预约演示

更新于：2025-08-16

Escitalopram

依地普仑

更新于：2025-08-16

概要

基本信息

简介艾司西酞普兰是一种选择性血清素再摄取抑制剂（SSRI），用作抗抑郁和抗焦虑药物。它是Lundbeck和Forest Laboratories合作开发的。最早于2002年8月获得美国食品和药物管理局（FDA）批准，由Forest Laboratories获得批准，后来该公司被Allergan收购，现已成为AbbVie的一部分。现在，艾司西酞普兰以多个品牌名称上市，包括Lexapro，Cipralex和Seroplex，以片剂和口服溶液形式供应。其作用机制涉及抑制大脑内神经递质血清素的再摄取，导致突触裂隙中血清素水平升高和血清素能神经递质传递的增强。这最终导致情绪改善和焦虑症状减轻。艾司西酞普兰最初被开发和批准用于治疗重度抑郁症（MDD）。此后，它也获得了治疗广泛性焦虑症（GAD）的批准。

药物类型

小分子化药

别名

Escitalopram (INN)、艾斯西酞普兰、Esertia

靶点

SERT

作用方式-

作用机制

5-羟色胺重摄取抑制剂

治疗领域

神经系统疾病

在研适应症-

非在研适应症

抑郁症

原研机构

Aquestive Therapeutics, Inc.

在研机构

University of Oxford

非在研机构

Aquestive Therapeutics, Inc.

权益机构-

最高研发阶段临床1/2期

首次获批日期-

最高研发阶段(中国)-

特殊审评-

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结构/序列

分子式C20H21FN2O

InChIKeyWSEQXVZVJXJVFP-FQEVSTJZSA-N

CAS号128196-01-0

关联

项与依地普仑相关的临床试验

NCT06696482

/ Not yet recruiting临床1/2期IIT

Effort and Antidepressant Study Test

The aim of this study is to investigate the behavioural effects and neural correlates of increasing serotonin levels in healthy volunteers, through a 7-day course of the SSRI escitalopram, on an effort-based decision-making task measuring self-benefiting and prosocial behaviours.

开始日期2025-01-01

申办/合作机构

University of Oxford

[+1]

IRCT20240803062623N1

/ RecruitingN/AIIT

Bioequivalence study of two Escitalopram 20 mg FC Tablet manufactured by tadbir kalaye jam company in comparison with Brand

开始日期2024-11-05

申办/合作机构-

CTRI/2024/08/072643

/ Not yet recruiting临床2/3期IIT

A Comparative Study between Escitalopram (Modern Medicine) and Jyotishmati (Ayurveda) in Depressive Disorder - Treatment Trial

开始日期2024-08-22

申办/合作机构-

100 项与依地普仑相关的临床结果

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100 项与依地普仑相关的转化医学

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100 项与依地普仑相关的专利（医药）

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4,960

项与依地普仑相关的文献（医药）

2025-12-01·MOLECULAR BIOLOGY REPORTS

Antidepressant-like and neuroprotective effect of hydroalcoholic extract of Aloysia citriodora in animals subjected to childhood stress

Article

作者: Nicolleti, Ana Olivia Albino ; da Silva, Gilnei Bruno ; Amaral, Severina Silva ; Manica, Daiane ; Soares, Silvio José Batista ; da Silva, Brunna Varela ; Ibrahim, Hélio Jungkenn ; Roman Junior, Walter Antônio ; Ignácio, Zuleide Maria ; Schuh, Laysa Anacleto ; Bertollo, Amanda Gollo ; Mingoti, Maiqueli Eduarda Dama ; Kreuz, Kelli Maria ; Bagatini, Margarete Dulce ; Bohnen, Lilian Caroline ; de Medeiros, Jesiel

BACKGROUND:

Stress in childhood can harm brain development, leading to biological and systemic dysfunctions that, along with genetic factors, may contribute to major depressive disorder (MDD) in adulthood. MDD treatment is complex, with current drugs taking time to show effects and not working for many patients. As a result, medicinal plants, like Aloysia citriodora (A. citriodora), are being studied as treatments for resistant depression. The main objective of this proposal was to evaluate the treatment with the hydroalcoholic extract of the medicinal species A. citriodora Palau on depressive-like behaviors in rats subjected to chronic stress in childhood and on mechanisms involved in neuroprotection through the evaluation of neuroinflammation and oxidative stress.

METHODS:

The maternal deprivation (MD) protocol was used during the first ten days of life. At the beginning of adulthood, the animals were treated for fourteen days. At the end of the treatments, the animals underwent the forced swimming behavioral test and were then euthanized for analysis of oxidative stress and inflammation markers.

RESULTS:

The stress caused by the MD protocol in rats culminated in a significant increase in depressive-like behaviors in adulthood, an increase in the expression of inflammatory substances IL-1 β and IL-6 in the animals' hippocampus, and an increase in the activity of oxidative stress parameters, such as myeloperoxidase (MPO) and thiobarbituric acid reactive substances (TBARS), in serum and hippocampus. The treatment with A. citriodora reduced depressive-like behaviors similar to the group treated with escitalopram. Regarding markers of inflammation in nervous tissue, it was observed that animals treated with A. citriodora had lower levels than those treated with escitalopram and the control group, and even more significantly when compared to the MD group treated with saline. The treatments reduced MPO activity in the serum of animals that underwent the MD protocol. TBARS was decreased in the serum and ultimately reversed in the hippocampus. Moreover, molecular docking studies have demonstrated that baicalein and quercetin-7-O-glucoside interact efficiently with IL-1β and IL-6.

CONCLUSION:

PM stress increased depressive-like behavior and increased markers of oxidative stress and inflammation. Treatment with the Aloysia citriodora extracts significantly reduced depressive-like behavior and markers of oxidative stress and inflammation, suggesting an antidepressant, antioxidant, and anti-inflammatory effect.

2025-11-01·JOURNAL OF AFFECTIVE DISORDERS

Consistent differential effects of bupropion and mirtazapine in major depression

Article

作者: Strobl, Eric V

BACKGROUND:

Patients with major depression exhibit heterogeneous symptom profiles and variable responses to antidepressants. Most clinical trials rely on aggregate outcomes such as total symptom severity or remission rates, which often obscure meaningful differences in treatment response.

