apoptogenic proteins from mitochondria. Forms fibers with BAX and also with BID, inducing BAX and BID conformational changes and sequestering them into the fibers which prevents their activation. Can also suppress apoptosis by interacting with BIM isoform BimEL, inhibiting BimEL-induced activation of BAX, blocking oligomerization of BAX and BAK, and preventing release of apoptogenic proteins from mitochondria. Plays a role in up-regulation of anti-apoptotic protein BIRC6/APOLLON, leading to inhibition of neuronal cell death. Binds to IGFBP3 and specifically blocks IGFBP3-induced cell death. Competes with importin KPNB1 for binding to IGFBP3 which is likely to block IGFBP3 nuclear import. Induces chemotaxis of mononuclear phagocytes via FPR2/FPRL1. Reduces aggregation and fibrillary formation by suppressing the effect of APP on mononuclear phagocytes and acts by competitively inhibiting the access of FPR2 to APP. Protects retinal pigment epithelium (RPE) cells against oxidative stress-induced and endoplasmic reticulum (ER) stress-induced apoptosis. Promotes mitochondrial biogenesis in RPE cells following oxidative stress and promotes STAT3 phosphorylation which leads to inhibition of CASP3 release. Also reduces CASP4 levels in RPE cells, suppresses ER stress-induced mitochondrial superoxide production and plays a role in up-regulation of mitochondrial glutathione. Reduces testicular hormone deprivation-induced apoptosis of germ cells at the nonandrogen-sensitive stages of the seminiferous epithelium cycle. Protects endothelial cells against free fatty acid-induced inflammation by suppressing oxidative stress, reducing expression of TXNIP and inhibiting activation of the NLRP3 inflammasome which inhibits expression of proinflammatory cytokines IL1B and IL18. Protects against high glucose-induced endothelial cell dysfunction by mediating activation of ERK5 which leads to increased expression of transcription factor KLF2 and prevents monocyte adhesion to endothelial cells. Inhibits the inflammatory response in astrocytes. Increases the expression of PPARGC1A/PGC1A in pancreatic beta cells which promotes mitochondrial biogenesis. Increases insulin sensitivity.
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TMPH-01503 | Humanin Protein, Human, Recombinant (hFc) | Human | HEK293 Cells | ||
Plays a role as a neuroprotective factor. Protects against neuronal cell death induced by multiple different familial Alzheimer disease genes and amyloid-beta proteins in Alzheimer disease. Mediates its neuroprotective effect by interacting with a receptor complex composed of IL6ST/GP130, IL27RA/WSX1 and CNTFR. Also acts as a ligand for G-protein coupled receptors FPR2/FPRL1 and FPR3/FPRL2. Inhibits amyloid-beta protein 40 fibril formation. Also inhibits amyloid-beta protein 42 fibril formation. Suppresses apoptosis by binding to BAX and preventing the translocation of BAX from the cytosol to mitochondria. Also suppresses apoptosis by binding to BID and inhibiting the interaction of BID with BAX and BAK which prevents oligomerization of BAX and BAK and suppresses release of apoptogenic proteins from mitochondria. Forms fibers with BAX and also with BID, inducing BAX and BID conformational changes and sequestering them into the fibers which prevents their activation. Can also suppress apoptosis by interacting with BIM isoform BimEL, inhibiting BimEL-induced activation of BAX, blocking oligomerization of BAX and BAK, and preventing release of apoptogenic proteins from mitochondria. Plays a role in up-regulation of anti-apoptotic protein BIRC6/APOLLON, leading to inhibition of neuronal cell death. Binds to IGFBP3 and specifically blocks IGFBP3-induced cell death. Competes with importin KPNB1 for binding to IGFBP3 which is likely to block IGFBP3 nuclear import. Induces chemotaxis of mononuclear phagocytes via FPR2/FPRL1. Reduces aggregation and fibrillary formation by suppressing the effect of APP on mononuclear phagocytes and acts by competitively inhibiting the access of FPR2 to APP. Protects retinal pigment epithelium (RPE) cells against oxidative stress-induced and endoplasmic reticulum (ER) stress-induced apoptosis. Promotes mitochondrial biogenesis in RPE cells following oxidative stress and promotes STAT3 phosphorylation which leads to inhibition of CASP3 release. Also reduces CASP4 levels in RPE cells, suppresses ER stress-induced mitochondrial superoxide production and plays a role in up-regulation of mitochondrial glutathione. Reduces testicular hormone deprivation-induced apoptosis of germ cells at the nonandrogen-sensitive stages of the seminiferous epithelium cycle. Protects endothelial cells against free fatty acid-induced inflammation by suppressing oxidative stress, reducing expression of TXNIP and inhibiting activation of the NLRP3 inflammasome which inhibits expression of proinflammatory cytokines IL1B and IL18. Protects against high glucose-induced endothelial cell dysfunction by mediating activation of ERK5 which leads to increased expression of transcription factor KLF2 and prevents monocyte adhesion to endothelial cells. Inhibits the inflammatory response in astrocytes. Increases the expression of PPARGC1A/PGC1A in pancreatic beta cells which promotes mitochondrial biogenesis. Increases insulin sensitivity.
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