The goal of this study is to better understand the underlying neurobiological basis of anxiety that emerges during abstinence in patients with alcohol use disorder (AUD). The main questions it aims to answer are:
1. To characterize anxiety itself as well as anxiety related-neurobiological circuitry in early abstinence in AUD
2. To examine how anxiety and anxiety related-neurobiological circuitry change over the course of abstinence in AUD
Researchers will recruit both participants with AUD and healthy volunteers.
The participants with AUD will be prescribed disulfiram, a medication that helps participants with AUD stay abstinent. Healthy volunteers will not receive antabuse. Patients with AUD will undergo fMRI scanning both after 1 week and 3 months of disulfiram treatment. Healthy volunteers will undergo fMRI once.

开始日期2025-06-01

申办/合作机构

The Trustees of Columbia University in The City of New York

[+1]

CTRI/2025/04/083861

/ Not yet recruiting临床4期IIT

ultrasound evaluation of radial artery size and ease of cannulation post subcutaneous infiltration of nitroglycerine and lignocaine versus lignocaine in prospective comparative study - nil

开始日期2025-04-29

申办/合作机构-

CTRI/2025/04/084788

/ Not yet recruiting临床2/3期IIT

To evaluate the role of subcutaneous nitroglycerin in preventing radial artery spasm during transradial diagnostic cerebral angiography - NIL

开始日期2025-04-23

申办/合作机构-

100 项与 ALDH 相关的临床结果

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100 项与 ALDH 相关的转化医学

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0 项与 ALDH 相关的专利（医药）

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13,860

项与 ALDH 相关的文献（医药）

2025-12-31·Renal Failure

Combining mitochondrial proteomes and Mendelian randomization to identify novel therapeutic targets for diabetic nephropathy

Article

作者: Zhang, Jiaai ; Liu, Yang ; Zhou, Junan ; Zhou, Zhelun ; Wu, Rong ; Wang, Xiaoyi

Diabetic nephropathy (DN) is a common microvascular complication of diabetes. Mitochondrial dysfunction in the kidney caused by diabetes has previously been linked to the pathogenesis of DN. By mass spectrometry, we identified characteristic proteins of DN from the renal mitochondria in mouse model. To identify the core proteins among them, Mendelian randomization (MR) analysis, microarray data validation, and drug-target interaction analysis were employed. MR analysis found that 189 candidate targets had a causal link with DN risk factors (estimated glomerular filtration rate (eGFR), urinary albumin excretion, and serum creatinine). After systematic analysis, we validated that SLC25A16, CTNND1, C2CD2L, ALDH3A2, NEU1, APEH, CORO1A, NUDT19, and NDUFA4L2 are the core proteins with promising druggability in DN. This study suggests the feasibility of using MR analysis for DN drug target screening, and provides potential insights into mitochondrial dysfunction research, which may contribute to further DN pathogenesis exploration.

2025-12-31·Epigenetics

Acetaldehyde-driven mRNA methylation and expression changes in ethanol-metabolizing enzyme genes

Article

作者: Zhan, Qiansheng ; Zhang, Huiping ; Koo, Ji Sun

This study examines how the alcohol metabolite acetaldehyde modulates mRNA methylation and expression of ethanol-metabolizing genes, uncovering its epigenetic role in ethanol metabolism. Using neuron-like (SH-SY5Y) and non-neuronal (SW620) cellular models, we examined the effects of chronic intermittent acetaldehyde (CIA) exposure and subsequent withdrawal (CIA+WD) on global RNA m6A modifications and the methylation and expression of three brain ethanol-metabolizing genes: CAT (catalase), CYP2E1 (cytochrome P450 2E1), and ALDH2 (aldehyde dehydrogenase 2). A 3-week CIA exposure, with or without 24-hour withdrawal, did not significantly alter global m6A methylation levels in either cell line. However, acetaldehyde exposure/withdrawal induced hypermethylation at the mRNA stop codon regions of ALDH2 (CIA: p = 0.002; CIA+WD: p = 0.055) and CAT (CIA: p = 0.077; CIA+WD: p = 0.036) in SH-SY5Y cells, but not in SW620 cells. Furthermore, ALDH2 mRNA expression was significantly upregulated in both cell types following exposure (SH-SY5Y: p = 0.073 [CIA] and 0.00002 [CIA+WD]; SW620: p = 0.0009 [CIA] and 0.00008 [CIA+WD]). In contrast, CYP2E1 mRNA methylation and the expression of CYP2E1 and CAT remained unchanged. These findings highlight the cell-specific epigenetic effects of acetaldehyde, particularly its role in modulating mRNA methylation and expression of ALDH2, a key enzyme in alcohol metabolism.

