Attempts to quit cigarette smoking are often accompanied by negative mood and problems in attention and memory. These effects, in turn, may contribute to smoking relapse. This exploratory/developmental project examines the effects of a novel medication, GTS-21, on individuals interested in smoking cessation. It is hypothesized that GTS-21 will reduce negative affect, improve cognition and/or reduce smoking relapse in healthy adult men and women who are chronic cigarette smokers.

开始日期2018-09-29

申办/合作机构

University of Florida

[+1]

NCT02458313

/ Completed临床1期IIT

Nicotinic Agonist Effects on BMI and Neuronal Response in Overweight/Obese Adults

Obesity is a serious and growing health problem in the United States. Obesity is associated with health problems such as type-2 diabetes and cardiovascular disease, leading to decreased quality of life and increased mortality. Given the health and quality-of-life effects of obesity, developing effective treatments clearly is an important goal.
This study plans to learn more about the effects of an investigational new drug (DMXB-A (3-(2,4-dimethoxybenzylidene anabaseine)) and its effects on obesity. The study drug has similar effects to nicotine. Since nicotine has been found to affect appetite, the investigators are interested in studying effects of the study drug, which has some similarities to nicotine, on how your brain responds to such things as pictures of food. The study drug has not been approved by the Food and Drug Administration (FDA), and is considered experimental.

开始日期2016-04-14

申办/合作机构

University of Colorado Denver

NCT02538081

/ Withdrawn临床1/2期IIT

Nicotinic Receptors and Schizophrenia

This study proposes to conduct a clinical trial comparison of olanzapine and the combination of a nicotinic cholinergic agonist, 3-[2,4-Dimethoxybenzylidene]anabaseine (DMXB-A) with a dopamine D2 receptor antagonist, the mechanism common to all antipsychotic drugs, to test the hypothesis that 7-nicotinic receptor agonism may be an additional necessary factor that enhances the efficacy of olanzapine that allows its slight superiority to risperidone. This trial would enroll patients taking olanzapine and record baseline measurements of clinical symptoms, cognition, metabolic parameters, and extrapyramidal side effects. The subjects would then be randomized to receive either risperidone or risperidone plus DMXB-A for 6 weeks and then would again have measurements of clinical symptoms, cognition, metabolic parameters and extrapyramidal side effects.

开始日期2015-08-01

申办/合作机构

VA Office of Research and Development

[+1]

100 项与 DMXB-Anabaseine 相关的临床结果

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100 项与 DMXB-Anabaseine 相关的转化医学

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100 项与 DMXB-Anabaseine 相关的专利（医药）

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项与 DMXB-Anabaseine 相关的文献（医药）

2026-03-01·EXPERIMENTAL NEUROLOGY

Alpha 7 nicotinic acetylcholine receptor contributes to long-term cognitive recovery following ischemic stroke

Article

作者: Tan, Chunfeng ; Hall, Cassandra ; Chauhan, Anjali ; Mendoza, Kate ; Nguyen, Dustin T

Stroke is associated with autonomic dysfunction and reduced acetylcholine (ACh), a neurotransmitter critical for cognition. ACh signals in part through the alpha-7 nicotinic acetylcholine receptor (α7nAChR), a ligand-gated ion channel involved in synaptic plasticity, learning, and memory. Impaired α7nAChR signaling has been linked to heightened neuroinflammation and poor acute stroke recovery. Here, we investigated whether α7nAChR contributes to post-stroke cognitive recovery in young male mice. Wild-type (WT) and α7nAChR knockout (α7n⁰KO) mice underwent 60-min middle cerebral artery occlusion (MCAO). In a pharmacology cohort, the α7nAChR agonist GTS-21 was administered immediately after reperfusion and then daily for 20 days. Cognitive performance was assessed by novel object recognition (day 10), object location (day 20), and Barnes maze and open field testing (day 28). Mass spectrometry at 24 h quantified brain ACh. Flow cytometry at 24 h, 7 days, and 30 days measured microglial and brain F4/80 macrophages. Immunohistochemistry at day 30 evaluated gliosis and neurogenesis. WT mice showed reduced ipsilateral ACh and α7nAChR⁺ microglia with increased TNF-α versus sham. Compared with WT, α7n⁰KO mice exhibited greater myeloid infiltration at 24 h, fewer IL-6⁺microglia and F4/80⁺macrophages with impaired STAT3/SOCS3 signaling at day 7, and by day 30, reduced reparative microglia, fewer F4/80⁺ macrophages, greater tissue loss, demyelination, gliosis, reduced SVZ neurogenesis, and impaired cognitive recovery. GTS-21 treatment improved cognition and reduced gliosis, supporting a protective role for α7nAChR activation. In conclusion, α7nAChR signaling supports reparative immune programs and promotes neurorepair after stroke, thereby enhancing long-term cognitive recovery.

