A Phase 1b/2, Multicenter, Adaptive, Double-blind, Randomized, Placebo-controlled Study to Assess the Safety, Tolerability, Immunogenicity, and Pharmacodynamic Effects of ACI-24.060 in Subjects With Prodromal Alzheimer's Disease and in Adults With Down Syndrome (ABATE)

The purpose of this study is to assess the safety, tolerability, immunogenicity and pharmacodynamic effects of ACI-24.060 in subjects with prodromal Alzheimer's disease and in non-demented adults with Down syndrome.

开始日期2022-06-21

申办/合作机构

AC Immune SA

[+1]

NCT04373616

/ Withdrawn临床2期

A Phase 2 Double-blind, Randomized, Placebo-controlled Study to Assess the Safety, Tolerability and Target Engagement of ACI-24 in Adults With Down Syndrome

This study is a prospective multicenter, placebo-controlled, double-blind, randomized study to assess the effect of one dose ACI-24 versus placebo over a 74-week treatment period and 26-week safety follow-up period.

开始日期2021-10-01

申办/合作机构

AC Immune SA

EUCTR2018-000445-39-FI

/ Completed临床2期

A Phase II Double-Blind, Randomized, Placebo-Controlled, Adaptive Design Study to Assess the Safety, Tolerability, Immunogenicity and Target Engagement of ACI-24 Formulations in Patients with Mild Alzheimer’s Disease

开始日期2018-06-19

申办/合作机构

AC Immune SA

100 项与 ACI-24 相关的临床结果

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100 项与 ACI-24 相关的转化医学

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100 项与 ACI-24 相关的专利（医药）

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项与 ACI-24 相关的文献（医药）

2022-06-01·JAMA neurology1区 · 医学

Safety, Tolerability, and Immunogenicity of the ACI-24 Vaccine in Adults With Down Syndrome

1区 · 医学

Article

作者: Evans, A. Carol ; Pfeifer, Andrea ; Streffer, Johannes ; Beth, Gregory ; Rafii, Michael S. ; dos Santos, Antonio Melo ; Sabbagh, Marwan N. ; Hliva, Valerie ; Delpretti, Saskia ; Skotko, Brian G. ; Sol, Olivier ; Rissman, Robert A. ; Evans, Casey ; Feldman, Howard H. ; Kosco-Vilbois, Marie ; Fournier, Nicolas ; Gray, Julian A. ; Yuan, Shauna H. ; Burke, Anna D. ; Vukicevic, Marija ; Mobley, William C. ; Pulsifer, Margaret

Importance:

Individuals with Down syndrome (DS) are at high risk of developing Alzheimer disease due to an increased dose of the amyloid precursor protein gene, APP, which leads to increased levels of full-length APP and its products, including amyloid-β (Aβ). The liposome-based antiamyloid ACI-24 vaccine is intended to treat neurological disorders caused by misfolded Aβ pathological protein. However, the safety, tolerability, and immunogenicity of the ACI-24 vaccine among adults with DS have not been fully examined.

Objective:

To assess the safety and tolerability of the ACI-24 vaccine among adults with DS as well as its ability to induce immunogenicity measured by anti-Aβ immunoglobulin G titers.

Design, Setting, and Participants:

This multicenter double-blind placebo-controlled dose-escalation phase 1b randomized clinical trial was conducted at 3 US academic medical centers with affiliated Down syndrome clinics between March 30, 2016, and June 29, 2020. A total of 20 adults with DS were screened; of those, 16 adults were eligible to participate. Eligibility criteria included men or women aged 25 to 45 years with cytogenetic diagnosis of either trisomy 21 or complete unbalanced translocation of chromosome 21. Between April 27, 2016, and July 2, 2018, participants were randomized 3:1 into 2 dose-level cohorts (8 participants per cohort, with 6 participants receiving the ACI-24 vaccine and 2 receiving placebo) in a 96-week study. Participants received 48 weeks of treatment followed by an additional 48 weeks of safety follow-up.

Interventions:

Participants were randomized to receive 7 subcutaneous injections of ACI-24, 300 μg or 1000 μg, or placebo.

Main Outcomes and Measures:

Primary outcomes were measures of safety and tolerability as well as antibody titers.

Results:

Among 16 enrolled participants, the mean (SD) age was 32.6 (4.4) years; 9 participants were women, and 7 were men. All participants were White, and 1 participant had Hispanic or Latino ethnicity. Treatment adherence was 100%. There were no cases of meningoencephalitis, death, or other serious adverse events (AEs) and no withdrawals as a result of AEs. Most treatment-emergent AEs were of mild intensity (110 of 132 events [83.3%]) and unrelated or unlikely to be related to the ACI-24 vaccine (113 of 132 events [85.6%]). No amyloid-related imaging abnormalities with edema or cerebral microhemorrhage and no evidence of central nervous system inflammation were observed on magnetic resonance imaging scans. Increases in anti-Aβ immunoglobulin G titers were observed in 4 of 12 participants (33.3%) receiving ACI-24 (2 receiving 300 μg and 2 receiving 1000 μg) compared with 0 participants receiving placebo. In addition, a greater increase was observed in plasma Aβ1-40 and Aβ1-42 levels among individuals receiving ACI-24.

Conclusions and Relevance:

In this study, the ACI-24 vaccine was safe and well tolerated in adults with DS. Evidence of immunogenicity along with pharmacodynamic and target engagement were observed, and anti-Aβ antibody titers were not associated with any adverse findings. These results support progression to clinical trials using an optimized formulation of the ACI-24 vaccine among individuals with DS.

Trial Registration:

ClinicalTrials.gov Identifier: NCT02738450.

2022-01-04·Brain communications

An amyloid beta vaccine that safely drives immunity to a key pathological species in Alzheimer’s disease: pyroglutamate amyloid beta

Article

作者: Depretti, S. ; Rentero, I. ; Donati, P. ; Rincon-Restrepo, M. ; Siegert, S. ; Beuzelin, M. ; Giriens, V. ; Rivot, S. ; Gesbert, A. ; Pfeifer, A. ; Fiorini, E. ; Lopez-Deber, P. ; Vukicevic, M. ; Kosco-Vilbois, M. H. ; Morici, C. ; Babolin, C. ; Ayer, M. ; Piot, N. ; Bravo-Veyrat, S. ; Streffer, J. ; Carpintero, R.

