Tinnitus can have different causes. From a peripheral point of view, the sensation of hearing a not present sound can be indicative of damage in the cells of the cochlea. Damage at this level can arise from traumatic, vascular, toxic origins or be caused by systemic pathologies. However, all the previous causes have a common denominator, the presence of reactive oxygen species (ROS), in the cochlea which determines the damage and the consequent death of the hair cells into the ear. The sound (tinnitus) that the patient perceives is generated by the spontaneous movement of the cilia of the hair cells; this phenomenon arises when these cells begin to be damaged.
Tinnitus can be also caused by a retrocochlear disorder such as damage of the auditory nerve (inflammatory and tumor cause). In case of an inflammatory origin, the factors released during inflammation can locally damage the nerves and spread into the cochlea destroying the hair cells.
Tinnitus can also originate from damage in the central auditory pathway. In this case, the problem persistent. It is important to keep in mind that although initially the tinnitus may originate from a damage inside the cochlea, after 6 months of persistence chronicizes causing an activation (without stimulus) of the upper auditory areas. This zone of "hypersensitivity" is therefore responsible for chronic tinnitus.
In addition to the overmentioned medical causes, tinnitus can also be sign of psychiatric/psychological disorders, in those cases in whom there is an involvement of the hypothalamus, as showed by neuropsychological studies. Tinnitus can be temporary and disappear spontaneously or, in the most of cases, be persistent and extremely annoying/stressful for the patient. At night in particular, in the absence of noise, the patient suffers more the presence of this ghost sound, which in some occasions prevents sleep. Insomnia negatively impacts on tinnitus increasing its duration and intensity, thus establishing a perpetual cycle of stress into the brain. The latter phenomenon worses and chronicizes the symptom .
Stress causes inflammation with ROS increase, which can affect both the peripheral and central auditory pathways. Recently, it has been shown that tinnitus can be a symptom of neuro-inflammatory pathologies such as, for example, Multiple Sclerosis.
The effects of inflammation on the hair cells are identifiable only through electrophysiological studies or from the temporal bone.
Keeping on mind inflammation and neuro-inflammation and considering the exchange between cerebrospinal fluid and perilymph , we speculate that the use of a molecule capable of reducing inflammation and modulating the action of mast cells and microglia, could be an effective tool to resolve tinnitus; moreover, thanks to its powerful action at the level of neuro-inflammation, it could reduce the hyper-activity in the upper auditory tracts, thus reducing/abolishing noise.
umPeaLut combines palmitoylethanolamide, which modulates the activity of mast cells, macrophages and microglia and luteolin, a bioflanoid extracted from fruits with anti-oxidant properties, able to improve microcirculation. Because the alterations of the ear microcirculation can be an additional cause of tinnitus, we believe that luteolin content can be an ulterior benefit.
Although various attempts have been made to use a mono-molecule, recent studies have shown that combination of several elements could reduce tinnitus ; PeaLut, in its ultra-micronized form with high bioavailability, could be the perfect solution.
This study aims at evaluating the efficacy of umPEALUT as a therapeutic treatment of tinnitus in a sample of adults.

开始日期2026-04-20

申办/合作机构

University of Campania Luigi Vanvitelli

ACTRN12625000876493

/ Completed临床1/2期

A Phase 1b, Randomized, Double-Blind, Placebo-Controlled Evaluation of selected Pharmacodynamic Biomarkers in Cerebrospinal Fluid (CSF) Following 24-hour Intravenous Infusion of EVX-301 in Adults with Depression Receiving Stable Antidepressant Treatment

开始日期2026-01-15

申办/合作机构-

NCT05401032

/ Recruiting临床2期IIT

TryptoBPH - Proof-of-concept Study to Evaluate the Safety and Efficacy of Tryptophan in Patients with BPH

Benign prostatic hyperplasia (BPH) is one of the most prevalent human diseases and a major cause of lower urinary tract symptoms (LUTS). Some men respond to current medical treatment (mainly α-1 adrenoreceptor antagonists and 5 α-reductase inhibitors), but a large proportion of patients continues to need a surgical procedure to treat resistant LUTS or even more serious complications of BPH, creating the emerging necessity for novel pharmacological therapies.
Oxitriptan may have a possible positive effect on BPH associated symptoms with probably no impact in sexual function (which is a common side effect of the current drugs for BPH associated symptoms). Also, improvement in symptoms could be higher than that of current drugs used for this condition.
This is a single-center parallel group, randomized clinical trial. The study will take place in Hospital de Braga (Urology department). Eligible patients will be randomized to receive tamsulosin 0.4mg (once a day, q.d.) or 5-HTP (5-hidroxitriptophan) 100mg (three times a day, t.i.d.), for 6 months.

