A Phase 2, Randomized, Placebo-Controlled, Double-Blind Study of XPro1595 in Patients With Mild Cognitive Impairment (MCI) With Biomarkers of Inflammation

The goal of this Phase 2 MCI study is to determine whether 1.0 mg/kg XPro1595 is superior to placebo at improving measures of cognition, functioning and brain quality in individuals with MCI and biomarkers associated with neuroinflammation (APOE4) and to evaluate safety, tolerability, and efficacy of XPro1595.

开始日期2023-06-01

申办/合作机构

INmune Bio, Inc.

NCT05522387

/ Terminated临床2期

An Open Label Extension of XPro1595 in Patients With Alzheimer's Disease That Have Completed a Phase 1 or Phase 2 Study With XPro1595

The goal of this Phase 2 Open Label study is to evaluate long-term safety, tolerability, and efficacy of XPro1595 on measures of cognition, function and brain quality in individuals with Alzheimer's Disease.

开始日期2023-02-21

申办/合作机构

INmune Bio, Inc.

NCT05318976

/ Completed临床2期

A Randomized, Placebo-Controlled, Double-Blind Study of XPro1595 in Patients With Early Alzheimer's Disease With Biomarkers of Inflammation

The goal of this Phase 2 Alzheimer's study is to determine whether 1.0 mg/kg XPro1595 confers a benefit on cognition, function, and biomarkers of white matter and to further evaluate safety and tolerability. The objectives of this study are to determine the safety, tolerability, and efficacy of XPro1595 in patients with early ADi.

开始日期2022-02-28

申办/合作机构

INmune Bio, Inc.

100 项与 INB-03 相关的临床结果

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100 项与 INB-03 相关的转化医学

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100 项与 INB-03 相关的专利（医药）

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项与 INB-03 相关的文献（医药）

2026-02-01·JOURNAL OF PHYSIOLOGY-LONDON

Targeting necroptosis protects against astrocyte death and hippocampal sclerosis in experimental temporal lobe epilepsy

Article

作者: Lukas Henning ; Christian Steinhäuser ; Zhou Wu ; Peter Bedner

Abstract:

Temporal lobe epilepsy (TLE) is the most common and severe form of adult focal epilepsy and is frequently associated with hippocampal sclerosis (HS). Accumulating evidence suggests that brain inflammation plays an important pathophysiological role in TLE. A key pro‐inflammatory mediator is tumour necrosis factor α (TNFα), which can trigger necroptosis pathways regulated by RIPK1, RIPK3 and MLKL through binding to the TNF receptor 1 (TNFR1). Previously, we detected activation of RIPK1, RIPK3 and MLKL in hippocampal CA1 astrocytes, along with a reduction in astrocyte density, during the early stages of experimentally induced TLE‐HS, providing strong evidence for necroptotic astrocytic cell death. Using immunohistochemistry, pharmacology and long‐term EEG recording, here we unravel the mechanisms underlying necroptosis induction in astrocytes and its role in epileptogenesis. The results show that pharmacological inhibition of necroptosis using Nec‐1s, a specific inhibitor of RIPK1, or selective inhibition of soluble TNFα by XPro1595, as well as genetic knockout of TNFR1, effectively rescued CA1 astrocyte loss caused by kainate‐induced status epilepticus. Furthermore, targeting necroptosis by Nec‐1s administration attenuated CA1 astrogliosis, degeneration of pyramidal neurons, granular cell dispersion and shrinkage of the CA1 subfield. In contrast, Nec‐1s did not affect acute and chronic epileptic activity in the TLE‐HS model. Our findings demonstrate that TNFα‐induced necroptotic astrocyte death is involved in the pathogenesis of TLE. image

Key points:

In the early stage of experimental temporal lobe epilepsy with hippocampal sclerosis (TLE‐HS), we observed activation of RIPK1, RIPK3 and MLKL in CA1 astrocytes, along with a reduction in astrocyte density, providing evidence for necroptotic cell death.Pharmacological inhibition of necroptosis (Nec‐1s), blockade of soluble tumour necrosis factor α (XPro1595) or genetic knockout of TNFR1 prevented astrocyte loss after status epilepticus.Continuous telemetric EEG recordings showed that Nec‐1s has no effect on acute or chronic epileptic activity in the TLE‐HS model.Immunohistochemical analysis revealed that Nec‐1s treatment reduced the extent of hippocampal sclerosis in experimental TLE‐HS.Our results provide further insights into the molecular mechanisms underlying the development and progression of TLE.

2026-01-01·Neurobiology of pain (Cambridge, Mass.)

Xpro®1595 alleviates neuropathic pain by targeting spinal dorsal horn ADAM17-mediated inflammation

Article

作者: Li, Li ; Yao, Wei-Wei ; Sun, Yan-Yan ; Sun, Ling-Ling ; Su, Yidie

A disintegrin and metalloprotease 17 (ADAM17) mediates the shedding of key pro-inflammatory cytokines, yet its specific contribution to neuropathic pain remains elusive. Here, we investigated the role of ADAM17 in the rat spinal nerve ligation (SNL) model. Following nerve injury, ADAM17 expression was significantly upregulated in the spinal dorsal horn (SDH) and dorsal root ganglion (DRG). Specifically, ADAM17 colocalized with TRPV1 and IB4 positive afferents in the superficial SDH, and with IB4, CGRP, and TRPV1 positive neurons in the DRG. Intrathecal administration of exogenous ADAM17 to naive rats recapitulated neuropathic pain behaviors-inducing mechanical and thermal hypersensitivity-and significantly increased the levels of TNF-α, IL-1β, and IL-6 in the SDH. Conversely, therapeutic treatment with Xpro®1595 markedly attenuated SNL-induced pain behaviors. This analgesic effect correlated with the suppression of injury-induced ADAM17 upregulation and a consequent reduction in proinflammatory cytokines. These findings demonstrate that ADAM17 is a critical driver of the neuroinflammatory cascade in neuropathic pain. Moreover, our data suggest that the analgesic efficacy of Xpro®1595 is mediated, at least in part, by disrupting this ADAM17-dependent inflammatory feedback loop.