METHODS:

We applied the Supervised Varimax (SV) algorithm to identify outcome dimensions that maximally differentiate antidepressants based on symptom-level effects. We analyzed all relevant levels of the STAR*D trial and validated findings in the independent CO-MED study. We assessed statistical significance using permutation testing with familywise error rate (FWER) correction.

RESULTS:

SV consistently identified interpretable and statistically significant differences between bupropion, mirtazapine, and other antidepressants. In STAR*D, bupropion monotherapy produced greater improvement in hypersomnia than venlafaxine in Levels 2 and 2 A (n=686, difference = 0.384, p_FWER=0.007). Bupropion augmentation outperformed buspirone augmentation for increased weight, increased appetite, and fatigue in Level 2 (n=520, difference = -0.322, p_FWER=0.005). Mirtazapine monotherapy outperformed nortriptyline for insomnia, decreased weight, and decreased appetite in Level 3 (n=214, difference = 0.401, p_FWER=0.022), and venlafaxine with mirtazapine similarly outperformed tranylcypromine in Level 4 (n=102, difference = -0.722, p_FWER=0.004). In CO-MED, escitalopram with bupropion and venlafaxine with mirtazapine demonstrated complementary symptom-specific benefits (n=640, difference = -0.302, p_FWER=0.022).

CONCLUSION:

Bupropion is most effective for hypersomnia, increased weight, increased appetite, or fatigue, while mirtazapine is preferable for insomnia, decreased weight, or decreased appetite. SV enables statistically rigorous, symptom-level differentiation using only treatment assignment, offering a scalable and clinically aligned framework for guiding antidepressant selection from individual clinical trials.

2025-09-01·JOURNAL OF AFFECTIVE DISORDERS

A randomized controlled trial comparing mindfulness to escitalopram for anxiety: In-person and remote, synchronous delivery pre and post COVID-19 pandemic

Article

作者: Szuhany, Kristin L ; Hoge, Elizabeth A ; Baker, Amanda W ; Armstrong, Caroline H ; Mete, Mihriye ; Dutton, Mary Ann ; Bui, Eric ; Simon, Naomi M ; Steinberg, Margot H

BACKGROUND:

During the pandemic, a randomized controlled trial (RCT) of Mindfulness-Based Stress Reduction (MBSR) versus the antidepressant, escitalopram (ESC) added a second phase using a synchronous, videoconference (VC) format for both interventions, enabling randomized and naturalistic comparisons. The original in-person RCT demonstrated non-inferiority of MBSR to ESC. In the second phase, we hypothesized that MBSR-VC would be non-inferior to ESC-VC, and that MBSR-VC would be non-inferior to in-person MBSR (MBSR-IN).

METHODS:

Adults with anxiety disorders were recruited for a 3-center RCT. Primary (Clinical Global Impression of Severity: CGIS) and secondary outcomes (satisfaction, other measures for anxiety subtypes) were compared between MBSR-IN vs MBSR-VC, ESC-IN vs ESC-VC and MBSR-VC vs ESC-VC.

RESULTS:

MBSR-VC (n = 100) and ESC-VC (n = 102) did not significantly differ in mean CGI-S change at endpoint (1.39 vs 1.51, p = 0.17) but non-inferiority of MBSR-VC was not supported. MBSR did not vary by delivery format (VC: 1.3 vs. IN: 1.3, p = 0.77) and MBSR-VC's non-inferiority to MBSR-IN was demonstrated within the pre-specified margin of -0.40 (95 % CI: -0.34 to 0.25). ESC-IN and ESC-VC were not significantly different in CGI-S change in unadjusted comparisons (1.4 vs 1.5, p = 0.53), but the average CGI-S at endpoint was significantly lower in the ESC-VC group in a multivariable longitudinal model. Other findings included in-person treatments having a greater impact on social anxiety compared to their VC version, ESC-VC having higher satisfaction ratings and a greater impact on panic symptoms than MBSR-VC.

CONCLUSIONS:

Remotely delivered MBSR demonstrated comparable effectiveness to in-person MBSR for anxiety disorders, providing support for this delivery approach. Social anxiety symptoms improved more with in-person care.

TRIAL REGISTRATION:

Clinicaltrials.gov: NCT03522844.

