目录号 | 产品详情 | 靶点 | |
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T60909 | |||
SSAO inhibitor-3 (Compound 2) 可用于研究动脉粥样硬化、糖尿病及其并发症、肥胖症、中风、慢性肾病、视网膜病变、慢性阻塞性肺病 (COPD)、自身免疫性疾病、多发性硬化等。SSAO inhibitor-3 是一种氨基脲敏感性胺氧化酶 (SSAO) 的抑制剂,对人 AOC1 和SSAO 的IC50分别为 0.1-10 μM 和 <10 nM 。 | |||
T37669 | |||
The A1, A2A, A2B, and A3 adenosine receptors (ARs) are ubiquitous G protein-coupled receptors. The four AR subtypes have been implicated in several areas of therapeutic interest such as stroke and other ischemic conditions, as well as inflammation, neurodegenerative diseases, diabetes, and sleep regulation. A3 AR antagonists are of interest as therapeutic agents in glaucoma agents and inflammation. CAY10498 is a potent and selective A3 AR antagonist exhibiting a Ki of 37 nM with 60 and 200-fold selectivity over A1 and A2A adenosine receptors, respectively. CAY10498 is also a structural analog of reversine, a dedifferentiation agent of embryonic progenitor cells. However, no dedifferentiation effects or any connection between A3 AR antagonism and dedifferentiation have been demonstrated. | |||
T60640 | |||
SSAO inhibitor-2 (Compound 1) 可用于动脉粥样硬化、糖尿病及其并发症、肥胖、中风、慢性肾病、视网膜病变、慢性阻塞性肺病 (COPD)、自身免疫性疾病、多发性硬化等的研究。SSAO inhibitor-2 是氨基脲敏感性胺氧化酶 (SSAO) 抑制剂,其对人 SSAO 和 MAO-A 的IC50分别为 <10 nM 和 10-100 μM。 | |||
T80419 | Apoptosis | ||
TAT-NEP1-40 TFA 是一种能够穿透血脑屏障的多肽。它能够保护 PC12 细胞抵御缺氧和葡萄糖剥夺 (OGD) 的损害,并促进神经突的生长。此外,TAT-NEP1-40 TFA 可通过减少缺血性脑损伤中的细胞凋亡,以改善神经系统功能。该化合物在中枢神经系统损伤,包括中风后轴突再生及功能恢复的研究中具有潜在应用价值。 | |||
T80418 | Apoptosis | ||
TAT-NEP1-40是一种能够穿透血脑屏障的多肽。它能够保护PC12细胞不受缺氧和葡萄糖剥夺(OGD)所致的损伤,同时促进神经突的生长。此外,TAT-NEP1-40通过阻断缺血性脑损伤中的细胞凋亡,对缺血后的神经功能恢复具有积极作用。该化合物适用于中枢神经系统损伤,特别是中风后的轴突再生与功能恢复方面的研究。 | |||
T82663 | |||
CU06-1004 (Sac-1004) 是一种口服活性的内皮功能障碍阻滞剂。它通过降低过度的渗透性和炎症来改善内皮功能障碍,有效抑制了包括糖尿病视网膜病变、中风、癌症和炎症性肠病在内的多种动物模型中的血管渗漏和炎症。此外,CU06-1004 对CDAA 诱导的 NASH 模型的小鼠也具有改善作用,并能够提升心脏功能。 | |||
T83730 | |||
Tat-M2NX是一种瞬时受体电位麦拉斯汀2(TRPM2)的肽类拮抗剂。在25到100µM的浓度范围内,能够抑制表达人类TRPM2的HEK293细胞中氢过氧化物诱导的钙离子流入。在体内,Tat-M2NX(20 mg/kg)通过在中大脑动脉阻塞(MCAO)诱导的中风模型中,如果在阻塞前或阻塞后3小时内给药,能减少雄性小鼠的脑梗塞体积,但对雌性小鼠无效。 | |||
T83695 | |||
Myelin Oligodendrocyte Glycoprotein (MOG) peptide 是 MOG 的一种内源性肽段截取,存在于髓鞘的细胞外表面。当与抗原血清型HLA-DR2结合时,MOG peptide 在通过中脑动脉阻塞(MCAO)诱导的缺血性中风模型中,能减少皮层和纹状体梗死体积,降低管-角转测试中的感觉运动障碍,增加对新奇气味的探索时间,以及增加雌性(但不是雄性)小鼠对笼伴侣发出的呼叫持续时间。 | |||
T36482 | |||
Water-soluble salt of lamotrigine . Displays anticonvulsant effects and inhibits glutamate release, possibly through inhibition of Na+, K+ and Ca2+ currents. Leach et al (1991) Neurochemical and behavioral aspects of lamotr. Epilepsia 32 S4 PMID:1685439 |Smith and Meldrum (1995) Cardioprotective effect of lamotr. after focal ischemia in rats. Stroke 26 117 PMID:7839380 |Zona and Avoli (1997) Lamotrigine reduces voltage-gated sodium currents in rat central neurons in culture. Epilepsia 38 522 PMID:9184596 |Grunze et al (1998) Modulation of calcium and potassium currents by lamotr. Neuropsychobiology 38 131 PMID:9778600 | |||
T83729 | |||
