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更新于：2025-07-05
Trifluoperazine Hydrochloride
盐酸三氟拉嗪
更新于：2025-07-05
概要
基本信息
原研机构 |
在研机构 |
权益机构- |
最高研发阶段批准上市 |
首次获批日期 美国 (1959-04-16), |
最高研发阶段(中国)批准上市 |
特殊审评- |
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结构/序列
分子式C21H26Cl2F3N3S |
InChIKeyBXDAOUXDMHXPDI-UHFFFAOYSA-N |
CAS号440-17-5 |
关联
7
项与 盐酸三氟拉嗪 相关的临床试验IRCT20200329046892N1
Evaluation of Trifluoperazine Effectiveness in Treatment Process, Survival rate and Cure rate of COVID-19 Patients
IRCT20200408046992N1
Evaluation of the Effect of Trifluoperazin in Treatment of Patients with Confirmed 2019 Novel Coronavirus(COVID- 19): An Open-Label Randomized Clinical Trial
CTRI/2020/03/023823
Prescriber Based, Active Post Marketing Surveillance Study (PMS) to Generate the Safety & Efficacy Data of Chlordiazepoxide and Trifluoperazine In the Treatment of Chronic Anxiety & Insomnia in Actual Field Conditions of Use
100 项与 盐酸三氟拉嗪 相关的临床结果
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100 项与 盐酸三氟拉嗪 相关的转化医学
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100 项与 盐酸三氟拉嗪 相关的专利（医药）
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7,338
项与 盐酸三氟拉嗪 相关的文献（医药）2025-06-16GLIA
Trifluoperazine Elevates Intracellular Ca2+ Levels and Locks Open the Store-Operated Calcium Entry Channels in Astrocytes.
Article
作者: Lim, Jiwoon ; Youn, Wongu ; Lee, C Justin
Trifluoperazine (TFP), a known inhibitor of Ca2+-bound calmodulin (Ca2+/CaM), has been reported to elevate cytosolic Ca2+ levels by disinhibiting inositol 1,4,5-triphosphate receptor 2 (IP3R2), thereby suppressing glioblastoma invasion and inducing apoptosis. Interestingly, TFP induces a sustained Ca2+ plateau, sensitive to extracellular Ca2+, suggesting involvement of Ca2+ entry such as store-operated calcium entry (SOCE). However, the underlying molecular mechanism remains elusive. Here, we report that TFP induces sustained Ca2+ signals by blocking the Ca2+/CaM-dependent desensitization of SOCE channels in cortical astrocyte cultures. TFP induces a prolonged Ca2+ response, with distinct kinetics compared to other Ca2+ modulators such as TFLLR-NH2 (a Gαq-coupled GPCR agonist) and thapsigargin (a sacro/endoplasmic reticulum Ca2+-ATPase inhibitor). Under extracellular Ca2+-free conditions, Ca2+ levels increase without reaching a plateau, suggesting that the sustained Ca2+ signal relies on Ca2+ influx. Pharmacological analysis shows that sustained Ca2+ signals by TFP are CaM-dependent. Gene silencing targeting STIM1 and Orai1-3 confirmed their essential roles in the sustained response. We find that TFP effectively "locks open" SOCE channels by inhibiting their desensitization, maintaining SOCE activity. This effect is also observed in ex vivo hippocampal dentate gyrus astrocytes. Structural modeling supports a mechanism in which TFP disrupts the interaction between Ca2+/CaM and the SOAR domain of STIM1. Together, these findings indicate that TFP elevates cytosolic Ca2+ levels by maintaining SOCE activation, offering novel insights into the molecular actions of this drug. TFP can be a pharmacological tool for SOCE research as it locks SOCE channels open.
