目录号 | 产品详情 | 靶点 | |
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TP2083L | Others | ||
Ac9-25 acetate 通过 FPR 激活中性粒细胞还原的烟酰胺腺嘌呤二核苷酸磷酸氧化酶。 | |||
T80799 | MAO | ||
WAY-620147 为N-(2-morpholinoethyl)nicotinamide的衍生物,能够抑制单胺氧化酶(Monoamine Oxidase)。WAY-620147 对MAO-A及MAO-B的IC50值分别为26 μM和55 μM,可用于研究神经系统疾病。 | |||
T1880 | Others | ||
P7C3 是一种 aminopropyl carbazole 类化合物,具有口服活性,可透过血脑屏障,具有神经保护作用。它可用于神经退行性疾病,如帕金森病的研究。 | |||
T1365 | Antibiotic | ||
Thioisonicotinamide (Isothionicotinamide) 是一种可用于药物合成的合成中间体。 | |||
T33565 | |||
NAAD sodium salt (NAAD Na salt) 是烟酰胺腺嘌呤二核苷酸合酶的底物,可用于研究底物的特异性和动力学。 | |||
T22446 | Others | ||
NADP disodium salt (Disodium NADP) 是一种氧化还原辅助因子,是一种烟酰胺腺嘌呤二核苷酸。它是代谢中电子转移的关键辅因子,可以被交替氧化 (NADP+) 和还原 (NADPH)。 | |||
T11143 | PARP | ||
EB-47 是一种有效的 PARP-1/ARTD-1 选择性抑制剂,IC50 值为 45 nM,对 ARTD5 的IC50 值为 410 nM,表现出温和的药效。EB-47 模拟底物 NAD+,从烟酰胺延伸至腺苷亚区结合。 | |||
T8760 | Others | ||
NNMTi (5-Amino-1-methylquinolinium) 是烟酰胺 N -甲基转移酶的抑制剂 (IC50=1.2 μM),可选择性地结合 NNMT 底物结合位点残基。它能诱导体外成肌细胞分化,提高老年小鼠肌肉干细胞融合和再生能力。 | |||
T66582 | Endogenous Metabolite | ||
6-Methylnicotinamide 是烟酰胺的衍生物,是一种内源性代谢物。在脑出血 (ICH) 急性期, 6-Methylnicotinamide 突然增加会加剧神经损伤。6-Methylnicotinamide 可用于制作共晶体/盐。 | |||
T8106 | Others | ||
JBSNF-000088 是一种烟酰胺的类似物,是一种 NNMT(烟酰胺 N-甲基转移酶) 抑制剂,可作用于人 NNMT (IC50:1.8 µm)、猴 NNMT(IC50:2.8 µm) 和小鼠 NNMT (IC50:5.0 µm)。在代谢性疾病的动物模型中,它能够抑制 NNMT 活性,降低 MNA 水平并驱动胰岛素增敏,调节葡萄糖和减轻体重。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-02577 | NAMPT Protein, Human, Recombinant (His & GST) | Human | Baculovirus-Insect Cells | ||
Nicotinamide phosphoribosyltransferase (NAMPT), also known as pre-B-cell colony-enhancing factor 1 (PBEF1) or visfatin, is an enzyme belonging to the family of glycosyltransferases, to be specific, the pentosyltransferases. This enzyme participates in nicotinate and nicotinamide metabolism. This enzyme catalyzes the condensation of nicotinamide with 5- phosphoribosyl-1- pyrophosphate to yield nicotinamide mononucleotide, one step in the biosynthesis of nicotinamide adenine dinucleotide. NAMPT is also considered as an essential enzyme mediating granulocyte colony-stimulating factor (G-CSF)-triggered granulopoiesis in healthy individuals and individuals with severe congenital neutropenia. Intracellular NAMPT and NAD+amounts in myeloid cells, as well as plasma NAMPT and NAD+levels, were increased by G-CSF treatment of both healthy volunteers and individuals with congenital neutropenia.
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TMPY-03406 | NMNAT1 Protein, Human, Recombinant (His) | Human | Baculovirus-Insect Cells | ||
NMNAT, also known as NMNAT1, is a member of the Nicotinamide-nucleotide adenylyltransferases. It is widely expressed with high levels in skeletal muscle, heart, liver, and kidney. NMNAT appears to have the ability to protect against axonal degeneration following mechanical or toxic insults. The coenzyme NAD and its derivatives are involved in hundreds of metabolic redox reactions and are utilized in protein ADP-ribosylation, histone deacetylation, and in some Ca(2+) signaling pathways. NMNAT enzyme is vital for NAD biosynthesis, catalyzing the condensation of nicotinamide mononucleotide (NMN) or nicotinic acid mononucleotide (NaMN) with the AMP moiety of ATP to form NAD or NaAD.