2025-12-31·Annals of Medicine

Identification of ALDH7A1 as a DNA-methylation-driven gene in lung squamous cell carcinoma

Article

作者: He, Jinxian ; Zhang, Liang ; Yu, Kaizhong ; Shen, Weiyu ; Chen, Tian ; Liang, Gaofeng

BACKGROUNDDeoxyribose nucleic acid (DNA) methylation is an important epigenetic modification that plays an important role in the occurrence and development of tumors. Identifying key methylation-driven genes that affect the prognosis of lung squamous cell carcinoma (LUSC) can provide direction for targeted therapy research.METHODS AND RESULTSMethylation and RNA-seq data were downloaded from The Cancer Genome Atlas (TCGA). The MethylMix package was used to integrate and analyze the methylation and gene expression data from TCGA, and the LUSC dataset (GSE37745) was downloaded from GEO for validation. Forty-five DNA-methylation-driven genes (MDGs) were obtained, and 3 genes (TRIM61, SMIM22, and ALDH7A1) were significantly associated with survival by using univariate and multivariate Cox regression. A risk model was constructed. KM analysis showed that patients with high-risk scores had poor survival. A nomination plot for prognosis prediction of LUSC patients was constructed, which showed a good predictive efficiency for tumor prognosis. The high expression of ALDH7A1 was an independent risk factor for poor prognosis in LUSC. The expression of ALDH7A1 in LUSC was negatively correlated with its methylation status (COR = -0.655). GSEA analysis showed that high expression of ALDH7A1 could activate multiple signaling pathways (JAK-STAT signaling pathway and mTOR signaling pathway). In vitro cell experiments confirmed that in LUSC, silencing ALDH7A1 could inhibit tumor progression, while overexpression of ALDH7A1 could promote tumor progression.CONCLUSIONOur results indicated that ALDH7A1, a newly discovered MDG in LUSC, could act as an independent prognostic factor for OS in LUSC, with the potential to become a potential target for LUSC diagnosis and treatment. High expression of ALDH7A1 in LUSC could promote the occurrence and development of tumors. Signaling pathways, such as JAK-STAT and mTOR signaling pathways, might regulate the high expression of ALDH7A1.