项与依地普仑相关的新闻（医药）

2025-07-24

·奇点网

《柳叶刀》子刊：复发风险减半！研究表明，抗抑郁药和氯氮平联用与难治性精神分裂症的复发风险降低51%有关

*仅供医学专业人士阅读参考在精神分裂症患者中，治疗抵抗通常指对两种一线抗精神病药物在足量足疗程使用后仍无显著疗效。约25%的初发精神分裂症患者会发展为治疗抵抗精神分裂症（又称为难治性精神分裂症，TRS），而在多次复发的患者中，这一比例可能高达40%。氯氮平是当前治疗TRS最有效的药物，但是也只有40%-50%的TRS患者对氯氮平治疗产生充分反应。一些随机对照试验表明，在氯氮平基础上联合抗抑郁药可能有助于TRS患者症状改善，但是整体证据质量有限，且缺乏长期随访数据。来自东芬兰大学的研究人员基于芬兰和瑞典的全国性队列研究，讨论了联合抗抑郁药物对氯氮平治疗TRS的有效性和安全性。研究结果发表在《柳叶刀·精神病学》杂志上。研究共纳入了23206名氯氮平使用者，结果显示，氯氮平联合标准剂量的舍曲林（30-45mg/天），与TRS复发风险降低51%有关，艾司西酞普兰、度洛西汀等联合使用也与TRS复发风险显著降低有关，且在低剂量或标准剂量使用时未观察到躯体原因住院风险增加。研究数据来自芬兰和瑞典的全国性患者登记系统或住院出院登记系统，随访起始时间为精神分裂症确诊日期或首次使用氯氮平日期（取较晚值），随访结束时间为死亡、移民或数据截止时间。采用个体内分析，每位受试者为自身对照，最大程度减少偏倚，主要暴露因素为特定抗抑郁药物联合氯氮平的使用情况。药物使用数据来自处方药登记系统，抗抑郁药物联合治疗期间，患者同时使用氯氮平和一种抗抑郁药（本研究覆盖的抗抑郁药包括西酞普兰、艾司西酞普兰、氟西汀、帕罗西汀、舍曲林、度洛西汀等）。研究主要结局为精神分裂症复发（指因精神病性症状住院），次要结局为躯体原因住院（非精神障碍相关的躯体原因住院）。研究队列共包括23206名受试者，41%为女性，平均年龄为41.3岁，芬兰组和瑞典组中分别有约50%的受试者使用了抗抑郁药。最常用的抗抑郁药为西酞普兰、舍曲林和艾司西酞普兰。芬兰组和瑞典组的中位随访时间分别为12.1年和11.4年，分别有9243名（65.8%）和4671名（51.0%）受试者发生复发，两种主要抗抑郁药物类型，选择性血清素再摄取抑制剂（SSRI）和去甲肾上腺素-血清素再摄取抑制剂（SNRI）均与精神分裂症复发风险下降有关，其中，舍曲林和度洛西汀与氯氮平联用，复发风险下降最显著。调整混杂因素后，舍曲林、度洛西汀和艾司西酞普兰仍然与精神分裂症复发风险下降显著相关。按照剂量对抗抑郁药物进行分析，30-54mg/天的舍曲林、6-10mg/天的艾司西酞普兰和18-32mg/天的度洛西汀的复发风险最低，这些药物低剂量使用时（<0.6 DDDs/天），也可以观察到与复发风险下降有关。安全性方面，氯氮平与安非他酮联用与较低的躯体原因住院风险有关，但是与艾司西酞普兰联用与住院风险较高有关。将抗抑郁药物按照剂量等级分类时，所有药物在低剂量或标准剂量下，均与躯体原因住院风险无关；但是中高剂量（1.1-2.1 DDDs/天）或高剂量（≥2.1 DDDs/天）与躯体原因住院风险增加有关。总的来说，研究表明，氯氮平与标准剂量的SSRI或SNRI联合使用，与精神分裂症复发风险降低有关，并且未发现严重躯体不良反应风险增加。但是，联合使用过程中，尚不清楚SSRI和SNRI会增加哪些具体的不良反应。高剂量抗抑郁药的使用可能本身代表抑郁症状加重或躯体状况恶化，因此也可能部分解释住院风险增加的结果。从安全性和疗效角度来看，应当谨慎使用高剂量抗抑郁药物。参考文献：Taipale H, Siskind D, Tanskanen A, Mittendorfer-Rutz E, Correll CU, Tiihonen J. Real-world effectiveness of clozapine augmentation with antidepressants: within-subject data evidence from two European nationwide cohorts. Lancet Psychiatry. 2025;12(8):568-578. doi:10.1016/S2215-0366(25)00163-4本文作者丨王雪宁