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TMPJ-00968 | NAMPT Protein, Human, Recombinant (His) | Human | E. coli | ||
Pre-B cell colony enhancing factor (PBEF) was originally identified as a cytokine that potentiated the clonal expansion and differentiation of pre-B cells, but it is also acknowledged to be the ubiquitous intracellular enzyme nicotinamide phosphoribosyltranferase (NAMPT) and the adipokine “visfatin”. PBEF is constitutively expressed in the fetal membranes where its greatest expression is in the amnion. It has intracellular and extracellular forms. Most of the intracellular functions of PBEF are due to its role as a Nampt which can induce angiogenesis through upregulation of VEGF and VEGFR and secretion of MCP-1. Extracellular PBEF has been shown to increase inflammatory cytokines, such as TNF-α, IL-1β, IL-16, and TGF-β1. PBEF also increases the production of IL-6, TNF-α, and IL-1β in CD14+ monocyctes, macrophages, and dendritic cells, enhances the effectiveness of T cells.
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TMPH-02811 | NRK1 Protein, Mouse, Recombinant (His) | Mouse | E. coli | ||
Catalyzes the phosphorylation of nicotinamide riboside (NR) and nicotinic acid riboside (NaR) to form nicotinamide mononucleotide (NMN) and nicotinic acid mononucleotide (NaMN).
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TMPH-03450 | Nicotinamidase/PNC1 Protein, S. cerevisiae, Recombinant | Saccharomyces cerevisiae | E. coli | ||
Catalyzes the deamidation of nicotinamide, an early step in the NAD(+) salvage pathway. Positively regulates SIR2-mediated silencing and longevity by preventing the accumulation of intracellular nicotinamide, an inhibitor of SIR2, during times of stress. Acts also on nicotinyl hydroxamate.
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TMPH-03449 | Nicotinamidase/PNC1 Protein, S. cerevisiae, Recombinant (His) | Saccharomyces cerevisiae | E. coli | ||
Catalyzes the deamidation of nicotinamide, an early step in the NAD(+) salvage pathway. Positively regulates SIR2-mediated silencing and longevity by preventing the accumulation of intracellular nicotinamide, an inhibitor of SIR2, during times of stress. Acts also on nicotinyl hydroxamate.
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TMPH-00673 | NADH pyrophosphatase Protein, E. coli O157:H7, Recombinant (His) | E. coli | E. coli | ||
mRNA decapping enzyme that specifically removes the nicotinamide adenine dinucleotide (NAD) cap from a subset of mRNAs by hydrolyzing the diphosphate linkage to produce nicotinamide mononucleotide (NMN) and 5' monophosphate mRNA. The NAD-cap is present at the 5'-end of some mRNAs and stabilizes RNA against 5'-processing. Has preference for mRNAs with a 5'-end purine. Catalyzes the hydrolysis of a broad range of dinucleotide pyrophosphates.
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TMPH-03761 | NAMPT Protein, Mouse, Recombinant (HA & His) | Mouse | E. coli | ||
The secreted form behaves both as a cytokine with immunomodulating properties and an adipokine with anti-diabetic properties, it has no enzymatic activity, partly because of lack of activation by ATP, which has a low level in extracellular space and plasma. Catalyzes the condensation of nicotinamide with 5-phosphoribosyl-1-pyrophosphate to yield nicotinamide mononucleotide, an intermediate in the biosynthesis of NAD. It is the rate limiting component in the mammalian NAD biosynthesis pathway. Plays a role in the modulation of circadian clock function. NAMPT-dependent oscillatory production of NAD regulates oscillation of clock target gene expression by releasing the core clock component: CLOCK-ARNTL/BMAL1 heterodimer from NAD-dependent SIRT1-mediated suppression.
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TMPH-03760 | NAMPT Protein, Mouse, Recombinant | Mouse | E. coli | ||
The secreted form behaves both as a cytokine with immunomodulating properties and an adipokine with anti-diabetic properties, it has no enzymatic activity, partly because of lack of activation by ATP, which has a low level in extracellular space and plasma. Catalyzes the condensation of nicotinamide with 5-phosphoribosyl-1-pyrophosphate to yield nicotinamide mononucleotide, an intermediate in the biosynthesis of NAD. It is the rate limiting component in the mammalian NAD biosynthesis pathway. Plays a role in the modulation of circadian clock function. NAMPT-dependent oscillatory production of NAD regulates oscillation of clock target gene expression by releasing the core clock component: CLOCK-ARNTL/BMAL1 heterodimer from NAD-dependent SIRT1-mediated suppression.
