目录号 | 产品详情 | 靶点 | |
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T40377 | Others | ||
Nicotredole (Tryptamide) 是一种口服有效的消炎剂,与 Phenylbutazone 的抗炎作用相当。它仅具有弱的致溃疡活性。它可用于缓解疼痛方面的研究。 | |||
TN1712 | NF-κB S6 Kinase | ||
Gossypin 是一种从Hibiscus vitifolius 中分离得到的黄酮,能够抑制NF-κB 和 NF-κB 的调节基因表达。在小鼠原代骨髓细胞和 RAW264.7 细胞中,它也可抑制 RANKL 诱导的破骨细胞形成。它具有抗氧化、抗炎、抗癌、抗衰老、抗糖尿病和保护肝脏的活性。 | |||
T0778 | COX | ||
Phenacetin (Acetophenetidin) 是一种非阿片类解热化合物,可用于缓解疼痛的研究。它是一种选择性的COX-3抑制剂,能作为人肝微粒体和大鼠体内 CYP1A2 的探针。 | |||
T0044 | HBV Sodium Channel | ||
Oxethazaine (Oxetacaine) 是一种具有耐酸性和口服活性试剂,是芬特明的酸性前体,有潜力缓解消化性溃疡疾病或食管炎引起的疼痛。 | |||
T1787 | Sodium Channel | ||
Levobupivacaine 是一种氨基酰胺类局麻药,属于n-alkylsubstituted pipecoloxylidide 家族。它是bupivacaine 的 S-对映异构体。 | |||
T4542 | Others | ||
Clonixin (Clonixic acid) 是一种非甾体抗炎药,具有口服活性。 | |||
T5460 | COX | ||
Mofezolac 是一种非甾体类抗炎药,可缓解疼痛并具有抗炎活性,抑制 COX-1和COX-2的IC50为 1.44 和 447 nM。 | |||
T1421 | COX | ||
Aceclofenac (Preservex) 是一种可口服的非甾体抗炎药,可用于缓解疼痛、骨关节炎、强直性脊柱炎、类风湿性关节炎的研究。 | |||
T22360 | TRP/TRPV Channel | ||
MDR-652是瞬时受体电位香草酸亚型 1 的选择性激动剂,对 hTRPV1 和 rTRPV1 的Ki 分别为 11.4 和 23.8 nM,EC50分别为 5.05 和 93 nM。MDR-652在缓解疼痛方面有研究的价值。 | |||
T10152 | COX Drug Metabolite | ||
4-Methylamino antipyrine 是 Metamizole 的活性代谢产物,可用于疼痛和发烧的研究。Metamizole 是吡唑啉酮类非甾体抗炎药,可抑制COX。 |
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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