临床研究临床结果

2025-07-21

·药学进展

独家原创|赵雪主治医师：抗精神病药、抗抑郁药与不宁腿综合征

“点击蓝字关注我们赵雪毕业于上海交通大学医学院。上海市精神卫生中心主治医师、上海市精神心理疾病临床医学研究中心秘书。主要研究方向为精神药物遗传药理学。主持上海市精神卫生中心院级课题、上海交通大学“医工交叉”等科研项目多项。作为主要研究人员参与国家自然科学基金、上海市申康医院发展中心“促进市级医院临床技能与临床创新三年行动计划”等多项纵向科研课题。作为研究骨干参与多项国际多中心和国内多中心（牵头）临床试验。以第一（含共一）作者发表多篇中英文学术论文。抗精神病药、抗抑郁药与不宁腿综合征 PPS 郭瑛睿1，钱瑞仪1，禹顺英2，沈一峰3，赵雪3*（1.上海交通大学医学院附属精神卫生中心精神科，上海 200030；2.上海交通大学医学院附属精神卫生中心遗传室，上海 200030；3.上海交通大学医学院附属精神卫生中心临床研究中心，上海 200030）[摘要] 不宁腿综合征（restless legs syndrome,RLS）是抗精神病药和抗抑郁药的常见不良反应之一，影响患者夜间睡眠、加重精神症状、降低患者生活质量，但其在临床实践尚未受到广泛重视。针对抗精神病药和抗抑郁药的 RLS 发生风险，这两类药物导致 RLS 的可能机制及相关治疗手段进行综述，以期为 RLS 的临床治疗提供参考。不宁腿综合征（restless legs syndrome，RLS）又称不安腿综合征，是临床常见的运动感觉性神经系统疾病，主要表现为强烈、迫切想要移动肢体的冲动或欲望，常常伴随着肢体深处不舒服或难以描述的感觉，夜间睡眠或安静时出现或加重，具有昼夜节律性，按摩或活动后缓解，可导致严重睡眠障碍。在《精神障碍诊断与统计手册（第 5 版）》（the fifith edition of the diagnostic and statistical manual of mental disorders，DSM-5）中， RLS属于睡眠-觉醒障碍中异常睡眠的一类疾病。一般人群中RLS的发病率为 3%~19%，女性发病率更高[1]，其中约有2.5%的患者症状严重到需要接受医疗干预[2]。根据病因不同，RLS可分为原发性和继发性2种类型。原发性RLS通常在40岁之前发病，主要与遗传因素有关。继发性RLS伴发于各类躯体疾病，如神经系统疾病、铁缺乏症、慢性肾功能衰竭、糖尿病、自身免疫性疾病、甲状腺疾病、血管疾病、精神疾病等[1, 3-4]。RLS也是精神类药物的不良反应之一。据报道，抗精神病药、抗抑郁药和抗癫痫药是引起RLS最常见的3类药物[1]。早在1999年，1例病案报告指出奥氮平可能导致RLS[5]，此后越来越多的精神类药物被报道能够诱发RLS这一不良反应，不同药物发生RLS的风险有所不同。如上所述，引起RLS的精神类药物主要为抗精神病药及抗抑郁药，故本文主要针对抗精神病药和抗抑郁药引起RLS的发生风险，这两类药物导致RLS的可能机制及相关治疗手段进行综述。1抗精神病药、抗抑郁药与不宁腿综合征 Elrassas等[6]开展的横断面研究结果显示，200名接受抗抑郁药和抗精神病药治疗的患者中，服用第1代抗精神病药（除氟哌啶醇外）的患者发生RLS比例最高（58.7%），其次是选择性5-羟色胺再摄取抑制剂（selective serotonin reuptake inhibitors，SSRIs）类药物（52.6%）和阿立哌唑（46.4%），接受曲唑酮（24.2%）和氟哌啶醇（31%）治疗的患者发生RLS可能性最小。 1.1 抗精神病药与不宁腿综合征有研究结果显示，与对照组（9.3%）相比，接受抗精神病药治疗的精神分裂症患者发生RLS的概率（21.4%）明显更高[7]。在各类抗精神病药中，奥氮平、喹硫平和氯氮平引起RLS的报道最多[1]，利培酮、鲁拉西酮等药物引起RLS的报道相对较少（见表1[5,8-29]）。也有部分研究结果显示，喹硫平和阿立哌唑能够改善其他抗精神病药引起的RLS症状[11,30]，可能是因为相对于多巴胺D2受体，这2种药物对5-羟色胺（5-hydroxytryptamine，5-HT）受体具有更高亲和力。另有研究报道，抗精神病药与抗抑郁药联用，如喹硫平与文拉法辛[31] 或帕罗西汀[18] 联用会导致RLS，停用2种药物中的一种会改善RLS症状。1.2 抗抑郁药与不宁腿综合征在多种抗抑郁药中，SSRIs、5-HT和去甲肾上腺素再摄取抑制剂（ serotonin-norepinephrine reuptake inhibitors，SNRIs）、四环类非典型抗抑郁药米氮平导致RLS的报道较多（见表2[32-46]）。Cetin Erdem 等[47]报道，在198名接受4~8周SSRIs/SNRIs药物治疗的门诊患者中，RLS的发生率为25%。与女性相比，男性使用抗抑郁药后发生RLS的风险增加[48]。Kolla等[49]报道，在各种抗抑郁药中，米氮平可能与较高的RLS发生率有关，也会恶化患者原有的RLS症状[50]，其次是文拉法辛，而安非他酮可能会减轻RLS症状。当联合使用2种或2种以上药物时，如氟西汀与米氮平联用[51]、帕罗西汀与度洛西汀联用[52]、艾司西酞普兰与锂盐或喹硫平联用[53]，患者发生RLS的风险也会相应增加。关于新型抗抑郁药伏硫西汀是否增加RLS风险的研究结果并不一致，有研究发现其可减轻RLS症状[54-55]，但也有研究报道伏硫西汀可诱发RLS[45]。2抗精神病药、抗抑郁药引起不宁腿综合征的可能机制2.1 多巴胺功能紊乱既往神经影像学研究表明，RLS患者脑内存在多巴胺能活性低下表现[56]。RLS包括运动和感觉异常两个维度的症状表现，感觉和运动回路受脊髓投射至大脑的相关区域控制，这些区域与不同神经递质有关，包括背区（5-HT）、丘脑区（去甲肾上腺素）和下丘脑后方的A11区（多巴胺）[57]。多巴胺受体激动剂是治疗RLS的一线药物，多巴胺拮抗剂（如抗精神病药）则会诱发RLS，提示多巴胺活性在RLS中的重要作用。抗精神病药与抗抑郁药增加RLS风险的具体机制目前尚不明确，多巴胺能活性降低被认为可能是抗精神病药诱发RLS的主要原因。阿立哌唑为多巴胺（D2、D3、D4）受体部分激动剂，正电子发射断层显像（positron emission tomography，PET）研究表明在治疗剂量下阿立哌唑受体占有率为95%[58]，阿立哌唑通过激动多巴胺受体改善RLS症状，该效果与罗匹尼罗和普拉克索等多巴胺受体激动剂相似。然而，与其他非典型抗精神病药物（如利培酮）相比，氯氮平和喹硫平的D2受体占有率较低，如果多巴胺功能降低能够诱发RLS，这些药物诱发RLS的可能性应该较小，这与多数研究报道不符。另有研究者认为，喹硫平因其镇静催眠作用，常在夜间使用可改善患者睡眠，而夜间多巴胺受体敏感性较白天增加[59]；另外，喹硫平常被用来与抗抑郁药（如SSRIs、米氮平等）合用改善情感症状，而抗抑郁药能够通过增加5-HT功能减少多巴胺释放 [60]，增加RLS发生风险。此外，有研究表明泌乳素（prolactin，PRL）水平可能在抗精神病药所致 RLS中起重要作用。多巴胺受体激动剂如左旋多巴和卡麦角林能够降低泌乳素水平，这2种药物均可以治疗RLS[61]。抗精神病药（如利培酮、奥氮平）能够增加PRL水平[62]，可能是引起RLS症状的间接原因。阿立哌唑可以降低抗精神病药引起的高泌乳素血症[63]，可能是阿立哌唑能够缓解RLS症状的另一原因 [23]。2.2 铁缺乏有研究发现，RLS患者脑脊液中铁蛋白含量减少[64] 及转铁蛋白含量升高；脑影像学研究也发现，RLS患者大脑中铁含量减少[65]；RLS患者尸检脑神经胶质细胞中铁含量较低[66]。外周铁水平正常的RLS患者补充铁剂也能改善RLS症状，可能是因为血脑屏障使大脑中铁水平独立于外周铁水平[67]。此外，脑内铁水平降低也会导致多巴胺代谢和D2受体状态改变，尤其是在黑质和壳核区域[9]。目前有研究发现，抗精神病药能够影响体内铁稳态[68]和肝脏铁代谢[69]，引起低铁血症。目前仍缺乏直接证据表明使用抗精神病或抗抑郁药出现RLS的患者是否存在外周或中枢铁代谢异常，仍需更多研究证据来明确这一可能机制。 2.3 遗传因素遗传因素是RLS的重要致病因素，大部分家族性RLS呈常染色体显性遗传，少数家族则呈常染色体隐性遗传或非孟德尔遗传模式[70]。既往遗传学研究多集中于原发性 RLS，全基因组关联研究发现位于不同染色体的 RLS 风险基因，包括BTBD9基因（位于染色体6p21）、MEIS1基因（位于染色体2p14）、PTPRD 基因（位于染色体9p24.1-p23）、MAP2K5/SKOR1 基因（位于染色体15q23）和TOX3/BC034767 基因（位于染色体 16q12.1）[71]。