目录号 | 产品详情 | 靶点 | |
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T74817 | |||
JNK3inhibitor-7 是一种有效的口服活性JNK3抑制剂,能穿过血脑屏障,其对JNK3、JNK2、JNK1的IC50值分别为53、973、1039 nM。该化合物表现出显著的神经保护作用,并具备研究阿尔茨海默病(AD)潜力。 | |||
TN7240 | ROS | ||
Erinacine A 是一种可从猴头菇中提取出的抗癌化合物,能够通过活性氧类 (ROS) 的产生促使癌细胞死亡。Erinacine A 可能通过参与信号通路的调节从而发挥其抗癌活性。Erinacine A 具有抗癌、抗肿瘤和神经保护活性。 | |||
T61206 | |||
AChE/BChE/BACE-1-IN-1 (Compound 4k) is an orally active inhibitor that targets acetylcholinesterase (AChE), butyrylcholinesterase (BChE), and β-site amyloid precursor protein cleaving enzyme 1 (BACE-1). It displays IC50 values of 0.058 μM, 0.082 μM, and 0.115 μM against hAChE, hBChE, and hBACE-1, respectively. AChE/BChE/BACE-1-IN-1 exhibits significant binding affinity with PAS-AChE, excellent ability to cross the blood-brain barrier, potential disassembly of amyloid-beta (Aβ) aggregates, and neuroprotective properties against Aβ-induced stress. Moreover, AChE/BChE/BACE-1-IN-1 demonstrates remarkable antioxidant capabilities [1]. | |||
T74818 | |||
JNK3inhibitor-8是一种高效、选择性且具口服活性的JNK3抑制剂,能穿透血脑屏障。其对JNK3、JNK2、JNK1的IC50值依次为21, 2203, >10000 nM。JNK3inhibitor-8展现出显著的神经保护性能,并具备研究阿尔茨海默病(AD)的可能性。 | |||
T13036 | Mitophagy | ||
Sulfosuccinimidyl oleate (Sulfo-N-succinimidyl oleate) (Sulfo-N-succinimidyl oleate) 是一种长链脂肪酸,可抑制脂肪酸运输到细胞。Sulfosuccinimidyl oleate 是一种有效且不可逆的线粒体呼吸链抑制剂。Sulfosuccinimidyl oleate 与小胶质细胞表面上的CD36受体结合,具有抗炎效果。 | |||
TP2019 | |||
Highly potent GIP receptor agonist (EC50 = 630 ± 119 pM). Displays equivalent cAMP stimulating properties and improved resistance to enzymatic degradation compared to native GIP in cells expressing wild type GIP receptor. Improves glucose tolerance, insul | |||
T73912 | |||
Maysin 是一种具有神经保护作用的 C-糖基黄酮,可以从玉米须中分离得到。Maysin 对 Syn 淀粉样蛋白聚集体-低聚物和原纤维引起的损伤具有保护作用。Maysin 可防止氧化应激和细胞内钙稳态失衡,激活自噬降解过程。Maysin 可用于帕金森病(PD) 的研究。 | |||
T13112 | NO Synthase iGluR | ||
Tat-NR2B9c (NA-1) 是一种突触后密度-95(PSD-95)抑制剂,具有神经保护和抗癫痫作用。Tat-NR2B9c 可抑制PSD-95d2、 PSD-95d1 和 PSD-95,可阻止NMDA诱导的神经元NADPH氧化酶的激活,从而阻断超氧化物的产生,可减少中风后急性期的缺血性损伤。 | |||
T78596 | |||
CAD031,一种针对阿尔茨海默病 (AD) 的J147衍生物,展现了神经保护和记忆增强的特性。它能增强小鼠的记忆力,优化树突结构,并促进老年小鼠大脑生发区细胞的分裂。相较于J147,CAD031在人类神经干细胞测定中显示出更高的活性。 | |||
T78954 | Neurotensin Receptor | ||
hNTS1R agonist-1 (Compound 10)为能穿透血脑屏障的hNTS1R全激动剂(Ki:6.9 nM)。它能提升帕金森病(PD)模型小鼠的运动能力及记忆。作为一种Neurotensin(8-13)类似物,hNTS1R agonist-1同时具有神经保护作用。 |
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-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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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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