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.

162

项与 INB-03 相关的新闻（医药）

2026-07-20

·GlobeNewswire-Health Care

INmune Bio Completes Commercial Manufacturing Milestone Supporting Planned Global Registration Filings for CORDStrom™ Platform

Commercial-Ready Manufacturing Now Supports Planned Phase 3 Confirmation Trial, and US, EU and UK Regulatory Submissions for Future Commercial Supply. Company Expresses Support for MHRA Draft Rare Disease Therapies Regulatory Framework BOCA RATON, Fla, July 20, 2026 (GLOBE NEWSWIRE) -- INmune Bio Inc. (NASDAQ: INMB) (the “Company”), a late-stage biotechnology company focused on inflammation and immunology, today announced a significant manufacturing milestone for its CORDStrom™ platform. The Company has successfully processed its first commercial-ready umbilical cord tissue at the Cell and Gene Therapy Catapult (CGT Catapult) Manufacturing Innovation Centre in Stevenage, UK, under its commercial agreement with Anthony Nolan Cord Blood Bank. This achievement marks the successful transfer of the mesenchymal stromal cell (MSC) isolation stage for the manufacture of master cell banks (MCBs) into INmune Bio’s commercial manufacturing facility. The process is now commercial-ready to MHRA, EMA and FDA standards, including maternal blood samples infectious disease testing in US-CLIA-accredited laboratories. The successful technology transfer positions the Company to generate its first US tested master cell banks for Ebstrocel™, the RDEB-specific investigational product derived from the CORDStrom™ platform, in support of its planned Phase 3 confirmation clinical trial and future commercial supply. “Completing this manufacturing transfer is one of the most important operational milestones for the CORDStrom platform. We now have the manufacturing infrastructure required to generate master cell banks that support our planned Phase 3 program and future commercial production using a process designed to satisfy both UK and U.S. regulatory expectations. I am hugely proud of the team for getting to this milestone so quickly,” said Professor Mark W. Lowdell, PhD, FRCPath, FRSB, Chief Scientific Officer of INmune Bio. “This important milestone reflects the strength of collaboration between Anthony Nolan, the Cell and Gene Therapy Catapult, and INmune Bio, and marks another critical step towards commercial delivery of Ebstrocel™,” said Dr. Ben Weil, MBA, EngD, Head of UK Operations at INmune Bio. “Everyone involved in the CORDStrom™ platform understands the urgency and criticality of developing potentially life-changing medicines to children living with RDEB and other rare diseases. Building a reliable, scalable, and commercial ready manufacturing platform is only possible through the commitment and expertise of all our suppliers and service partners.” With commercial manufacturing established, pediatric strategy approved, regulatory alignment completed and the MAA preparation underway, INmune Bio believes Ebstrocel™ has entered the final stage of development before planned commercialization in the United Kingdom. Alignment with MHRA Draft Rare Disease Therapies Regulatory Framework INmune Bio’s approach to developing Ebstrocel™ for recessive dystrophic epidermolysis bullosa (RDEB), an ultra-rare disease, is directly aligned with the principles recently outlined in the UK Medicines and Healthcare products Regulatory Agency (MHRA) draft rare disease therapies regulatory framework. The Company believes the principles proposed within the draft framework validate the regulatory strategy it has already established with the MHRA for Ebstrocel™. Specifically, the framework emphasizes flexible evidence generation, advanced statistical methodologies, patient-centered outcomes and lifecycle evidence development, principles reflected in the Company's recent written MHRA guidance supporting its planned Conditional Marketing Authorization application. "Commercial manufacturing is often one of the largest execution risks facing cell therapy companies. Today's milestone demonstrates that we have successfully transitioned from clinical manufacturing toward a scalable commercial process that supports our planned regulatory filings and long-term commercialization strategy. Combined with our recent regulatory alignment from the MHRA and the evolving UK rare disease framework, we believe CORDStrom is exceptionally well positioned for the next stage of development," said David Moss, CEO and co-founder of INmune Bio. Stakeholders are encouraged to review and respond to the consultation, available at: https://www.gov.uk/government/consultations/draft-rare-disease-therapies-regulatory-framework. Note that this is currently a discussion document and does not yet constitute final guidelines. 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 and EU EMA in 2026, 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 www.inmunebio.com. Forward Looking Statements Clinical trials are in early stages 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 trial results, 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 US 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.comDaniel Carlson Head of Investor Relations (415) 509-4590 dcarlson@inmunebio.com