2025-12-23·BIOSCIENCE REPORTS

The effect of the nonselective TNF inhibitor etanercept and of the selective TNF inhibitor XPro1595 on lesioned supraspinatus muscle

Article

作者: Nasseri, Sohail ; Aboo, Christopher ; Jensen, Peter Toft ; Ditzel, Nicholas ; Ding, Ming ; Hejbøl, Eva Kildall ; Stensballe, Allan ; Lambertsen, Kate Lykke ; Frich, Lars Henrik ; Schrøder, Henrik Daa ; Linh Ta, Thi My

The cytokine tumor necrosis factor (TNF), a major regulator of inflammatory responses, exists in both a membrane-bound form and a soluble form. We used the nonselective TNF inhibitor etanercept and the selective inhibitor XPro1595 and compared supraspinatus muscle cytokine levels, histology, and proteomic signatures in mice after supraspinatus tendon tear. The aim was to investigate the effect of anti-TNF treatment on the early inflammatory response in the muscle after tendon tear. In addition, the effect on body composition and bone mineral content was compared in naive mice after 2 months of treatment with either etanercept or XPro1595 using dual-energy X-ray absorptiometry (DEXA) and micro-CT. Inhibition of TNF did not significantly affect DEXA indexes of body composition nor bone microarchitecture, apart from increased structure model index and decreased bone surface density at 14 days, and bone surface to volume ratio at 2 months. Supraspinatus tendon tear caused extensive inflammatory changes in the supraspinatus muscle and initiated a regenerative response. However, TNF inhibition did not significantly affect these processes recorded as density in the lesioned supraspinatus muscle of macrophages and myogenin-positive nuclei. Although both inhibitors had an effect on mitochondrial proteins, particularly etanercept tended to modulate mitochondrial function, and eternacept also influenced NF-κB signaling. Modulation of the mitochondrial proteome and the influence on NF-κB signaling seen after etanercept treatment could correspond with its known effect on apoptosis.

170

项与 INB-03 相关的新闻（医药）

2026-08-26

·BioSpace

INmune Bio Advances Ebstrocel™ Toward European Marketing Authorization with EMA Regulatory Filings

Orphan Drug Designation application and pre-MAA Scientific Advice package submitted for Ebstrocel™ in RDEB Filings support a planned EU MAA in Q1 2027; orphan designation, if granted and maintained through approval, may provide regulatory incentives and 10 years of market exclusivity BOCA RATON, Fla., Aug. 26, 2026 (GLOBE NEWSWIRE) -- INmune Bio Inc. (NASDAQ: INMB) ("INmune Bio" or the "Company"), a late-stage biotechnology company focused on inflammation and immunology, today announced that it has submitted two regulatory packages to the European Medicines Agency (EMA) for Ebstrocel™: an application for Orphan Drug Designation and a Scientific Advice package to streamline the upcoming Marketing Authorization Application (MAA ) in Europe. Ebstrocel™, the first product from the Company’s CORDStrom™ platform, is an investigational pooled, allogeneic, umbilical cord-derived mesenchymal stromal cell therapy being developed as a systemic treatment for recessive dystrophic epidermolysis bullosa (RDEB). The EMA filings are intended to support the Company’s planned EU MAA in Q1 2027 and form part of a coordinated global registration strategy that includes a planned UK MAA in Q4 2026 and a planned U.S. Biologics License Application (BLA) in Q1 2027. “These EMA submissions are another execution milestone as we move Ebstrocel from late-stage clinical development toward potential commercialization,” said David Moss, co-founder and Chief Executive Officer of INmune Bio. “Our focus is on converting the clinical, regulatory and manufacturing progress achieved to date into a defined sequence of registration milestones across the UK, European Union and United States. Each step advances Ebstrocel toward patients and provides an opportunity to validate the broader regulatory and commercial potential of the CORDStrom platform.” Regulatory and Strategic Highlights EU orphan designation: The application seeks orphan medicinal product designation for Ebstrocel™ in RDEB in Europe to align with the ODD already granted in USA. If granted, sponsors may receive incentives that include protocol assistance and fee reductions. If Ebstrocel™ later receives marketing authorization and maintains orphan status, the approved orphan indication may benefit from 10 years of EU market exclusivity, subject to applicable requirements. Pre-MAA engagement: The Scientific Advice package is intended to support dialogue with EMA on scientific, regulatory and procedural requirements before the planned MAA, helping the Company identify and address key questions earlier in the filing process. Defined global catalyst sequence: The Company is targeting a UK MAA in Q4 2026, followed by planned EU MAA and U.S. BLA submissions in Q1 2027. Platform leverage: Ebstrocel™ is the first disease-specific CORDStrom™ product to advance toward potential marketing authorization. Progress with Ebstrocel™ is expected to inform development of additional scalable, off-the-shelf therapies from the platform. RDEB and the Ebstrocel™ Opportunity RDEB is a rare, debilitating genetic disease characterized by extreme skin fragility, chronic wounds, scarring and significant systemic complications. Ebstrocel™ is being developed as a systemic therapy intended to address disease manifestations beyond topical wound care. “RDEB is a systemic disease with substantial unmet need beyond the visible manifestations of skin injury,” said Mark Lowdell, Ph.D., Chief Scientific Officer of INmune Bio and inventor of the CORDStrom™ platform. “Advancing Ebstrocel through European regulatory pathways is important for patients and for CORDStrom. Ebstrocel is our first opportunity to demonstrate how a pooled, scalable, off-the-shelf stromal cell platform can progress through late-stage regulatory development.” About the European Regulatory Submissions Orphan Drug Designation in the European Union is intended to support the development of medicines for rare, serious conditions. If granted, the designation can provide access to regulatory incentives during development. Market exclusivity is available only after marketing authorization and maintenance of orphan status at the time of approval. The pre-MAA Scientific Advice process is designed to facilitate interaction with EMA in advance of an MAA submission and to help sponsors address scientific, regulatory and procedural considerations as they prepare a marketing authorization package. About Ebstrocel™ and CORDStrom™ Ebstrocel™ is the RDEB-specific investigational product from INmune Bio’s proprietary CORDStrom™ platform. CORDStrom™ is a platform of pooled, allogeneic, human umbilical cord-derived mesenchymal stromal cell therapies designed to reduce donor variability and manufacturing inconsistency. The Company’s fully closed, semi-automated manufacturing approach is intended to support scalable, reproducible and off-the-shelf products that can be tailored for different therapeutic applications and routes of administration. INmune Bio plans to continue its interactions with European regulators as it advances toward the planned MAA for Ebstrocel™. About INmune Bio Inc. INmune Bio Inc. is a publicly traded (NASDAQ: INMB), late-stage biotechnology company focused on developing treatments that target the innate immune system to fight disease. Moving beyond early-stage exploration, the Company’s clinical-development strategy centers on advanced precision medicine, matching drug mechanisms directly to patient biology to optimize clinical outcomes. INmune Bio is actively advancing two late-stage product platforms toward registrational milestones: CORDStrom™: A proprietary, pooled, allogeneic, human umbilical cord-derived mesenchymal stromal cell platform engineered to address the historical clinical challenges of donor variability and manufacturing inconsistency. Following successful clinical readouts in RDEB, the platform is transitioning to regulatory filing phases, with a UK MAA planned for 2026 and an EU MAA and U.S. BLA planned for Q1 2027. XPro1595™: A Dominant-Negative Tumor Necrosis Factor (DN-TNF) platform that selectively neutralizes soluble TNF (sTNF) to eliminate neuroinflammation without compromising protective immune function. Backed by FDA Fast Track designation and regulatory alignment from an End-of-Phase 2 meeting, XPro1595™ is positioned for an integrated Phase 2b/3 seamless adaptive registrational program in neuroinflammation-enriched early Alzheimer’s disease. To learn more about INmune Bio’s pipeline and its approach to harnessing the innate immune system, please visit . Forward Looking Statements The Company’s product candidates are in clinical development and there is no assurance that any specific outcome will be achieved. Any statements contained in this press release related to the development or commercialization of product candidates and other business and financial matters, including without limitation, trial results and data, including the timing of key milestones, future plans or expectations, and the prospects for receiving regulatory approval or commercializing or selling any product or drug candidates, may constitute forward-looking statements as that term is defined in the Private Securities Litigation Reform Act of 1995. Any forward-looking statements contained herein are based on current expectations but are subject to several risks and uncertainties. Actual results and the timing of certain events and circumstances may differ materially from those described by the forward-looking statements because of these risks and uncertainties. CORDStrom™, XPro1595™ (XPro™, pegipanermin), and INKmune™ have either finished clinical trials, are still in clinical trials or are preparing to start clinical trials and have not been approved by the U.S. Food and Drug Administration (FDA), the UK MHRA or any regulatory body and there cannot be any assurance that they will be approved by the FDA, the UK MHRA or any regulatory body or that any specific results will be achieved. The factors that could cause actual future results to differ materially from current expectations include, but are not limited to, risks and uncertainties relating to the Company’s ability to produce more drug for clinical trials; the availability of substantial additional funding for the Company to continue its operations and to conduct research and development, clinical studies and future product commercialization; and the Company’s business, research, product development, regulatory approval, marketing and distribution plans and strategies. These and other factors are identified and described in more detail in the Company’s filings with the Securities and Exchange Commission, including the Company’s Annual Report on Form 10-K, the Company’s Quarterly Reports on Form 10-Q and the Company’s Current Reports on Form 8-K. The Company assumes no obligation to update any forward-looking statements to reflect any event or circumstance that may arise after the date of this release. INmune Bio Contacts David Moss Chief Executive Officer (561) 710-0512 info@inmunebio.com Daniel Carlson Head of Investor Relations (415) 509-4590 dcarlson@inmunebio.com