122

项与 ALDH 相关的新闻（医药）

2025-04-29

·生物世界

癌症研究专题1：值得阅读的结直肠癌、乳腺癌研究高分文献分享

结直肠癌与乳腺癌作为全球高发恶性肿瘤，其发病机制复杂且治疗需求迫切，其发病机制与治疗耐药是研究热点。近期高分文献揭示：结直肠癌：QKI 蛋白通过调控 PABPN1 的液-液相分离影响 RNA 加工，其低表达与癌细胞增殖相关；FOXC1 介导丝氨酸代谢重编程，激活 ERK1/2 通路促进 5-FU 耐药，联合丝氨酸限制与靶向治疗或为新策略。三阴性乳腺癌（TNBC）：天然化合物 Pristimerin 靶向 HSPA8 激活 VAV1/ERK 通路，诱导自噬与凋亡，抑制转移并增变化疗敏感性；BCA2 通过 TLR4/NF-κB 通路上调 SOX9，促进干细胞特性，为克服耐药提供新靶点。这些研究从分子机制到治疗策略层层突破，为两类癌症的精准医疗提供了创新思路。文献分享一论文题目：BiFC and FACS-based CRISPR screening revealed that QKI promotes PABPN1 LLPS in colorectal cancer cells（BiFC 和 FACS-based CRISPR 筛选揭示 QKI 促进 PABPN1 的液-液相分离）期刊名：Protein & Cell论文总结：该研究开发了一种基于双分子荧光互补（BiFC）和荧光激活细胞分选（FACS）的 CRISPR 筛选平台，鉴定出肿瘤抑制因子 QKI 可促进 RNA 结合蛋白 PABPN1 的液-液相分离（LLPS）。在结直肠癌细胞中，QKI 表达降低及核定位减少会削弱 PABPN1 的 LLPS，进而促进近端多聚腺苷酸化（APA），增强癌细胞增殖和迁移能力。机制上，QKI 通过 KH 结构域与 PABPN1 直接结合，提升其 RNA 结合亲和力，调控 APA 过程。研究为 QKI 在结直肠癌中的抑癌作用提供了新视角，揭示了 LLPS 在肿瘤发生中的关键作用。胎牛血清产品货号：FSP500（南美优级胎牛血清）/ExCell Bio论文链接：https://doi.org/10.1093/procel/pwaf022文献分享二论文题目：Pristimerin Promotes Ubiquitination of HSPA8 and Activates the VAV1/ERK Pathway to Suppress TNBC Proliferation（Pristimerin 促进 HSPA8 泛素化并激活 VAV1/ERK 通路抑制三阴性乳腺癌）期刊名：Advanced Science论文总结：该研究发现，天然化合物 Pristimerin 通过靶向热休克蛋白 HSPA8，促进其泛素化降解，进而激活下游 VAV1/ERK 信号通路，诱导三阴性乳腺癌（TNBC）细胞自噬和凋亡。机制上，Pristimerin 抑制 HSPA8 介导的 VAV1 降解，增强 ERK 磷酸化，促进自噬起始并阻滞细胞周期于 G2/M 期。体内外实验显示，Pristimerin 显著抑制 TNBC 细胞增殖、迁移和侵袭，并增强其对阿霉素的敏感性，且无明显毒副作用。该研究为 TNBC 提供了一种靶向 HSPA8 的天然药物治疗策略。