Abstract:

Pyroglutamate amyloid beta3–42 (pGlu-Abeta3–42), a highly amyloidogenic and neurotoxic form of Abeta, is N-terminally truncated to form a pyroglutamate and has recently been proposed as a key target for immunotherapy. Optimized ACI-24, a vaccine in development for the treatment and prevention of Alzheimer’s disease, focuses the antibody response on the first 15 N-terminal amino acids of Abeta (Abeta1–15). Importantly, clinical data with an initial version of ACI-24 incorporating Abeta1–15, established the vaccine’s safety and tolerability with evidence of immunogenicity. To explore optimized ACI-24’s capacity to generate antibodies to pGlu-Abeta3–42, pre-clinical studies were carried out. Vaccinating mice and non-human primates demonstrated that optimized ACI-24 was well-tolerated and induced an antibody response against Abeta1–42 as expected, as well as high titres of IgG reactive with pyroGlu-Abeta. Epitope mapping of the polyclonal response confirmed these findings revealing broad coverage of epitopes particularly for Abeta peptides mimicking where cleavage occurs to form pGlu-Abeta3–42. These data are in striking contrast to results obtained with other clinically tested Abeta targeting vaccines which generated restricted and limited antibody diversity. Taken together, our findings demonstrate that optimized ACI-24 vaccination represents a breakthrough to provide a safe immune response with a broader Abeta sequence recognition compared to previously tested vaccines, creating binders to pathogenic forms of Abeta important in pathogenesis including pGlu-Abeta3–42.

2003-03-01·Vaccine3区 · 医学

Reduction of β-amyloid plaques in brain of transgenic mouse model of Alzheimer’s disease by EFRH-phage immunization

3区 · 医学

Article

作者: Frenkel, Dan ; Dewachter, Ilse ; Van Leuven, Fred ; Solomon, Beka

Antibodies to the epitope EFRH, representing residues 3-6 within the beta-amyloid (Abeta) sequence, were previously shown to affect the solubility and disaggregation of Abeta fibrils in vitro. Here, we describe a novel method of immunization, using as antigen the EFRH peptide displayed on the surface of the filamentous phage. The EFRH phage evoked effective auto-immune antibodies in amyloid precursor protein [V717I] (APP[V717I]) transgenic mice that recapitulate the amyloid plaques and vascular pathology of Alzheimer's disease (AD). The immunization provoked a considerable reduction in the number of Abeta amyloid plaques in the brain of the transgenic mice and may serve as the basis for anti-Abeta vaccine.

项与 ACI-24 相关的新闻（医药）

2026-04-30

·BioSpace

AC Immune Initiates Final Cohort in Ongoing Phase 1b/2 ABATE Trial of Anti-Abeta Active Immunotherapy to Treat Alzheimer’s Disease

AC Immune Initiates Final Cohort in Ongoing Phase 1b/2 ABATE Trial of Anti-Abeta Active Immunotherapy to Treat Alzheimer's Disease Treatment of first patient in Cohort AD4 in ABATE trial triggers $12 million milestone payment Allows evaluation of potential for precision prevention of neurodegenerative diseases Data from ABATE Cohorts AD1, AD2 and AD3 after 12 months treatment expected Q2 2026 Lausanne, Switzerland, April 30, 2026 -- AC Immune SA (NASDAQ: ACIU), a clinical-stage biopharmaceutical company pioneering precision therapeutics for neurodegenerative diseases, today announced it dosed the first patients in Cohort AD4 in the ongoing Phase 1b/2 ABATE trial. As a result, AC Immune will receive a $12 million milestone payment from Takeda under the partners’ exclusive, worldwide option and license agreement for AC Immune’s active immunotherapies targeting toxic forms of amyloid beta (Abeta), including ACI-24 for the treatment of Alzheimer’s disease (AD). ABATE is assessing ACI-24 in subjects with prodromal AD and in adults with Down syndrome (DS). AD4 includes subjects with prodromal AD. Dr. Andrea Pfeifer, CEO of AC Immune SA , said: “This milestone underscores the progress in our Phase 1b/2 ABATE trial of ACI-24. AD4 will build on the encouraging early safety and immunogenicity data to date. It allows further evaluation of the potential of ACI-24 and, more broadly, our precision prevention approach to neurodegenerative diseases, which encompasses a pipeline of active immunotherapies and intracellular-targeted small-molecule therapeutics to intervene at the earliest stages of disease.” ACI-24 is an anti-Abeta active immunotherapy candidate designed to induce a robust antibody response against the toxic forms of Abeta believed to drive plaque formation and AD progression. By inducing plaque clearance and efficiently inhibiting plaque formation in the brain, ACI-24 has the potential to delay or slow AD progression. ACI-24 is being investigated in the ongoing ABATE randomized, double-blind, placebo-controlled Phase 1b/2 trial to assess its safety, tolerability, immunogenicity and pharmacodynamic effects. Data so far show that ACI-24 is generally safe and well tolerated, and that it has generated anti-Abeta antibody responses at all tested doses. Cohorts AD1, AD2 and AD3 enrolled a total of 74 patients who received ACI-24 at escalating dose levels. The 12-month data readouts from Cohorts AD1, AD2 and AD3 are expected later in Q2 2026. Cohort AD4 will include an initial group of 36 patients treated for 12 months, with follow-up of 6 months, significantly expanding the safety and biomarker efficacy data set. A subsequent expansion of the AD4 cohort could potentially see the total number of subjects reach approximately 112 patients. AC Immune is responsible for conducting the ABATE trial. Following the potential option exercise, Takeda would conduct and fund all further clinical development and be responsible for all global regulatory activities as well as worldwide commercialization. Under the terms of the agreement with Takeda, AC Immune received an upfront payment of $100 million and is eligible to receive an option exercise fee and additional potential development, commercial and sales-based milestones of up to approximately $2.1 billion, if all related milestones are achieved over the course of the agreement. Upon commercialization, AC Immune will be entitled to receive tiered double-digit royalties on worldwide net sales. About ACI-24 This product is AC Immune’s anti-Abeta active immunotherapy candidate. The ABATE randomized, double-blind, placebo-controlled Phase 1b/2 trial of ACI-24 for treatment of Alzheimer’s disease (AD) continues fully blinded ( NCT05462106 ). Enrolled patients are required to have a diagnosis of prodromal AD: MCI due to AD according to the National Institute on Aging Alzheimer’s Association (NIA-AA) criteria, and a PET scan at screening must be consistent with the presence of amyloid pathology. Patients will be randomized to one of several doses of ACI-24 or placebo. Following multiple data safety monitoring board (DSMB) reviews, no safety concerns have been raised to date, consistent with previous results. Very encouraging immunogenicity has been shown with clear evidence of anti-Abeta antibody responses against toxic Abeta species observed in the blinded data. About AC Immune SA AC Immune SA is a clinical-stage biopharmaceutical company and a global leader in precision prevention for neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, and NeuroOrphan indications driven by misfolded proteins. The Company’s two clinically validated technology platforms, SupraAntigen® and Morphomer®, fuel its pipeline of first- and best-in-class assets, which currently features a range of therapeutic and diagnostic programs, including candidates in Phase 2 and Phase 3 development. AC Immune has a strong track record of securing strategic partnerships with leading global pharmaceutical companies, resulting in substantial non-dilutive funding to advance its proprietary programs and >$4.5 billion in potential milestone payments plus royalties. SupraAntigen® is a registered trademark of AC Immune SA in the following territories: AU, EU, CH, GB, JP, RU, SG and USA. Morphomer® is a registered trademark of AC Immune SA in CA, CN, CH, EU, GB, JP, KR, NO, RU and SG. The information on our website and any other websites referenced herein is expressly not incorporated by reference into, and does not constitute a part of, this press release. For further information, please contact: SVP, Investor Relations & Corporate Communications Gary Waanders, Ph.D., MBA AC Immune Phone: +41 21 345 91 91 Email: gary.waanders@acimmune.com International Media Chris Maggos Cohesion Bureau Phone: +41 79 367 6254 Email: chris.maggos@cohesionbureau.com Forward looking statements This press release contains statements that constitute “forward-looking statements” within the meaning of Section 27A of the Securities Act of 1933 and Section 21E of the Securities Exchange Act of 1934. Forward-looking statements are statements other than historical fact and may include statements that address future operating, financial or business performance or AC Immune’s strategies or expectations. In some cases, you can identify these statements by forward-looking words such as “may,” “might,” “will,” “should,” “expects,” “plans,” “anticipates,” “believes,” “estimates,” “predicts,” “projects,” “potential,” “outlook” or “continue,” and other comparable terminology. Forward-looking statements are based on management’s current expectations and beliefs and involve significant risks and uncertainties that could cause actual results, developments and business decisions to differ materially from those contemplated by these statements. These risks and uncertainties include those described under the captions “Item 3. Key Information – Risk Factors” and “Item 5. Operating and Financial Review and Prospects” in AC Immune’s Annual Report on Form 20-F and other filings with the Securities and Exchange Commission. Forward-looking statements speak only as of the date they are made, and AC Immune does not undertake any obligation to update them in light of new information, future developments or otherwise, except as may be required under applicable law. All forward-looking statements are qualified in their entirety by this cautionary statement. Attachment 20260429__ACIU Takeda AD4 milestone-final