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TMPH-02810 | NAMPT Protein, Mouse, Recombinant (His) | Mouse | Yeast | ||
The secreted form behaves both as a cytokine with immunomodulating properties and an adipokine with anti-diabetic properties, it has no enzymatic activity, partly because of lack of activation by ATP, which has a low level in extracellular space and plasma. Catalyzes the condensation of nicotinamide with 5-phosphoribosyl-1-pyrophosphate to yield nicotinamide mononucleotide, an intermediate in the biosynthesis of NAD. It is the rate limiting component in the mammalian NAD biosynthesis pathway. Plays a role in the modulation of circadian clock function. NAMPT-dependent oscillatory production of NAD regulates oscillation of clock target gene expression by releasing the core clock component: CLOCK-ARNTL/BMAL1 heterodimer from NAD-dependent SIRT1-mediated suppression.
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TMPY-02519 | BLVRB Protein, Human, Recombinant (His) | Human | E. coli | ||
Biliverdin reductase (hBVR) is a serine/threonine kinase that catalyzes reduction of the heme oxygenase (HO) activity product, biliverdin, to bilirubin. BVR consists of an N-terminal dinucleotide-binding domain (Rossmann-fold) and a C-terminal domain that contains a six-stranded β-sheet that is flanked on one face by several α-helices. The C-terminal and N-terminal domains interact extensively, forming the active site cleft at their interface. Biliverdin reductase (BVR) catalyzes the last step in heme degradation by reducing the γ-methene bridge of the open tetrapyrrole, biliverdin IXα, to bilirubin with the concomitant oxidation of a β-nicotinamide adenine dinucleotide (NADH) or β-nicotinamide adenine dinucleotide phosphate (NADPH) cofactor. It is now recognized that human BVR (hBVR) is a dual-specificity kinase (Ser / Thr and Tyr) upstream activator of the insulin/insulin growth factor-1 (IGF-1) and mitogen-activated protein kinase (MAPK) signaling pathways. Human BVR (hBVR) is essential for MAPK-extracellular signal-regulated kinase (ERK)1/2 (MEK)-eukaryotic-like protein kinase (Elk) signaling and has been identified as the cytoplasm-nuclear heme transporter of ERK1/2 and hematin, the key components of stress-responsive gene expression.
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TMPJ-00462 | NADK Protein, Human, Recombinant (His) | Human | E. coli | ||
NAD Kinase (NADK) is an enzyme that belongs to the NAD Kinase family. It is a widely expressed enzyme, but it is not detected in skeletal muscle. NADK converts Nicotinamide Adenine Dinucleotide (NAD+) into NADP+, through phosphorylating the NAD+ coenzyme. NADP+ is an essential coenzyme in metabolism and provides reducing power to biosynthetic processes such as fatty acid biosynthesis. The structure of the NADK from the archaean Archaeoglobus fulgidus has been determined.
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TMPH-00207 | PTX S1 Protein, Bordetella pertussis, Recombinant (His) | Bordetella pertussis | Yeast | ||
S1 is an NAD-dependent ADP-ribosyltransferase, which plays a crucial role in the pathogenesis of B.pertussis causing disruption of normal host cellular regulation. It catalyzes the ADP-ribosylation of a cysteine in the alpha subunit of host heterotrimeric G proteins. In the absence of G proteins it also catalyzes the cleavage of NAD(+) into ADP-ribose and nicotinamide. It irreversibly uncouples the G-alpha GTP-binding proteins from their membrane receptors.
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TMPJ-00848 | NCF1 Protein, Human, Recombinant (His) | Human | E. coli | ||
Neutrophil cytosol factor 1( NCF1) is a 47 kDa cytosolic subunit of neutrophil NADPH oxidase. This oxidase is characterized as a multicomponent enzyme which is activated to produce superoxide anion. NCF2, NCF1, and a membrane bound cytochrome b558 are required for the activation of the latent NADPH oxidase. The human NCF1 gene encodes a 390 amino acids protein without a signal peptide. The NCF1 gene interacts with other subunits of nicotinamide adenine dinucleotide phosphate-oxidase (NADPH) and plays an important role in innate immunity, producing reactive oxygen species and reducing the severity and duration of parasitic infection and autoimmune disease. NCF1 also has a role in T cell activation.
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TMPJ-00473 | QPRTase Protein, Human, Recombinant (His) | Human | E. coli | ||
Nicotinate-Nucleotide Pyrophosphorylase (QPRT) belongs to the nadC/modD family. QPRT plays an improtant role in catabolism of quinolinate which acts as a potent endogenous exitotoxin to neurons. In addition, QPRT serves as an an intermediate in the Tryptophan-Nicotinamide Adenine Dinucleotide pathway. QPRT participates in some pathways including Cofactor biosynthesis, NAD(+) biosynthesis and the Nicotinate D-Ribonucleotide from Quinolinate. In addition, QPRT is involved in the catabolism of Quinolinic Acid (QA). The activity toward QA is slightly repressed by phosphoribosylpyrophosphate (PRPP) in both a competitive and a non-competitive manner.