2025-05-24Journal of biomolecular structure & dynamics
Integration analysis of PLAUR as a sunitinib resistance and macrophage related biomarker in ccRCC, an in silicon and experimental study
Article
作者: Gan, Sishun ; Li, Lin ; Jiang, Aimin ; Chu, Jian ; Yang, Qiwei ; Cao, Jianwei ; Ye, Fangdie ; Tian, Yijun
Sunitinib remains the preferred systemic treatment option for specific patients with advanced RCC who are ineligible for immune therapy. However, it's essential to recognize that Sunitinib fails to elicit a favourable response in all patients. Moreover, most patients eventually develop resistance to Sunitinib. Therefore, identifying new targets associated with Sunitinib resistance is crucial. Utilizing multiple datasets from public cohorts, we conducted an exhaustive analysis and identified a total of 8 microRNAs and 112 mRNAs displaying significant expression differences between Sunitinib responsive and resistant groups. A particular set of six genes, specifically NIPSNAP1, STK40, SDC4, NEU1, TBC1D9, and PLAUR, were identified as highly significant via WGCNA. To delve deeper into the resistance mechanisms, we performed additional investigations using cell, molecular, and flow cytometry tests. These studies confirmed PLAUR's pivotal role in fostering Sunitinib resistance, both in vitro and in vivo. Our findings suggest that PLAUR could be a promising therapeutic target across various cancer types. In conclusion, this investigation not only uncovers vital genes and microRNAs associated with Sunitinib resistance in RCC but also introduces PLAUR as a prospective therapeutic target for diverse cancers. The outcomes contribute to advancing personalized healthcare and developing superior therapeutic strategies.
2025-05-01TRENDS IN PHARMACOLOGICAL SCIENCES
Repurposing trifluoperazine for glioblastoma treatment
Review
作者: Gan, Hui K ; Bardy, Cedric ; De Silva, Manam Inushi
Glioblastoma (GBM) remains a therapeutic challenge due to its heterogeneity and plasticity, which drive treatment resistance, especially when compounded by interactions with the brain microenvironment. Recent preclinical evidence indicates that trifluoperazine (TFP) inhibits treatment-induced malignant reprogramming of tumour cells, potentially helping to reduce tumour plasticity. TFP targets calmodulin, dopamine receptors, and stress-responsive proteins (nuclear protein 1, NUPR1). Through these mechanisms, TFP has been shown to reduce tumour growth, sensitise tumours to chemoradiotherapy, and prolong survival in xenograft animal models. The clinical safety profile of TFP is well known from its use as an antipsychotic, and recent preclinical evidence further indicates that TFP has low toxicity to healthy neurons and glia despite transient functional effects on dopamine receptors. This Opinion explores TFP mechanisms of action and clinical activity to assess its suitability as a repurposed therapeutic option for GBM.
100 项与 盐酸三氟拉嗪 相关的药物交易
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研发状态
10 条最早获批的记录, 后查看更多信息
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 抑郁症 | 中国 | 1995-01-01 | |
| 精神分裂症 | 中国 | 1995-01-01 | |
| 焦虑症 | 美国 | 1959-04-16 |
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临床结果
临床结果
适应症
分期
评价
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临床1/2期 | 2 | 網鑰顧膚遞築繭夢窪鏇 = 壓築繭築窪醖膚鬱積餘 衊窪窪簾鏇構範壓願鹽 (願醖構膚顧築壓觸鑰齋, 鬱憲遞觸糧鹽構襯襯鏇 ~ 膚艱廠壓淵觸積蓋鏇廠) 更多 | - | 2022-12-14 | |||
N/A | - | - | 餘願艱構構鹹選憲蓋鹹(觸夢築築選餘窪繭壓鏇) = 齋膚鏇壓鹹齋選鑰鹽夢 糧憲顧構鑰選襯衊鏇淵 (願觸衊窪範顧憲鏇積繭 ) | - | 2012-05-20 | ||
(Ionizing radiation) | 餘願艱構構鹹選憲蓋鹹(觸夢築築選餘窪繭壓鏇) = 齋簾顧願衊鹽鏇齋衊鏇 糧憲顧構鑰選襯衊鏇淵 (願觸衊窪範顧憲鏇積繭 ) |
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