Tat-CIRP是一种肽类抑制剂,用于抑制髓样分化2蛋白(MD-2,亦称淋巴细胞抗原96 [LY96])与寒冷诱导的RNA结合蛋白(CIRP)之间的蛋白-蛋白相互作用。它通过与MD-2结合,干扰MD-2与CIRP之间的相互作用,这一作用在共免疫沉淀实验中得到证实。在体内实验中,Tat-CIRP (10及20 mg/kg) 能够减少由中脑动脉闭塞(MCAO)引发的小鼠脑梗死体积。同样,在通过血栓引发脑梗死的恒河猴模型中,Tat-CIRP同样能减少脑梗死体积,并缩短患中风一侧手臂抓取并放下食物的时间。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-01075 | Von Willebrand Factor/vWF Protein, Human, Recombinant (His) | Human | CHO Cells | ||
Von Willebrand Factor (VWF) is a multimeric glycoprotein involved in hemostasis in blood, binds receptors on the surface of platelets and in connective tissue, thereby mediating the adhesion of platelets to sites of vascular injury. From studies it appears that VWF protein uncoils under these circumstances, decelerating passing platelets. VWF protein is deficient or defective in von Willebrand disease (VWD) and is involved in a large number of other diseases, including thrombosis, thrombotic thrombocytopenic purpura, Stroke, Heyde's syndrome, possibly hemolytic-uremic syndrome and so on.
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TMPY-00344 | ARL6IP6 Protein, Human, Recombinant (mFc) | Human | HEK293 Cells | ||
It had been found that a homozygous truncating mutation in ARL6IP6 as the likely cause of a syndromic form of CMTC associated with major dysmorphism, developmental delay, transient ischemic attacks and cerebral vascular malformations. This gene was previously implicated by genome wide association study (GWAS) as a susceptibility locus to ischemic stroke in young adults. We identify ARL6IP6 as a novel candidate gene for a syndromic form of CMTC. This suggests that ischemic stroke or transient ischemic attacks (TIA) may represent, at least in some cases, the mild end of a phenotypic spectrum that has at its severe end autosomal recessive CMTC. This finding contributes to a growing appreciation of the continuum of Mendelian and common complex diseases.
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TMPY-00410 | EPHX2 Protein, Human, Recombinant (His) | Human | Baculovirus Insect Cells | ||
Genetic variation in EPHX2 was significantly associated with risk of incident CHD in Caucasians, implicating EPHX2 as a potential cardiovascular disease-susceptibility gene. Single nucleotide polymorphisms (SNPs) in the human EPHX2 gene had been implicated in susceptibility to cardiovascular disease, including stroke. The human EPHX2 mutations may in part explain the genetic variability in sensitivity to ischemic brain injury and stroke outcome. Epoxide hydrolase is involved in metabolism of vasoactive and anti-inflammatory epoxyeicosatrienoic acids to their corresponding diols. Consequently, epoxide hydrolase 2 (EPHX2) is a candidate cardiovascular disease (CVD) gene. Genetic variation in EPHX2 is associated with forearm vasodilator responses in a bradykinin receptor- and endothelium-independent manner, suggesting an important role for soluble epoxide hydrolase in the regulation of vascular function in humans. EPHX2 variants may mediate EETs levels, and low levels of EETs may be a predictor for END in acute MIS.
