所有图片(3)
About This Item
经验公式（希尔记法）:
C21H21N·HCl·1.5H2O
CAS号:
分子量:
350.88
EC號碼:
分類程式碼代碼:
12352200
PubChem物質ID:
NACRES:
NA.77
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化驗
≥98% (TLC)
形狀
solid
顏色
white to slightly yellow
溶解度
ethanol: soluble
methanol: soluble
起源
Merck & Co., Inc., Kenilworth, NJ, U.S.
SMILES 字串
Cl.CN1CCC(\CC1)=C2/c3ccccc3C=Cc4ccccc24
InChI
1S/2C21H21N.2ClH.3H2O/c2*1-22-14-12-18(13-15-22)21-19-8-4-2-6-16(19)10-11-17-7-3-5-9-20(17)21;;;;;/h2*2-11H,12-15H2,1H3;2*1H;3*1H2
InChI 密鑰
ZEAUHIZSRUAMQG-UHFFFAOYSA-N
基因資訊
human ... HRH1(3269) , HTR2A(3356) , HTR2B(3357) , HTR2C(3358)
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應用
盐酸赛庚啶倍半水合物已被用于：
降钙素基因相关肽（CGRP）的抑制
- 检测5-羟色胺受体（5-HT）诱导的炎症中的抗炎活性
- 螃蟹中体内和体外生物检测中5-HT的抑制
- 胚胎生理性实验中5-HT的抑制
降钙素基因相关肽（CGRP）的抑制
生化／生理作用
赛庚啶盐酸盐倍半水合物是一种血清素受体（5-HT2 / 5-HT1C）拮抗剂、H1组胺受体拮抗剂和止痒剂。赛庚啶对5-HT的抑制作用可改善精神分裂症的认知功能。赛庚啶对治疗功能性胃肠道疾病（FGID）有效。食品药品监督管理局（FDA）批准的赛庚啶具有抗抑郁和抗血小板功能。它可有效地治疗血栓栓塞性疾病。赛庚啶能够抑制赖氨酸甲基转移酶7/9（Set7/9），导致乳腺癌细胞中雌激素受体（ERα）的表达减少和生长停滞。
特點和優勢
该化合物是由Merck & Co., Inc., Kenilworth, NJ, U.S.开发的。想要浏览其他由制药公司开发的化合物以及已批准药物/候选药物清单， 请单击此处。
訊號詞
Danger
危險分類
Acute Tox. 3 Oral - Eye Irrit. 2 - Skin Irrit. 2 - STOT SE 3
標靶器官
Respiratory system
儲存類別代碼
6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects
水污染物質分類（WGK）
WGK 3
個人防護裝備
dust mask type N95 (US), Eyeshields, Faceshields, Gloves
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S Kimura et al.
Immunological investigations, 27(6), 379-393 (1998-12-09)
For the immunopharmacological characterization of murine passive anaphylactic shock, the effects of antihistaminics and/or anti-platelet-activating factor (anti-PAF) agents were studied on the shock mediated by allogeneic monoclonal IgE and IgG1 antibodies and hyperimmune serum. IgE antibody-mediated shock was strongly suppressed
The antidepressant 5-HT2A receptor antagonists pizotifen and cyproheptadine inhibit serotonin-enhanced platelet function
Lin OA, et al.
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Anti-inflammatory activity of bartogenic acid containing fraction of fruits of Barringtonia racemosa Roxb. in acute and chronic animal models of inflammation
Patil KR and Patil CR
Journal of traditional and complementary medicine, 7(1), 86-93 (2017)
E O Okoro
The Journal of pharmacy and pharmacology, 51(8), 953-957 (1999-09-30)
We have previously shown that elimination of buffer Ca2+ markedly reduced maximum 5-HT-induced contractions. We have now investigated the effect of L-type Ca2+-channel blockers and 5-HT2 receptor antagonists on 5-HT- and K+-induced contractions in rat aorta to explore the possibility
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