目录号 | 产品详情 | 靶点 | |
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T70073 | |||
Fabomotizole, also known as Afobazole, Obenoxazine and CM346, is an anxiolytic drug launched in Russia in the early 2000s. It produces anxiolytic and neuroprotective effects without any sedative or muscle relaxant actions. Its mechanism of action remains poorly defined however, with GABAergic, NGF- and BDNF-release-promoting, MT1 receptor agonism, MT3 receptor antagonism, and sigma agonism suggested as potential mechanisms. Fabomotizole was shown to inhibit MAO-A reversibly and there might be also some involvement with serotonin receptors. | |||
T21772 | |||
Reserpine hydrochloride 是一种从催吐萝芙木的根中发现的生物碱。它抑制去甲肾上腺素吸收到储存囊泡中,导致中枢和外周轴突末端的儿茶酚胺和血清素耗尽。它可作为抗高血压药和抗精神病药以及研究工具。 | |||
T61011 | |||
Izuforant (JW1601) (Compound 24) 具有有效的抗炎和止痒活性。 Izuforant 对人血清素3受体 (h5-HT3R) 具有结合亲和力,IC50值为 9.1 μM。它也是组胺 H4 受体 (H4R) 的口服活性拮抗剂,对人 H4R 的IC50值为 36 nM。 | |||
TMIH-0582 | |||
Trazodone-d8 hydrochloride 是 Trazodone hydrochloride 的氘代化合物。Trazodone hydrochloride 的 CAS 号为 25332-39-2。Trazodone hydrochloride 是5 羟色胺受体拮抗剂和重吸收抑制剂,用作抗抑郁药,可治疗失眠和焦虑。 | |||
TMIH-0001 | |||
(+/-)-Venlafaxine-d6 HCl 是 (+/-)-Venlafaxine HCl 的氘代化合物。(+/-)-Venlafaxine HCl 的 CAS 号为 99300-78-4。Venlafaxine hydrochloride 是一种口服有效的 5-羟色胺 (5-HT)/去甲肾上腺素 (NE) 重摄取的双重抑制剂,具有抗抑郁活性。 | |||
T73715 | |||
Risperidone-d4是 Risperidone 的氘代物。Risperidone 是5-HT2受体的阻断剂,P-糖蛋白(P-Glycoprotein)的抑制剂 和dopamine D2受体的拮抗剂,其对 5-HT2A 和 dopamine D2受体的Ki 值分别为 4.8,5.9 nM。 | |||
T69129 | |||
Clozapine HCl is a tricylic dibenzodiazepine, classified as an atypical antipsychotic agent. It binds several types of central nervous system receptors, and displays a unique pharmacological profile. Clozapine is a serotonin antagonist, with strong binding to 5-HT 2A/2C receptor subtype. It also displays strong affinity to several dopaminergic receptors, but shows only weak antagonism at the dopamine D2 receptor, a receptor commonly thought to modulate neuroleptic activity. Agranulocytosis is a major adverse effect associated with administration of this agent. | |||
T61846 | |||
CM398 is an orally active chemical compound that acts as a highly selective ligand for the sigma-2 receptor (K i =0.43 nM), demonstrating a significant ratio of selectivity between sigma-1 and sigma-2 receptors (1000-fold). Moreover, CM398 exhibits notable affinity towards dopamine (K i =32.90 nM) and serotonin transporters (K i =244.2 nM). In addition, CM398 has shown promising efficacy as an anti-inflammatory analgesic in a mouse model of inflammatory pain induced by formalin [1]. | |||
T38055 | |||
Salvinorin A propionate is a selective partial agonist at κ1-opioid receptors (KOR) with a Ki value of 32.6 nM. It inhibits adenylate cyclase (EC50 = 4.7 nM) in HEK293 cells transfected with human KOR. It is selective for KORs over μ, δ, and ORL-1 opioid receptors and has no effect at serotonin, dopamine, muscarinic, or adrenergic receptors. In mice, salvinorin A propionate (13 μg, i.c.v.) reduces nociceptive responses in a radiant heat tail-flick assay, though not as potently as salvinorin A . | |||
T71211 | |||
Rizatriptan-d6 is intended for use as an internal standard for the quantification of rizatriptan by GC- or LC-MS. Rizatriptan is an agonist of the serotonin receptor subtypes 5-HT1B and 5-HT1D. It is selective for 5-HT1B and 5-HT1D receptors over 5-HT1A receptors. Rizatriptan induces vasoconstriction in isolated human middle meningeal arteries. In vivo, rizatriptan reduces head grooming, the number of oculotemporal strokes, eye blinking, and one-eye closures in a Cacna1a mutant transgenic mouse model of migraine. Formulations containing rizatriptan have been used in the treatment of migraine. |
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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