近期有研究发现7个全新的RLS易感基因位点：RLS1（位于染色体12q12-q21）、RLS2（位于染色体 14q13-q21）、RLS3（位于染色体 9p24-p22）、RLS4（位于染色体 2q33）、RLS5（位于染色体20p13）、RLS6（位于染色体 19p13）及RLS7（位于染色体16p12.1）[72-73]。截至目前，抗精神病药或抗抑郁药所致RLS的遗传学研究仍较少。有研究发现，MAOA基因VNTR与MAOB基因A644g多态的单倍型频率与抗精神病药引起RLS严重程度有关[74]。另一项研究显示，MAP2K5基因多态性增加了抗精神病药物诱发RLS的风险[75]。3抗精神病药、抗抑郁药引起不宁腿综合征的治疗RLS的治疗分为非药物治疗和药物治疗。非药物治疗包括：消除或减少继发性因素的影响，如尽量避免使用能够诱发或加重RLS的药物（如多巴胺受体拮抗剂、抗抑郁药、抗组胺药等）；保持良好的睡眠卫生习惯；加强体育锻炼；结合物理治疗（如重复经颅磁刺激、重复经颅电刺激）等。药物治疗包括：多巴胺激动剂（如罗匹尼罗、罗替戈汀、普拉克索），α2δ钙通道配体类药物（如普瑞巴林、加巴喷汀-恩那卡比、加巴喷汀），这些药物均为治疗RLS的一线用药 [76]，也可使用苯二氮䓬类镇静药[77] 和抗癫痫药[78] 等。治疗抗精神病药或抗抑郁药引起的RLS具有一定挑战性，目前仍缺乏高水平临床研究或相关指南指导医生用药。在既往相关病例报道中，临床医生一般采取减量或停用现用药物，加用多巴胺受体激动剂或α2δ钙通道配体类药物（具体病例处理方式可参考表1和表2），上述策略均能够有效改善患者RLS症状。值得注意的是，多巴胺受体激动剂和α2δ钙通道配体类药物可能会导致患者精神症状波动或病情复发。在既往病案报道中，加用小剂量阿立哌唑也是改善 RLS症状的常用手段，阿立哌唑剂量为1~10 mg·d-1[23,30]，在临床实践中医生可根据患者具体情况探索使用阿立哌唑的剂量。铁缺乏是RLS病理生理学中重要假说之一。在患者出现RLS症状后，医生可以通过相关检测指标（包括铁蛋白、转铁蛋白、血清铁、总铁结合力、转铁蛋白饱和度等）评估患者外周铁储存情况。如果患者确实存在缺铁表现，可采用铁替代疗法，如口服硫酸亚铁，若患者不能耐受或有效吸收口服铁剂，也可考虑静脉补铁，同时补充维生素C有助于促进消化道对铁的吸收[76]。在补充铁剂后，需动态观察患者RLS症状改善和评估外周铁相关指标变化。4结语精神障碍患者常合并睡眠障碍，而RLS会进一步加重患者睡眠问题，同时伴有强烈心理不适感。此外，RLS能够增加肥胖、抑郁症、焦虑症、高血压及其他心血管疾病的发生风险，显著降低患者生活质量、延缓患者康复[79]。Cetin Erdem等[47]的研究显示，服用抗抑郁药发生RLS的患者生活质量显著下降。一项回顾性队列研究发现，自杀和自残风险与RLS呈正相关[80]。尽管在临床实践中，使用抗精神病药或抗抑郁药后出现RLS的病例并不少见，但与其他药物不良反应（如心血管不良反应、代谢综合征等）相比，RLS仍未得到有效识别和广泛重视。尤其在患者用药后出现新发睡眠问题时，不能简单地归结为疾病症状的一部分，应仔细识别是否存在RLS的可能性。目前关于精神类药物引起RLS的各方面研究仍较少，后续需要更多关注和探索，从而更好地为患者及临床服务。参考文献：[1]Patatanian E, Claborn M K. 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Nat Sci Sleep, 2023, 15: 779-784.[31] Michopoulos I, Ferentinos P, Oulis P, et al. Restless legs syndrome associated with the combined use of quetiapine and venlafaxine[J]. J Clin Psychopharmacol, 2014, 34(1): 159-161.[32] Makiguchi A, Nishida M, Shioda K, et al. Mirtazapine-induced restless legs syndrome treated with pramipexole[J]. J Neuropsychiatry Clin Neurosci, 2015, 27(1): e76.[33] Chopra A, Pendergrass D S, Bostwick J M. Mirtazapine-induced worsening of restless legs syndrome (RLS) and ropinirole-induced psychosis: challenges in management of depression in RLS[J]. Psychosomatics, 2011, 52(1): 92-94.[34] Park Y M, Lee H J, Kang S G, et al. Resolution of pregabalin and mirtazapine associated restless legs syndrome by bupropion in a patient with major depressive disorder[J]. Psychiatry Investig, 2009, 6(4): 313-315.[35] Pae C U, Kim T S, Kim J J, et al. Re-administration of mirtazapine could overcome previous mirtazapine- associated restless legs syndrome [J]. Psychiatry Clin Neurosci, 2004, 58(6): 669-670.[36] Ağargün M Y, Kara H, Ozbek H, et al. Restless legs syndrome induced by mirtazapine[J]. J Clin Psychiatry, 2002, 63(12): 1179.[37] Bahk W M, Pae C U, Chae J H, et al. Mirtazapine may have the propensity for developing a restless legs syndrome? A case report[J]. Psychiatry Clin Neurosci, 2002, 56(2): 209-210.[38] Hargrave R, Beckley D J. Restless leg syndrome exacerbated by sertraline[J]. Psychosomatics, 1998, 39(2): 177-178.[39] Oztürk O, Eraslan D, Kumral E. Oxcarbazepine treatment for paroxetine-induced restless leg syndrome[J]. Gen Hosp Psychiatry, 2006, 28(3): 264-265.[40] Sanz-Fuentenebro F J, Huidobro A, Tejadas-Rivas A. Restless legs syndrome and paroxetine[J]. Acta Psychiatr Scand, 1996, 94(6): 482- 484.[41] Bakshi R. Fluoxetine and restless legs syndrome[J]. J Neurol Sci,1996, 142(1/2): 151-152.[42] Nader P, Coralie L, Baleydier B, et al. Restless legs syndrome induced by citalopram: a psychiatric emergency[J]. Gen Hosp Psychiatry, 2007, 29(1): 72-74.[43] Page R L 2nd, Ruscin J M, Bainbridge J L, et al. Restless legs syndrome induced by escitalopram: case report and review of the literature[J]. Pharmacotherapy, 2008, 28(2): 271-280.[44] Yilbaş B. Restless legs syndrome due to the use of trazodone: a case report[J]. Turk Psikiyatri Derg, 2022, 33(1): 70-72.