目录号 | 产品详情 | 靶点 | |
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T2S2109 | Others | ||
Skimmianine (Chloroxylonine) 是一种呋喹啉类生物碱,主要存在于芸香科,具有抗炎、抗痉挛和抗血小板聚集活性。它对多种癌细胞系具有细胞毒性和基因毒性。 | |||
T4503 | Chloride channel COX N-Acetylglucosaminyltransferase Anion Exchanger | ||
Talniflumate (Somalgen) 是一种钙激活氯离子通道 (hCLCA1/mCLCA3) 阻滞剂,可减少动物模型和细胞培养中的粘蛋白合成和释放。它通过抑制环氧合酶,并抑制 Cl-/HCO3- 交换活性,具有抗炎作用。它还增加了远端肠梗阻综合征囊性纤维化小鼠模型的存活率。 | |||
T4561 | Others COX | ||
Tiaprofenic acid (Acido tiaprofenico) 是可口服的非甾体抗炎药,通过抑制环氧化酶抑制前列腺素合成,可用于风湿性疾病的研究。 | |||
T1039 | AChR | ||
Choline chloride (Biocoline) 是一种必需营养素,可激活 α7 烟碱受体,具有抗炎、镇痛的活性。对动脉粥样硬化、神经系统疾病和肝脏疾病等具有影响。 | |||
T11147 | Epoxide Hydrolase | ||
EC5026 (BPN-19186) 是首创的,非阿片类的,可溶性环氧水解酶 (sEH) 抑制剂,它可有效缓解发炎性和神经性疼痛。 | |||
T6737 | COX | ||
Zaltoprofen (Soleton) 是一种非甾体类抗炎剂,具有强大的抗炎作用和对炎性疼痛的止痛作用。它是可口服的COX-2抑制剂,对COX-1和COX-2的IC50值分别为 1.3 和 0.34 μM。 | |||
T30937 | COX | ||
Cimicoxib (UR8880) 是一种有效的、选择性的 COX-2 抑制剂,具有抗炎和镇痛活性。 | |||
T27635 | Others | ||
Isoxepac (Olopatadine USP Related Compound C) 是非甾体抗炎剂,显示出抗炎、镇痛和解热活性,已在多种动物模型中进行了相关研究。 | |||
T6464 | Adrenergic Receptor | ||
Detomidine hydrochloride (MPV-253 AII) 是咪唑衍生物,是有效的 α2-肾上腺素能 (α2-adrenergic) 激动剂,可用于促进安定、缓解疼痛的研究。 | |||
T7416 | TRP/TRPV Channel | ||
WS-12 是有效的TRPM8激动剂,EC50为 39 nM。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPH-00055 | Alpha-toxin Amm8 Protein, Androctonus mauritanicus, Recombinant (His & Myc) | Androctonus mauritanicus | Baculovirus | ||
Alpha toxins bind voltage-independently at site-3 of sodium channels (Nav) and inhibit the inactivation of the activated channels, thereby blocking neuronal transmission. The toxin principally slows the inactivation process of TTX-sensitive sodium channels. It discriminates neuronal versus muscular sodium channel, as it is more potent on rat brain Nav1.2/SCN2A (EC(50)=29 nM) than on rat skeletal muscle Nav1.4/SCN4A (EC(50)=416 nM). It also shows a weak activity on Nav1.7/SCN9A (EC(50)=1.76 uM). In vivo, the toxin produces pain hypersensibility to mechanical and thermal stimuli.(PubMed:23685008). It also exhibits potent analgesic activity (when injected intraperitoneally), increasing hot plate and tail flick withdrawal latencies in a dose-dependent fashion. This paradoxical analgesic action, is significantly suppressed by opioid receptor antagonists, suggesting a pain-induced analgesia mechanism that involves an endogenous opioid system. This led to hypothesis that pain relief induced by peripheral administration of Amm VIII may result from sensitization of primary afferent neurons and subsequent activation of an opioid-dependent noxious inhibitory control.
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