开始日期2024-12-20

申办/合作机构

The Clinical Academic Center of Braga

100 项与羟色氨酸相关的临床结果

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100 项与羟色氨酸相关的转化医学

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100 项与羟色氨酸相关的专利（医药）

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3,758

项与羟色氨酸相关的文献（医药）

2026-08-01·MOLECULAR GENETICS AND METABOLISM

Molecular heterogeneity in AADC deficiency: Variant-dependent effects on AADC activity

Article

作者: Poznański, Jarosław ; Bisello, Giovanni ; Głogowska, Natalia ; Szymańska, Krystyna ; Sykut-Cegielska, Jolanta ; Kamińska, Julia Zuzanna ; Ślusarczyk, Klaudia ; Drożak, Jakub ; Kuśmierska, Katarzyna ; Bertoldi, Mariarita ; Rygiel, Agnieszka Magdalena

Aromatic L-amino acid decarboxylase (AADC), encoded by DDC gene, catalyzes the final step in dopamine and serotonin biosynthesis. Pathogenic DDC variants cause AADC deficiency, a severe neurometabolic disorder. This study aimed to elucidate previously uninvestigated DDC variant combinations: p.Pro47Ala/p.Arg447Cys and p.Cys261Phe/p.Gly354Ser, with respect to structural and functional characteristics. Recombinant heterodimeric and homodimeric AADC proteins were expressed in Escherichia coli and purified. Enzymatic activity was quantified via ion-pair reversed-phase HPLC with photodiode detection, while structural changes were analyzed using circular dichroism and molecular modelling. Functional characterization revealed that p.Pro47Ala, p.Gly354Ser, and p.Arg447Cys homodimers showed marked loss of activity towards both L-DOPA (88%, 97% and >99%, respectively) and L-5-hydroxytryptophan (88%, 99%, >99%, respectively), whereas p.Cys261Phe retained substantial activity (82% for L-DOPA and 75% for L-5-hydroxytryptophan). Kinetic analysis indicated a mild to severe decrease in substrate affinity for all homodimers, particularly for p.Arg447Cys. Furthermore, heterodimeric combinations showed positive complementation effects on decarboxylase reaction for both heterodimers. Surprisingly, p.Cys261Phe/p.Gly354Ser also restored the wild-type activity with L-DOPA and regained 43% of L-5-hydroxytryptophan activity, whereas p.Pro47Ala/p.Arg447Cys was 15% and 10% active towards L-DOPA and L-5-hydroxytryptophan with respect to the wild-type. Our results indicate that the pathogenicity of AADC variants depends on structural combination, complementation effects in heterodimeric species, and residual activity of homodimers, highlighting the complexity of polypeptide chain interactions in compound heterozygotes.

2026-08-01·CURRENT OPINION IN BIOTECHNOLOGY

Recent advances in microbial production of stress-relieving nutraceuticals

Review

作者: Ren, Yuyao ; Cai, Peng ; Zhou, Yongjin J

The fast-paced modern life exerts great pressure to individuals. Nutritional interventions for stress management have gained increasing attention due to its favorable safety profiles, multiple health benefits, and suitability for vulnerable populations. Microbial production of stress-relieving nutraceuticals represents a sustainable alternative to natural extraction and chemical synthesis, while meeting the growing market demand for natural-labeled and consumer-preferred products. This review provides an overview of the recent progress in engineering microorganisms to produce common stress-relieving biomolecules, such as: γ-aminobutyric acid, ʟ-theanine, 5-hydroxytryptophan and its derivatives, and vitamin B. Key bottlenecks limiting the bioproduction of each molecules and targeted strategies, including chassis selection, enzyme engineering, pathway rewiring and bioprocess regulation, are discussed.