2025-05-01·INTERNATIONAL IMMUNOPHARMACOLOGY

GTS-21 alleviates sepsis-induced atrial fibrillation susceptibility by modulating macrophage polarization and Neuregulin-1 secretion

Article

作者: Liu, Qiming ; Li, Shunyi ; Wu, Keke ; Zhang, Yusha ; Li, Fanqi ; Zhou, Jiabao ; Zhu, Jiayi ; Zhou, Yong ; Lin, Qiuzhen ; Zhang, Zixi ; Wan, Cancan ; Tu, Tao ; Ma, Yingxu ; Tan, Siyuan ; Zeng, Gaoming

OBJECTIVE:

Sepsis-induced atrial fibrillation (AF) is driven by systemic inflammation and macrophage-mediated atrial remodeling, with proinflammatory M1 macrophages playing a key role. This study investigates whether GTS-21, an α7nAChR agonist, can reduce AF susceptibility by promoting macrophage polarization towards the anti-inflammatory M2 phenotype.

METHODS:

A mouse model of lipopolysaccharide (LPS) (10 mg/kg)-induced sepsis was used to explore the relationship between atrial inflammation and AF. GTS-21 (20 mg/kg) was administered to assess its impact on 48-h survival and AF incidence. Cardiac function was evaluated using echocardiography. Markers of myocardial injury, including CK-MB, LDH, and cTnI, were measured. Macrophage polarization and atrial inflammation were assessed using immunofluorescence, flow cytometry, RT-qPCR, and western blotting. Oxidative stress and mitochondrial function were evaluated using reactive oxygen species (ROS) measurements, electron microscopy, and mitochondrial protein expression analysis. Calcium dynamics were studied using western blotting and confocal microscopy.

RESULTS:

In LPS-induced septic mice, GTS-21 improved 48-h survival rates and reduced the induction rate and duration of AF (P < 0.05). Echocardiography showed a preserved left ventricular ejection fraction and enhanced diastolic function. Mechanistically, it promoted M2 macrophage polarization, inhibited the NF-κB P65/NLRP3/C-caspase 1 pathway to reduce IL-1β release, and alleviated oxidative stress. Additionally, mitochondrial structure was restored by reversing fission and promoting fusion, while calcium-handling proteins (NCX-1, RYR2, and SERCA2a) were regulated to prevent intracellular calcium overload, reducing AF susceptibility.

CONCLUSION:

GTS-21 mitigated atrial inflammation and reduced the incidence of AF in mice with sepsis by regulating macrophage polarization, reducing oxidative stress, and preserving mitochondrial and calcium dynamics in cardiomyocytes. These findings highlight the therapeutic potential of GTS-21 in treating sepsis-induced AF.

2025-04-01·Zhonghua wei zhong bing ji jiu yi xue

[Research progress on the potential mechanisms and effects of the cholinergic anti-inflammatory pathway in sepsis].