2026-04-22

·丁香园神经时间

APOE4 高风险人群如何破局？一文读懂阿尔茨海默病诊疗现状与研发新进展

引言阿尔茨海默病（简称 AD）是一种常见的神经退行性疾病，主要表现为记忆力下降、认知功能减退、行为异常，以及日常生活能力逐渐丧失。在我国，65 岁以上人群中 AD 患病率已达 6.0%，约每 17 人就有 1 人患有 AD，疾病负担远超全球平均水平 [1]。在临床上，AD 的两大核心病理特征是：大脑中出现 β-淀粉样蛋白（Aβ）沉积形成的「斑块」，以及 tau 蛋白过度磷酸化形成的「神经纤维缠结」[1]。但长期以来，AD 的治疗只能暂时缓解症状，无法延缓疾病进展。近年来，靶向 Aβ 的单克隆抗体药物取得了突破，但仍面临疗效争议、安全风险和临床应用不便等挑战 [2-3]。如何开发更安全、更有效、更方便的新疗法，已成为全球 AD 药物研发的核心目标。 AD 机制研究不断深入，精准生物标志物仍需突破 AD 的发病机制非常复杂，至今尚未明确。对于 AD 的发病机制的研究，目前较为公认的包括「Aβ 假说」和「tau 蛋白假说」。「Aβ 假说」认为，Aβ 生成过多或清除不足是 AD 的关键驱动因素。在 Aβ 形成斑块之前，可溶性的 Aβ 寡聚体会损伤神经元之间的连接（突触），并产生神经毒性 [2]。而「tau 蛋白假说」则强调，过度磷酸化的 tau 蛋白在神经细胞内形成神经纤维缠结，也是 AD 的标志性病理改变之一 [2]。除了上述机制，遗传因素也扮演重要角色。载脂蛋白 E ε4（APOE ε4）是目前已知 AD 最常见的遗传风险基因，约 50% 的散发性 AD 病例与之相关 [2]。携带一个 APOE ε4 拷贝的个体，患病风险高于非携带者；携带两个拷贝（即纯合子）的个体，患病风险则更高 [2]。APOE ε4 携带者脑内 Aβ 和 tau 蛋白的异常积聚速度更快，认知功能下降和海马体（大脑的记忆中枢）萎缩也更早出现 [8]，因此这类患者面临更为迫切的治疗需求。图 1：AD 核心病理机制和遗传风险基因 [2] 诊断方式上，在精准医疗时代，AD 的诊断正从单纯看症状，转向采用生物标志物（可测量的生物学指标）进行精准判断 [1]。目前，通过腰椎穿刺获取脑脊液并检测生物学标志物（如 Aβ42/Aβ40 比值、p-tau181/Aβ42 比值）具备高诊断准确性，但受限于穿刺取样的有创性，难以大规模推广 [1]。相比之下，血液生物标志物检测（如血浆 Aβ42/Aβ40 比值、血浆 p-tau217 等）操作简便、创伤小，更适合大规模筛查。目前，血浆 Aβ42/Aβ40 比值和血浆 p-tau217 等血液生物指标，已可用于 AD 的早期筛查与疗效监测，为更早发现疾病、更早干预提供了有力工具。更多新型标志物和影像学指标仍在持续研究中。 AD 治疗进入「疾病修饰」阶段，新药选择仍待丰富过去很长时间里，AD 的治疗主要依赖两类传统药物：胆碱酯酶抑制剂和 NMDA 受体拮抗剂 [4]，但这些药物都只能暂时改善症状，无法改变疾病进程 [3]。近些年，两款靶向清除脑内 Aβ 的新型单抗药物相继在国内外获批，标志着 AD 治疗进入了疾病修饰治疗（DMT）的新阶段，即能够延缓疾病进展、改变病程的疗法 [1,4]。研究显示，抗 Aβ 单抗可以显著降低大脑中的 Aβ 负荷，有效延缓认知和功能衰退 [3,5]。然而这类药物可能引起 Aβ 相关影像异常（ARIA），主要表现为伴有水肿的 ARIA（ARIA-E）和伴有含铁血黄素沉积的 ARIA（ARIA-H）。ARIA 通常无症状，但有极小的可能发生罕见的严重事件 [3-4]。研究还发现，ARIA 的发生与 APOE 基因型密切相关。其说明书提示，与 ApoE ε4 杂合子和非携带者相比，接受抗 Aβ 单抗治疗的 ApoE ε4/4 纯合子患者的 ARIA 发生率更高，包括症状性和严重 ARIA [3-4]。抗 Aβ 疗法的获批是 AD 治疗领域的一个重要里程碑，但临床上仍需更多新型疾病修饰药物，以丰富治疗用药选择。 AD 药物研发新格局：多条路径齐头并进如今，AD 新药研发呈现出多元化格局：从口服小分子抑制剂、下一代抗体，到靶向 Aβ、tau 蛋白以及神经保护机制，多条路径同步推进。一、靶向 Aβ 的新一代疗法由于抗 Aβ 单抗治疗存在 ARIA 风险，且需要静脉输注给药，不够便捷，推动了口服小分子 Aβ 抑制剂的研发热潮兴起。这类药物旨在从 Aβ 级联反应的上游进行干预，阻止 Aβ 单体错误折叠和聚集 [6]。 01 从希望到转折，ALZ-801 研发带来新启示 ALZ-801 是高牛磺酸的前体药物，通过抑制 Aβ42 寡聚体形成发挥作用 [6]。在针对 APOE ε4/4 纯合子和杂合子早期 AD 患者的 Ⅱ 期试验中，该药表现良好：84 例患者治疗 2 年后，血浆 p-tau181 水平显著降低 31%（P = 0.045），海马萎缩得到缓解，且整个研究期间未观察到血管源性脑水肿事件 [7]。 APOE ε4 携带者因基因原因，Aβ 和 tau 病理加速沉积、认知下降更快、海马萎缩更严重，治疗需求尤为迫切。上述 ALZ-801 的 Ⅱ 期研究结果，曾为这部分患者带来治疗的希望 [8]。然而，2025 年公布的 Ⅲ 期 APOLLOE4 研究结果却增添了不确定性 [9]。在 325 例早期 AD 患者（均为 APOE ε4/4 纯合子，包括轻度认知障碍和轻度 AD）中，ALZ-801 治疗 78 周后，主要认知终点（ADAS-Cog13 量表）未能达到统计学显著性（仅延缓 11%，P = 0.607）[9]。尽管在总体人群中未达到主要认知终点，但预设的亚组分析中却出现了令人振奋的不同结果：在轻度认知障碍（MCI）亚组（125 例）中，ALZ-801 展现出显著且一致的临床获益，认知衰退延缓（ADAS-Cog13）52%（P = 0.041），日常功能衰退（痴呆残疾评估量表）延缓 96%（P = 0.016）[9]。这意味着，在更早期的 MCI 阶段就开始用药的患者，认知功能衰退被有效延缓了一半以上。图 2：MCI 亚组中认知功能和日常生活能力获益显著 [9] 更值得关注的是，部分患者在治疗 78 周后，海马体积不仅没有萎缩，反而出现了增长，这类患者被称为「超级应答者」[10-11]。在 APOLLOE4 研究中，活性药物治疗组有 16% 的患者属于超级应答者，而安慰剂组只有 3%[10]。与整体早期 AD 人群相比，这些超级应答者年龄更小、基线认知评分更高、基线海马体积更大[10]，提示早期干预可能是 APOE ε4/4 纯合子实现疾病修饰治疗获益的关键。随后公布的 ALZ-801 4 年开放标签扩展研究结果，为这份临床获益提供了坚实的长期证据[8]：在该研究的 MCI 亚组中，APOE ε4/4 纯合子携带者经 ALZ-801 治疗 4 年后，认知状态（MMSE 评分）稳定的比例高达 67%（8/12），而 APOE ε3/4 杂合子携带者中这一比例仅为 46%（6/13）[8]。 02 国内创新药 RP902：直接瞄准获益优势人群——MCI 患者 RP902 是润佳医药自主研发的小分子 Aβ 抑制剂，与 ALZ-801 类似，均在牛磺酸结构基础上优化，但 RP902 是氘代高牛磺酸的前体药物，体内转化为氘代高牛磺酸后起效，进一步优化了药代动力学特性[12]。RP902 可抑制大脑中与 AD 患者认知功能下降直接相关的可溶性 Aβ 寡聚体的形成，消除或降低 Aβ 对神经细胞的毒性，对血脑屏障损伤也有一定的缓解和保护作用[12-13]。该药于 2022 年 12 月获得中国 NMPA 临床试验批件，是我国首个进入临床试验的小分子 Aβ 抑制剂[13]。临床前研究显示，RP902 在 AD 模型小鼠中能改善形象识别记忆、空间记忆和长期记忆障碍，降低 Aβ 沉积以及可溶性和不溶性 Aβ1-40/1-42 水平。