2026-06-30·LANGMUIR

Elucidating the Adverse Interactions of L -Tryptophan and 5-Hydroxytryptophan Self-Assemblies with Prebiotic Membranes and Neuronal Cells: An Investigation Using Fluorescence Spectroscopy and Lifetime Imaging Microscopy

Article

作者: Nandi, Pratyush Kiran ; Paul, Somdatta ; Sarkar, Nilmoni ; Maity, Arijit ; Hazra, Ritwik ; Layek, Souvik ; Debnath, Ananya

L-tryptophan (l-Trp) and 5-Hydroxytryptophan (5-HTP) are essential precursors in serotonin biosynthesis and widely used as over-the-counter dietary supplements. We hypothesize that, due to prolonged uptake and accumulation in the human body, these amino acids can spontaneously form fibrillar self-assemblies at higher concentrations, capable of interacting with model membranes, possibly constituting the underlying mechanistic basis for their cytotoxicity and associated neurodegenerative risks. The self-assemblies of l-Trp and 5-HTP were characterized using field emission scanning electron microscopy (FESEM) and fluorescence lifetime imaging microscopy (FLIM). We investigated their interfacial interactions with fatty acid model membranes, evaluating structural perturbations using fluorescence spectroscopy, molecular dynamics (MD) simulations, dynamic light scattering (DLS), and FLIM, and complementing these with in vitro cellular viability assays using SH-SY5Y cell lines. Self-assembly of l-Trp and 5-HTP formed distinct flake-like and rod-like structures, respectively, with different rigidity. Fluorescence spectroscopy and FLIM analyses demonstrated that these assemblies altered local microenvironmental polarity and significantly compromised bilayer integrity─a disruptive integration further corroborated by atomistic MD simulations. Crucially, in vitro assays linked these interfacial interactions to a marked decrease in SH-SY5Y cell viability, establishing membrane disruption as a plausible mechanism driving the neurotoxicity of these assemblies at biointerfaces.

项与羟色氨酸相关的新闻（医药）

2026-09-19

·药学进展

学科前沿 | 北京协和医学院王琰研究员团队揭示YZG-331通过肠道菌与药物相互作用改善失眠的分子机制

“ 点击蓝字关注我们北京协和医学院王琰研究员团队揭示YZG-331通过肠道菌与药物相互作用改善失眠的分子机制 PPS 近日，药物所王琰研究员、石建功研究员团队与北京协和医院孙劲旅教授合作，共同在药学知名期刊Acta Pharmaceutica Sinica B在线发表了“Molecular mechanisms of YZG-331 ameliorated insomnia based on the gut microbiota-drug interaction”（YZG-331基于肠道菌群-药物相互作用改善失眠的分子机制）的研究论文，揭示了创新药物YZG-331通过肠道菌与药物相互作用改善失眠的分子机制。失眠是一种以入睡困难、睡眠维持障碍和睡眠质量下降为主要表现的常见睡眠障碍，长期失眠不仅影响情绪和认知功能，还可增加多种慢性疾病风险。YZG-331是由药物所研发的具有自主知识产权的1.1类化学药品，目前已获得《国家药品监督管理局药物临床试验批准通知书》，而YZG-331如何改善失眠的分子机制尚需进一步阐明。越来越多数据证明，肠道菌及其代谢产物能够通过肠-脑通路参与“睡眠-觉醒”调控，为药物治疗失眠的机制研究提供了新方向。该研究首次揭示了YZG-331通过肠道菌-药物双向互作改善失眠的分子机制。结果表明，BALB/c 小鼠口服YZG-331后肠道内乳杆菌属（Lactobacillus）和鼠杆菌科（Muribaculaceae）菌群的丰度显著增加，其中罗伊氏乳杆菌在YZG-331的代谢转化和刺激5-HT生成的过程中发挥了重要作用。肠道菌通过升高四氢生物蝶呤（辅酶）的含量增加了色氨酸羟化酶（TPH）活性，进而促进5-HT生成而改善睡眠；同时，肠道菌表达的核糖核苷水解酶RihC可水解YZG-331生成活性代谢产物M2，YZG-331及M2均能增加丁酸等短链脂肪酸产生，从而显著降低小鼠海马Orexin A（食欲素A）水平而改善了睡眠。此外，人源化肠道菌移植小鼠的动物模型进一步证实YZG-331可改善失眠患者菌群所诱导的睡眠异常，并恢复5-HTP和5-HT水平。综上所述，该研究首次阐明了YZG-331通过调控肠道与脑之间的“色氨酸-5-HT”和“丁酸-Orexin A”代谢通路而改善失眠的作用机制，为揭示天然药物如何通过肠道菌的小分子代谢物发挥药效的分子机制提供了重要的科学依据，同时也为失眠患者的临床精准治疗方案提出有价值的参考策略。国家自然科学基金重大项目（82293685），中国医学科学院医学与健康创新工程（2021-I2M-1-028）和“创新药临床前研发药代-药效关键技术”北京市重点实验室等项目资助了该研究。药物所2023级博士生左恒通、郭庆兰副研究员、2022级直博生鲁金月以及北京协和医院赵彬主任药师为该文共同第一作者，药物所王琰研究员、石建功研究员、北京协和医院孙劲旅教授为该文共同通讯作者。文章来源：北京协和医学院药物研究所美编排版：方正文章审核：周碧远方正罗琪【免责声明】以上内容来源于互联网，不代表本平台立场或观点；如有侵犯作者著作权，请及时与我们联系（Tel：025-83271227，或直接在微信平台留言），我们将及时更正或删除。《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1.311，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“第七届药学前沿学术论坛暨《药学进展》编委会会议” 聚力前沿赛道，共启学术新程：第七届药学前沿学术论坛在南京隆重启幕承学术匠心，启时代新章：《药学进展》第七届编委会、第三届青年编委会成立大会在宁召开聚焦“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