Review

作者: Sun, Bin ; Luo, Xiaoyan

Sepsis is a common clinical syndrome in intensive care unit (ICU) with high morbidity and high mortality, making it a global health issue. The estimated global incidence of sepsis is 437/100 000, with an in-hospital mortality of 17%, which is higher in developing countries and underdeveloped regions. Despite some progress in sepsis treatment in recent years, the complexity of its pathophysiology limits therapeutic effectiveness. The cholinergic anti-inflammatory pathway (CAP), a neuro-immune regulatory pathway, plays a crucial role in sepsis through key components such as the vagus nerve, central M-type muscarinic receptor, the spleen and splenic sympathetic nerves, acetylcholine, and the α7 subunit of the nicotinic acetylcholine receptor (α7nAChR). This article explores the potential mechanisms and roles of CAP in sepsis, focusing on CAP-related cell signaling pathways, including nuclear factor-κB (NF-κB) signaling pathway, Janus kinase/signal transducer and activator of transcription 3 (JAK/STAT3) signaling pathway, phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway, and cyclooxygenase (COX) and prostaglandin E2 (PGE2) signaling pathways. Potential applications of CAP in sepsis treatment include stimulating the vagus nerve (e.g., through pharmacological, electrical, or acupuncture stimulation), using α7nAChR agonists (e.g., nicotine, GTS-21, and PNU-282987), adrenergic receptor agonists (e.g., dexmedetomidine and salbutamol), or other drugs and bioactive substances (e.g., buprenorphine and traditional Chinese medicine components). These approaches aim to activate CAP, suppress inflammatory responses, and improve sepsis prognosis, providing a theoretical basis for treatment and promoting the development of related drugs.