目前，RP902 已完成 Ⅰ 期临床研究，其 Ⅱ/Ⅲ 期试验已获 CDE 批准，针对携带 APOE ε4 等位基因的阿尔茨海默病源性 MCI 阶段患者，临床正在启动中 [14]。 03 其他口服小分子 PRI-002（RD2）：通过将 Aβ 寡聚体分解为单体，降低神经毒性，恢复突触可塑性，目前处于 Ⅱ 期临床阶段[15-16]。 ALX-001 / BMS-9894923：通过阻断 Aβ 与 mGluR5 相互作用，防止突触丢失，Ⅰ 期试验进行中[17]。 04 下一代抗 Aβ 单抗新一代抗体致力于解决现有药物的局限性 [18]。 Trontinemab：利用转铁蛋白受体技术实现跨血脑屏障转运，提高脑内药物浓度，Ⅲ 期临床正在招募[19-20]。 Remternetug：多奈单抗的后续产品，支持皮下注射，给药更便捷，Ⅱ/Ⅲ 期研究进行中[18,21]。 Sabirnetug：选择性靶向可溶性 Aβ 寡聚体，Ⅰ 期已完成，Ⅱ 期研究招募中[22-23]。二、靶向 Tau 蛋白的药物由于 tau 蛋白病理负荷与 AD 认知下降密切相关，靶向 tau 的治疗正成为研发热点 [5]。 Bepranemab：抗 tau 单抗，Ⅱ 期临床已完成 [5,24]。 BIIB080（MAPTRx）：首款靶向 tau 的反义寡核苷酸药物，通过抑制 tau 蛋白生成发挥作用。Ⅰb 期探索性分析显示认知和功能下降速度持续减缓，Ⅱ 期研究进行中 [25]。三、神经保护机制疗法这类策略旨在支持神经元存活、增强突触可塑性，延缓神经退行性变。但这一方向的临床有效性仍需大型随机对照研究验证。 AR1001：口服 PDE5 抑制剂，通过提高细胞内 cGMP 水平，激活下游信号通路，从而增强突触可塑性并促进神经细胞存活。该药的 Ⅱ 期临床试验未达主要终点，Ⅲ 期临床试验正在进行中 [26]。 GSK4527226（AL101）：靶向 sortilin 的单抗，通过调节小胶质细胞功能增强对 Aβ 和 tau 的清除，Ⅱ 期进行中 [27]。四、其他前沿方向基因疗法：针对 APOE4 的多重策略——包括靶向抗体清除有害蛋白、病毒载体导入保护性 APOE2 基因、CRISPR 基因编辑降低 APOE4 表达等，均处于临床前或早期临床阶段 [5]。主动免疫疫苗： ACI-24.060：靶向 Aβ，诱导针对 Aβ 寡聚体和原纤维的多克隆抗体应答，Ⅰb/Ⅱ 期研究正在进行中 [28]。 ACI-35.030 和 JACI-35.054：靶向磷酸化 tau 蛋白的脂质体疫苗，通过诱导针对病理性 tau 的免疫应答，阻止 tau 聚集，Ⅰb/Ⅱa 期临床试验数据支持诱导更快速持久的 ACI-35.030 进入下一阶段 Ⅱb 期临床研究阶段 [29]。结语：精准预防与早期干预，AD 治疗的新希望随着血液生物标志物的普及和疾病修饰疗法的问世，AD 药物研发正从「症状期干预」向「临床前阶段预防」前移 [4]。目前已有多个临床试验在探索这一策略。小分子 Aβ 抑制剂凭借良好的安全性和口服便捷性，在破解 APOE ε4 携带者（高风险人群）的治疗困境方面展现出巨大潜力 [8-11]。未来，通过高灵敏度的血液生物标志物精准识别高危个体，在神经元尚未发生不可逆损伤的临床前阶段，采用安全、便捷的口服药物进行早期干预，有望从源头上延缓甚至阻止 AD 的发生。将干预窗口前移至临床前阶段，结合生物标志物指导的精准预防，已成为 AD 领域值得期待的发展方向。 ✩ 本文仅供医疗卫生等专业人士参考内容策划：郭青青项目审核：唐静题图来源：图虫创意参考文献 [1] 中国微循环学会神经变性病专业委员会, 王盼, 刘帅, 等. 阿尔茨海默病诊断规范共识 [J]. 中国现代神经疾病杂志,2026,26(02):112-128. [2] Fu C, Li X, Liu X, et al. Psychoactive substances: novel molecular insights and therapeutic potential for Alzheimer's disease. Transl Neurodegener. 2025 Jul 25;14(1):38. [3] 刘雨辉, 卜先乐, 马辛, 等. 阿尔茨海默病药物治疗指南 [J]. 阿尔茨海默病及相关病杂志,2025,8(01):8-16. [4] Wu CK, Fuh JL. A 2025 update on treatment strategies for the Alzheimer's disease spectrum. J Chin Med Assoc. 2025 Jul 1;88(7):495-502. [5] Guo X, Yue R, Cui Z, et al. Advances of therapeutic strategies for Alzheimer's disease. J Neurol. 2025 Oct 17;272(10):705. [6] Hey JA, Kocis P, Hort J, et al. Discovery and Identification of an Endogenous Metabolite of Tramiprosate and Its Prodrug ALZ-801 that InhⅠbits Beta Amyloid Oligomer Formation in the Human Brain. CNS Drugs. 2018 Sep;32(9):849-861. [7] Hey JA, Abushakra S, Blennow K,et al. Effects of Oral ALZ-801/Valiltramiprosate on Plasma Biomarkers, Brain Hippocampal Volume, and Cognition: Results of 2-Year Single-Arm, Open-Label, Phase 2 Trial in APOE4 Carriers with Early Alzheimer's Disease. Drugs. 2024 Jul;84(7):811-823. [8] J Patrick Kessiak, et al. Biomarker-Positive APOE4 Carriers with MCI Show Disease Stability over 4-Years of Valiltramiprosate/ALZ-80I Treatment: MMSE Responder Analysis from the ALZ-801 Phase 2 Long-Term Extension Study. Poster 01 326. Presented at AD/PD 2026. [9] Abushakra S, Power A, Watson D, et al. Clinical Efficacy, Safety and Imaging Effects of Oral Valiltramiprosate in APOEε4/ε4 Homozygotes with Early Alzheimer's Disease: Results of the Phase III, Randomized, Double-Blind, Placebo-Controlled, 78-Week APOLLOE4 Trial. Drugs. 