目录号 | 产品详情 | 靶点 | |
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T19950 | |||
Paliperidone is a dopamine antagonist and 5-HT2A antagonist of the atypical antipsychotic class of medications. Paliperidone has an antagonist effect at α1 and α2 adrenergic receptors and at H1 histamine receptors. In addition, it binds with dopamine and | |||
T71537 | |||
Tofenacin hydrochloride is an antidepressant drug with a tricyclic-like structure. It acts as a serotonin-norepinephrine reuptake inhibitor, and based on its close relation to orphenadrine, may also possess anticholinergic and antihistamine properties. Tofenacin is also the major active metabolite of orphenadrine and likely plays a role in its beneficial effects against depressive symptoms seen in Parkinson's disease patients. | |||
T83888 | |||
(S)-5-羟基-6-甲氧基Duloxetine是(S)-duloxetine的一个活性代谢物,主要通过对血清素(5-HT)和去甲肾上腺素的再摄取进行抑制。它通过(S)-duloxetine经过一个5-或6-羟基Duloxetine中间体以及一个儿茶酚Duloxetine中间体形成,这些中间体由细胞色素P450 (CYP)同型酶CYP1A2和CYP2D6形成。(S)-5-羟基-6-甲氧基Duloxetine在脂质膜中抑制5-HT转运体(SERT)、去甲肾上腺素转运体(NET)和多巴胺转运体(DAT),其对人类转运体的抑制常数(Kis)分别为266、920和2,814 nM。 | |||
T61008 | |||
(±)-Duloxetine ((Rac)-Duloxetine) hydrochloride 是 Duloxetine hydrochloride 的外消旋物。Duloxetine hydrochloride 可用于研究糖尿病性神经性疼痛、纤维肌痛和重度抑郁症,它是 5-羟色胺去甲肾上腺素再摄取的抑制剂。 | |||
T73977 | |||
(S)-Dehydro Venlafaxine 是 Dehydro Venlafaxine 的非活性 S-对映异构体。Dehydro Venlafaxine 是 Venlafaxine 的杂质。Venlafaxine (Wy 45030) 是有效的 5-羟色胺 (5-HT) / 去甲肾上腺素 (NE) 再摄取双重抑制剂。 | |||
T65390 | |||
Fluvoxketone is trifluoromethyl-substituted aryl ketone compound useful as an intermediate in the synthesis of Fluvoxamine, which is a selective serotonin reuptake inhibitor. In the synthesis of Fluvoxamine, the ketone carbonyl of Fluvoxketone is elaborated to an oxime.In vitro,the inhibitory effect of fluvoxamine on actin polymerization was concentration dependent, and its IC50 was approximately 30 μM.In vivo,fluvoxamine treated EAE rats showed a decrease in IFN-γ serum levels and an increase in IL-4, pro- and anti-inflammatory cytokines respectively. | |||
T74668 | |||
Zicronapine (Lu 31-130) fumarate 是抗精神病药,主要通过拮抗多巴胺D1/D2受体和5-HT2A受体发挥作用,在动物模型中显示出显著的前认知效果,展现出治疗多种神经和精神疾病的可能性。 | |||
T78446 | |||
Phenosafranine是一种吩嗪染料,具有较高的三链RNA结合亲和力,相较于双链RNA。该染料通过嵌入机制与这两种RNA结合。Phenosafranine用途包括植物细胞染色,以及血红蛋白、多巴胺、血清素等的检测。 | |||
T37167 | |||
Reduced haloperidol is an active metabolite of haloperidol . It is formed via reduction of haloperidol by ketone reductase. Reduced haloperidol inhibits radioligand binding to sigma-1 and dopamine D2 receptors (Kis = 1.4 and 31 nM, respectively) and stimulates brain-derived neurotrophic factor (BDNF) secretion from CCF-SSTG1 and U87MG astrocytic glial cells. It also inhibits norepinephrine, dopamine, and serotonin (5-HT) reuptake (Kis = 21, 25, and 33 μM, respectively, in COS-7 cells expressing the human transporters). Reduced haloperidol (0.5 mg/kg) increases latency to paw withdrawal in mouse models of capsaicin- but not force-induced mechanical hypersensitivity. | |||
T71302 | |||
Norfluoxetine-d5 is intended for use as an internal standard for the quantification of norfluoxetine by GC- or LC-MS. Norfluoxetine is an active metabolite of the antidepressant fluoxetine. It is formed from fluoxetine by the cytochrome P450 (CYP) isoforms CYP2C9, CYP2C19, and CYP3A. Norfluoxetine inhibits serotonin (5-HT) uptake in rat brain synaptosomal membrane preparations (Ki = 44.7 nM) and isolated human platelets (IC50 = ~15 nM). It has been found in the tissues of fish exposed to wastewater effluent. |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPH-02099 | AANAT Protein, Human, Recombinant (GST & His) | Human | E. coli | ||
AANAT Protein, Human, Recombinant (GST & His) is expressed in E. coli.
