目录号 | 产品详情 | 靶点 | |
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T38838 | |||
QS-21, an immunostimulatory saponin, is a powerful vaccine adjuvant that stimulates both Th2 humoral and Th1 cell-mediated immune responses by interacting with antigen presenting cells (APCs) and T cells. Additionally, QS-21 activates the NLRP3 inflammasome, leading to the release of cytokines IL-1β and IL-18, which are dependent on caspase-1. | |||
T61709 | |||
AMS-17 is a potent NLRP3 inhibitor, which effectively suppresses microglia activation both in vitro and in vivo. Additionally, AMS-17 exhibits inhibitory effects on various cytokines, such as caspase-1, TNF-α, IL-1β, and inducible nitric oxide synthase (iNOS), in N9 cells. Given these properties, AMS-17 holds promise as a valuable tool for investigating inflammation-associated neurological disorders [1]. | |||
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。 | |||
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。 | |||
T60868 | |||
NF-κB-IN-4 (化合物 17) 是有效的NF-κB 通路抑制剂,可透过血脑屏障(BBB)。NF-κB-IN-4 具有潜在的抗神经炎症活性,毒性低,可用于研究神经炎症相关疾病。NF-κB-IN-4 可阻断 IκBα 的活化及磷酸化,降低 NLRP3 的表达,从而抑制NF-κB 的激活。 | |||
T79446 | NOD-like Receptor (NLR) | ||
INF200(compound 5)是一种磺酰脲衍生的抑制剂,既能抑制NLRP3也能抑制NLRP3介导的焦亡(pyroptosis)。在HFD诱导的大鼠模型上,INF200对心脏代谢表现出有益效果,并且在(10 μM)浓度下减少了人巨噬细胞中IL-1β的释放,表现出抗炎特性。它还能改善血糖控制和脂质水平,降低全身炎症和心功能障碍的标志物(尤其是BNP水平)。此外,INF200在血流动力学评估中还可提升心肌损伤后的缺血/再灌注损伤(IRI)恢复。 | |||
T79738 | |||
CYP51/PD-L1-IN-1(compound L11)是一种具有抗真菌活性的喹唑啉化合物,作为CYP51(IC50: 0.884 μM)和PD-L1(IC50: 0.083 μM)的双重抑制剂,能够在细胞周期早期引发真菌细胞的凋亡。该化合物还能有效减少IL-2、NLRP3、NF-κBp65等蛋白的细胞内水平,诱导线粒体损伤及ROS积聚,进而导致真菌细胞的破裂和死亡。 | |||
T79740 | |||
CYP51/PD-L1-IN-3(compound L21)是一种具有抗真菌活性的喹唑啉化合物。作为CYP51(IC50: 0.205 μM) 和PD-L1(IC50: 0.039 μM) 的双重抑制剂,它能够引发真菌细胞在细胞周期早期的凋亡。此外,CYP51/PD-L1-IN-3 还能显著降低IL-2、NLRP3、NF-κBp65 蛋白的细胞内水平,并诱导线粒体损害及ROS 聚集,进而导致真菌细胞的裂解与死亡。 | |||
T79739 | |||
CYP51/PD-L1-IN-2(compound L20)是一种具有抗真菌活性的喹唑啉化合物。它作为CYP51(IC50:0.263 μM)和PD-L1(IC50:0.017 μM)的双重抑制剂,能够在细胞周期的早期引发真菌细胞凋亡。CYP51/PD-L1-IN-2进一步显著降低IL-2、NLRP3、NF-κBp65等蛋白水平,触发线粒体损伤及ROS积累,终致真菌细胞裂解和死亡。 | |||
T83962 | |||
C 101248是一种选择性且强效的小鼠和人类串联孔道卤素抑制K+通道1(THIK-1, IC50= 50 nM)抑制剂,对K2P家族成员TREK-1和TWIK-2以及Kv2.1无活性。C 101248能够阻断小鼠海马微胶质细胞中THIK-1 K+电流的整细胞膜片钳记录中的音调和ATP激发的电流。C 101248通过防止NLRP3依赖性IL-1β的释放,从而减少在分离的微胶质细胞中的神经炎症。 |
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 | ||
NLRP3 Protein, Human, Recombinant (His) is expressed in E. coli expression system with N-6xHis tag. The predicted molecular weight is 27.7 kDa and the accession number is Q96P20.
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TMPH-02796 | NLRP3 Protein, Mouse, Recombinant (His & SUMO) | Mouse | E. coli | ||
NLRP3 Protein, Mouse, Recombinant (His & SUMO) is expressed in E. coli expression system with N-6xHis-SUMO tag. The predicted molecular weight is 34.2 kDa and the accession number is Q8R4B8.
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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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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-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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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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