[45] Romigi A, Vitrani G, Caccamo M, et al. Restless legs syndrome related to vortioxetine: a case report[J]. J Clin Psychopharmacol, 2019, 39(5): 514-516.[46] Abdul Karim M, Al-Baz N, Ouanes S, et al. Suspected agomelatineinduced restless legs syndrome: a case report[J]. BMC Psychiatry, 2021, 21(1): 180.[47] Cetin Erdem H, Kara H, Ozcelik O, et al. Frequency, risk factors,and impacts on quality of life of the restless legs syndrome and side effects among antidepressant users in a tertiary hospital: an observational cross-sectional study[J]. Int Clin Psychopharmacol, 2023, 38(4): 209-215.[48] Odabaş F Ö, Uca A U. Is there any association between antidepressants and restless legs syndrome in a large Turkish population receiving mono or combined treatment? A cross-sectional comparative study[J]. Psychiatry Clin Psychopharmacol, 2019, 29(4): 565-569.[49] Kolla B P, Mansukhani M P, Bostwick J M. The influence of antidepressants on restless legs syndrome and periodic limb movements: a systematic review[J]. Sleep Med Rev, 2018, 38: 131- 140.[50] Teive H A G, de Quadros A, Barros F C, et al. Worsening of autosomal dominant restless legs syndrome after use of mirtazapine: case report[J]. Arq Neuropsiquiatr, 2002, 60(4): 1025-1029.[51] Prospero-Garcia K A, Torres-Ruiz A, Ramirez-Bermudez J, et al. Fluoxetine-mirtazapine interaction may induce restless legs syndrome: report of 3 cases from a clinical trial[J]. J Clin Psychiatry, 2006, 67(11): 1820.[52] Nikolaou K N, Michopoulos I, Douzenis A, et al. Restless legs syndrome associated with the combined use of duloxetine plus paroxetine[J]. J Clin Psychopharmacol, 2015, 35(3): 345-346.[53] Chen P H. Restless leg syndrome induced by escitalopram and lithium combined with quetiapine treatment in bipolar II disorder: a case report[J]. Clin Neuropharmacol, 2016, 39(2): 118-119.[54] Alıcı Y H, Kumcu M K. Potential effect of vortioxetine on restless leg syndrome[J]. Clin Psychopharmacol Neurosci, 2023, 21(3): 599-603.[55] Yılbas B. The use of vortioxetine in major depression disorder accompanying restless legs syndrome: a case report[J]. Arch Neuropsychiatry, 2022: 27827.[56] Cervenka S, Pålhagen S E, Comley R A, et al. Support for dopaminergic hypoactivity in restless legs syndrome: a PET study on D2-receptor binding[J]. Brain, 2006, 129(Pt 8): 2017-2028[57] Kocar T D, Müller H P, Kassubek J. Differential functional connectivity in thalamic and dopaminergic pathways in restless legs syndrome: a meta-analysis[J]. Ther Adv Neurol Disord, 2020, 13: 1756286420941670.[58] Grunder G, Carlsson A, Wong D F. Mechanism of new antipsychotic medications: occupancy is not just antagonism[J]. Arch Gen Psychiatry, 2003, 60(10): 974-977.[59] Garcia-Borreguero D, Larrosa O, Granizo J J, et al. Circadian variation in neuroendocrine response to L-dopa in patients with restless legs syndrome[J]. Sleep, 2004, 27(4): 669-673.[60] Zhou F M, Liang Y, Salas R, et al. Corelease of dopamine and serotonin from striatal dopamine terminals[J]. Neuron, 2005, 46(1): 65-74.[61] Trenkwalder C, Benes H, Grote L, et al. Cabergoline compared to levodopa in the treatment of patients with severe restless legs syndrome: results from a multi-center, randomized, active controlled trial[J]. Mov Disord, 2007, 22(5): 696-703.[62] Koch M T, Carlson H E, Kazimi M M, et al. Antipsychotic-related prolactin levels and sexual dysfunction in mentally ill youth: a 3-month cohort study[J]. J Am Acad Child Adolesc Psychiatry, 2023, 62(9): 1021-1050.[63] Jiang Q, Li T, Zhao L, et al. Treatment of antipsychotic-induced hyperprolactinemia: an umbrella review of systematic reviews and meta-analyses[J]. Front Psychiatry, 2024, 15: 1337274.