胎牛血清产品货号：FSP500（南美优级胎牛血清）/ExCell Bio论文链接：https://doi.org/10.1002/advs.202413174文献分享三论文题目：E3 ubiquitin ligase BCA2 promotes breast cancer stemness by up-regulation of SOX9 by LPS（E3 泛素连接酶 BCA2 通过 LPS 诱导 SOX9 上调促进乳腺癌干性）期刊名：International Journal of Biological Sciences文章总结：研究揭示 BCA2 作为 E3 泛素连接酶，通过增强 TLR4 与 MyD88 的相互作用，抑制 MyD88 与去泛素化酶 OTUD4 的结合，激活 LPS 介导的 NF-κB 信号通路，从而上调 SOX9 表达，促进三阴性乳腺癌（TNBC）干细胞（BCSCs）的干性维持。BCA2 敲除显著减少 ALDH + 和 CD44high/CD24low BCSCs 比例，抑制肿瘤球形成和体内成瘤能力。临床样本分析显示，BCA2 与 SOX9 表达呈正相关，且 BCA2 高表达与 TNBC 患者不良预后相关。该研究阐明了 BCA2 通过调控 TLR4/MyD88/NF-κB/SOX9 轴促进肿瘤干性的机制，为靶向 BCSCs 提供了新靶点。胎牛血清产品货号：FSD500（南美超级胎牛血清）/ExCell Bio论文链接：https://doi.org/10.7150/ijbs.92338文献分享四论文题目：FOXC1-mediated serine metabolism reprogramming enhances colorectal cancer growth and 5-FU resistance under serine restriction（FOXC1 介导的丝氨酸代谢重编程在丝氨酸缺乏条件下增强结直肠癌生长和 5-FU 耐药性）期刊名：Cell Communication and Signaling论文总结：该研究发现，丝氨酸缺乏条件下，结直肠癌细胞通过激活 ERK1/2-p-ELK1 信号轴上调转录因子 FOXC1，进而促进丝氨酸合成通路（SSP）关键酶 PHGDH、PSAT1、PSPH 的表达，维持丝氨酸生成，支持肿瘤生长并增强 5 - 氟尿嘧啶（5-FU）耐药性。FOXC1 通过直接结合 SSP 基因启动子促进其转录，同时调控嘌呤代谢和 DNA 损伤修复。体内外实验表明，抑制 FOXC1 或阻断 ERK1/2 通路可协同丝氨酸限制，显著抑制肿瘤生长并提高 5-FU 敏感性。该研究揭示了 FOXC1 介导的代谢重编程机制，为结直肠癌的代谢靶向治疗提供了 “饮食限制 + 靶向药物” 联合策略的理论依据。胎牛血清产品货号：FSD500（南美超级胎牛血清）/ExCell Bio论文链接：https://biosignaling.biomedcentral.com/articles/10.1186/s12964-024-02016-8依科赛胎牛血清南美正宗，厂家直供，非贴牌、可审厂、手续全、可免税，采用国际先进的胎牛血清生产工艺，建立严苛的质控标准，从源头上把控供应与质量，安全且正规的进口，给客户细胞培养提供坚实的质量保障。点击下方阅读原文，免费申请试用装