2026-09-18

·今日头条

候选药YZG-331助眠，肠道菌群是功臣 | 热心肠日报

本文要点背景与核心设计针对具有镇静催眠作用的候选药物YZG-331口服生物利用度低的问题，利用伪无菌、人源化菌群小鼠及多组学技术解析其治疗失眠的肠脑轴机制。总体概述 YZG-331通过双向菌药互作驱动色氨酸代谢与短链脂肪酸生成，决定了其改善睡眠及修复肠屏障的药效，为失眠治疗提供新机制。菌群依赖性药效伪无菌小鼠中YZG-331延长睡眠时长的能力显著下降，伴随5-羟基色氨酸（5-HTP）与5-羟色胺（5-HT）升高的效应被阻断，证实菌群是其药效必需介质。水解代谢机制基因工程证实，富集的罗伊氏乳杆菌通过表达核糖核苷水解酶RihC，直接催化YZG-331水解生成代谢物M2。羟基化与5-HT合成 YZG-331经菌群羟基化驱动BH₄积累，进而激活色氨酸羟化酶，显著促进色氨酸向5-HTP及5-HT转化。丁酸与食欲素通路 YZG-331及其代谢物M2显著提升肠道丁酸水平，伴随下丘脑食欲素A表达下调，从而发挥镇静催眠作用。人源化模型验证移植失眠患者菌群的小鼠重现睡眠障碍，YZG-331干预显著恢复5-HT水平，提示该机制在人源菌群中保守。核心关键词 YZG-331　　药理学　　药物-菌群互作　　失眠　　肠道菌群　　色氨酸代谢　　5-羟色胺　　罗伊氏乳杆菌　　色氨酸羟化酶　　丁酸　　肠-脑轴科普解读许多人都有过这样的夜晚：身体疲惫不堪，大脑却像高速运转的马达无法停机。长期失眠不仅意味着第二天精神萎靡，更被证实与抑郁症、心血管病乃至卵巢癌的风险激增有关。临床上，现有的镇静催眠药物常伴随成瘾性或次日残留效应，寻找更安全的方案一直是神经药理学界的核心挑战。而一个前沿的思路正逐渐清晰：调控我们体内那套“第二大脑”——肠道菌群，或许能开辟一条全新的助眠路径。近期，来自中国医学科学院北京协和医学院的王琰团队、石建功团队，以及北京协和医院的孙劲旅团队，在学术期刊 Acta Pharmaceutica Sinica B 上发表了一项研究，揭示了一种名为YZG-331的化合物改善失眠的全新机制。YZG-331是中药天麻中主要镇静活性成分的优化衍生物。研究发现，这种药物的催眠效应高度依赖肠道菌群的存在，它通过一种名为“羟化反应”的特殊代谢过程，巧妙地激活了菌群合成 5-羟色胺的通路，从而经“肠-脑轴”传递睡眠信号。锁定肠道的“化学信使” 在实验中，团队利用PCPA（一种色氨酸羟化酶抑制剂）构建了小鼠失眠模型。数据显示，口服YZG-331能显著缩短入睡时间并延长睡眠时长，且效果优于腹腔注射。这提示药物的核心作用位点可能在肠道，而非仅靠进入大脑起作用。通过对小鼠粪便和血清进行非靶向代谢组学分析，研究人员注意到，失眠模型小鼠的色氨酸代谢通路发生了严重紊乱。在接受YZG-331治疗后，肠道中5-羟色胺的直接前体——5-羟色氨酸（5-HTP）和5-羟色胺（5-HT）的水平显著回升。相关性分析进一步证实，这些代谢物的增加与睡眠的改善呈现极强的正相关。这意味着，YZG-331在肠道内重新激活了“色氨酸-5-羟色胺”这条关键的生化流水线。菌群是疗效的“必要中介” 为了验证肠道菌群在其中是否扮演了决定性角色，团队构建了伪无菌小鼠模型——即用广谱抗生素清空了肠道菌群。结果颇具戏剧性：在无菌群的小鼠体内，YZG-331的助眠效果大打折扣，睡眠时长缩短了约 56% ，且粪便、血清及脑组织中的5-羟色胺水平均未能有效恢复。