快速通道孤儿药临床研究免疫疗法细胞疗法

2026-08-20

·CNSight

Nature子刊揭示阿尔茨海默病免疫新机制，神经免疫正在成为CNS药物研发新战场

阿尔茨海默病过去几十年的药物研发，基本围绕Aβ和Tau两条主线展开。如今，这个研发格局正在出现一个越来越清晰的变化：真正决定疾病是否持续进展的，可能不仅是异常蛋白本身，还包括大脑免疫系统如何应对这些异常蛋白。 2026年8月，《Nature Genetics》发表的一项人脑研究，对1607名供者的83万余个髓系细胞进行了系统分析，发现衰老和阿尔茨海默病进程中，小胶质细胞与脑血管周围巨噬细胞存在高度动态的状态变化；与此同时，《Nature Communications》另一项研究则直接证明，特定状态的小胶质细胞可以通过吞噬突触造成认知损害。这两项研究的重要性并不只是“发现了一种新的细胞状态”。它们正在把阿尔茨海默病的神经免疫研究，从过去的相关性研究推进到细胞状态—分子通路—突触损伤—认知功能的因果链条。而这条链条正在迅速转化成药物研发。截至2026年，全球阿尔茨海默病临床研发管线已经达到192项临床试验、158个候选药物，其中疾病修饰疗法占73%。这意味着，阿尔茨海默病已经不再是一个只有Aβ抗体的单一路径市场，而正在进入多靶点、多机制竞争阶段。神经免疫，正在成为下一场CNS药物研发竞争的重要战场。 01 从“炎症存在”到“哪些免疫细胞、处于什么状态”：Nature Genetics把研究推进了一步长期以来，神经炎症已经被认为参与阿尔茨海默病发生发展，但真正限制药物开发的一个问题是：我们过去知道“大脑有炎症”，却并不知道究竟是哪一群细胞、处于什么状态、在疾病的哪个阶段发挥作用。 Nature Genetics（2026-08-11） DOI:https://doi.org/10.1038/s41588-026-02716-6 《Nature Genetics》的这项研究，正是在解决这个问题。研究团队对1607名供者的前额叶皮层进行了单细胞层面的系统分析，总计获得832,505个人类髓系细胞，并按照细胞转录特征划分出6个主要亚类和13个具有不同转录特征的细胞亚型，覆盖从正常衰老到不同程度阿尔茨海默病病理负荷的人群。研究最值得关注的发现，是一种与疾病相关的小胶质细胞亚型。这类细胞具有较高的GPNMB表达，而且携带更多与阿尔茨海默病遗传风险相关的特征。随着阿尔茨海默病病理负荷增加，这一细胞亚群明显扩张，并表现出增强的吞噬能力。但研究并没有简单地把这种小胶质细胞定义为“坏细胞”。相反，研究进一步发现，这一细胞状态具有一定的神经保护作用，而这种保护效应依赖TREM2信号。研究团队进一步通过细胞间通讯分析，将APOE–SORL1和APOE–TREM2信号轴确定为与疾病进展密切相关的关键通讯关系，并利用人类样本和小鼠模型验证了TREM2在这一保护性小胶质细胞状态中的作用。这实际上改变了过去对“小胶质细胞”的简单理解。问题可能不是小胶质细胞到底该不该被激活，而是它在什么时候、以什么状态、通过什么通路被激活。这一区别对药物研发非常关键。因为如果小胶质细胞同时具有清除病理蛋白、维持组织稳态和造成炎症损伤等多种功能，那么简单地“把小胶质细胞关掉”很可能并不是正确的治疗策略。真正有价值的药物，需要做的是重新编程小胶质细胞的功能状态。这也是TREM2、CD33、SIGLEC10、NLRP3等靶点近年来受到关注的根本原因。 02 Nature Communications进一步证明：小胶质细胞甚至可以直接“吃掉”突触如果说《Nature Genetics》解决的是“哪些小胶质细胞状态与疾病相关”，那么7月发表在《Nature Communications》的研究则进一步追问：这种异常的免疫状态究竟如何造成认知功能下降？ Nature Communications（2026-07-09） DOI:https://doi.org/10.1038/s41467-026-74904-1 答案指向了突触。研究人员在小鼠皮层损伤模型中发现，慢性阶段的丘脑出现了一类具有高度吞噬活性的CD9^hi小胶质细胞。单细胞RNA测序显示，这类细胞富集了与吞噬和溶酶体功能相关的基因程序。进一步实验发现，丘脑中的谷氨酸能突触数量明显下降，而小胶质细胞溶酶体内可以检测到PSD95等突触后结构蛋白，直接提示其正在吞噬突触。更重要的是，研究建立了从免疫信号到行为表型的因果关系。研究人员发现，皮层损伤后，血脑屏障发生破坏，IgG从血管外渗进入丘脑，并通过FcγRIII信号诱导CD9^hi小胶质细胞形成。这些细胞随后大量吞噬突触，导致丘脑神经元活动下降，最终造成识别记忆障碍。 Nature Communications（2026-07-09） DOI:https://doi.org/10.1038/s41467-026-74904-1 当研究人员在丘脑局部阻断CD9，或者选择性破坏小胶质细胞中的CD9后，突触丢失得到改善，神经元活动恢复，动物的识别记忆也随之改善。阻断FcγRIII同样可以减少吞噬性小胶质细胞、突触损失和认知障碍。这里真正值得药物研发人员关注的，不是“CD9是一个新靶点”这么简单。它证明了一件更重要的事情：神经免疫异常可以位于认知损伤的上游，而且可以通过直接改变突触数量来造成认知障碍。这意味着，如果未来能够精准阻断这种异常的突触吞噬，而不是全面抑制小胶质细胞，那么理论上就有可能在神经元死亡之前，阻断认知功能继续恶化。这也是神经免疫从基础研究走向临床开发的重要一步。 03 再把Tau和线粒体放进来，一条完整的疾病链条开始出现最近《Science》报道的另一项研究，又把这条链条向神经元内部推进了一步。研究发现，Tau不仅形成神经原纤维缠结，还能够进入线粒体并干扰其能量代谢，使神经元的“能量工厂”出现功能障碍。于是，过去看似分散的几个研究方向开始出现交叉： Aβ和Tau提供持续的病理刺激；小胶质细胞和脑血管周围巨噬细胞感知这些异常信号；免疫细胞发生状态重塑；部分小胶质细胞增强吞噬，造成突触丢失；慢性炎症进一步影响神经元和线粒体；最终形成神经元功能障碍和认知下降。因此，今天再用简单的“Aβ→Tau→神经元死亡”解释阿尔茨海默病，已经越来越难以覆盖疾病的全部生物学过程。更接近当前研究前沿的理解，是把阿尔茨海默病看成病理蛋白、神经免疫、突触和细胞代谢相互作用的动态网络疾病。这也是为什么神经免疫正在成为新的药物研发方向。 04 但真正进入临床后，神经免疫并没有想象中那么容易机制越来越清楚，并不意味着药物已经成功。恰恰相反，神经免疫领域目前已经出现了一个非常重要的临床教训：调节免疫系统不是简单的“抗炎”。最典型的例子就是TREM2。TREM2是小胶质细胞的重要受体，遗传学研究早已证明，TREM2功能异常与阿尔茨海默病风险增加有关。因此，增强TREM2信号一度被认为是非常有吸引力的治疗策略。 Alector开发的AL002就是针对TREM2的激动性抗体，也是这一领域最重要的临床验证项目之一。但INVOKE-2Ⅱ期研究纳入381例早期阿尔茨海默病患者后，AL002并没有达到减缓疾病临床进展的主要目标。这项失败非常值得行业重视。因为它并没有简单证明“TREM2没有价值”，而是暴露了神经免疫药物开发最核心的问题：同一个免疫靶点，在不同疾病阶段、不同细胞状态甚至不同患者中，可能发挥完全不同的作用。