目录号 | 产品详情 | 靶点 | |
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T81072 | |||
Suffruticosol A是一种从P. lactiflora种子中分离得到的神经保护剂,能够逆转由Scopolamine诱导的细胞神经退行性损伤。该化合物还能改善海马体胆碱能缺陷并部分增强BDNF信号传导,从而在Scopolamine诱导模型中显示出改善神经功能的作用,可恢复小鼠记忆与认知行为。 | |||
T74860 | Monoamine Oxidase | ||
MAO-B-IN-21是一种有效的MAO-B抑制剂,该化合物表现出抗氧化和抗Aβ聚集的活性。该化合物还可螯合金属离子,抗神经炎症(如NO、TNF-α),具有神经保护作用,并可穿透BBB。在Aβ1-42诱导的阿尔茨海默病小鼠模型中,MAO-B-IN-21显著改善了记忆与认知功能。 | |||
T76536 | |||
Pinealon是一种由三个氨基酸构成的肽,展现出神经保护属性。该化合物能够抑制ROS(活性氧)的积累和ERK1/2活化,激发脑组织主要细胞成分的活跃性,减缓自发性细胞凋亡率。此外,Pinealon对于防护大鼠后代免遭产前高同型半胱氨酸血症的影响亦显著。 | |||
T72824 | |||
RAGE/SERT-IN-1 是一种 RAGE 和 SERT 抑制剂,口服活性良好,IC50 分别为 8.26 μM 和 31.09 nM。它对 Aβ25-35 诱发的神经元损伤具有显著神经保护效果,并可缓解小鼠抑郁症状。RAGE/SERT-IN-1 适用于阿尔茨海默病与抑郁症并发症的研究。 | |||
T62598 | |||
Pitavastatin (NK-104) sodium 是一种有效的羟甲基戊二酰-CoA(HMG-CoA) 还原酶抑制剂,也是一种高效的肝细胞低密度脂蛋白胆固醇 (LDL-C) 受体诱导剂。Pitavastatin sodium 在 HepG2 细胞中,能够抑制乙酸合成胆固醇 (IC50: 5.8 nM) 。Pitavastatin sodium 表现出抗动脉粥样硬化、抗哮喘、抗骨关节炎、神经保护、抗肿瘤、肝保护和肾保护作用。 | |||
T37671 | |||
N-Methyl-D-aspartate (NMDA) receptors are Ca2+ permeable ligand-gated channels of the central nervous system that are activated after binding of the co-agonists glutamate and glycine. CAY10608 is a propanolamine that potently, selectively, and non-competitively antagonizes the NR2B subunit of NMDA receptors (IC50 = 50 nM). It does not inhibit NR1, NR2A, NR2C, and NR2D subunits and has no significant effects on α-amino-3-hydroxy-5-methyl-4-isoxazolepropioinic acid (AMPA) or kainate receptors. CAY10608 is neuroprotective, since it prevents NMDA-triggered release of lactate dehydrogenase from cultured cortical neurons. Also, CAY10608, when administered intraperitoneally, reduces brain infarct volume resulting from transient ischemia via carotid artery occlusion. | |||
T63873 | |||
Anti-Aβ agent 1A 是有效的抗淀粉样蛋白-β (amyloid-β) 剂。Anti-Aβ agent 1A 可明显抑制 LPS 诱导的 IL-1β、IL-6 和 TNF-α 水平,并能够利用线粒体途径减少 H2O2诱导的 SH-SY5Y 细胞凋亡,表现出抗氧化、抗炎、抗 Aβ 毒性和神经保护活性。Anti-Aβ agent 1A 能够用于研究阿尔兹海默症。 | |||
T79716 | Bcr-Abl | ||
c-ABL-IN-5是一种选择性c-Abl抑制剂,具有神经保护功能。该化合物显示出血脑屏障渗透性、代谢稳定性和优良的药物动力学特性。经[18F]标记的c-ABL-IN-5(化合物[18F]3)可用作PET示踪剂,以评估疾病改善的功效。此外,c-ABL-IN-5适用于帕金森病(PD)等神经退行性疾病的研究。 | |||
T63990 | |||
AChE-IN-12 是有效的、能够透过血脑屏障 (BBB) 的乙酰胆碱酯酶 (AChE) 抑制剂,能够作用于大鼠 AChE (IC50: 0.41 μM) 和电鳗 AChE (IC50: 1.88 μM)。AChE-IN-12 是一种良好的抗氧化剂 (ORAC: 3.3eq)、选择性金属螯合剂及 huMAO-B 抑制剂 (IC50: 8.8 μM)。AChE-IN-12 能够显著抑制 Cu2+诱导的 Aβ1-42 的聚集,表现出良好的神经保护效果,能够用于阿尔兹海默症的研究。 | |||
T81485 | |||
Phoenixin-14 (PNX-14) TFA 是具抗焦虑、心脏保护及神经保护效果的穿透大脑屏障神经肽。它通过上调GnRH受体mRNA调控垂体促性腺激素分泌,并促进胰岛素释放。此外,Phoenixin-14 TFA保护小鼠免受缺血/再灌注(IR)伤害,通过降低ROS、提高GSH减缓氧化应激。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPK-00810 | tPA Protein, Mouse, Recombinant (His) | Mouse | HEK293 Cells | ||
Tissue plasminogen activator (tPA) is the predominant plasminogen activator present in the vascular and nervous systems.t tPA is not only neuroprotective for postnatal primary cortical neurons, but also that the
predominant route for enhancing cell survival is via an mTORdependent mechanism.
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TMPH-03391 | TRIM2 Protein, Rat, Recombinant (His) | Rat | E. coli | ||
E3 ubiquitin-protein ligase that mediates the ubiquitination of phosphorylated BCL2L11. Also mediates the UBE2D1-dependent ubiquitination of NEFL. Plays a neuroprotective function. May play a role in neuronal rapid ischemic tolerance. TRIM2 Protein, Rat, Recombinant (His) is expressed in E. coli expression system with N-6xHis tag. The predicted molecular weight is 85.5 kDa and the accession number is D3ZQG6.
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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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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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TMPJ-00990 | S100B Protein, Mouse, Recombinant (His) | Mouse | E. coli | ||
S100-B, is an acidic protein with a molecular weight of 21 kDa belonging to the S100 family. S100-B contains two EF-hand-type calcium-binding motifs separated by a hinge region with a hydrophobic cleft. S100-B plays an important role in neurodevelopment, differentiation, and brain construction. S100-B has neuroprotective effects, but at high concentrations S100-B is neurotoxic. Extracellular concentration of S100-B increases following brain damage, which easily penetrates into cerebrospinal fluid in brain damage and then into the blood. S100-B is expressed and produced by astrocytes in vertebrate brains and in the CNS, and the astrocytes are the major cells producing S100-B protein in gray matter, as well as oligodendrocytes are the predominant S100-B in protein producing cells in white matter. The major advantage of using S100-B is that elevations in serum or CSF levels provide a sensitive measure for determining CNS injury at the molecular level before gross changes develop, enabling timely delivery of crucial medical intervention before irreversible damage occurs. In addition, S100-B, which is also present in Mouse melanocytes, is a reliable marker for melanoma malignancy both in bioptic tissue and in serum.
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