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TMPJ-01022 | SUMO3 Protein, Human, Recombinant (HEK293, His) | Human | HEK293 Cells | ||
Small ubiquitin-like modifier (SUMO), also known as SUMO homologue and SMT3, is a member of the superfamily of ubiquitin-like polypeptides that become covalently attached to various intracellular target proteins as a way to alter their function, location, and/or half-life. Small ubiquitin-like modifiers include SUMO1, SUMO2, SUMO3, and SUMO4. Except for SUMO4, all other SUMOs are ubiquitously expressed, including in the brain. In human, SUMO2 and SUMO3 are two highly homologous proteins, collectively called SUMO2/3. Several studies suggest that SUMO3 are associated with pathogenesis in several neurological diseases, including Alzheimer's disease, Parkinson's disease, and cerebral ischemia/stroke.
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TMPY-01481 | FLAP Protein, Human, Recombinant (His) | Human | Baculovirus Insect Cells | ||
Arachidonate 5-Lipoxygenase-Activating Protein (ALOX5AP), also known as FLAP, belongs to the MAPEG family. ALOX5AP/FLAP is an essential partner of 5-LO for this process. The FLAP (ALOX5AP) gene has been linked to risk for myocardial infarction, stroke and restenosis, reigniting pharmaceutical interest in this target. It had been found that ALOX5AP/FLAP is a key enzyme in leukotriene formation, in both human pulmonary microvascular endothelial cells and a transformed human brain endothelial cell line. In addition, the protein FLAP has recently been identified as an emerging target in metabolic disease. In fact, FLAP is overexpressed in the adipose tissue of patients and experimental animals with obesity.
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TMPY-02298 | ACYP2 Protein, Human, Recombinant (GST) | Human | E. coli | ||
Recent genome-wide association studies have identified genetic variants in ACYP2 and WFS1 that are associated with cisplatin-induced ototoxicity. We sought to explore the role of these genetic susceptibility factors to cisplatin-induced ototoxicity in patients with testicular cancer. Telomere length, as a marker of biological aging, has been reported to influence the risk of several age-related diseases, including ischemic stroke. Recent studies have identified the genetic variant within ACYP2 and TSPYL6 associated with shorter telomere length. The research showed that that the G allele of rs11896604 and the A allele of rs12615793 within ACYP2 gene, rs12615793- smoking interaction, and rs11896604-alcohol drinking interaction were all associated with increased IS risk.
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TMPY-02376 | BNIP3L Protein, Human, Recombinant | Human | E. coli | ||
The deletion of BNIP3L results in retention of mitochondria during lens fiber cell remodeling, and that deletion of BNIP3L also results in the retention of endoplasmic reticulum and Golgi apparatus. BNIP3L localizes to the endoplasmic reticulum and Golgi apparatus of wild-type newborn mouse lenses and is contained within mitochondria, endoplasmic reticulum and Golgi apparatus isolated from adult mouse liver. As the cells become packed with keratin bundles, Bnip3L expression triggers mitophagy to rid the cells of the last remaining 'living' characteristic, thus completing the march from 'living' to 'dead' within the hair follicle. during retinal development tissue hypoxia triggers HIF1A/HIF-1 stabilization, resulting in increased expression of the mitophagy receptor BNIP3L/NIX. BNIP3L-dependent mitophagy results in a metabolic shift toward glycolysis essential for RGC neurogenesis. BNIP3L could be a potential therapeutic target for ischemic stroke
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TMPJ-00857 | Thrombomodulin Protein, Mouse, Recombinant (His) | Mouse | HEK293 Cells | ||
Thrombomodulin is also known as CD141 antigen and blood dendritic cell antigen 3 (BDCA3), which is encoded by the THBD gene. The deduced amino acid sequence of mouse THBD predicts a signal peptide (aa 1 to 16) and a mature chain (aa 17 to 577) that consists of the following domains: C-type lectin, EGF-like, transmembrane and cytoplasmic. Mouse THBD is corresponding to the extracellular portion of the type I membrane protein. Predominantly synthesized by vascular endothelial cells, THBD inhibits coagulation and fibrinolysis. It functions as a cell surface receptor and an essential cofactor for active thrombin, which in turn activates protein C and thrombinactivatable fibrinolysis inhibitor (TAFI), also known as carboxypeptidase B2 (CPB2). In addition, THBD gene polymorphisims are associated with human disease and THBD plays a role in thrombosis, stroke, arteriosclerosis, and cancer.