最新研究也提示，TREM2在疾病早期可能有利于小胶质细胞清除病理、维持神经保护状态，但持续或过度激活又可能推动炎症和Tau相关病理。因此，未来的神经免疫药物很可能不会采用“一刀切”的免疫抑制策略，而需要进一步进行患者分层和疾病阶段分层。 05 全球已经出现一批真正进入临床的“神经免疫药物” 从目前管线来看，神经免疫已经从实验室进入临床验证阶段，而且形成了几条非常清晰的路线。第一条路线：选择性阻断炎症信号 INmune Bio的XPro1595是目前值得关注的代表。它并不是简单阻断全部TNF，而是选择性中和具有神经毒性的可溶性TNF，同时保留跨膜TNF的生理信号。其Ⅱ期MINDFuL研究纳入早期AD患者，并特别加入炎症生物标志物进行患者富集。总体mITT人群中，主要认知终点没有达到统计学显著差异；但在同时满足Aβ阳性和高炎症负荷的ADi亚组中，认知、神经精神症状以及pTau217、GFAP等指标均出现一致方向的改善信号。更值得注意的是，这家公司已经与FDA就生物标志物富集的Ⅱb/Ⅲ期注册路径形成监管沟通结果，意味着神经免疫药物正在从“广泛招募AD患者”转向“只治疗真正存在炎症异常的AD患者”。这可能是未来神经免疫药物商业化最重要的模式之一。第二条路线：直接调节神经免疫细胞 Tiziana Life Sciences开发的鼻喷抗CD3抗体Foralumab，是另一种完全不同的策略。它通过鼻腔给药调节T细胞和中枢免疫环境，目前已经进入ADⅡ期临床，研究不仅观察认知变化，同时利用TSPO-PET直接观察脑内神经炎症，并探索与lecanemab或donanemab联合治疗的可能性。这个设计本身就很有产业意义：未来神经免疫药物很可能不是替代Aβ药物，而是与Aβ药物联合。先清除Aβ，再降低持续的免疫损伤，可能比单独清除Aβ更接近疾病真实的病理网络。第三条路线：NLRP3炎症小体 NLRP3是目前神经炎症药物研发中最活跃的靶点之一。 AC Immune今年启动了脑穿透型NLRP3抑制剂ACI-19764的Ⅰ期临床。该药为口服小分子，重点观察安全性、药代动力学、脑脊液暴露以及IL-1β抑制等靶点参与指标，首批临床数据预计在2026年下半年公布。第四条路线：重新“编程”小胶质细胞 OncoC4的ONC-841则代表了另一条路线。它是一种靶向SIGLEC10的抗体，最初在肿瘤领域开发，目前已经进入阿尔茨海默病Ⅰ/Ⅱ期临床。其AD研发逻辑并不是简单抑制免疫，而是希望恢复小胶质细胞清除病理蛋白的能力。这条路线与此次《Nature Genetics》研究的逻辑高度契合：不是消灭小胶质细胞，而是把它重新调整到正确的功能状态。 06 国内的机会可能不在“复制Aβ”，而在下一代免疫靶点如果从全球竞争格局来看，中国在Aβ单抗商业化和临床开发上已经进入快速追赶阶段。目前国内已经有仑卡奈单抗、仑卡奈单抗等国际产品进入临床使用，同时国内企业也在推进Aβ相关创新药。但在神经免疫领域，情况有所不同。目前全球真正进入临床验证阶段的TREM2、NLRP3、TNF、SIGLEC10等项目数量仍然有限，国内尚未形成与国际头部企业相当的成熟神经免疫AD后期管线。反而是ISM8969这样的项目，让国内企业第一次在全球竞争中进入了一个尚未形成明确赢家的新赛道。这对中国CNS药物研发具有特殊意义。因为Aβ已经进入商业化竞争阶段，临床价值、疗效、安全性和给药成本都开始决定市场格局；而神经免疫仍处于机制验证和临床PoC阶段，未来谁能够首先证明“精准调节免疫可以改变疾病进程”，谁就可能拥有下一代AD治疗的重要话语权。 07 未来的商业化机会不只是一个新靶点，而是“免疫分型+精准治疗” 神经免疫药物最大的商业化挑战，也恰恰来自疾病异质性。如果一个药物只对“高炎症负荷”的患者有效，那么传统的AD临床试验设计就会稀释疗效。 XPro1595的MINDFuL研究已经给出了一个非常典型的案例：总体人群没有达到主要终点，但炎症富集亚组出现了一致的临床和生物标志物方向信号。这意味着未来AD药物开发可能出现新的组合：血液标志物负责筛选患者，PET负责确认病理（点击可查看之前已发布的相关文章），神经炎症标志物负责判断免疫状态，药物负责精准调节特定免疫通路。这将直接改变CNS临床试验的设计方式。过去是：“所有早期AD患者都进组。”未来可能变成：“Aβ阳性+Tau阳性+炎症高负荷+特定免疫表型患者进组。”而这也意味着，神经免疫药物未来的商业价值可能不仅来自药物本身，还会延伸到伴随诊断、PET显像、血液标志物和患者分层平台。 08 阿尔茨海默病的下一场战争，可能从“清除什么”转向“调节什么” 从Leqembi和Kisunla开始，Aβ清除已经证明了疾病修饰治疗可以真正进入临床。但Aβ清除并没有终结阿尔茨海默病。相反，它让行业更加清楚地看到：减少一种病理蛋白，并不意味着整个疾病网络都会停止。Tau仍然存在，突触仍然会丢失，线粒体仍然可能发生功能障碍，神经免疫也可能继续维持在异常状态。因此，阿尔茨海默病下一阶段真正值得关注的，不再是“谁能够找到另一个Aβ”，而是谁能够证明：改变神经免疫状态，能够真正改变疾病进程。 2026年《Nature Genetics》和《Nature Communications》的两项研究，把这一问题进一步从“相关性”推向了细胞状态和因果机制；而TREM2、TNF、NLRP3、SIGLEC10等临床项目，则正在把这些机制推向人体验证。现在还不能说“阿尔茨海默病的答案就是神经免疫”。但可以越来越明确地说：阿尔茨海默病药物研发已经进入一个不再只有Aβ和Tau的时代，而神经免疫，很可能就是下一场CNS创新药竞争最重要的战场之一。参考资料： Nature Genetics（2026-08-11） DOI:https://doi.org/10.1038/s41588-026-02716-6 Nature Communications（2026-07-09） DOI:https://doi.org/10.1038/s41467-026-74904-1 Science（2026） https://www.science.org/doi/10.1126/sciadv.aeg0515 https://www.science.org/content/article/una-investigaci%C3%B3n-de-science-arroja-dudas-sobre-genes-prometedores-para-prevenir-la npj Dementia（2026） ClinicalTrials.gov Alzheimer's Association 2026 Alzheimer's Disease Drug Development Pipeline AC Immune Nmune Bio Tiziana Life Sciences OncoC4 本文收录于阿尔茨海默病话题中，欢迎交流讨论。【近期热点】重磅：阿尔茨海默病影像诊断革命来了！FDA批准新型Tau-PET，揭示大脑代谢新规律神经退行性疾病重大突破：中国科学家重新定义细胞“垃圾清运系统” CNS信息差｜霍德生物完成近2亿元C轮融资首关;阿尔茨海默病新药仑卡奈单抗新剂型获批 CNS信息差｜石药集团长效精神分裂症药物获批上市;国产帕金森病口服1类新药获批临床