基因疗法快速通道临床3期细胞疗法

2026-07-15

·Tanomics

AAIC 2026 伦敦直击：Leqembi皮下自动注射器达成生物等效，阿尔茨海默病治疗迎来居家给药新时代

2026年7月12日至15日，全球最大的阿尔茨海默病学术会议——阿尔茨海默病协会国际会议（AAIC® 2026）在英国伦敦ExCel会展中心隆重举行。来自全球的8000余名研究者、临床医师和痴呆领域专业人士汇聚一堂，分享推动阿尔茨海默病诊断、风险降低和治疗领域的最新突破性研究发现。本届AAIC最引人瞩目的焦点之一，是Leqembi（lecanemab）皮下自动注射器（SC-AI）的关键临床数据首次公开展示，标志着阿尔茨海默病靶向治疗从静脉输液中心走向居家自我给药的历史性跨越。Leqembi皮下自动注射器：生物等效性达成，居家给药可期 7月12日，BioArctic的合作伙伴卫材（Eisai）在AAIC“Developing Topics”专题会议“Lecanemab Subcutaneous Formulation in Early Alzheimer‘s Disease: Emerging Clinical Evidence and Practical Use Considerations”（Session #1-32-FRS-C）上，正式公布了Leqembi皮下自动注射器研发项目的完整数据。核心数据——生物等效性达成：每周一次500 mg SC-AI方案与已获批的静脉输注起始方案（10 mg/kg，每两周一次）达成了生物等效性，暴露比为104%（90%置信区间：99.1%–109%）。暴露水平在不同体重四分位数间保持一致，证实了该固定剂量方案在广泛患者群体中具有稳定的药代动力学特征。关键发现：疗效由暴露量驱动，而非给药途径：通过淀粉样蛋白PET测量的淀粉样蛋白清除、通过CDR-SB测量的临床疗效以及ARIA-E（淀粉样蛋白相关影像学异常-水肿/渗出）的发生率均由lecanemab的暴露量驱动，而非给药途径。500 mg SC-AI起始方案达到了与IV起始方案相当的暴露水平，支持其具有可比的疗效和安全性预期。各患者人群结果一致：500 mg SC-AI起始方案在不同体重组中均表现出一致的暴露水平、淀粉样蛋白清除、临床疗效和安全性。淀粉样蛋白清除和临床结局不受体重的显著影响，支持固定剂量方案的合理性。灵活给药选项：患者可根据需要在IV和SC给药之间切换；若错过一次剂量，可在次日或最晚六天内补用，大幅提升了Leqembi给药的灵活性和便利性。安全性特征与IV制剂一致： SC-AI的总体安全性与IV制剂基本一致。500 mg SC-AI起始方案的ARIA-E发生率预计与IV起始方案相似。注射部位反应多为局部反应，全身性反应较少见。抗药物抗体发生率仅为1.4%，未观察到中和抗体，证实SC-AI制剂保持了低免疫原性特征。真实世界患者体验：来自美国两个治疗中心的真实世界数据显示，在接受至少六个月皮下维持治疗后，91%的可评估患者（11例中的10例）在MMSE认知评估中保持稳定或改善。患者和照护伙伴的满意度达75%至97%，92%至100%表示愿意推荐该治疗。卫材临床研究高级副总裁兼阿尔茨海默病与脑健康部门负责人Michael Irizarry博士在会议中表示：“数据证实，疗效和安全性由药物暴露量驱动，而非给药途径。” 监管进展：美国FDA已于2025年8月批准LEQEMBI IQLIK®（360 mg）用于每周一次皮下维持治疗。针对500 mg皮下起始剂量的补充生物制剂许可申请（sBLA）已获FDA优先审评资格，PDUFA目标日期为2026年8月24日。2026年1月，卫材在中国的皮下制剂生物制剂许可申请已获受理，并于2月被指定为优先审评。 Leqembi目前已获53个国家批准，另有6个国家正在审评中。皮下自动注射器的获批将有望通过减少输液中心就诊需求，大幅扩大可治疗患者群体——这对主要影响老年患者、常需依赖照护者安排交通的阿尔茨海默病而言意义重大。礼来：16篇摘要聚焦Kisunla长期安全性与P-tau217血液检测礼来公司在本次AAIC上共呈报了16篇摘要，涵盖Kisunla（donanemab-azbt）的长期安全性数据、P-tau217血液生物标志物检测的診断性能，以及影像科学、卫生经济学、真实世界处方证据和患者中心结局等多个维度。 Kisunla长期扩展安全性数据：来自TRAILBLAZER-ALZ 6和TRAILBLAZER-ALZ 2长期扩展试验的研究结果在会议上展示，回答了关于改良滴定方案和糖皮质激素预处理的安全性及生物标志物持久性等临床关键问题。Lars Raket博士还讨论了TRAILBLAZER-ALZ 2长期扩展中外部对照与内部外推的方法学问题。 P-tau217血液检测诊断性能：礼来高级研究科学家Samantha Burnham博士于7月15日展示的数据表明，P-tau217血液生物标志物检测在识别认知未受损个体的阿尔茨海默病病理方面，表现出与淀粉样蛋白PET相当的强效“rule-in”（确诊）性能。这一发现为未来用可扩展、可及的血液检测替代专业化影像检查提供了有力支持。其他展示还包括应用自然语言处理算法识别美国电子病历中颅内出血和ARIA的研究，以及用于预测血浆P-tau217升高状态和临床前期疾病进展过程中医疗资源利用驱动因素的预测算法。