临床1期临床结果引进/卖出

2025-04-12

·梅斯医学

夜深人静，灯光昏黄，一杯小酒在手，独处时的仪式感瞬间拿捏了。有人说，“小酌怡情，不醉不归”，仿佛人生就该微醺着过；也有人摇头叹气，“酒是穿肠毒，喝多伤肝肾”，一句话浇灭了浪漫的泡泡。可最近，关于“深夜这一杯”到底是福是祸，竟扯上了一个意想不到的角色——胆固醇。哈佛大学研究团队发表于JAMA Network Open一项覆盖超5万名日本人、长达10年追踪的大型研究[1]揭晓了一个颇为反转的结论：适量喝酒的人，坏胆固醇（低密度脂蛋白胆固醇，LDL-C）水平降了、好胆固醇（高密度脂蛋白胆固醇，HDL-C）水平升了；而戒了酒的人，胆固醇水平反而变差了。十年追踪，酒精撬动的血脂变奏如果把血管比作城市中的道路，那血脂中的两种主要成分——LDL-C和HDL-C——就像在道路上穿梭的不同“交通工具”，负责运输胆固醇等物质。就像城市交通要想顺畅，就得有秩序；我们的血管也一样，血脂的“运作”必须维持在一个平衡的状态。其中，LDL-C更像是一群“不守规矩”的货车，它们把胆固醇从肝脏运往身体的各个角落，但如果数量太多，就容易在“沿路”乱丢货物——胆固醇会沉积在血管壁上，形成斑块，久而久之堵塞血管，所以它也被称为“坏胆固醇”。相比之下，HDL-C则是“城市环卫车”，负责把多余的胆固醇从血管壁清理干净，送回肝脏处理，是名副其实的“好胆固醇”。问题来了，喝酒，到底是让这些“交通工具”更加有序，还是彻底打乱了交通秩序？喝多喝少，胆固醇“反应”各不同研究人员首先把目光锁定在那些“开始喝酒”的人身上（队列1），看看每天多喝一杯（约含10g纯酒精）会不会对血脂造成什么影响。结果令人很意外，这些刚开始喝酒的人，“坏胆固醇”（LDL-C）下降了，“好胆固醇”（HDL-C）反而上升了。而且无论是啤酒、葡萄酒还是烈性酒，都表现出类似的效果。换句话说，不挑酒，关键在于“喝”了没。不过，研究团队并不满足于知道“喝与不喝”的区别，他们进一步“掰开揉碎”来分析不同饮酒量的效果，结果发现饮酒量和血脂水平之间，藏着一条剂量-反应曲线。更为形象地来理解，这好比一场“胆固醇的交通改造工程”：每天多喝一杯酒，路上的“堵车货车”（LDL-C）就会减少一点，而“城市环卫车”（HDL-C）则越来越多。本想靠戒酒“回血”，结果血脂先“翻车？话说回来，如果喝酒能让“好胆固醇”提升，那戒酒会不会反过来让血脂变差？在我们的传统认知中，戒酒几乎等同于“重获新生”：肝脏清爽了，皮肤好了，血脂也该恢复元气了吧？但这项研究的结果再次让人“震碎三观”。当人们停止每天1杯酒的饮用习惯后，LDL-C（坏胆固醇）不降反升，HDL-C（好胆固醇）则会下降。而且这种趋势也并不取决于酒的种类，只要戒酒，血脂就有可能“跑偏”。简而言之：戒酒与LDL-C水平升高和HDL-C降低相关。之前喝得越多，戒得越猛，血脂波动也越大。对于其中潜在的机制，研究人员指出，在酒精依赖人群中，戒酒会降低IGFBP-1（一种与脂代谢相关的蛋白），从而影响HDL-C的水平。看到这里可能会有点懵：那到底还要不要戒酒？别误会，戒酒从长远来看仍然对身体有益，尤其是肝脏、胰腺和癌症风险等方面。总的来看，这项研究向我们展示了一个有趣的现象：开始喝酒的人，LDL-C有所下降，而HDL-C则上升；而一旦戒酒，这两个指标反而朝着相反方向变化——LDL-C上升、HDL-C下降，并且这种变化还呈现出“剂量-反应关系”。大脑的“保护伞”，但要“点到为止”这听起来或许让人有些意外，但其实也并不是孤例。关于“适度饮酒可能带来健康益处”的讨论，在科学界早已有过不少声音。比如，来自山东大学齐鲁医学院的研究团队就对91万余名成年人长达12年的追踪研究，探讨了喝酒量与健康风险的关联[2]。该研究表明，当前轻度至中度喝酒者（女性每周≤7杯、男性≤14杯）的全因死亡风险较终身不喝酒者降低13％-23％，心血管疾病、阿尔茨海默症及流感相关死亡风险降幅显著。[注：这里的1杯酒相当于含有14g酒精≈490-700mL啤酒（酒精度数为3.5％）≈210mL红酒（酒精度数为13％）≈70mL烈酒（酒精度数为40％）]从下图来看，当每日饮酒量在1杯左右的时候，全因死亡风险达到最低值，约降低20％。而哈佛大学的另一项曾发表在《美国心脏病学会杂志》上的研究[3]发现，相比不喝酒或极少喝酒（每周少于1杯）的人，轻度到中度饮酒者（每周1至14杯）发生主要心血管不良事件的风险要低22％。研究者进一步指出，适量饮酒似乎可以长期降低大脑的压力信号水平，从而减轻心血管系统的负担。值得关注的是，JAMA Network Open上曾发表的一项涵盖超393万人的全国回顾性队列研究[4]又道出了适量饮酒的另一好处：与不喝酒的群体相比，持续轻度和中度喝酒的人罹患全因痴呆症的风险降低。