2026-08-07

·BioSpace

INmune Bio Inc. Announces Second Quarter 2026 Results and Highlights Regulatory, Manufacturing and Clinical Progress

Company to Host Conference Call Today, August 6th, at 4:30pm ET BOCA RATON, Fla., Aug. 06, 2026 (GLOBE NEWSWIRE) -- INmune Bio Inc. (NASDAQ: INMB) (the “Company”), a late-stage biotechnology company focused on inflammation and immunology, today announced its financial results for the quarter ended June 30, 2026 and provided a business update. “The second quarter and subsequent weeks were defined by execution across both of our late-stage platforms,” said David Moss, Chief Executive Officer of INmune Bio. “For Ebstrocel™, we secured MHRA alignment, PIP approval and commercial-ready manufacturing, materially reducing regulatory and operational risk ahead of our planned UK MAA submission. For XPro™, FDA Fast Track designation and statistically significant MRI findings strengthened the clinical and regulatory foundation for a registrational Phase 2b/3 program in early Alzheimer’s disease that we believe establishes XPro™ as a first-in-class, late-stage neuroimmunology program in CNS disease. Looking ahead, our core priority is clear: driving Ebstrocel efficiently through regulatory filing and approval to bring this critical therapy to patients in need while delivering long-term value for our shareholders.” Second Quarter and Recent Corporate Highlights ezstandalone.cmd.push(function () { ezstandalone.showAds(131); }); CORDStrom™ Platform (Ebstrocel for RDEB): Completed a key commercial manufacturing milestone by successfully processing the first commercial-ready umbilical cord tissues at the Cell and Gene Therapy Catapult Manufacturing Innovation Centre in Stevenage, UK. The transferred process is designed to meet MHRA, EMA and FDA standards and supports planned Phase 3 confirmatory development, global regulatory submissions and future commercial supply. Received formal MHRA written alignment across the CMC, non-clinical and clinical elements of the planned UK MAA, providing a clear regulatory path toward a Conditional Marketing Authorization application for Ebstrocel™ in RDEB. Obtained MHRA approval of the Ebstrocel™ Pediatric Investigation Plan in less than three months, preserving the Company’s planned 2026 UK MAA timetable and incorporating the agency’s feedback into the planned open-label Phase 3 confirmatory trial. Completed preparations for the Phase 3 trial of Ebstrocel in RDEB remaining on track for first patient treatment in Q4 2026. Advanced the CORDStrom™ platform patent application into the U.S. national phase following a favorable international Written Opinion. If granted, the patent family is expected to provide broad platform protection, including composition-of-matter and method-of-treatment claims, extending into at least 2045. Expanded the Company’s agreement with Anthony Nolan Cord Blood Bank, securing long-term access to high-quality umbilical cord tissue to support scalable global development and commercialization of the CORDStrom™ platform. Established a Scientific Advisory Board comprising internationally recognized leaders in MSC biology, clinical translation, manufacturing, potency assessment and rare pediatric skin disease. Chaired by Professor Mark Lowdell, the working SAB will support Ebstrocel’s late-stage regulatory and clinical development, including Phase 3 design, biomarkers, manufacturing consistency and product-release criteria, while helping prioritize additional indications for the CORDStrom platform. The SAB adds substantial independent expertise as the Company advances Ebstrocel toward regulatory submissions and expands CORDStrom into additional disease-specific cell therapies. XPro1595 Platform Highlights (XPro™): Reported a statistically significant treatment effect on a white matter myelin MRI biomarker in the Phase 2 MINDFuL trial. XPro™ demonstrated an effect in the full modified intent-to-treat population (p=0.0028; Cohen’s d=0.46; n=200), with a larger effect in the biomarker-enriched population (p=0.0098; d=0.59; n=100), supporting the precision-medicine strategy for the planned registrational program. Published the Phase 2 MINDFuL results in NPJ Dementia . In the pre-specified, protocol-defined Alzheimer’s Disease with inflammation (ADi) subgroup, XPro™ showed directionally consistent benefit across cognitive, global, functional, behavioral and biomarker endpoints over 24 weeks, with zero ARIA-E and zero ARIA-H observed. Presented expanded Phase 2 imaging analyses at the Alzheimer’s Association International Conference showing concordant treatment-related effects across independent white matter and cortical gray matter measures at Week 24, strengthening evidence of early biologic activity and tissue-level target engagement. Received FDA Fast Track designation for XPro™ (pegipanermin) for early Alzheimer’s disease, encompassing mild cognitive impairment due to Alzheimer’s disease and mild Alzheimer’s disease dementia, enabling more frequent FDA interactions and potential eligibility for expedited review mechanisms. Published a Department of Defense-funded, peer-reviewed Journal of Neurotrauma study showing that XPro1595 prevented the injury-induced rise in amyloid pathology and improved early cognitive and pain-related outcomes in a preclinical model linking traumatic brain injury to Alzheimer’s disease. Presented AACR 2026 preclinical data showing that INB03 (XPro1595 for oncology) enhanced the activity of HER2-targeted tyrosine kinase inhibitors and reduced metastatic spread to the brain, lungs and liver in HER2-positive breast cancer models. Corporate: Received an approximately US$4.2 million research and development tax rebate from Australia during July 2026, providing non-dilutive capital to support ongoing development activities. Announced it has been named a founding member of the American Biotech Innovation Alliance (ABIA). The newly launched national coalition brings together biotechnology leaders with the shared objective of defining a national strategy to sustain and extend U.S. leadership in biotech innovation. Upcoming Events and Milestones: Submit the Ebstrocel™ Marketing Authorization Application to the UK MHRA by the end of Q3 or early Q4 2026, followed by a planned European Union submission to the EMA in Q1 2027. Ebstrocel™ Biologics License Application (BLA) submission to the FDA expected in Q1 2027. Submit the registrational Phase 2b/3 protocol for XPro™ in early Alzheimer’s disease to the FDA in [Q4 2026]. Submit for publication the Phase 2 MINDFuL imaging analyses, including the white matter and cortical gray matter findings presented at AAIC 2026. Financial Results for the Second Quarter Ended June 30, 2026: Net loss attributable to common stockholders for the quarter ended June 30, 2026 was approximately $1.3 million, compared to approximately $24.5 million for the quarter ended June 30, 2025. The prior-year period included a $16.5 million impairment charge related to acquired in-process research and development intangible assets. Research and development expenses totaled approximately $(0.8 million) for the quarter ended June 30, 2026, compared to approximately $5.8 million for the quarter ended June 30, 2025. The research and development benefit during the 2026 period was primarily due to the recognition of additional Australian research and development tax rebate. General and administrative expenses were approximately $2.3 million for each of the quarters ended June 30, 2026 and June 30, 2025. As of June 30, 2026, the Company had cash and cash equivalents of approximately $18.4 million. As of August 6, 2026, the Company had approximately 27.8 million common shares outstanding. Earnings Call Information To participate in this event, dial approximately 5 to 10 minutes before the beginning of the call. Please ask for the INmune Bio Second Quarter Conference Call when reaching the operator. Date: August 6 th , 2026 Time: 4:30 PM Eastern Time Participant Dial-in: 1-800-717-1738 Participant Dial-in (international): +1-646-307-1865 Conference ID: INMUNE A live audio webcast of the call can be accessed by clicking here or using this link: A transcript will follow approximately 24 hours from the scheduled call. A replay will also be available through September 21st, 2026 by dialing 1-844-512-2921 or 1-412-317-6671 (international) and entering PIN 1166817. About INmune Bio Inc. INmune