目录号 | 产品详情 | 靶点 | |
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T21700 | NOS | ||
NOS-IN-1 (2-Imino-4-methylpiperidine acetate) 是有效的、具有口服活性的一氧化氮合酶 (NOS) 的抑制剂。NOS-IN-1抑制人 iNOS (hiNOS),hnNOS 和 heNOS 的 IC50 分别为 0.1 μM,0.2 μM 和1.1 μM。 | |||
T37696 | NOS | ||
NOS1-IN-1(nNOS Inhibitor I) 是一种强效、选择性和细胞渗透性 nNOS 抑制剂(Ki:120 nM)。NOS1-IN-1 对 eNOS 的 Ki 值为 39 μM,对 iNOS 的 Ki 值为 325 μM。 | |||
T14286 | Others | ||
ANB-NOS is a alkyl/ether-based linker for PROTACs which joins two essential ligands, crucial for forming PROTAC molecules. This linker enables selective protein degradation by leveraging the ubiquitin-proteasome system within cells. | |||
TQ0301 | NO Synthase | ||
Kuwanon A 抑制一氧化氮的产生 (IC50: 10.5 μM)。Kuwanon A 是从桑树 (Morus alba L.) 中分离出来的黄酮衍生物。 | |||
T6S1665 | Others NO Synthase | ||
Irisflorentin 是天然存在的异黄酮,是大量存在于 Rhizoma Belamcandae 中的活性成分。它明显抑制了诱导型一氧化氮合酶的转录和翻译以及 NO 产生。 | |||
T6S2023 | Others COX NO Synthase | ||
Harpagoside 是从爪钩草中分离出来的一种天然产物,可抑制COX-1和COX-2活性,并抑制 NO 的产生。 | |||
T7474 | NOS | ||
7-Nitroindazole 是一种具有抗损伤及心血管作用的选择性nNOS 抑制剂,也是评价一氧化氮在中枢神经系统中生物学效应的有效工具。 | |||
T7682 | Endogenous Metabolite NO Synthase NOD | ||
Asymmetric dimethylarginine 是内源性一氧化氮合成酶抑制剂,可以作为内皮功能障碍的标志。 | |||
T2S0765 | NO Synthase Prostaglandin Receptor | ||
Epibetulinic acid 对细菌内毒素刺激的小鼠巨噬细胞 (RAW 264.7) 中 NO 和前列腺素 E(2) 的产生具有有效的抑制作用,IC50分别为 0.7 和 0.6 μM,具有抗炎活性。 | |||
T3847 | Others NO Synthase | ||
Asperuloside (Asperulosid) 是一种来源于蛇舌草的环烯醚萜,具有抗炎作用。它可抑制诱导型一氧化氮合酶,抑制 NF-κB 和 MAPK 信号通路。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPH-01733 | DDAH2 Protein, Human, Recombinant (GST & His) | Human | E. coli | ||
Hydrolyzes N(G),N(G)-dimethyl-L-arginine (ADMA) and N(G)-monomethyl-L-arginine (MMA) which act as inhibitors of NOS. Has therefore a role in the regulation of nitric oxide generation.
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TMPH-01732 | DDAH1 Protein, Human, Recombinant (His & Myc) | Human | E. coli | ||
Hydrolyzes N(G),N(G)-dimethyl-L-arginine (ADMA) and N(G)-monomethyl-L-arginine (MMA) which act as inhibitors of NOS. Has therefore a role in the regulation of nitric oxide generation.
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TMPY-03172 | Argininosuccinate lyase Protein, Human, Recombinant (His & GST) | Human | Baculovirus-Insect Cells | ||
The recycling of citrulline by argininosuccinate synthase 1 (ASS1) and argininosuccinate lyase (ASL) is crucial to maintain arginine availability and nitric oxide (NO) production. Nitric oxide (NO) plays an established role in numerous physiological and pathological processes, but the specific cellular sources of NO in disease pathogenesis remain unclear, preventing the implementation of NO-related therapy. Argininosuccinate lyase (ASL) is the only enzyme able to produce arginine, the substrate for NO generation by nitric oxide synthase (NOS) isoforms. Induction of endogenous NO production by enterocytes with supplements that upregulate ASL expression and complement its substrates results in improved epithelial integrity and alleviation of colitis and of inflammation-associated colon cancer.