此外，如果从不喝酒逐渐培养起轻至中度饮酒的习惯，也能表现出全因痴呆症和阿尔茨海默病（AD）患病风险下降。也就是说，每天喝一点，反而可能对大脑有“保护”作用。更有意思的是，如果一个人原本滴酒不沾，但后来养成了“偶尔小酌”的习惯，也能看到风险下降的趋势。研究团队进一步指出，轻至中度喝酒可能通过激活某些“促生存”通路、减少神经炎症，从而对认知功能起到保护作用。这就像是为大脑撑了一把伞，帮它们抵御时间和病变的侵袭。不过，看到这里，“无酒不欢”的“喝酒党”们先别着急举杯庆祝。研究也明确指出，一旦饮酒量过大，风险就开始“反转”。重度饮酒者患痴呆的风险不降反升。而且，“适量”这两个字，说起来容易，做起来难。每个人的“安全剂量”并不一样——性别、体重、基因代谢能力（比如乙醛脱氢酶的活性）都会影响酒精在体内的代谢速度。即便是“适度”，也可能悄悄给身体带来其他伤害，比如增加癌症风险。并且研究[2]也能看出“小酌”虽怡情，但“大饮”真伤身。具体而言，相较于终身不喝酒的群体，重度喝酒的人（女性每周喝酒量> 7杯，男性每周喝酒量>14杯）患癌死亡风险增加了24％，甚至远高于轻度喝酒者。所以，本篇内容并不是在鼓励大家为了健康而去喝酒，尤其是节假日聚会扎堆的时节，切记“不过量、不劝酒、不硬喝”，别把“适量”变成“失控”。仍需指出的是，上述几项研究均不能直接推断因果关系。参考资料：[1]Suzuki T,Fukui S, Shinozaki T, et al. Lipid Profiles After Changes in Alcohol Consumption Among Adults Undergoing Annual Checkups. JAMA Netw Open. 2025;8(3):e250583. doi:10.1001/jamanetworkopen.2025.0583[2]Tian Y, Liu J, Zhao Y, Jiang N, Liu X, Zhao G, Wang X. Alcohol consumption and all-cause and cause-specific mortality among US adults: prospective cohort study. BMC Med. 2023 Jun 7;21(1):208. doi: 10.1186/s12916-023-02907-6. PMID: 37286970; PMCID: PMC10249162.[3] Mezue K, Osborne MT, Abohashem S, Zureigat H, Gharios C, Grewal SS, Radfar A, Cardeiro A, Abbasi T, Choi KW, Fayad ZA, Smoller JW, Rosovsky R, Shin L, Pitman R, Tawakol A. Reduced Stress-Related Neural Network Activity Mediates the Effect of Alcohol on Cardiovascular Risk. J Am Coll Cardiol. 2023 Jun 20;81(24):2315-2325. doi: 10.1016/j.jacc.2023.04.015. PMID: 37316112; PMCID: PMC10333800.[4] Jeon KH, Han K, Jeong SM, Park J, Yoo JE, Yoo J, Lee J, Kim S, Shin DW. Changes in Alcohol Consumption and Risk of Dementia in a Nationwide Cohort in South Korea. JAMA Netw Open. 2023 Feb 1;6(2):e2254771. doi: 10.1001/jamanetworkopen.2022.54771. PMID: 36745453.撰文 | 木白编辑 | 木白● 热议！大三甲科主任被同事悬赏式举报挪用公款、大额财产来源不明！已停职调查！网友：有些主任职场霸凌、滥用权力、不干不净，该管管了● 益生菌别乱吃！多项研究：不仅促进癌症生长，甚至诱导肠道致病菌毒性飙升，引爆感染危机！● 热议！院领导集体痛哭：发不出下个月工资了！江西一医院突然停诊！浙江一骨科医生在岗期间猝死，年仅35岁！当医生又穷又累，以后咋办？版权说明：梅斯医学（MedSci）是国内领先的医学科研与学术服务平台，致力于医疗质量的改进，为临床实践提供智慧、精准的决策支持，让医生与患者受益。欢迎个人转发至朋友圈，谢绝媒体或机构未经授权以任何形式转载至其他平台。点击下方「阅读原文」立刻下载梅斯医学APP！

