目录号 | 产品详情 | 靶点 | |
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T2334 | PDE | ||
Avanafil (TA1790) 是一种高活性PDE-5抑制剂,IC50=5.2 nM,对PDE1,PDE6和PDE11活性较低。 | |||
T7206L | NOS NO Synthase | ||
2-Iminobiotin hydrobromide (Guanidinobiotin) 是生物素 (维生素 H 或 B7) 类似物。它是一种可逆的 NO 合酶抑制剂,可作用于小鼠 iNOS(Ki:21.8 μM)和大鼠 n-cNOS(Ki:37.5 μM)。它和低温环境均可以保护人类神经细胞,使其免受缺氧诱导的细胞损伤。 | |||
T1479 | Others NO Synthase | ||
Isosorbide dinitrate (Isordil) 是 NO 供体,可预防心肌梗死 (MI) 引起的左室重构及心功能退化。 | |||
T12808 | NO Synthase | ||
S-Nitroso-N-acetyl-DL-penicillamine (SNAP) 是一种稳定的血小板聚集抑制剂,是一氧化氮的供体。 | |||
TN1373 | TNF NOS COX | ||
α-Humulene (Alpha-caryophyllene) 是 Tanacetum vulgareL. 精油的主要成分,显示出抗炎作用,IC50=15±2 μg/mL。它抑制 iNOS 和COX-2表达。 | |||
T7030 | p38 MAPK NF-κB MEK COX NO Synthase | ||
Anemarsaponin B 是一种甾体皂苷,可降低iNOS 和COX-2的蛋白和 mRNA 水平,减少促炎细胞因子的表达和产生。它通过阻断 IκBα 的磷酸化来抑制NF-κB 的 p65 亚基的核转位,还抑制 MAP 激酶激酶 3/6 (MKK3/6) 和混合谱系激酶 3 的磷酸化。 | |||
T19916 | NOS | ||
TRIM (1-(2-Trifluoromethylphenyl)imidazole) 是一氧化氮合酶抑制剂。它在体外能够抑制小鼠小脑 nNOS (IC50:28.2 µM),以及大鼠肺 iNOS (IC50:27.0 µM)。它拥有抗焦虑以及抗抑郁的能力。 | |||
T3198L | Sigma receptor | ||
PRE-084 hydrochloride 是 σ1 的选择性激动剂在sigma 受体检测中,IC50值为44 nM。 | |||
T5681 | NF-κB COX PGE Synthase NO Synthase | ||
Ethyl Caffeate (ETHYL 3,4-DIHYDROXYCINNAMATE) 是从鬼针草分离的一种酚类天然产物,在体外或在小鼠皮肤中抑制NF-κB 活化及其下游炎症介质的诱导型一氧化氮合酶、环氧合酶 2 和前列腺素 E2。 | |||
T5684 | Apoptosis Others Reactive Oxygen Species HIF/HIF Prolyl-Hydroxylase NO Synthase Autophagy | ||
Ethyl 3,4-dihydroxybenzoate 是从花生种子的种皮中发现的脯氨酰羟化酶抑制剂,是一种抗氧化剂。它是胶原蛋白合成抑制剂,具有骨骼保护作用。它通过激活 NO 合酶并产生线粒体 ROS 来保护心肌,可诱导 ESCC 细胞自噬和凋亡。 |
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-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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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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