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TMPH-02526 | Arginase-2/ARG2 Protein, Mouse, Recombinant (His & SUMO) | Mouse | E. coli | ||
May play a role in the regulation of extra-urea cycle arginine metabolism and also in down-regulation of nitric oxide synthesis. Extrahepatic arginase functions to regulate L-arginine bioavailability to nitric oxid synthase (NOS). Arginine metabolism is a critical regulator of innate and adaptive immune responses. Seems to be involved in negative regulation of the survival capacity of activated CD4(+) and CD8(+) T cells. May suppress inflammation-related signaling in asthmatic airway epithelium. May contribute to the immune evasion of H.pylori by restricting M1 macrophage activation and polyamine metabolism. May play a role in promoting prenatal immune suppression. Regulates RPS6KB1 signaling, which promotes endothelial cell senescence and inflammation and implicates NOS3/eNOS dysfunction. Can inhibit endothelial autophagy independently of its enzymatic activity implicating mTORC2 signaling. Involved in vascular smooth muscle cell senescence and apoptosis independently of its enzymatic activity.
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TMPH-02524 | Arginase-1/ARG1 Protein, Mouse, Recombinant (His) | Mouse | Yeast | ||
Key element of the urea cycle converting L-arginine to urea and L-ornithine, which is further metabolized into metabolites proline and polyamides that drive collagen synthesis and bioenergetic pathways critical for cell proliferation, respectively; the urea cycle takes place primarily in the liver and, to a lesser extent, in the kidneys.; Functions in L-arginine homeostasis in nonhepatic tissues characterized by the competition between nitric oxide synthase (NOS) and arginase for the available intracellular substrate arginine. Arginine metabolism is a critical regulator of innate and adaptive immune responses. Involved in an antimicrobial effector pathway in polymorphonuclear granulocytes (PMN). Upon PMN cell death is liberated from the phagolysosome and depletes arginine in the microenvironment leading to suppressed T cell and natural killer (NK) cell proliferation and cytokine secretion. In group 2 innate lymphoid cells (ILC2s) promotes acute type 2 inflammation in the lung and is involved in optimal ILC2 proliferation but not survival. Plays a role in the immune response of alternatively activated or M2 macrophages in processes such as wound healing and tissue regeneration, immune defense against multicellular pathogens and parasites, and immune suppression and allergic inflammation; the regulatory outcome seems to be organ specific. In tumor-infiltrating dendritic cells (DCs) and myeloid-derived suppressor cells (MDSCs) plays a role in suppression of T cell-mediated antitumor immunity.
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TMPH-02525 | Arginase-1/ARG1 Protein, Mouse, Recombinant (His & SUMO) | Mouse | E. coli | ||
Key element of the urea cycle converting L-arginine to urea and L-ornithine, which is further metabolized into metabolites proline and polyamides that drive collagen synthesis and bioenergetic pathways critical for cell proliferation, respectively; the urea cycle takes place primarily in the liver and, to a lesser extent, in the kidneys.; Functions in L-arginine homeostasis in nonhepatic tissues characterized by the competition between nitric oxide synthase (NOS) and arginase for the available intracellular substrate arginine. Arginine metabolism is a critical regulator of innate and adaptive immune responses. Involved in an antimicrobial effector pathway in polymorphonuclear granulocytes (PMN). Upon PMN cell death is liberated from the phagolysosome and depletes arginine in the microenvironment leading to suppressed T cell and natural killer (NK) cell proliferation and cytokine secretion. In group 2 innate lymphoid cells (ILC2s) promotes acute type 2 inflammation in the lung and is involved in optimal ILC2 proliferation but not survival. Plays a role in the immune response of alternatively activated or M2 macrophages in processes such as wound healing and tissue regeneration, immune defense against multicellular pathogens and parasites, and immune suppression and allergic inflammation; the regulatory outcome seems to be organ specific. In tumor-infiltrating dendritic cells (DCs) and myeloid-derived suppressor cells (MDSCs) plays a role in suppression of T cell-mediated antitumor immunity.
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