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TMPY-01959 | Tryptophan Hydroxylase 1/TPH-1 Protein, Human, Recombinant (His) | Human | E. coli | ||
Tryptophan 5-hydroxylase 1, also known as Tryptophan 5-monooxygenase 1, Tryptophan hydroxylase 1, TPH1, TPH and TPRH, is an enzyme that belongs to the biopterin-dependent aromatic amino acid hydroxylase family. TPH1 contains one ACT domain. Tryptophan hydroxylase catalyzes the biopterin-dependent monooxygenation of tryptophan to 5-hydroxytryptophan (5HT), which is subsequently decarboxylated to form the neurotransmitter serotonin. It is the rate-limiting enzyme in the biosynthesis of serotonin. It is the rate-limiting enzyme in the biosynthesis of serotonin. TPH1 expression is limited to a few specialized tissues: raphe neurons, pinealocytes, mast cells, mononuclear leukocytes, beta-cells of the islets of Langerhans, and intestinal and pancreatic enterochromaffin cells. The tryptophan hydroxylase 1 (TPH1) gene is also reported to be associated with suicidal behavior. Polymorphisms of TPH1 may assist in identifying a subgroup of mood disorder patients that is at higher risk for suicidal behavior.
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TMPH-02958 | Tryptophan Hydroxylase 1 Protein, Mouse, Recombinant (His & SUMO) | Mouse | E. coli | ||
Oxidizes L-tryptophan to 5-hydroxy-l-tryptophan in the rate-determining step of serotonin biosynthesis. Tryptophan Hydroxylase 1 Protein, Mouse, Recombinant (His & SUMO) is expressed in E. coli expression system with N-6xHis-SUMO tag. The predicted molecular weight is 67.3 kDa and the accession number is P17532.
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TMPY-03452 | PTS Protein, Human, Recombinant (His) | Human | E. coli | ||
PTS(6-pyruvoyltetrahydropterin synthase) belongs to the PTPS family. It catalyzes the elimination of inorganic triphosphate from dihydroneopterin triphosphate, which is the second and irreversible step in the biosynthesis of tetrahydrobiopterin from GTP. Tetrahydrobiopterin, also known as BH(4), is an essential cofactor and regulator of various enzyme activities, including enzymes involved in serotonin biosynthesis and NO synthase activity. Mutations in this gene result in hyperphenylalaninemia. PTS is involved in the biosynthesis of tetrahydrobiopterin, an essential cofactor of aromatic amino acid hydroxylases. PTS also catalyzes the transformation of 7,8-dihydroneopterin triphosphate into 6-pyruvoyl tetrahydropterin. Defects in PTS are the cause of BH4-deficient hyperphenylalaninemia type A (HPABH4A), also called 6-pyruvoyl-tetrahydropterin synthase deficiency (PTS deficiency) or hyperphenylalaninemia tetrahydrobiopterin-deficient due to PTS deficiency. HPABH4A is an autosomal recessive disorder characterized by depletion of the neurotransmitters dopamine and serotonin, and clinically by severe neurological symptoms unresponsive to the classic phenylalanine-low diet.