项与 DMXB-Anabaseine 相关的新闻（医药）

2025-12-02

·结直肠肛门外科杂志

【综述】胆碱能抗炎通路在炎症性肠病治疗中的研究进展

高江波1，李文萱1，倪敏2△ 1 南京中医药大学 2 南京中医药大学附属南京中医院肛肠中心引用信息：高江波, 李文萱，倪敏. 胆碱能抗炎通路在炎症性肠病治疗中的研究进展[J]. 结直肠肛门外科, 2025, 31(5): 481-484. 摘要炎症性肠病包括溃疡性结肠炎和克罗恩病，是一种慢性肠道炎症性疾病，其病理生理机制涉及免疫失衡、遗传易感与肠道菌群紊乱等多重因素，尚未完全阐明。近年来，胆碱能抗炎通路的发现为炎症性肠病治疗提供了新方向，该通路通过迷走神经调节免疫反应，抑制促炎性细胞因子的产生，从而减轻肠道炎症。本文系统回顾了胆碱能抗炎通路的生物学机制及其在炎症性肠病中的作用，对靶向该通路治疗炎症性肠病的研究进展作一综述，以期为炎症性肠病的治疗提供新的策略与理论依据。［关键词］炎症性肠病；胆碱能抗炎通路；迷走神经；α7烟碱型乙酰胆碱受体炎症性肠病（inflammatory bowel disease，IBD）是一组以慢性、反复发作的肠道炎症为特征的疾病，可波及回肠、结肠乃至直肠，常见症状包括腹泻、腹痛、便血和体重下降等，可分为溃疡性结肠炎（ulcerative colitis，UC）和克罗恩病（Crohn’s disease，CD）这两型[1]。近年来，IBD的全球发病率持续攀升，目前全球约有超过2 000万的IBD患者[2]。临床上，主要依赖糖皮质激素、免疫抑制剂及生物制剂等对IBD进行治疗，但长期使用后往往伴随严重的药物副作用，如出现免疫抑制、感染风险增加和耐药性等[3]，因此亟需探索更为安全有效的新型治疗方式。在此背景下，作为“炎症反射”核心效应通路的胆碱能抗炎通路（cholinergic anti-inflammatory pathway，CAP）为IBD的治疗提供了全新视角。该通路通过迷走神经释放神经递质乙酰胆碱（acetylcholine，ACh），ACh与免疫细胞表面的α7烟碱型乙酰胆碱受体（α7 nicotinic acetylcholine receptor，α7nAChR）结合后，能有效抑制TNF-α等关键促炎因子的产生。本文结合文献资料，对CAP的生物学机制在IBD中的作用及靶向该通路的前沿治疗策略作一综述，以期为IBD的治疗提供新的理论依据与干预思路。 1 CAP的生物学机制及在IBD发病机制中的作用 CAP由Borovikova等[4]在2000年首次提出，该研究阐明了迷走神经通过释放ACh有效调控系统性炎症反应的病理进程，并据此构建了“炎症反射”的理论框架。之后，Murray等[5]对该通路进行了系统梳理，强调CAP兼具传入、整合与传出三条反射弧，并指出α7nAChR是执行抑炎效应的分子枢纽。 CAP在机体中发挥作用的具体过程如下：当炎症反应发生时，炎性因子会激活迷走神经的传入纤维，该信号经由延髓孤束核中继，最终通过迷走神经的传出纤维，作用于支配脾脏的儿茶酚胺能纤维，从而促进去甲肾上腺素（norepinephrine，NE）的释放。经脾脏生成的一种表达胆碱乙酰转移酶的T细胞上存在β2肾上腺素能受体，NE与其结合后释放ACh。之后，ACh通过作用于免疫细胞表面的α7nAChR，一方面抑制NF-κB的信号转导，另一方面激活细胞内的JAK2/STAT3信号通路，共同抑制炎性因子的释放，从而实现抗炎效果[5-6]。因此，α7nAChR的激活在CAP介导的抗炎过程中具有核心调节作用，被视为外周免疫系统感知胆碱能信号的“主开关”[7-9]。Lv等[10]等针对自身免疫性风湿病进行研究，发现激活α7nAChR不仅可以抑制NF‑κB和JAK‑STAT信号通路，还能重塑树突状细胞与调节性T细胞之间的平衡，进一步拓展了CAP的免疫学内涵。 IBD的核心病理环节为免疫失衡与肠上皮屏障破坏[11-12]，根据现有报道，CAP可以通过直接参与抑制这两个病理过程，在维持肠道稳态、抑制IBD发展方面发挥重要作用。在免疫层面，CAP是一个关键的内源性负向调节通路，迷走神经被刺激后释放的ACh与巨噬细胞和树突状细胞表面的α7nAChR结合，可抑制NF-κB与NLRP3炎症小体活化，降低TNF-α、IL-6等促炎因子的表达并重塑Th17/Treg细胞比例，进而限制炎症反应的发展[13-15]。除此之外，CAP经α7nAChR-AMPK/mTOR-自噬轴上调Occludin、Claudin-1等紧密连接蛋白的表达，降低肠上皮通透性与细菌移位，维持黏膜完整与免疫稳态[16-18]。 2 靶向CAP的IBD治疗策略 2.1 神经调控技术随着对CAP机制理解的逐步深入，神经调控技术在IBD治疗领域的应用潜力逐渐成为研究热点。其中，迷走神经刺激（vagus nerve stimulation，VNS）通过电刺激激活连接大脑与内脏的中枢—外周神经免疫轴，并借助其传入与传出纤维的双重作用来抑制促炎性细胞因子的分泌，目前已在多种IBD动物模型中显示出良好的抗炎效果[19-21]。Meroni等[22]发现，VNS可通过促进上皮细胞增殖、抑制细胞凋亡、减少促炎细胞因子（如TNF-α和CXCL1）表达，从而改善肠上皮屏障功能。非侵入式耳迷走神经刺激（transcutaneous auricular vagus nerve stimulation，ta-VNS）同样有助于改善结肠炎症并减少促炎因子的释放[23]。低强度超声（low-intensity ultrasound，LIUS）作为另一种非侵入性神经调控技术，能同时激活迷走神经与脾神经，促进α7nAChR的表达[24]。临床上，Bonaz等[25]发现，在6个月的随访时间内，VNS可显著降低CD患者的克罗恩病活动指数（Crohn’s disease activity index，CDAI）及C-反应蛋白水平。Sinniger等[26]进行的一项为期12个月的临床研究结果显示，在纳入的9例CD患者中，采用VNS治疗后，5例患者实现了临床缓解，6例患者在内镜检查下提示已达到缓解状态。此外，6例患者的C-反应蛋白和5例患者的粪钙卫蛋白水平均降低。D’Haens等[27]发布的一项多中心前瞻性研究进一步指出，短程程序化VNS能同步下调CD患者粪钙卫蛋白与血清TNF-α的表达，并使60%患者达到临床缓解。总之，目前国内外关于CAP介入治疗IBD的临床研究多以VNS为主要干预手段，未来进一步规范刺激参数、扩大样本量并完善长期随访，将有助于全面评估CAP在IBD治疗中的实际价值及其临床应用前景。 2.2 胆碱能药物胆碱能药物通过激活α7nAChR或抑制ACh的降解，从而靶向CAP发挥作用。Ye等[16]在UC小鼠模型中发现，α7nAChR激动剂GTS-21可通过上调紧密连接蛋白（如ZO-1和Occludin）的表达增强肠黏膜的屏障功能，进而减轻结肠的炎症损伤。