[64] Clardy S L, Earley C J, Allen R P, et al. Ferritin subunits in CSF are decreased in restless legs syndrome[J]. J Lab Clin Med, 2006, 147(2): 67-73.[65] Allen R P, Barker P B, Wehrl F W, et al. MRI measurement of brain iron in patients with restless legs syndrome[J]. Neurology, 2001, 56(2): 263-265.[66] Connor J R, Boyer P J, Menzies S L, et al. Neuropathological examination suggests impaired brain iron acquisition in restless legs syndrome[J]. Neurology, 2003, 61(3): 304-309.[67] Yu P, Chang Y Z. Brain iron metabolism and regulation[J]. Adv Exp Med Biol, 2019, 1173: 33-44.[68] Schoretsanitis G, Nikolakopoulou A, Guinart D, et al. Iron homeostasis alterations and risk for akathisia in patients treated with antipsychotics: a systematic review and meta-analysis of crosssectional studies[J].Eur Neuropsychopharmacol, 2020, 35: 1-11.[69] May M, Barlow D, Ibrahim R, et al. Mechanisms underlying antipsychotic-induced NAFLD and iron dysregulation: a multi-omic approach[J]. Biomedicines, 2022, 10(6): 1225.[70] Jiménez-Jiménez F J, Alonso-Navarro H, García-Martín E, et al.Genetics of restless legs syndrome: an update[J]. Sleep Med Rev, 2018, 39: 108-121.[71] Akçimen F, Sarayloo F, Liao C, et al. Transcriptome-wide association study for restless legs syndrome identifies new susceptibility genes[J]. Commun Biol, 2020, 3(1): 373.[72] Estiar M A, Senkevich K, Yu E, et al. Lack of causal effects or genetic correlation between restless legs syndrome and Parkinson’s disease[J]. Mov Disord, 2021, 36(8): 1967-1972.[73] Lin W S. The conundrum of the origin of restless legs syndrome[J].Sleep, 2022, 45(5): zsac018.[74] Kang S G, Park Y M, Choi J E, et al. Association study between antipsychotic-induced restless legs syndrome and polymorphisms of monoamine oxidase genes in schizophrenia[J]. Human Psychopharmacology, 2010, 25(5): 397-403.[75] Kang S G, Lee Y J, Park Y M, et al. Haplotype association of the MAP2K5 gene with antipsychotics-induced symptoms of restless legs syndrome among patients with schizophrenia[J]. Psychiatry Investig, 2018, 15(1): 84-89.[76] Liu Z, Guan R, Pan L. Exploration of restless legs syndrome under the new concept: a review[J]. Medicine (Baltimore), 2022, 101(50): e32324.[77] Walters A S, Spruyt K, Ba D M, et al. A historical overview of the role of benzodiazepines including clonazepam in the treatment of adult restless legs syndrome and periodic limb movements in sleep[J]. Tremor Other Hyperkinet Mov (N Y), 2024, 14: 21.[78] Al-Kassmy J, Alsalmi M, Kang W, et al. Anticonvulsant agents for treatment of restless legs syndrome: a case report with lamotrigine and a review of the literature[J]. Neurologist, 2024, 29(3): 173- 178.[79] Shen Y, Liu H, Dai T, et al. Association between restless legs syndrome and hypertension: a meta-analysis of nine population-based studies[J]. Neurol Sci, 2018, 39(2): 235-242.[80] Zhuang S, Na M, Winkelman J W, et al. Association of restless legs syndrome with risk of suicide and self-harm[J]. JAMA Netw Open, 2019, 2(8): e199966.美编排版：覃冰冰感谢您阅读《药学进展》微信平台原创好文，也欢迎各位读者转载、引用。本文选自《药学进展》2025年第 6 期。《药学进展》杂志由教育部主管、中国药科大学主办，中国科技核心期刊（中国科技论文统计源期刊）。刊物以反映药学科研领域的新方法、新成果、新进展、新趋势为宗旨，以综述、评述、行业发展报告为特色，以药学学科进展、技术进展、新药研发各环节技术信息为重点，是一本专注于医药科技前沿与产业动态的专业媒体。《药学进展》注重内容策划、加强组稿约稿、深度挖掘、分析药学信息资源、在药学学科进展、科研思路方法、靶点机制探讨、新药研发报告、临床用药分析、国际医药前沿等方面初具特色；特别是医药信息内容以科学前沿与国家战略需求相合，更加突出前瞻性、权威性、时效性、新颖性、系统性、实战性。根据最新统计数据，刊物篇均下载率连续三年蝉联我国医药期刊榜首，复合影响因子1.216，具有较高的影响力。《药学进展》编委会由国家重大专项化学药总师陈凯先院士担任主编，编委由新药研发技术链政府监管部门、高校科研院所、制药企业、临床医院、CRO、金融资本及知识产权相关机构近两百位极具影响力的专家组成。联系《药学进展》↓↓↓编辑部官网：pps.cpu.edu.cn；邮箱：yxjz@163.com；电话：025-83271227。欢迎投稿、订阅！往期推荐聚焦“兴药为民·2023生物医药创新融合发展大会”“兴药为民·2023生物医药创新融合发展大会”盛大启幕！院士专家齐聚杭城，绘就生物医药前沿赛道新蓝图“兴药强刊”青年学者论坛暨《药学进展》第二届青年编委会议成功召开“兴药为民·2023生物医药创新融合发展大会”路演专场圆满收官！校企合作新旅程已启航我知道你在看哟