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TMPH-00862 | HTR1F Protein, Human, Recombinant (His & SUMO) | Human | E. coli | ||
G-protein coupled receptor for 5-hydroxytryptamine (serotonin). Also functions as a receptor for various alkaloids and psychoactive substances. Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of down-stream effectors, such as adenylate cyclase. Signaling inhibits adenylate cyclase activity. HTR1F Protein, Human, Recombinant (His & SUMO) is expressed in E. coli expression system with N-10xHis-SUMO tag. The predicted molecular weight is 60.2 kDa and the accession number is P30939.
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TMPY-02948 | SULT1A3 Protein, Human, Recombinant (His) | Human | E. coli | ||
SULT1A3 belongs to the sulfotransferase 1 family. Sulfotransferase enzymes catalyze the sulfate conjugation of many hormones, neurotransmitters, drugs, and xenobiotic compounds. They are different in their tissue distributions and substrate specificities while their gene structure (number and length of exons) is similar. SULT1A3 gene encodes a phenol sulfotransferase with thermolabile enzyme activity. Four sulfotransferase genes are located on the p arm of chromosome 16; this gene and SULT1A4 arose from a segmental duplication. It is the most centromeric of the four sulfotransferase genes. Exons of this gene overlap with exons of a gene that encodes a protein containing GIY-YIG domains (GIYD1). SULT1A3 is expressed in liver, colon, kidney, lung, brain, spleen, small intestine, placenta and leukocyte. SULT1A3 is a sulfotransferase that utilizes 3'-phospho-5'-adenylyl sulfate (PAPS) as sulfonate donor to catalyze the sulfate conjugation of phenolic monoamines (neurotransmitters such as dopamine, norepinephrine and serotonin) and phenolic and catechol drugs.
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TMPH-01248 | ADAR Protein, Human, Recombinant (His & SUMO) | Human | E. coli | ||
Catalyzes the hydrolytic deamination of adenosine to inosine in double-stranded RNA (dsRNA) referred to as A-to-I RNA editing. This may affect gene expression and function in a number of ways that include mRNA translation by changing codons and hence the amino acid sequence of proteins; pre-mRNA splicing by altering splice site recognition sequences; RNA stability by changing sequences involved in nuclease recognition; genetic stability in the case of RNA virus genomes by changing sequences during viral RNA replication; and RNA structure-dependent activities such as microRNA production or targeting or protein-RNA interactions. Can edit both viral and cellular RNAs and can edit RNAs at multiple sites (hyper-editing) or at specific sites (site-specific editing). Its cellular RNA substrates include: bladder cancer-associated protein (BLCAP), neurotransmitter receptors for glutamate (GRIA2) and serotonin (HTR2C) and GABA receptor (GABRA3). Site-specific RNA editing of transcripts encoding these proteins results in amino acid substitutions which consequently alters their functional activities. Exhibits low-level editing at the GRIA2 Q/R site, but edits efficiently at the R/G site and HOTSPOT1. Its viral RNA substrates include: hepatitis C virus (HCV), vesicular stomatitis virus (VSV), measles virus (MV), hepatitis delta virus (HDV), and human immunodeficiency virus type 1 (HIV-1). Exhibits either a proviral (HDV, MV, VSV and HIV-1) or an antiviral effect (HCV) and this can be editing-dependent (HDV and HCV), editing-independent (VSV and MV) or both (HIV-1). Impairs HCV replication via RNA editing at multiple sites. Enhances the replication of MV, VSV and HIV-1 through an editing-independent mechanism via suppression of EIF2AK2/PKR activation and function. Stimulates both the release and infectivity of HIV-1 viral particles by an editing-dependent mechanism where it associates with viral RNAs and edits adenosines in the 5'UTR and the Rev and Tat coding sequence. Can enhance viral replication of HDV via A-to-I editing at a site designated as amber/W, thereby changing an UAG amber stop codon to an UIG tryptophan (W) codon that permits synthesis of the large delta antigen (L-HDAg) which has a key role in the assembly of viral particles. However, high levels of ADAR1 inhibit HDV replication.
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