2025-04-02

·PRNewswire

Amygdala Neurosciences Selects ANS-858 for Clinical Development as a Novel ALDH2 Inhibitor for Substance Use Disorder

The discovery and preclinical efficacy of ANS-858, a proprietary, selective, reversible, orally bioavailable ALDH2 inhibitor will be presented at 48th Annual Scientific Meeting of the Research Society on Alcohol. SAN FRANCISCO, April 2, 2025 /PRNewswire/ -- Amygdala Neurosciences, Inc., a biopharmaceutical company dedicated to the research and development of novel therapies for addiction and compulsive overeating disorders, has announced a significant milestone in its drug development pipeline. The company has selected ANS-858 as its lead clinical candidate. This marks a crucial step forward in bringing a potentially transformative treatment to patients suffering from these debilitating conditions. ANS-858 is a new, proprietary, small molecule inhibitor of aldehyde dehydrogenase 2 (ALDH2). By inhibiting ALDH2, ANS-858 aims to reduce the rewarding effects associated with alcohol and other substances, thereby mitigating the risk of relapse and offering a path toward abstinence while also reducing anxiety. The selection of ANS-858 follows an extensive preclinical evaluation demonstrating strong efficacy, selectivity, and a favorable safety profile. ALDH2 inhibition represents a promising mechanism for reducing consumption of addictive drugs by affecting the mesolimbic dopamine reward pathway to reduce cravings. Unlike traditional therapies, ANS-858 is designed to provide greater tolerability, improved dosing flexibility, and optimized pharmacokinetics. "Amygdala Neurosciences is committed to advancing the treatment landscape for substance use disorder, a condition with significant unmet medical need," said Brent K Blackburn, PhD, CEO. "The selection of ANS-858 for clinical development marks a key milestone in our mission to develop safe and effective therapeutics for individuals struggling with SUD. Our team is preparing to initiate first-in-human clinical trials to evaluate ANS-858's potential in reducing addictive drug consumption and promoting recovery." One in five adult Americans, or 48 million people, have a diagnosis of a substance use disorder. Alcohol use disorder affects over 28 million adults in the United States, yet current treatment options remain limited. There are 1.2 million patients with cocaine use disorder, where no medical treatment options are available. ANS-858 is designed to provide a targeted, pharmacological approach to modulating dopamine biosynthesis in the brain without affecting basal levels, offering a novel alternative to existing therapies. Amygdala Neurosciences plans to submit an Investigational New Drug (IND) application to the U.S. Food and Drug Administration (FDA) and advance ANS-858 into Phase 1 clinical trial. Amygdala Neurosciences to present at the Research Society on Alcohol. The Annual Scientific Meeting of the Research Society on Alcohol (RSA) aims to bring together alcohol researchers from various disciplines to share their latest findings and stay updated on new research developments. It fosters both professional and personal interactions in a collaborative environment. The meeting is being held in New Orleans, LA, June 21-25, 2025. About ANS-858 ANS-858, a proprietary new chemical entity, works in the brain's 'neural interface between motivation and action' to reduce the dopamine surge responsible for craving. Inhibition of ALDH2 has been shown to reduce drug seeking behavior in preclinical studies against multiple addictive agents and has the potential for use as pharmacotherapy for substance use disorders (SUD), binge-eating, and anxiety. Amygdala Neurosciences is developing ANS-858 for the safe treatment of SUD that includes alcohol and cocaine use disorders. About Amygdala Neurosciences, Inc . Amygdala Neurosciences is developing ANS-858 to curb craving. Its mission is to treat individuals who experience harmful cravings associated with chemicals of addiction and food. The company was formed based on technology discovered and developed by members of the companies' leadership team while at CV Therapeutics and acquired from Gilead Sciences. Research reported in this press release was supported by the National Institute On Alcohol Abuse And Alcoholism of the National Institutes of Health under Award Numbers U43AA030689 and R43AA029311. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. SOURCE Amygdala Neurosciences Inc. WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

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