临床研究

2025-04-14

·奇点网

JAMA子刊：“双药联手”谁更强？艾司氯胺酮联合传统抗抑郁药的5年真实世界数据发布

*仅供医学专业人士阅读参考艾司氯胺酮是氯胺酮的S-对映体，是一种快速起效的抗抑郁药，以鼻腔喷雾剂形式给药，于2019年获得美国FDA批准治疗难治性抑郁症（TRD），同年在中国获批。TRD患者对传统口服抗抑郁药，如选择性5-羟色胺再摄取抑制剂（SSRI）和去甲肾上腺素-5-羟色胺再摄取抑制剂（SNRI）的治疗无反应，临床上，患者可以选择艾司氯胺酮与SSRI或SNRI联合使用。与其他真实世界中的联合用药策略相比，艾司氯胺酮联合SSRI或SNRI通常在6个月后表现出显著的功能改善。但是，有效的TRD治疗还应该考虑患者的临床特征。确定最佳联合用药方案，使疗效最大化和不良反应最小化，是当前研究的重要方向。鉴于TRD的慢性特征，研究结局不应局限于治疗反应，还应包括住院率、死亡风险和自杀倾向等。来自意大利罗马大学的研究团队评估了艾司氯胺酮联合SSRI或SNRI治疗TRD的临床结局差异。研究结果显示，接受艾司氯胺酮联合SNRI治疗的患者全因死亡率、住院率和抑郁复发率显著低于接受艾司氯胺酮联合SSRI治疗的患者，但是后者的自杀企图发生率略低。研究发表在《JAMA·精神病学》杂志上。研究使用了TriNetX数据库中的数据进行回顾性研究，通过逻辑回归进行倾向性评分分配（PSM）。根据治疗方案进行分组，艾司氯胺酮+SSRI组包括艾司氯胺酮联合西酞普兰、艾司西酞普兰、氟西汀、氟伏沙明、帕罗西汀、舍曲林或维拉佐酮；艾司氯胺酮+SNRI组包括艾司氯胺酮联合文拉法辛、米那普仑、度洛西汀、去甲文拉法辛或左旋米那普仑。将首次艾司氯胺酮处方作为观察期起点时间，持续5年。主要结局包括全因死亡、住院、抑郁复发和自杀企图。死亡定义为观察期内发生的任何死亡事件。研究最终纳入55480名TRD患者，每个治疗组包括27740名个体，女性比例约为58%，平均年龄约为46岁。主要研究结局在5年观察期内，总体来说，所有患者的全因死亡率为7.20%，住院率为0.10%，抑郁复发率为17.78%，自杀企图发生率为0.39%。分别来看，艾司氯胺酮联合SNRI组的临床结局优于艾司氯胺酮联合SSRI组。与艾司氯胺酮联合SNRI相比，接受艾司氯胺酮联合SSRI与全因死亡风险升高72%有关（9.1% vs 5.3%），与住院风险升高201%有关（0.2% vs 0.1%），与抑郁复发风险升高43%有关（21.2% vs 14.8%）。但是，艾司氯胺酮联合SSRI组在5年内的自杀企图发生率较低，为0.3%，艾司氯胺酮联合SNRI组为0.5%，RR为0.70。Kaplan-Meier生存分析显示，艾司氯胺酮联合SNRI组的5年生存率高于SSRI组（91.4% vs 86.9%），差异具有统计学意义，RR为1.68。Kaplan-Meier生存曲线事实上，在全部研究样本中，艾司氯胺酮联合SSRI或SNRI在所有结局中都表现出持续低风险，年死亡率仅为1.4%；年住院率为0.02%，低于TRD患者通常报告的0.3%；抑郁年复发率为3.5%，远低于此前报告的TRD患者6个月内复发率70%；自杀企图年发生率为0.08%，而TRD患者自杀企图年发生率估计为4.66%。研究从全球真实世界数据出发，综合展示了两种用药方案的差异化结局。虽然无法确定艾司氯胺酮联合SNRI在真实世界中优于其他治疗方案的潜在原因，但依然对优化个体治疗策略具有重要意义。参考文献：Del Casale A, Spirito S, Arena J F, et al. Esketamine Combined With SSRI or SNRI for Treatment-Resistant Depression[J]. JAMA psychiatry, 2025. 本文作者丨王雪宁

临床结果

100 项与依地普仑相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D07913	依地普仑	N06AB10	DB01175

研发状态

10 条进展最快的记录,

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适应症	最高研发状态	国家/地区	公司	日期
抑郁症	临床前	-	Aquestive Therapeutics, Inc.	-

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临床结果

适应症

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT05470465 (CTgov)	临床1期	高碳酸血症	27	Placebo+Oxycodone (Treatment A: Placebo)	餘廠鹽鹹蓋鬱製齋鑰鏇(願網齋蓋遞廠鬱憲壓艱) = 襯憲遞壓壓壓簾構醖範艱鹽獵選簾製齋築廠壓 (窪淵淵鑰選齋鹽醖選鏇, 夢鏇齋夢衊壓淵夢糧繭 ~ 觸構顧簾醖淵衊憲構鏇) 更多	-	2025-05-22
				Paroxetine+Oxycodone (Treatment B: Paroxetine)	餘廠鹽鹹蓋鬱製齋鑰鏇(願網齋蓋遞廠鬱憲壓艱) = 艱獵構糧簾齋壓製糧餘艱鹽獵選簾製齋築廠壓 (窪淵淵鑰選齋鹽醖選鏇, 齋製艱廠糧選選鏇簾蓋 ~ 窪築糧鏇鏇艱夢簾觸窪) 更多
NCT03429075 (Psilodep-RCT, CTgov)	临床2期	重度抑郁症	59	Psilocybin + Placebo (Psilocybin)	廠衊獵醖糧廠繭醖襯網(壓築構淵壓遞鹹壓網窪) = 膚築鹹襯憲衊鏇艱簾積壓簾鑰鹹憲艱網餘壓淵 (願網願齋襯淵構獵壓壓, 0.45) 更多	-	2024-10-24
				Psilocybin + Escitalopram (Escitalopram)	廠衊獵醖糧廠繭醖襯網(壓築構淵壓遞鹹壓網窪) = 淵觸夢鏇觸齋窪夢糧鬱壓簾鑰鹹憲艱網餘壓淵 (願網願齋襯淵構獵壓壓, 0.62) 更多
NCT03429075 (Literature) 人工标引	临床2期	中度重度抑郁症	59	Psilocybin combined with psychological support	製糧襯醖蓋鹹鑰願願窪(艱夢艱築夢簾鏇鹽壓憲): Difference = 1.51 (95% CI, -1.35 ~ 4.38), P-Value = 0.311 更多	积极	2024-09-21
				Escitalopram combined with psychological support
NCT00361218 (CTgov)	临床3期	重度抑郁症	72	SSRI+selective serotonin reuptake inhibitor+escitalopram+citalopram	製艱積壓鬱襯願獵壓窪(簾製廠遞夢遞簾觸顧憲) = 鹽廠構襯廠觸鹽蓋糧範淵觸蓋積壓網淵觸製積 (膚鏇艱範夢餘範遞齋網, 4371.67) 更多	-	2013-09-26