目录号 | 产品详情 | 靶点 | |
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T75436 | |||
Jatrorrhizine hydroxide, 一种从黄连中提取的生物碱,展现了神经保护、抗菌、抗疟原虫及抗氧化的活性。作为一种高效的乙酰胆碱酯酶(AChE)抑制剂(IC50=872 nM),其对BuChE的选择性高达115倍。此外,Jatrorrhizine hydroxide还能通过抑制uptake-2 transporter活性来减少血清素(5-HT)和去甲肾上腺素(NE)的摄取,表现出口服活性。 | |||
T62504 | |||
BChE-IN-8 (compound 20) 是一种能透过血脑屏障的、口服具有活力的 BChE (丁酰胆碱酯酶) 抑制剂,能够作用于 eqBChE (IC50: 0.15 nM)、hBChE (IC50: 45.2 nM)。BChE-IN-8 具有高度稳定性,有助于显著改善血液浓度和组织暴露。BChE-IN-8 能够利用胆碱能系统、Aβ 聚集、神经肽水平等多种调控机制,发挥神经保护和认知改善作用。BChE-IN-8 能够用于研究阿尔茨海默病 (AD)。 | |||
T61049 | |||
AChE-IN-11 (compound 5C) 可用于阿尔茨海默病的研究,它具有神经保护作用和良好的抗氧化活性 (ORAC = 2.5 eq) 。AChE-IN-11 是一种很好的多功能剂,其对于AChE、MAO-B 和 BACE1 的 IC 50 值分别为 7.9 μM、9.9 μM 和 8.3 μM。AChE-IN-11 具有混合型 AChE 抑制作用,可与结合AChE 的 CAS 和 PAS 结合。AChE-IN-11 也是一种选择性金属离子螯合剂。 | |||
T72506 | |||
Antioxidant agent-8是一种口服活性的Aβ1-42沉积抑制剂。其抑制原纤维聚集的IC50值为11.15 µM,促进原纤维分解的IC50值为6.87 µM。此外,Antioxidant agent-8对Cu2+诱导的Aβ1-42原纤维聚集有抑制作用(IC50=3.69 µM),并能促进Cu2+诱导的Aβ1-42原纤维分解(IC50=3.35 µM)。该化合物具备抗氧化活性、抗炎活性、生物安全性、血脑屏障通透性和神经保护作用。 | |||
T37215 | |||
5α,6β-Dihydroxycholestanol is an oxysterol metabolite of cholesterol formed from conversion of cholesterol epoxides by 5,6-epoxysterol hydrolase. It inhibits NMDA-mediated calcium influx in HEK293 cells expressing NR1/NR2B NMDA receptors in a concentration-dependent manner. It also binds to voltage-gated sodium (Nav) channels and decreases action potentials in hippocampal neurons in vitro when used at a concentration of 10 uM. It increases survival of spinal cord motoneurons, cortical neurons, and cerebellar granule neurons in vitro when used at concentrations ranging from 5 to 15 uM. 5α,6β-Dihydroxycholestanol is neuroprotective in a rat model of cerebral ischemia when administered at a dose of 12 mg/kg and increases latency to seizure onset and reduces severity of seizures induced by pentylenetetrazole in rats. 5α,6β-Dihydroxycholestanol has been used as a replacement for cholesterol in the study of cholesterol binding proteins. | |||
T60691 | |||
AChE/BChE/BACE-1-IN-2 (Compound 4o) 表现出显著的抗氧化潜力和对PAS-AChE 的强大的结合能力。AChE/BChE/BACE-1-IN-2 是口服有效的AChE、BACE-1和BChE 抑制剂,对 hAChE、hBACE-1 和hBChE 的IC50分别为 0.069、0.097 和0.127 μM。AChE/BChE/BACE-1-IN-2 显示出对潜在的 Aβ 聚集物的分解能力和针对 Aβ 诱导的应激的神经保护作用。 | |||
TN4291 | IL Receptor NOS | ||
Isofuranodiene protects GalN/LPS-induced liver injury in SD rats, it may be a potential functional food ingredient for the prevention and treatment of liver diseases. Isofuranodiene has anticancer activity, by inhibiting the proliferation and inducing apo | |||
TN2775 | MMP BCL IκB/IKK GSK-3 TNF NOS NF-κB Wnt/beta-catenin COX JAK STAT | ||
2-Methoxystypandrone displays an immunomodulatory effect in a cellular model, it blocks inflammatory responses by impairing NF-κB signaling to limit the inflammation and oxidative stress for preservation of BBB integrity. 2-Methoxystypandrone concomitant | |||
TP2019L | |||
[D-Ala2]-GIP (human) acetate(444073-04-5 Free base) 是一种高效的 GIP 受体激动剂 (EC50 = 630 ± 119 pM)。 在表达野生型 GIP 受体的细胞中,与天然 GIP 相比,[D-Ala2]-GIP (human) acetate 显示出同等的 cAMP 刺激特性,并提高了对酶促降解的抵抗力。 [D-Ala2]-GIP (human) acetate 可改善各种肥胖和糖尿病动物模型的葡萄糖耐量、胰岛素释放和认知功能。 [D-Ala2]-GIP (human) acetate 在 PD 的 MPTP 模型中显示出神经保护作用。 | |||
T60395 | |||
Nrf2-ARE/hMAO-B/QR2 modulator 1是一种新的基于白藜芦醇的多靶点定向配体(MTDL),显示出良好的平衡 MTDL 特征:细胞激活 Nrf2-ARE 通路(CD = 9.83 μM),选择性抑制 hMAO-B 和 QR2 (IC50s = 8.05和0.57 μM),并具有较佳的促进海马神经发生的能力。Nrf2-ARE/hMAO-B/QR2调节剂1在急性和慢性阿尔茨海默症模型中使用海马组织发挥神经保护和抗氧化作用。 |
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-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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