2025 Nov;85(11):1455-1472. [10] Jeremy Yu,et al. VALILTRAMIPROSATE REVERSES NEURODENEGERATION AND IMPROVES CLINICAL OUTCOMES IN SUBGROUP OF EARLY SYMPTOMATIC AD IN HOMOZYGOTES: RESULTS FROM 78 WEEK PHASE 3 APOLLOE4 TRIAL. ID:1299. Presented at AD/PD 2026. [11] Jeremy Yu,et al. Valiltramiprosate/ALZ-801 Prevents Hippocampal Atrophy and Clinical Decline in a Stage 2 AD Subpopulation in APOLLOE4 Phase 3 Study. Presented at AD/PD 2025. [12] 润佳医药官网. RP902 临床开发.http://www.risen-pharma.com/clinical/id-2.html [13] 润佳医药科技公众号. 重磅 | 润佳医药 RP902（靶向 Aβ）临床试验申请获得中国 NMPA 批准. https://mp.weixin.qq.com/s/JFsPorNIA-tmH-k9dwoG4A [14] 药物临床试验登记与信息公示平台. https://www.chinadrugtrials.org.cn/clinicaltrials.searchlist.dhtml [15] Kutzsche J, Cosma NC, Kauselmann G, et al. Oral PRI-002 treatment in patients with MCI or mild AD: a randomized, double-blind phase 1b trial. Nat Commun. 2025 May 6;16(1):4180. [16] ClinicalTrials. Study to Assess Safety and Efficacy of PRI-002 in Patients With MCI to Mild Dementia Due to Alzheimer's Disease (AD) (PRImus-AD). NCT06182085. [17] ClinicalTrials. A Study Evaluating the Potential of BMS-984923 to Alter the Systemic Exposure of Three Orally Administered Probe Substrates. NCT06632990. [18] Rafii MS, Aisen PS. Amyloid-lowering immunotherapies for Alzheimer disease: current status and future directions. Nat Rev Neurol. 2025 Sep;21(9):490-498. [19] Grimm HP, Schumacher V, Schäfer M, et al. Delivery of the Brainshuttle™ amyloid-beta antⅠbody fusion trontinemab to non-human primate brain and projected efficacious dose regimens in humans. MAbs. 2023 Jan-Dec;15(1):2261509. [20] ClinicalTrials. A Study of Trontinemab in Participants With Early Symptomatic Alzheimer's Disease (TRONTIER 1). NCT07169578 [21] ClinicalTrials. A Study of a Potential Disease Modifying Treatment in Individuals at Risk for or With a Type of Early Onset AD Caused by a Genetic Mutation (DIAN-TU-002). NCT06647498 [22] Cline EN, Antwi-Berko D, Sundell K, et al. Biofluid biomarker changes following treatment with sabirnetug (ACU193) in INTERCEPT-AD, a phase 1 trial in early Alzheimer's disease. J Prev Alzheimers Dis. 2025 Apr;12(4):100082. [23] ClinicalTrials. A Study to Evaluate Efficacy and Safety of Intravenous Sabirnetug in Participants With Early Alzheimer's Disease (ALTITUDE-AD) (ALTITUDE-AD). NCT06335173 [24] ClinicalTrials. A Study to Test the Efficacy, Safety, and Tolerability of Bepranemab (UCB0107) in Patients With Mild Cognitive Impairment or Mild Alzheimer's Disease (AD). NCT04867616 [25] Shulman M, Wu S, Ziogas N,et al. Exploratory analyses of clinical outcomes from the BIⅠB080 phase 1b study in mild Alzheimer's disease. Nat Aging. 2026 Feb;6(2):445-453. [26] Greeley D, Nash M, Herskowitz B, et al. A phase 2 randomized, placebo-controlled study on the efficacy and safety of AR1001, a phosphodiesterase-5 inhⅠbitor, in patients with mild-to-moderate Alzheimer's disease. J Prev Alzheimers Dis. 2025 Nov;12(9):100337. [27] Budda B, Mitra A, Park L, et al. Development of AL101 (GSK4527226), a progranulin-elevating monoclonal antⅠbody, as a potential treatment for Alzheimer's disease. Alzheimers Res Ther. 2025 Jul 25;17(1):174. [28] ClinicalTrials. A Study to Assess the Effects of ACI-24.060 in Alzheimer's Disease and in Down Syndrome (ABATE Study). NCT05462106 [29] Sol O, Mermoud J, Hallikainen M, et al. Safety and immunogenicity of two Tau-targeting active immunotherapies, ACI-35.030 and JACI-35.054, in participants with early Alzheimer's disease: a phase 1b/2a, multicentre, double-blind, randomised, placebo-controlled study. EBioMedicine. 2025 Oct;120:105940.