还有研究发现，α7nAChR的另一种激动剂PNU‑282987能够上调α7nAChR的表达水平，激活AMPK-mTOR-自噬通路，促进巨噬细胞向M2表型转化，下调TNF‑α、IL‑6表达水平，为IBD的治疗提供了新的治疗靶点[17]。Singh等[28]的研究认为，吡斯的明溴化物可以延长UC小鼠模型体内ACh的作用时间，间接激活CAP并增强抗炎效应，改善了肠道菌群失调状态，从而减轻肠道病理损伤。随着对CAP作用机制的解析逐步深入，以α7nAChR为靶点的创新药物研发有望持续拓展，为IBD临床治疗提供更具精准性的干预策略选择。 3 未来研究方向与挑战目前，关于CAP在IBD治疗中的研究仍面临一些局限性。首先，大部分疗效证据来自小规模的动物实验[29]；其次，神经刺激的参数设定（例如频率、波形）尚缺乏统一标准，即使采用相同的技术，不同研究报告的应答率仍存在差异[30]。未来的研究可以重点关注以下几个方向：第一，融合多种前沿技术手段，以深化对CAP在IBD中作用机理的理解。例如，可通过单细胞测序解析肠道细胞对CAP调节的反应，并结合代谢组学追踪ACh与肠道微生物代谢产物之间的相互作用[31]。第二，通过实时监测心率变异性来动态优化神经刺激参数，从而提升治疗效果[32]。第三，设计适应性临床试验，应用富集策略筛选基线迷走神经张力＞2.5 Ln[ms2]的高反应患者。有研究表明，此类患者的临床缓解率较未筛选人群更高[33]。VNS与生物制剂还存在协同作用，据报道，两者联合治疗能够使IBD黏膜愈合率由23%提升至48%[34]。在技术层面，神经刺激信号的特异性尚待提高，降低非靶信号（如胃肠道运动引起的伪信号）干扰对于精准治疗至关重要。另外，现有神经调控装置体积较大（植入设备体积＞8 cm3），设备的微型化和便携化需求迫切[30]。伦理方面的争议主要集中在神经调控应用的边界问题。例如，当在IBD缓解期采用VNS预防炎症复发时，应将其归类为“治疗”还是“功能增强”，目前尚无明确的法律界定[35]。此外，智能闭环系统所采集的自主神经数据可能会泄露患者的心理状态（如焦虑水平），因此需建立符合美国HIPAA（《健康保险可携性和责任法案》）标准的去识别化数据架构来保护患者隐私[32]。 4 小结 CAP的发现为IBD的治疗开辟了新的方向。通过调节CAP，包括VNS和胆碱能药物等，可以有效减轻肠道的炎症反应。尽管在动物模型中已取得突破性进展，但CAP相关疗法的临床转化仍面临多重挑战，包括给药途径优化、个体化治疗响应差异及长期安全性评估等关键瓶颈问题。未来仍需进行大规模、多中心的临床试验，以全面评估CAP在IBD治疗中的疗效与安全性。未来CAP有望成为IBD治疗的重要补充，为IBD患者提供新的治疗选择。利益冲突声明全体作者均声明不存在与本文相关的利益冲突。参考文献 [1] BRUNER L P, WHITE A M, PROKSELL S. Inflammatory bowel disease[J]. Primary care, 2023, 50(3): 411-427. [2] NG S C, SHI H Y, HAMIDI N, et al. Worldwide incidence and prevalence of inflammatory bowel disease in the 21st century: a systematic review of population-based studies[J]. The Lancet, 2017, 390(10114): 2769-2778. [3] KIRCHGESNER J, LEMAITRE M, CARRAT F, et al. Risk of serious and opportunistic infections associated with treatment of inflammatory bowel diseases[J]. Gastroenterology, 2018, 155(2): 337-346. e10. [4] BOROVIKOVA L V, IVANOVA S, ZHANG M, et al. Vagus nerve stimulation attenuates the systemic inflammatory response to endotoxin[J]. Nature, 2000, 405(6785): 458-462. [5] MURRAY K, REARDON C. The cholinergic anti-inflammatory pathway revisited[J]. Neurogastroenterology and motility, 2018, 30(3): e13288. [6] ALEN N V. The cholinergic anti-inflammatory pathway in humans: state-of-the-art review and future directions[J]. Neuroscience and biobehavioral reviews, 2022, 136: 104622. [7] BERTRAND D, LEE C H, FLOOD D, et al. Therapeutic potential of α7 nicotinic acetylcholine receptors[J]. Pharmacological reviews, 2015, 67(4): 1025-1073. [8] ROA-VIDAL N, RODRÍGUEZ-APONTE A S, LASALDE-DOMINICCI J A, et al. Cholinergic polarization of human macrophages[J]. International journal of molecular sciences, 2023, 24(21): 15732. [9] QIN Z, XIANG K, SU D F, et al. Activation of the cholinergic anti-inflammatory pathway as a novel therapeutic strategy for COVID-19[J]. Frontiers in immunology, 2021, 11: 595342. [10] LV J Q, JI X X, LI Z, et al. The role of the cholinergic anti-inflammatory pathway in autoimmune rheumatic diseases[J]. Scandinavian journal of immunology, 2021, 