这一实验直接说明，菌群的参与是YZG-331起效的必要条件。在重塑菌群结构方面，YZG-331显著提升了失眠小鼠肠道内乳酸杆菌属和Muribaculaceae的丰度。其中，团队重点考察了罗伊氏乳杆菌。体外实验表明，YZG-331不仅能直接促进这种菌的生长，更关键的是，在药物存在的条件下，罗伊氏乳杆菌代谢色氨酸并产出5-羟色胺的效率大幅提升。羟化反应驱动的“质子密码” 那么，YZG-331究竟是如何增强菌群合成5-羟色胺能力的？研究团队发现了一个精巧的化学耦合机制。肠道菌群在代谢YZG-331时，会对其分子结构进行“羟化反应”修饰，并在此过程中释放出质子。研究推测，这些质子恰好能为一种关键辅因子——四氢生物蝶呤（BH4）的再生提供动力。BH4是色氨酸羟化酶（TPH）必不可少的“激活钥匙”。当BH4水平升高，TPH酶活性随之增强，通向5-羟色胺合成的大门便被打开了。为了验证这一推断，团队使用羟化反应抑制剂后，不仅YZG-331的代谢产物减少，BH4水平、TPH活性以及下游的5-羟色胺产量也全线回落。这一连串的锁链反应证明，YZG-331通过自身在肠道的代谢，间接为5-羟色胺的合成提供了燃料。菌群代谢产物的“双通道”助攻除了调控5-羟色胺，研究还揭示了另一条保护路径。肠道菌群表达的一种核糖核苷水解酶（RihC），能将YZG-331水解为代谢产物M2。无论是原型药物YZG-331还是代谢物M2，都能显著提升肠道内丁酸的含量。丁酸作为一种重要的短链脂肪酸，不仅能修复失眠造成的肠屏障损伤，还能抑制大脑中促进觉醒的食欲素A信号。团队在关键的脑区—— 下丘脑中检测到食欲素A水平的下降，同时海马区的神经炎症也得到显著缓解。这表明，YZG-331对肠道屏障的物理修复和对中枢兴奋信号的化学抑制是同步进行的。为了验证这一机制的临床转化潜力，研究者利用失眠患者的粪便构建了“人源化”菌群小鼠模型。令人振奋的是，同样移植了失眠患者菌群的小鼠表现出睡眠紊乱和色氨酸代谢异常，而YZG-331干预不仅显著改善了它们的睡眠，还恢复了肠道内5-羟色胺水平及乳酸杆菌的丰度。这为将该药物推向临床精准治疗提供了来自肠道维度的有力证据。这项研究首次从分子层面描绘了“菌群-药物-代谢”的交互图景：一个源自天麻的化合物，通过在肠道菌群中引发特定的化学反应，最终让紊乱的“肠脑轴”重归宁静。关于YZG-331的I期临床试验已获批准，我们或许可以期待，未来的安眠策略将不仅仅是让大脑“强制关机”，而是从安抚肠道里的微观居民开始。图片摘要相关文章推荐 01 Advanced Science · IF: 14.1 湖大史峻峰团队：益生菌披上"甘草锌铠甲"，双效干预结肠炎 02 Nature Communications · IF: 18.1 NC：椰子油或可成为克罗恩病的新型膳食疗法 03 Molecular Psychiatry · IF: 10.4 浙大一院来建波/陈艺等：微生物单细胞测序揭示心境障碍中的肠菌"情绪"信号 04 Gut Microbes · IF: 15.3 肠菌的"兼职"游戏，跨物种基因如何联手促发肠癌？ 05 Cell Reports Medicine · IF: 14 Cell子刊：免疫治疗引发严重肠炎，粪菌移植有效改善原文链接 https://rbase.chinagut.cn/base/article/ff8fd7fb72a34fcba9b00dcd202e0f3f

