目录号 | 产品详情 | 靶点 | |
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T26645 | NMDAR | ||
Aptiganel (CNS-1102) 是一种非竞争性 NMDA 拮抗剂,是一种多肽,可用于研究急性缺血性卒中。 | |||
T26389 | Glutathione Peroxidase | ||
4-POBN (Myeloperoxidase Inhibitor 1) 是一种有效且不可逆的髓过氧化物酶抑制剂 (IC50 = 0.3 µM)。 4-POBN 可用于亚急性中风的研究。 | |||
T14842 | Prostaglandin Receptor | ||
BW 245C 是一种选择性的前列腺素类DP受体(DP1)激动剂,是一种前列腺素类似物,对胶原蛋白的聚集反应有抑制作用,可用于研究中风等疾病。 | |||
T24873 | PI3K | ||
TGX-115是一种细胞渗透性和有效的PI 3-K 异构体p110β/p110δ抑制剂(对p110β IC50值为 0.13 μM, 对p110δ值为0.63 μM),是一种调节血小板粘附过程的酶,可抑制磷酸肌苷(PI)3-激酶,可用来治疗冠状动脉闭塞、中风、急性冠状动脉综合征、急性心肌梗塞、血管再狭窄、动脉硬化和不稳定心绞痛等心血管疾病 。 | |||
T27830L | Sodium Channel | ||
Lifarizine FA 是一种钠通道阻滞剂,可用于治疗神经系统疾病和心血管疾病,研究脑卒中。 | |||
T7355 | Others iGluR | ||
IC87201 是 PSD95-nNOS 相互作用的抑制剂,可抑制 nMDAR 诱导的一氧化氮和 cGMP 的形成,可用于缺血性中风和疼痛的研究。 | |||
T3527 | HSP | ||
TRC051384 是一种热休克蛋白70 (HSP70) 诱导剂,可减少中风相关的神经元损伤并增加短暂性缺血性中风大鼠模型的存活率,激活热休克因子-1 并导致分子伴侣和抗炎活性升高,增强神经元和神经胶质细胞中 Hsp72 的表达。 | |||
T39463 | Factor Xa | ||
Asundexian (BAY-2433334) 是一种高效且具有口服活性凝血因子 FXIa 抑制剂,可直接且可逆地与FXIa 的活性位点结合,从而抑制其活性。Asundexian 对缓冲液中的人 FXIa 的 IC50 为 1 nM。Asundexian 具有抗肿瘤活性,可用于研究急性缺血性卒中、短暂性脑缺血发作和缺血性卒中。 | |||
T3871 | Glucosidase | ||
Daucosterol (Sitogluside) 是天然的甾醇体类化合物。 | |||
T22798 | NMDAR iGluR | ||
Gavestinel (GV 150526) 是一种非竞争性的 NMDA 受体拮抗剂,具有有效性、选择性和口服活性。Gavestinel 可与 NMDA 受体的甘氨酸位点结合,其结合亲和力(pKi 值)为 8.5。Gavestinel 可用于急性缺血性脑卒中研究。 |
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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