2026-03-13

·BioSpace

AC Immune Reports Full Year 2025 Financial Results and Provides a Corporate Update

AC Immune Reports Full Year 2025 Financial Results and Provides a Corporate Update Phase 2 interim results suggest treatment with active immunotherapy ACI-7104 may slow the progression of Parkinson’s disease NLRP3 inhibitor ACI-19764 Phase 1 trial initiated with first participants dosed Approaching multiple value-inflection points, including interim results of the AD3 cohort in the Phase 2 ABATE trial of ACI-24 in Alzheimer’s disease in H1 2026, and full 24-month data from Part 1 of the Phase 2 VacSYn trial of ACI-7104 in Q3 2026 Cash resources of CHF 91.4 million as of December 31, 2025, provide funding to the end of Q3 2027 before any potential milestone payments Lausanne, Switzerland, March 13, 2026 -- AC Immune SA (NASDAQ: ACIU), a clinical-stage biopharmaceutical company pioneering precision therapeutics for neurodegenerative diseases, today reported results for the full year ended December 31, 2025, and provided a corporate update. Dr. Andrea Pfeifer, CEO of AC Immune SA, commented: “We made significant progress towards delivering precision prevention of neurodegenerative diseases in 2025, exemplified by the exceptional interim data from the VacSYn trial of ACI-7104, our wholly-owned active immunotherapy targeting α-synuclein. Evidence that ACI-7104 appears to slow the rate of progression in early Parkinson’s disease (PD) further demonstrates the potential for active immunotherapies as disease-modifying treatments with the potential to slow or prevent neuronal damage.” “Our novel Morphomer® small-molecule therapeutics complement these programs by targeting intracellular mechanisms, enabling intervention at the earliest stages of disease. ACI-19764, a brain-penetrant NLRP3 inhibitor with potential to treat numerous diseases both within and beyond neurodegeneration, is now in a Phase 1 trial.” Full Year 2025 and Subsequent Highlights: ACI-7104 anti-α-synuclein active immunotherapy Reported positive interim safety and efficacy results from Part 1 of the Phase 2 VacSYn trial of our wholly-owned anti-α-synuclein active immunotherapy ACI-7104 in early PD. Results suggest, for the first time, that targeting underlying α-synuclein pathology with an active immunotherapy may slow the rate of progression of Parkinson’s disease. These results could translate into a shift from treating symptoms toward true disease modification in PD Clear safety pro no clinically relevant safety issues reported to date Targets met for immunogenicity (100% responder rate), pharmacodynamic effect, target engagement and clinical assessments Final data from Part 1 of the study expected in mid-2026. Morphomer-Tau small molecule program Progressed the Morphomer small molecule Tau aggregation inhibitors for the potential treatment of Alzheimer’s disease (AD) and other neurodegenerative diseases. Investigational New Drug (IND)-enabling studies are expected to begin in H1 2026. NLRP3 inhibitor, ACI-19764, small molecule program Dosed the first participants in a Phase 1 clinical trial of ACI-19764, a brain-penetrant small molecule targeting the NLRP3 inflammasome (NCT07463196). Our NLRP3 inhibitors have potential to intervene at the earliest stages of disease in neurodegenerative conditions, including AD, PD, amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. Potential additional indications include inflammatory disorders (e.g., multiple sclerosis, inflammatory bowel disease, gout), cancer, cardiovascular disease, metabolic disorders (e.g., Type 2 diabetes, obesity), skin inflammatory diseases (e.g. hidradenitis suppurativa) and rare genetic syndromes of autoimmunity such as Cryopyrin-associated periodic syndromes (CAPS). ACI-19764, an orally available, brain-penetrant NLRP3 inhibitor is a major addition to AC Immune’s growing intracellular targeting pipeline. Sharpened Pipeline Focus with Operational Efficiencies Extending Cash Runway Following a strategic review by executive management, sharpened investment on our most important assets. These include the three clinical-stage active immunotherapy programs ACI-7104, ACI-24 and ACI-35, the latter two of which are in ongoing pharma collaborations, and promising small molecule programs targeting NLRP3, Tau and α-synuclein. The Company reduced its workforce by around 30% and extended its cash for operations to the end of Q3 2027. AC Immune research results published in peer-reviewed journals and presented at conferences: Clinical results from the completed Phase 1b/2a trial of active immunotherapy ACI-35 (JNJ-2056) partnered with Janssen Pharmaceuticals, Inc., a Johnson & Johnson company, in eBioMedicine . Preclinical research demonstrating the in vivo activity of a vectorized (AAV9) anti-TDP-43 monoclonal antibody in a model of ALS/FTD, in Molecular Therapy . First-in-class positron emission tomography (PET) tracers for imaging TDP-43 pathology in the brain, including ACI-19626, that could enable a precision medicine approach to neurodegenerative diseases which are currently difficult to diagnose, in Nature Communications . Featured the company’s therapeutic and diagnostic programs in presentations at AD/PD™ 2025 where we also hosted an industry symposium highlighting the company’s leading pipeline of active immunotherapies for precision prevention of neurodegenerative diseases. Appointed Prof. Catherine Mummery , a renowned neurologist and expert in dementia clinical trials, as Chair of Ac Immune’s Clinical Advisory Board (CAB). Anticipated 2026 Milestones Program Milestone Expected in ACI-7104 anti-α-synuclein active immunotherapy Final data from Part 1 of the Phase 2 VacSYn trial in PD expected in mid-2026 H2 2026 ACI-24 anti-Abeta active immunotherapy Interim results from ABATE Phase 2 trial after reaching 12-month treatment timepoint in the AD3 cohort H1 2026 ACI-19764 NLRP3 inhibitor Results from Phase 1 trial in healthy volunteers H2 2026 Morphomer-Tau aggregation inhibitors Lead declaration and initiation of IND-enabling studies H1 2026 Morphomer α-synuclein aggregation inhibitor Lead declaration H1 2026 Analysis of Financial Statements for the Full Year Ended December 31, 2025 Cash Position : The Company had total cash resources of CHF 91.4 million as of December 31, 2025, compared to total cash resources of CHF 165.5 million as of December 31, 2024. The Company’s cash balance provides sufficient capital resources into Q3 2027, assuming no other milestones. Contract Revenues : The Company recorded CHF 3.6 million in contract revenues for the year ended December 31, 2025, compared with CHF 27.3 million in the prior year. For the year ended December 31, 2025, our contract revenues of CHF 3.6 million were related to the efforts made under the agreement with Takeda for development, CMC, and regulatory activities. The decrease compared to the prior year relates to the recognition of the second ReTain-related milestone payment of CHF 24.6 million under the agreement with Janssen in 2024. R&D Expenditures : R&D expense decreased by CHF 6.1 million for the year ended December 31, 2025 to CHF 56.4 million, predominantly due to: Discovery and preclinical expenses : Decrease of CHF 1.6 million, primarily due to the completion of certain pre-clinical studies and our strategic focus on advancing clinical-stage programs. Clinical expenses : Decrease of CHF 4.4 million, primarily due to lower costs related to manufacturing activities for our Phase 2 VacSYn study evaluating ACI-7104 in early PD and certain non-recurring manufacturing costs in 2024. These changes were offset by increased costs associated with our NLRP3 inhibitor program, which entered