2026-09-15

·BioSpace

Evecxia Therapeutics Announces Positive Clinical Results From a Phase 1b Target Engagement Trial

The trial delivered POC that active compound 5-HTP at target plasma exposure (i) enters the brain, (ii) elevates biomarkers of serotonin synthesis, and (iii) elevates biomarkers of serotonin activity beyond the SSRI/SNRI effect The data corroborate the 5-HTP plasma exposure target of ~100 ng/mL and de-risk Phase 2 development RESEARCH TRIANGLE PARK, N.C.--(BUSINESS WIRE)--Evecxia Therapeutics, Inc.—a clinical-stage neuroscience company developing a novel class of Serotonin Synthesis Amplification therapies—today announced positive data from a Phase 1b PK/PD trial for brain serotonin target engagement in depression patients on selective serotonin reuptake inhibitor/serotonin-norepinephrine reuptake inhibitor (SSRI/SNRI) therapy. Phase 1b Target Engagement Trial Design: N=18 depression patients on SSRI/SNRI therapy were administered adjunctive placebo (N=6) or EVX-301 (IV 5-HTP, N=12) at a dose (1 mg/kg/24h) previously reported to produce a C Average of ~100 ng/mL plasma 5-HTP in humans, the putative therapeutic 5-HTP exposure target, with rapid onset (hours). Cerebrospinal fluid (CSF) 5-HTP, 5-HIAA (serotonin metabolite), and serotonin were determined at baseline and after placebo/EVX-301. Changes in serum cortisol, a validated neuroendocrine biomarker of brain synaptic serotonin release, and 5-HTP PK were included as ancillary measures. Results : EVX-301 elevated all CSF biomarkers and the serum cortisol biomarker, together indicating brain serotonin synthesis amplification and elevation of serotonin activity beyond the SSRI/SNRI effect. Taken together, the data corroborate the 5-HTP exposure target for Evecxia’s drug candidates, EVX-101 and EVX-301. Adjunctive EVX-301 was generally well tolerated; adverse events were mostly mild or moderate and consistent with elevation of brain serotonin activity. Trial site: The trial was conducted at PARC Clinical Research, Adelaide, Australia. “The Phase 1b PK/PD target engagement data further de-risk Phase 2 development of Evecxia’s drug candidates, including lead candidate EVX-101,” said Jacob Jacobsen, PhD, Chief Executive Officer and Co-founder of Evecxia Therapeutics. “EVX-101 is backed by Evecxia’s comprehensive data package and decades of peer-reviewed published clinical data, addresses multiple unmet needs in psychiatry, and would slot seamlessly into existing psychiatric care and reimbursement infrastructure, globally. EVX-101 Phase 2 initiation in OCD is targeted for 1H 2027.” About EVX-101 EVX-101 is an oral, gastro-retentive, sustained-release tablet formulation of 5-HTP (the natural immediate precursor to serotonin) and low-dose carbidopa (multiplies 5-HTP’s bioavailability). In Phase 1, EVX-101, as an adjunctive to SSRI therapy, transformed 5-HTP’s PK pro demonstrated favorable safety and tolerability. EVX-101 is the first drug candidate realizing the therapeutic potential of Serotonin Synthesis Amplification, a pharmacology risk-mitigated by decades of clinical data (J Clin Psychopharmacol 2026 46(4):462-475, Full text , Podcast ). Lead indication for EVX-101 is obsessive compulsive disorder (OCD) responding inadequately to SSRI therapy — a chronic, severe indication, with no FDA-approved drugs, affecting an estimated 2 million US patients. About EVX-301 EVX-301 is a proprietary intravenous infusion of 5-HTP designed to rapidly increase 5-HTP plasma exposure and produce fast-onset brain Serotonin Synthesis Amplification. EVX-301 is being positioned as rescue therapy for patients hospitalized with suicidal ideation. About Evecxia Therapeutics Evecxia is the first company dedicated to realizing the therapeutic potential of Serotonin Synthesis Amplification—building a stronger, more resilient brain serotonin system—to treat psychiatric indications. Evecxia’s lead candidate EVX-101 is being developed as next-line oral adjunctive (add-on) therapy for OCD and depression patients for whom monotherapy with first-line serotonin reuptake inhibitor antidepressants (e.g., SSRIs such as Prozac®) yields inadequate therapeutic relief. Contacts Jacob Jacobsen, PhD, CEO Evecxia Therapeutics, Inc. info@evecxia.com