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TMPJ-00836 | G6PD Protein, Human, Recombinant (His) | Human | Human Cells | ||
Glucose-6-Phosphate 1-Dehydrogenase (G6PD) is a cytosolic enzyme that belongs to the glucose-6-phosphate dehydrogenase family. G6PD participates in the pentose phosphate pathway that supplies reducing energy to cells by maintaining the level of the co-enzyme nicotinamide adenine dinucleotide phosphate (NADPH). G6PD produces pentose sugars for nucleic acid synthesis and main producer of NADPH reducing power. NADPH in turn maintains the level of glutathione in these cells that helps protect the red blood cells against oxidative damage. It is notable in humans that G6PD is remarkable for its genetic diversity. G6PD deficiency may cause neonatal jaundice, acute hemolysis, or severe chronic non-spherocytic hemolytic anemia.
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TMPH-01740 | SARM1 Protein, Human, Recombinant (His & Myc) | Human | Baculovirus | ||
NAD(+) hydrolase, which plays a key role in axonal degeneration following injury by regulating NAD(+) metabolism. Acts as a negative regulator of MYD88- and TRIF-dependent toll-like receptor signaling pathway by promoting Wallerian degeneration, an injury-induced form of programmed subcellular death which involves degeneration of an axon distal to the injury site. Wallerian degeneration is triggered by NAD(+) depletion: in response to injury, SARM1 is activated and catalyzes cleavage of NAD(+) into ADP-D-ribose (ADPR), cyclic ADPR (cADPR) and nicotinamide; NAD(+) cleavage promoting cytoskeletal degradation and axon destruction. Also able to hydrolyze NADP(+), but not other NAD(+)-related molecules. Can activate neuronal cell death in response to stress. Regulates dendritic arborization through the MAPK4-JNK pathway. Involved in innate immune response: inhibits both TICAM1/TRIF- and MYD88-dependent activation of JUN/AP-1, TRIF-dependent activation of NF-kappa-B and IRF3, and the phosphorylation of MAPK14/p38.
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TMPH-01741 | SARM1 Protein, Human, Recombinant (His & KSI) | Human | E. coli | ||
NAD(+) hydrolase, which plays a key role in axonal degeneration following injury by regulating NAD(+) metabolism. Acts as a negative regulator of MYD88- and TRIF-dependent toll-like receptor signaling pathway by promoting Wallerian degeneration, an injury-induced form of programmed subcellular death which involves degeneration of an axon distal to the injury site. Wallerian degeneration is triggered by NAD(+) depletion: in response to injury, SARM1 is activated and catalyzes cleavage of NAD(+) into ADP-D-ribose (ADPR), cyclic ADPR (cADPR) and nicotinamide; NAD(+) cleavage promoting cytoskeletal degradation and axon destruction. Also able to hydrolyze NADP(+), but not other NAD(+)-related molecules. Can activate neuronal cell death in response to stress. Regulates dendritic arborization through the MAPK4-JNK pathway. Involved in innate immune response: inhibits both TICAM1/TRIF- and MYD88-dependent activation of JUN/AP-1, TRIF-dependent activation of NF-kappa-B and IRF3, and the phosphorylation of MAPK14/p38.
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TMPH-03008 | ENR Protein, Mycobacterium tuberculosis, Recombinant (His) | Mycobacterium tuberculosis | E. coli | ||
Enoyl-ACP reductase of the type II fatty acid syntase (FAS-II) system, which is involved in the biosynthesis of mycolic acids, a major component of mycobacterial cell walls. Catalyzes the NADH-dependent reduction of the double bond of 2-trans-enoyl-[acyl-carrier protein], an essential step in the fatty acid elongation cycle of the FAS-II pathway. Shows preference for long-chain fatty acyl thioester substrates (>C16), and can also use 2-trans-enoyl-CoAs as alternative substrates. The mycobacterial FAS-II system utilizes the products of the FAS-I system as primers to extend fatty acyl chain lengths up to C56, forming the meromycolate chain that serves as the precursor for final mycolic acids.; Is the primary target of the first-line antitubercular drug isoniazid (INH) and of the second-line drug ethionamide (ETH). Overexpressed inhA confers INH and ETH resistance to M.tuberculosis. The mechanism of isoniazid action against InhA is covalent attachment of the activated form of the drug to the nicotinamide ring of NAD and binding of the INH-NAD adduct to the active site of InhA. Similarly, the ETH-NAD adduct binds InhA.
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