clinical development in 2026, and higher costs associated with our PET Tracer programs. Salary- and benefit-related costs : Decrease of CHF 0.7 million, primarily due to decreased share-based compensation in the current year. G&A Expenditures : G&A expenses decreased by CHF 1.1 million for the year ended December 31, 2025, to CHF 16.1 million. This decrease is primarily due to legal fees in 2024 which did not recur. Restructuring Expenditures : Expenses recognized as a result of the restructuring were CHF 0.5 million compared to nil for the year ended 2024. These expenses include CHF 2.1 million of termination benefits, offset by a CHF 1.8 million gain on curtailment in the defined benefit pension liability. The remaining balance pertains to other non-cash activities within share-based compensation. Financial Result : Net finance result was a CHF 1.1 million loss for the year ended December 31, 2025, compared with a CHF 1.5 million gain in 2024. This was due to lower interest received on net investments in short-term financial assets and foreign exchange differences caused by foreign currencies depreciating against CHF, predominantly the U.S. Dollar. IFRS Loss for the Period : The Company reported a net loss after taxes of CHF 70.5 million for the year ended December 31, 2025, compared with a net loss of CHF 50.9 million for the prior year. 2026 Financial Guidance For the full year 2026, the Company expects its total cash expenditure to be in the range of CHF 55-65 million. The Company defines total cash expenditure as operating expenditure adjusted to include capital expenditure and offset by significant non-cash items (including share-based compensation and depreciation expenses). About AC Immune SA AC Immune SA is a clinical-stage biopharmaceutical company and a global leader in precision prevention for neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, and NeuroOrphan indications driven by misfolded proteins. The Company’s two clinically validated technology platforms, SupraAntigen® and Morphomer®, fuel its pipeline of first- and best-in-class assets, which currently features a range of therapeutic and diagnostic programs, including candidates in Phase 2 and Phase 3 development. AC Immune has a strong track record of securing strategic partnerships with leading global pharmaceutical companies, resulting in substantial non-dilutive funding to advance its proprietary programs and >$4.5 billion in potential milestone payments plus royalties. SupraAntigen® is a registered trademark of AC Immune SA in the following territories: AU, EU, CH, GB, JP, RU, SG and USA. Morphomer® is a registered trademark of AC Immune SA in CA, CN, CH, EU, GB, JP, KR, NO, RU and SG. The information on our website and any other websites referenced herein is expressly not incorporated by reference into, and does not constitute a part of, this press release. For further information, please contact: SVP, Investor Relations & Corporate Communications Gary Waanders, Ph.D., MBA AC Immune Phone: +41 21 345 91 91 Email: gary.waanders@acimmune.com International Media Chris Maggos Cohesion Bureau Phone: +41 79 367 6254 Email: chris.maggos@cohesionbureau.com Forward looking statements This press release contains statements that constitute “forward-looking statements” within the meaning of Section 27A of the Securities Act of 1933 and Section 21E of the Securities Exchange Act of 1934. Forward-looking statements are statements other than historical fact and may include statements that address future operating, financial or business performance or AC Immune’s strategies or expectations. In some cases, you can identify these statements by forward-looking words such as “may,” “might,” “will,” “should,” “expects,” “plans,” “anticipates,” “believes,” “estimates,” “predicts,” “projects,” “potential,” “outlook” or “continue,” and other comparable terminology. Forward-looking statements are based on management’s current expectations and beliefs and involve significant risks and uncertainties that could cause actual results, developments and business decisions to differ materially from those contemplated by these statements. These risks and uncertainties include those described under the captions “Item 3. Key Information – Risk Factors” and “Item 5. Operating and Financial Review and Prospects” in AC Immune’s Annual Report on Form 20-F and other filings with the Securities and Exchange Commission. Forward-looking statements speak only as of the date they are made, and AC Immune does not undertake any obligation to update them in light of new information, future developments or otherwise, except as may be required under applicable law. All forward-looking statements are qualified in their entirety by this cautionary statement. AC Immune SA Consolidated Balance Sheets (Unaudited) (In CHF thousands) As of December 31, 2025 2024 Assets Non-current assets Property, plant and equipment 1,989 2,651 Right-of-use assets 4,540 5,437 Intangible asset 50,416 50,416 Long-term financial assets 584 415 Total non-current assets 57,529 58,919 Current assets Prepaid expenses 3,972 4,302 Accrued income 360 1,099 Other current receivables 978 1,104 Short-term financial assets 64,617 129,214 Cash and cash equivalents 26,795 36,275 Total current assets 96,722 171,994 Total assets 154,251 230,913 Shareholders' equity and liabilities Shareholders’ equity Share capital 2,253 2,226 Share premium 481,863 478,506 Treasury shares (218) (218) Currency translation differences 7 (5) Accumulated losses (439,021) (368,239) Total shareholders’ equity 44,884 112,270 Non-current liabilities Long-term deferred contract revenue 2,339 4,560 Long-term lease liabilities 3,689 4,401 Net employee defined benefit liabilities 8,646 8,844 Total non-current liabilities 14,674 17,805 Current liabilities Trade and other payables 2,068 2,658 Accrued expenses 8,067 12,098 Short-term deferred contract revenue 83,706 85,056 Short-term lease liabilities 852 1,026 Total current liabilities 94,693 100,838 Total liabilities 109,367 118,643 Total shareholders’ equity and liabilities 154,251 230,913 Consolidated Statements of Income/(Loss) (unaudited) ( In CHF thousands, except for per-share data) For the Year Ended December 31, 2025 2024 2023 Revenue Contract revenue 3,573 27,309 14,801 Total revenue 3,573 27,309 14,801 Operating expenses Research & development expenses (56,436) (62,570) (54,606) General & administrative expenses (16,094) (17,259) (15,305) Other operating income/(expense), net 94 142 1,486 Restructuring expenses, net (455) — — Total operating expenses (72,891) (79,687) (68,425) Operating loss (69,318) (52,378) (53,624) Financial income 1,865 3,196 1,044 Financial expense (191) (133) (176) Exchange differences (2,803) (1,598) (1,467) Finance result, net (1,129) 1,465 (599) Loss before tax (70,447) (50,913) (54,223) Income tax expense — (3) (10) Loss for the period (70,447) (50,916) (54,233) Loss per share: Basic and diluted loss for the period attributable to equity holders (0.70) (0.51) (0.64) Consolidated Statements of Comprehensive Income/(Loss) (unaudited) (In CHF thousands) For the Year Ended December 31, 2025 2024 2023 Loss for the period (70,447) (50,916) (54,233) Items that may be reclassified to income or loss in subsequent periods (net of tax): Currency translation differences 12 46 (61) Items that will not to be reclassified to income or loss in subsequent periods (net of tax): Remeasurement gains/(losses) on defined-benefit plans (net of tax) (1,353) (3,084) (1,669) Other comprehensive income/(loss) (1,341) (3,038) (1,730) Total comprehensive loss, net of tax (71,788) (53,954) (55,963) Attachment 20260313__ACIU Q4 2025 Earnings Final