Bio Inc. is a publicly traded (NASDAQ: INMB), late-stage biotechnology company focused on developing treatments that target the innate immune system to fight disease. Moving beyond early-stage exploration, the Company’s clinical-development strategy centers on advanced precision medicine, matching drug mechanisms directly to patient biology to optimize clinical outcomes. INmune Bio is actively advancing two late-stage product platforms toward registrational milestones: CORDStrom™: A proprietary, pooled, allogeneic, human umbilical cord-derived mesenchymal stromal cell platform engineered to address the historical clinical challenges of donor variability and manufacturing inconsistency. Following successful clinical readouts in RDEB, the platform is transitioning to regulatory filing phases, with an MAA planned for the UK MHRA in 2026 and EU EMA in 2027, alongside a planned U.S. Biologics License Application (BLA) submission. XPro1595™: A Dominant-Negative Tumor Necrosis Factor (DN-TNF) platform that selectively neutralizes soluble TNF (sTNF) to eliminate neuroinflammation without compromising protective immune function. Backed by recently granted FDA Fast Track designation and successful regulatory alignment from an End-of-Phase 2 meeting, XPro1595™ is positioned for an integrated Phase 2b/3 seamless adaptive registrational program in neuroinflammation-enriched early Alzheimer’s disease. To learn more about INmune Bio’s pipeline and its approach to harnessing the innate immune system, please visit . Forward Looking Statements The Company’s product candidates are in clinical development and there is no assurance that any specific outcome will be achieved. Any statements contained in this press release related to the development or commercialization of product candidates and other business and financial matters, including without limitation, trial results and data, including the timing of key milestones, future plans or expectations, and the prospects for receiving regulatory approval or commercializing or selling any product or drug candidates, may constitute forward-looking statements as that term is defined in the Private Securities Litigation Reform Act of 1995. Any forward-looking statements contained herein are based on current expectations but are subject to several risks and uncertainties. Actual results and the timing of certain events and circumstances may differ materially from those described by the forward-looking statements because of these risks and uncertainties. CORDStrom™, XPro1595™ (XPro™, pegipanermin), and INKmune™ have either finished clinical trials, are still in clinical trials or are preparing to start clinical trials and have not been approved by the U.S. Food and Drug Administration (FDA), the UK MHRA or any regulatory body and there cannot be any assurance that they will be approved by the FDA, the UK MHRA or any regulatory body or that any specific results will be achieved. The factors that could cause actual future results to differ materially from current expectations include, but are not limited to, risks and uncertainties relating to the Company’s ability to produce more drug for clinical trials; the availability of substantial additional funding for the Company to continue its operations and to conduct research and development, clinical studies and future product commercialization; and the Company’s business, research, product development, regulatory approval, marketing and distribution plans and strategies. These and other factors are identified and described in more detail in the Company’s filings with the Securities and Exchange Commission, including the Company’s Annual Report on Form 10-K, the Company’s Quarterly Reports on Form 10-Q and the Company’s Current Reports on Form 8-K. The Company assumes no obligation to update any forward-looking statements to reflect any event or circumstance that may arise after the date of this release. INmune Bio Contacts: David Moss Chief Executive Officer (561) 710-0512 info@inmunebio.com Daniel Carlson Head of Investor Relations (415) 509-4590 dcarlson@inmunebio.com The following tables summarize our results of operations for the periods indicated: INMUNE BIO INC. CONDENSED CONSOLIDATED BALANCE SHEETS (In thousands, except share and per share amounts) (Unaudited) June 30, 2026 December 31, 2025 ASSETS CURRENT ASSETS Cash and cash equivalents $ 18,411 $ 24,751 Research and development tax credit receivable 4,413 4,284 Other tax receivable 354 257 Prepaid expenses and other current assets 621 595 TOTAL CURRENT ASSETS 23,799 29,887 Equipment, net 1,262 955 Operating lease – right of use asset 1,247 914 Other assets 537 595 TOTAL ASSETS $ 26,845 $ 32,351 LIABILITIES AND STOCKHOLDERS’ EQUITY CURRENT LIABILITIES Accounts payable and accrued liabilities $ 5,053 $ 7,768 Accounts payable and accrued liabilities – related parties 25 25 Operating lease, current liabilities 812 623 TOTAL CURRENT LIABILITIES 5,890 8,416 Long-term operating lease liability 593 411 TOTAL LIABILITIES 6,483 8,827 COMMITMENTS AND CONTINGENCIES STOCKHOLDERS’ EQUITY Preferred stock, $0.001 par value, 10,000,000 shares authorized, 0 shares issued and outstanding - - Common stock, $0.001 par value, 200,000,000 shares authorized, 27,653,789 and 26,585,258 shares issued and outstanding, respectively 28 27 Additional paid-in capital 237,688 233,271 Subscription receivable (814 ) - Accumulated other comprehensive loss (823 ) (737 ) Accumulated deficit (215,717 ) (209,037 ) TOTAL STOCKHOLDERS’ EQUITY 20,362 23,524 TOTAL LIABILITIES AND STOCKHOLDERS’ EQUITY $ 26,845 $ 32,351 INMUNE BIO INC. CONDENSED CONSOLIDATED STATEMENTS OF OPERATIONS AND COMPREHENSIVE LOSS (In thousands, except share and per share amounts) (Unaudited) For the Three Months Ended June 30, For the Six Months Ended June 30, 2026 2025 2026 2025 REVENUE $ - $ - $ - $ 50 OPERATING EXPENSES General and administrative 2,279 2,253 4,450 4,569 Research and development (803 ) 5,804 2,838 13,443 Impairment of acquired in-process research and development intangible assets - 16,514 - 16,514 Total operating expenses 1,476 24,571 7,288 34,526 LOSS FROM OPERATIONS (1,476 ) (24,571 ) (7,288 ) (34,476 ) OTHER INCOME, NET 203 113 608 279 NET LOSS $ (1,273 ) $ (24,458 ) $ (6,680 ) $ (34,197 ) Net loss per common share – basic and diluted $ (0.05 ) $ (1.05 ) $ (0.25 ) $ (1.49 ) Weighted average common shares outstanding – basic and diluted 26,718,507 23,298,455 26,652,250 22,899,539 COMPREHENSIVE LOSS Net loss $ (1,273 ) $ (24,458 ) $ (6,680 ) $ (34,197 ) Other comprehensive loss – foreign currency translation (96 ) (153 ) (86 ) (188 ) Total comprehensive loss $ (1,369 ) $ (24,611 ) $ (6,766 ) $ (34,385 ) INMUNE BIO INC. CONDENSED CONSOLIDATED STATEMENTS OF CASH FLOWS (In thousands) (Unaudited) For the Six Months Ended June 30, 2026 2025 CASH FLOWS FROM OPERATING ACTIVITIES: Net loss $ (6,680 ) $ (34,197 ) Adjustments to reconcile net loss to net cash used in operating activities: Stock-based compensation 2,855 3,610 Gain on settlement of accounts payable (91 ) - Depreciation expense 118 - Impairment of acquired research and development intangible assets - 16,514 Changes in operating assets and liabilities: Research and development tax credit receivable (129 ) (424 ) Other tax receivable (97 ) (322 ) Prepaid expenses (26 ) (174 ) Other assets 58 (491 ) Accounts payable and accrued liabilities (2,624 ) 1,132 Accounts payable and accrued liabilities – related parties - 159 Deferred liabilities - (6 ) Operating lease liabilities 38 - Net cash used in operating activities (6,578 ) (14,199 ) CASH FLOWS FROM INVESTING ACTIVITIES: Purchase of equipment (430 ) (706 ) Net cash used in investing activities (430 ) (706 ) CASH FLOWS FROM FINANCING ACTIVITIES: Sale of common stock for cash 584 27,544 Exercise of warrants for cash 130 1 Exercise of stock options for cash 35 - Net cash provided by financing activities 749 27,545 Impact on cash from foreign currency translation (81 ) (188 ) NET (DECREASE) INCREASE IN CASH AND CASH EQUIVALENTS (6,340 ) 12,452 CASH AND CASH EQUIVALENTS AT BEGINNING OF PERIOD 24,751 20,922 CASH AND CASH EQUIVALENTS AT END OF PERIOD $ 18,411 $ 33,374 SUPPLEMENTAL DISCLOSURE OF CASH FLOWS INFORMATION: Cash paid for income taxes $ - $ - Cash paid for interest $ - $ - SUPPLEMENTAL NONCASH INVESTING AND FINANCING ACTIVITIES Right of use assets obtained in exchange for lease obligations $ 587 $ -