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TMPY-01303 | Serpin A3 Protein, Human, Recombinant (His) | Human | HEK293 Cells | ||
SerpinA3, also known as Alpha 1-antichymotrypsin (AACT), is a plasma alpha globulin glycoprotein, and is a member of serpin superfamily of the serine protease inhibitors consisting of at least 35 members. SerpinA3 has been demonstrated to inhibit the activity of certain serine proteases, such as cathepsin G found in neutrophils, and chymases present in mast cells, by inducing a major conformational rearrangement, and thus protects some tissues from damage caused by proteolytic enzymes. This enzyme is produced primarily in the liver, and is identified as an acute-phase inflammatory protein. SerpinA3 deficiency has been associated with liver disease, and mutations of this gene have been observed in patients with Parkinson disease and chronic obstructive pulmonary disease. Besides, ACT gene polymorphism has been implicated with Alzheimer’s disease (AD), cerebral amyloid angiopathy (CAA), as well as stroke, since SerpinA3 is a major constituent of the plaques in AD and an inhibitor of amyloid beta peptide degradation.
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TMPY-02043 | PARK7/DJ-1 Protein, Human, Recombinant (His) | Human | E. coli | ||
Parkinson's disease locus DJ-1 (PARK7) is a differentially expressed transcript. DJ-1 plays a physiologic role in protection of erythroid cells from oxidant damage, a function unmasked in the context of oxidative stress. PARK7 belongs to the peptidase C56 family of proteins. It acts as a positive regulator of androgen receptor-dependent transcription. It may also function as a redox-sensitive chaperone, as a sensor for oxidative stress, and it apparently protects neurons against oxidative stress and cell death. Mutations in the DJ-1 gene are associated with rare forms of autosomal recessive early-onset Parkinson's disease (PD). DJ-1/p53 interactions contribute to apoptosis resistance in clonal myeloid cells and may serve as a prognostic marker in patients with myelodysplastic syndromes (MDS). DJ-1 regulates redox signaling kinase pathways and acts as a transcriptional regulator of antioxidative gene batteries. Therefore, DJ-1 is an important redox-reactive signaling intermediate controlling oxidative stress after ischemia, upon neuroinflammation, and during age-related neurodegenerative processes. Augmenting DJ-1 activity might provide novel approaches to treating chronic neurodegenerative illnesses such as Parkinson's disease and acute damage such as stroke.
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TMPY-04467 | NME1 Protein, Human, Recombinant (His) | Human | E. coli | ||
NME1, also known as Nucleoside Diphosphate Kinase A (NDK-A), or NM23-H1, belongs to the NDK family. NM23-H1 is known to have a metastasis suppressive activity in many tumor cells. Recent studies have shown that the interacting proteins with NM23-H1 which mediate cell proliferation, may act as modulators of the metastasis suppressor activity. The interacting proteins with NM23-H1 can be classified into 3 groups. The first group of proteins can be classified as upstream kinases of NM23-H1 such as CKI and Aurora-A/STK15. The second group of proteins acts as downstream effectors for the regulation of specific gene transcriptions, GTP-binding protein functions, and signal transduction in the Erk signal cascade. The third group of proteins can be classified as bi-directionally influencing binding partners of NM23-H1. As a result, the interactions with NM23-H1 and binding partners have implications in the biochemical characterization involved in metastasis and tumorigenesis. NDKA is increased in human postmortem cerebrospinal fluid (CSF), a model of global brain insult, suggesting that measurement in CSF and, more importantly, in plasma may be useful as a biomarker of stroke. Additionally, NM23-H1 significantly reduces metastasis without effects on primary tumor size and was the first discovered metastasis suppressor gene.
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