100 项与羟色氨酸相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D07339	羟色氨酸	N06AX01	DB02959

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适应症	国家/地区	公司	日期
苯丙酮尿症	中国台湾	中国化学制药股份有限公司	1995-12-31
抑郁症	瑞士	-	-

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适应症	最高研发状态	国家/地区	公司	日期
自杀意念	临床1期	美国	Evecxia, Inc.	2023-04-20

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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


NCT05030129 (CTgov)	临床2期	脆性X综合征	15	Matching placebo for 5-Hydroxytryptophan+Ergoloid Mesylates (Ergoloid Mesylates (EM))	夢繭鹽築艱簾鹽窪鬱蓋 = 選夢糧網選鑰選膚範築鬱觸鏇蓋膚選構構廠願 (壓繭蓋膚選製願築膚選, 構襯鏇蓋構衊築醖憲觸 ~ 窪網衊夢廠衊餘醖簾餘) 更多	-	2024-09-19
NCT05030129 (CTgov)	临床2期	脆性X综合征	15	Ergoloid Mesylates+5-hydroxytryptophan (Ergoloid Mesylates (EM) and 5-hydroxytryptophan (5-HTP))	夢繭鹽築艱簾鹽窪鬱蓋 = 製製淵淵網蓋鹹鑰壓鹹鬱觸鏇蓋膚選構構廠願 (壓繭蓋膚選製願築膚選, 觸膚構選鹽鏇醖蓋醖窪 ~ 製鹽淵齋醖壓獵鑰窪獵) 更多	-	2024-09-19
NCT04395183 (CTgov)	临床2期	重度抑郁症	43	placebo matched to 5-HTP+5-Hydroxytryptophan 100 MG (5-HTP + Placebo)	網鏇蓋廠鹽構獵夢簾願 = 觸膚鏇鏇顧遞襯鑰觸蓋範鑰膚艱齋膚餘餘遞鏇 (淵窪糧網鹽齋範鹹餘選, 觸鹹艱醖淵憲醖構艱淵 ~ 鏇廠願醖獵遞蓋齋鹽遞) 更多	-	2024-07-23
NCT04395183 (CTgov)	临床2期	重度抑郁症	43	placebo matched to 5-HTP+Creatine monohydrate (Creatine + Placebo)	網鏇蓋廠鹽構獵夢簾願 = 壓築窪範觸餘遞構鬱繭範鑰膚艱齋膚餘餘遞鏇 (淵窪糧網鹽齋範鹹餘選, 膚簾艱構積衊積膚積鹹 ~ 鹹積淵鹹選淵鹽鑰製廠) 更多	-	2024-07-23
NCT03574948 (2017-005059-10, Pubmed \| Gastroenterology)	临床2期	炎症性肠病	166	5-hydroxytryptophan	鹽鏇範鏇窪襯鏇醖範範(遞窪廠繭餘製襯鬱鑰窪) = 糧壓糧鬱獵廠壓鏇憲餘鑰鏇製襯淵選選膚積衊 (餘範淵選夢築繭願醖遞, 1.97 ~ 4.03) 更多	不佳	2022-08-05
NCT02356107 (CTgov)	临床4期	缺氧 \| 重度抑郁症 \| 难治性抑郁症	15	Creatine monohydrate+5-hydroxytryptophan	築網艱鑰夢選獵壓齋願(齋網鏇鑰淵糧範簾範壓) = 壓鹽築網壓餘淵鏇獵鑰鬱繭鑰鏇餘網窪遞繭積 (繭觸範顧鬱製壓選網構, 2.5) 更多	-	2018-01-04