临床2期临床结果临床3期财报快速通道

100 项与 INB-03 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
并发症	临床3期	美国	INmune Bio, Inc.	2020-10-21
新型冠状病毒感染	临床3期	美国	INmune Bio, Inc.	2020-10-21
阿尔茨海默症	临床2期	澳大利亚	INmune Bio, Inc.	2022-02-28
阿尔茨海默症	临床2期	加拿大	INmune Bio, Inc.	2022-02-28
阿尔茨海默症	临床2期	捷克	INmune Bio, Inc.	2022-02-28
阿尔茨海默症	临床2期	法国	INmune Bio, Inc.	2022-02-28
阿尔茨海默症	临床2期	德国	INmune Bio, Inc.	2022-02-28
阿尔茨海默症	临床2期	波兰	INmune Bio, Inc.	2022-02-28
阿尔茨海默症	临床2期	西班牙	INmune Bio, Inc.	2022-02-28
阿尔茨海默症	临床2期	英国	INmune Bio, Inc.	2022-02-28

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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


NCT05318976 (MINDFuL, CTgov)	临床2期	阿尔茨海默症 \| 炎症 \| 轻度认知障碍	207	XPro1595 (1.0 mg/kg XPro1595)	遞選醖艱鏇窪繭醖鏇壓(製鏇鹹餘顧構遞襯蓋齋) = 膚夢鹹鑰觸壓膚衊觸艱鹽艱醖壓鏇鑰淵衊積蓋 (醖積淵構艱鏇壓製壓觸, 0.04) 更多	-	2026-06-29
				Placebo (1.0 mg/kg Placebo)	遞選醖艱鏇窪繭醖鏇壓(製鏇鹹餘顧構遞襯蓋齋) = 窪壓構廠夢鏇鬱簾製齋鹽艱醖壓鏇鑰淵衊積蓋 (醖積淵構艱鏇壓製壓觸, 0.05) 更多
NCT04370236 (CTgov)	临床2/3期	新型冠状病毒感染 \| 并发症	79	INB03 (INB03 + Standard of Care)	觸衊鑰餘積製壓醖構網 = 餘遞網膚襯窪築鏇簾壓製網壓膚齋積網糧顧壓 (選膚糧獵範壓夢築餘範, 獵壓鬱膚顧遞繭觸糧遞 ~ 夢襯觸築鏇艱衊艱製艱) 更多	-	2026-05-19
				Placebo (Placebo + Standard of Care)	觸衊鑰餘積製壓醖構網 = 願艱鹹糧積鬱淵遞淵鹽製網壓膚齋積網糧顧壓 (選膚糧獵範壓夢築餘範, 壓鑰艱簾鏇鑰製廠糧範 ~ 積夢鬱築醖願襯鬱糧窪) 更多
NCT05318976 (MINDFuL, GlobeNewswire) 人工标引	临床2期	阿尔茨海默症	208	XPro1595	範繭範鹹糧廠製淵簾獵(顧淵網餘齋鏇觸廠繭夢) = was not met 網鏇夢壓範衊觸鏇膚觸 (選壓繭廠艱顧廠襯網構 ) 未达到更多	积极	2025-07-24
				Placebo
NCT05318976 (MINDFuL, PipelineReview) 人工标引	临床2期	阿尔茨海默症	208	XPro™	選艱築顧醖簾糧餘鬱願(餘壓淵糧積簾遞糧繭築) = did not meet the primary cognitive endpoint. 憲製願鬱繭遞願廠鑰願 (艱醖顧憲齋積範艱蓋製 ) 未达到更多	不佳	2025-06-30
				Placebo
GlobeNewswire 人工标引	临床2期	阿尔茨海默症	7	XPro1595	窪鹽襯範獵遞糧鑰醖艱(糧糧獵積廠餘鹹鹽遞鹽) = statistically significant increase in Alpha wave frequency and power (p<0.05) 夢遞構糧範衊蓋選廠獵 (糧製夢蓋鏇襯襯選壓選 )	积极	2024-03-05
				placebo
NCT03943264 (CTAD2023)	临床1期	阿尔茨海默症	9	XPRO1595 0.3 mg/kg/wk	觸簾齋鏇膚齋積築襯糧(鬱鏇蓋齋衊鑰餘憲鹽構) = 鑰網醖獵餘構襯醖壓膚蓋齋淵鏇夢鏇襯窪範願 (觸衊糧餘遞獵艱夢網積 )	积极	2023-10-24
NCT03943264 (CTAD2023)	临床1期	阿尔茨海默症 inflammation	3	XPro1595	築齋淵襯願積鏇衊觸壓(餘繭鬱構製襯願鏇網鹽) = 餘膚獵製糧壓襯壓廠衊鏇範廠顧鹹餘齋壓醖蓋 (鬱蓋鏇願選淵壓齋製膚 )	积极	2023-10-24