94(4): e13092. [11] SHEN B, ABREU M T, COHEN E R, et al. Endoscopic diagnosis and management of adult inflammatory bowel disease: a consensus document from the American Society for Gastrointestinal Endoscopy IBD Endoscopy Consensus Panel[J]. Gastrointestinal endoscopy, 2025, 101(2): 295-314. [12] SINGH N, BERNSTEIN C N. Environmental risk factors for inflammatory bowel disease[J]. United European gastroenterology journal, 2022, 10(10): 1047-1053. [13] PU W Y, SU Z Z, WAZIR J, et al. Protective effect of α7 nicotinic acetylcholine receptor activation on experimental colitis and its mechanism[J]. Molecular medicine, 2022, 28(1): 104. [14] HE Y, ZHU Y R, GUO Y L, et al. α7nAChR activation promotes the generation of Treg cells by enhancing the dephosphorylation of Foxo1 via the IP3R/Ca2+/calcineurin pathway[J]. Biochemical pharmacology, 2025, 242(Pt 1): 117290. [15] ATES G, OZGUR I, SORMAZ I C. Paradoxical regulation of α7nAChR and NLRP3 inflammasome in gastrointestinal cancers and ulcerative colitis[J]. Metabolites, 2025, 15(9): 622. [16] YE Z P, ZHU Y J, TANG N N, et al. α7 nicotinic acetylcholine receptor agonist GTS-21 attenuates DSS-induced intestinal colitis by improving intestinal mucosal barrier function[J]. Molecular medicine, 2022, 28(1): 59. [17] SHAO B Z, WANG S L, FANG J, et al. α7 nicotinic acetylcholine receptor alleviates inflammatory bowel disease through induction of AMPK-mTOR-p70S6K-mediated autophagy[J]. Inflammation, 2019, 42(5): 1666-1679. [18] GUO L N, CHEN Q, GAO Y Y, et al. CDP-choline modulates cholinergic signaling and gut microbiota to alleviate DSS-induced inflammatory bowel disease[J]. Biochemical pharmacology, 2023, 217: 115845. [19] BONAZ B, SINNIGER V, PELLISSIER S. Anti-inflammatory properties of the vagus nerve: potential therapeutic implications of vagus nerve stimulation[J]. The journal of physiology, 2016, 594(20): 5781-5790. [20] BONAZ B, SINNIGER V, PELLISSIER S. Vagus nerve stimulation: a new promising therapeutic tool in inflammatory bowel disease[J]. Journal of internal medicine, 2017, 282(1): 46-63. [21] HOOVER D B. Cholinergic modulation of the immune system presents new approaches for treating inflammation[J]. Pharmacology & therapeutics, 2017, 179(1): 1-16. [22] MERONI E, STAKENBORG N, GOMEZ-PINILLA P J, et al. Vagus nerve stimulation promotes epithelial proliferation and controls colon monocyte infiltration during DSS-induced colitis[J]. Frontiers in medicine, 2021, 8: 694268. [23] HESAMPOUR F, TSHIKUDI D M, BERNSTEIN C N, et al. Exploring the efficacy of transcutaneous auricular vagus nerve stimulation in experimental models of colitis[J]. Bioelectronic medicine, 2024, 10(1): 29. [24] NUNES N S, CHANDRAN P, SUNDBY M, et al. Therapeutic ultrasound attenuates DSS-induced colitis through the cholinergic anti-inflammatory pathway[J]. EBioMedicine, 2019, 45(7): 495-510. [25] BONAZ B, SINNIGER V, HOFFMANN D, et al. Chronic