临床1期免疫疗法财报临床结果临床2期

100 项与 ACI-24 相关的药物交易

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适应症	最高研发状态	国家/地区	公司	日期
淀粉样蛋白斑	临床2期	美国	AC Immune SA	2022-06-21
淀粉样蛋白斑	临床2期	西班牙	AC Immune SA	2022-06-21
淀粉样蛋白斑	临床2期	英国	AC Immune SA	2022-06-21
唐氏综合征	临床2期	-	AC Immune SA	2021-10-01
阿尔茨海默症	临床2期	芬兰	AC Immune SA	2018-06-19

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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


NCT05462106 (ABATE, Company_Website) 人工标引	临床1/2期	阿尔茨海默症	-	ACI-24.060	壓壓糧廠壓鬱願鬱遞淵(淵願願鹹膚觸蓋鹹顧鹽) = ACI-24.060 was generally well tolerated with no safety concerns observed 選獵鬱廠觸艱顧製艱獵 (鏇顧選選淵鬱窪繭夢艱 ) 更多	积极	2023-01-26
NCT02738450 (3-Star, Pubmed \| JAMA Neurol) 人工标引	临床1期	唐氏综合征	16	ACI 24	糧鬱齋憲憲觸鹹觸夢網(夢鹹蓋蓋簾獵餘繭簾窪) = 鹹淵蓋齋繭遞餘壓製遞憲選餘鏇襯艱齋夢網鹹 (遞餘範製壓網鹽鹽糧糧 )	积极	2022-05-09
NCT02738450 (3-Star, Pubmed \| JAMA Neurol) 人工标引	临床1期	唐氏综合征	16	Placebo	糧鬱齋憲憲觸鹹觸夢網(夢鹹蓋蓋簾獵餘繭簾窪) = 齋憲夢選築遞顧範選獵憲選餘鏇襯艱齋夢網鹹 (遞餘範製壓網鹽鹽糧糧 )	积极	2022-05-09
NCT02738450 (3-Star, CTgov)	临床1期	唐氏综合征	20	Placebo	選窪糧醖願簾鹹遞窪窪(窪觸餘積膚淵憲淵淵範) = 廠窪選齋鹹鑰製蓋範鹹簾糧壓顧蓋鏇襯廠艱窪 (夢獵鏇獵構膚鑰顧壓夢, 84.5) 更多	-	2021-09-21