vagus nerve stimulation in Crohn’s disease: a 6-month follow-up pilot study[J]. Neurogastroenterology and motility, 2016, 28(6): 948-953. [26] SINNIGER V, PELLISSIER S, FAUVELLE F, et al. A 12-month pilot study outcomes of vagus nerve stimulation in Crohn’s disease[J]. Neurogastroenterology and motility, 2020, 32(10): e13911. [27] D’HAENS G, EBERHARDSON M, CABRIJAN Z, et al. Neuroimmune modulation through vagus nerve stimulation reduces inflammatory activity in Crohn’s disease patients: a prospective open-label study[J]. Journal of Crohn’s and colitis, 2023, 17(12): 1897-1909. [28] SINGH S P, CHAND H S, BANERJEE S, et al. Acetylcholinesterase inhibitor pyridostigmine bromide attenuates gut pathology and bacterial dysbiosis in a murine model of ulcerative colitis[J]. Digestive diseases and sciences, 2020, 65(1): 141-149. [29] DILIXIATI S, YAN J X, QINGZHUOGA D, et al. Exploring electrical neuromodulation as an alternative therapeutic approach in inflammatory bowel diseases[J]. Medicina (Kaunas), 2024, 60(5): 729. [30] HESAMPOUR F, BERNSTEIN C N, GHIA J E. Brain-gut axis: Invasive and noninvasive vagus nerve stimulation, limitations, and potential therapeutic approaches[J]. Inflammatory bowel diseases, 2024, 30(3): 482-495. [31] ALJERADAT B, KUMAR D, ABDULMUIZZ S, et al. Neuromodulation and the gut-brain axis: therapeutic mechanisms and implications for gastrointestinal and neurological disorders[J]. Pathophysiology, 2024, 31(2): 244-268. [32] LIU F J, WU J, GONG L J, et al. Non-invasive vagus nerve stimulation in anti-inflammatory therapy: mechanistic insights and future perspectives[J]. Frontiers in neuroscience, 2024, 18: 1490300. [33] GABALSKI A H, TYNAN A, TSAAVA T, et al. Circulating extracellular choline acetyltransferase regulates inflammation[J]. Journal of internal medicine, 2024, 295(3): 346-356. [34] IIZUKA M, ETOU T, SAGARA S, et al. Efficacy of cytapheresis in patients with ulcerative colitis showing insufficient or lost response to biologic therapy[J]. World journal of gastroenterology, 2022, 28(34): 4959-4972. [35] BUTT M F, ALBUSODA A, FARMER A D, et al. The anatomical basis for transcutaneous auricular vagus nerve stimulation[J]. Journal of anatomy, 2020, 236(4): 588-611. 点击此处，下载原文 RECOMMEND 往期推荐 ◆《结直肠肛门外科》杂志2025年第5期内容通告 ◆【《结直肠肛门外科》杂志“说文论道”云端学术厅公益讲座（2025年第五期）】——肛瘘外科治疗新进展 ◆【专题述评】复杂性肛瘘的诊疗进展及思考 ◆【专题论著】“存体寡损”思想指导下的高位肛瘘术后肛门功能研究 ◆【专题论著】带蒂组织瓣翻转肌间填塞闭合术在括约肌上型肛瘘外科治疗中的应用: 基于12例患者的回顾性分析 ◆【专题论著】括约肌外型肛瘘亚型及手术方式的临床研究：基于47例患者的回顾性分析 ◆【专题论著】经括约肌间瘘管结扎术治疗30例克罗恩病肛瘘患者的疗效分析 ◆【直播回看】“说文论道”云端学术厅公益讲座（2025年第五期）——肛瘘外科治疗新进展 ◆精选论文 | 专题论坛——肛瘘外科治疗新进展（2025年第5期） ◆【手术技术论坛】“主桅杆”式牵拉法在机器人结直肠手术中的应用 ◆【海外采风论坛】括约肌间复合体作为超低位直肠癌潜在转移部位的解剖学意义及其在经括约肌间切除术中完全切除对预后的影响 ◆【海外采风论坛】池诏丞(评论). 超低位直肠癌经括约肌间切除术与腹会阴联合切除术的长期有效性和短期结果比较 ◆【海外采风论坛】黄胜辉，阮浩杨(评论).采用双吻合技术的直肠癌和乙状结肠癌肠腔冲洗: 一项单中心前瞻性研究 ◆【海外采风论坛】局部进展期直肠癌全程新辅助治疗短程放疗后序贯卡培他滨加奥沙利铂联合信迪利单抗对比短程放疗后序贯卡培他滨加奥沙利铂 ◆【综述】肛管直肠测压在结直肠肛门疾病诊疗中的应用现状责编：韦佩茹校对：廖靖芳审核：马辉

100 项与 DMXB-Anabaseine 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
-	-	-	DB05708

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
注意缺陷障碍伴多动	临床2期	美国	CoMentis, Inc.	2007-02-01
阿尔茨海默症	临床2期	美国	CoMentis, Inc.	2006-11-01
精神分裂症	临床2期	美国	University of Colorado Denver	2005-01-01
认知障碍	临床2期	美国	CoMentis, Inc.	-
认知障碍	临床2期	-	The University of Colorado	-
自闭症	临床1期	美国	University of Colorado Denver	2015-06-01
血管迷走神经性晕厥	临床阶段不明	荷兰	CoMentis, Inc.	2008-08-01
心房颤动	临床前	-	中南大学	2025-05-01

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临床结果

适应症

分期

评价

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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


NCT02458313 (CTgov)	临床1期	肥胖	61	DMXB-A (DMXB-A)	廠淵願簾積鏇艱顧醖築(簾齋鑰餘獵壓製鏇網糧) = 醖獵襯襯廠繭齋範鬱繭鹹窪顧網繭壓艱觸餘憲 (餘選齋齋選觸衊膚構鏇, .073) 更多	-	2023-06-12
				Placebo (Placebo)	廠淵願簾積鏇艱顧醖築(簾齋鑰餘獵壓製鏇網糧) = 積鑰糧構簾獵蓋繭鹹網鹹窪顧網繭壓艱觸餘憲 (餘選齋齋選觸衊膚構鏇, .095) 更多
NCT00100165 (DMXB-A, CTgov)	临床2期	精神分裂症	29	Placebo	製鏇構鏇獵鹽膚範膚鏇(鹽積襯鑰窪衊鑰鹽夢淵) = 顧壓夢築鹽襯鏇簾壓觸夢蓋糧醖構醖淵夢淵觸 (廠積簾鑰齋淵膚醖範範, 7.3) 更多	-	2020-01-29
NCT01400477 (CTgov)	临床2期	分裂情感性障碍 \| 精神分裂症	97	DMXB-A-SR (DMXB-A-SR)	製觸醖鏇膚鹹鹹網鑰糧(衊願膚製糧製獵製鏇築) = 鏇繭鑰鏇網襯顧範繭窪鬱憲繭鹽淵餘憲構製獵 (襯窪齋繭鬱鏇鬱遞淵構, 5.8) 更多	-	2019-05-07
				Placebo (Arm #2: Placebo Comparator)	製觸醖鏇膚鹹鹹網鑰糧(衊願膚製糧製獵製鏇築) = 襯醖鑰範糧蓋鏇選構夢鬱憲繭鹽淵餘憲構製獵 (襯窪齋繭鬱鏇鬱遞淵構, 8.2) 更多