罗氏：trontinemab长期安全性数据与PrevenTRON Ⅲ期试验设计罗氏及其子公司基因泰克在AAIC上呈报了18篇口头报告和壁报，涵盖制药与诊断两大板块。 Trontinemab长期安全性数据：在一个90分钟的Featured Research Session中，五场口头报告集中展示了trontinemab——一种基于Brainshuttle™技术的双特异性2+1淀粉样蛋白-β靶向单克隆抗体——的最新进展。报告者分享了来自Phase Ib/IIa Brainshuttle AD开放标签扩展研究的新的长期安全性、淀粉样蛋白清除和生物标志物数据。该研究的建模数据已为正在进行的早期症状性阿尔茨海默病Ⅲ期TRONTIER 1和2研究的剂量方案提供了依据。 PrevenTRON Ⅲ期试验设计首次公布：罗氏首次公布了PrevenTRON的试验设计——一项在临床前阿尔茨海默病患者中研究trontinemab的Ⅲ期临床试验。PrevenTRON计划招募认知未受损但具有高进展风险的个体，研究者将使用罗氏的Elecsys® pTau217血液检测来帮助识别潜在研究参与者。此外，罗氏还受邀在AAIC上就NLRP3炎症小体在阿尔茨海默病中的作用进行了Perspectives Session专题报告，展示了NLRP3抑制剂在阿尔茨海默病和帕金森病等神经退行性疾病中的免疫调节效应的新兴临床前和临床数据。INmune Bio：XPro1595 II期髓鞘形成阳性成像数据 INmune Bio公司在AAIC上展示了XPro1595（pegipanermin）在早期阿尔茨海默病患者中的II期MINDFuL研究的扩展成像分析。报告标题为“Concordant White Matter and Cortical Treatment Effects in a Phase 2 Study of XPro1595 in Early Alzheimer‘s disease”，展示了白质髓鞘的完整χ-separation（χ-分离）分析，以及皮质结构紊乱测量（CDM）——一种先进的扩散MRI灰质微结构测量方法。 χ-separation是一种近期 validated 的成像技术，解决了传统MRI髓鞘测量的关键挑战，可在标准多中心临床基础设施中部署，无需专用扫描仪。两种技术依赖不同的MRI对比机制（χ-separation利用磁化率，CDM利用水扩散），采用不同的采集序列和处理流程。由于这两种方法学上独立的测量指标变化方向一致，其一致性支持了观察到的变化为治疗相关、反映脑微结构效应的解释。 INmune Bio此前报告，在MINDFuL研究中，χ-separation MRI显示XPro治疗组患者在全改良意向治疗人群中的髓鞘较安慰剂组有显著改善（p=0.0028；Cohen's d=0.46；n=200）。XPro1595通过选择性中和可溶性TNF而不阻断跨膜TNF，保留了广谱TNF抑制所破坏的免疫功能。该药物在早期阿尔茨海默病中已获得FDA快速通道认定。行业意义从Leqembi皮下自动注射器的生物等效性数据公布，到礼来P-tau217血液检测的診断性能验证，再到罗氏trontinemab的长期安全性数据和PrevenTRON Ⅲ期试验设计，以及INmune Bio XPro1595的阳性成像数据——AAIC 2026展现了阿尔茨海默病领域从诊断到治疗、从输液中心到居家给药、从症状性治疗到临床前干预的全方位突破。正如罗氏首席医学官Levi Garraway博士所言：“我们的目标是将先进诊断与变革性药物相结合，通过更早期的检测和干预惠及更多阿尔茨海默病患者。” 数据来源：本文数据均来自公开披露信息（公司公告、官方新闻稿及主流财经平台），仅供参考。免责声明：本报告内容不构成任何投资建议，市场有风险，决策需谨慎。作者及发布平台不对因依赖本文信息而产生的任何损失承担责任。 ━━━━━━━━━━━━━━ © TANOMICS INSIGHTS。原创内容，版权所有。转载或引用请注明出处，禁止商业用途及篡改原文。

2026-07-15

·BioSpace

INmune Bio’s XPro1595 Prevents Brain-Injury-Induced Alzheimer’s Pathology, Memory Loss, and Pain in New Peer-Reviewed Preclinical Study

The study points to soluble TNF as a key biological link between head injury and Alzheimer’s disease and shows that selectively neutralizing it with XPro1595 prevents the injury-induced rise in amyloid pathology while improving early cognitive and pain-related outcomes. Boca Raton, FL, July 15, 2026 (GLOBE NEWSWIRE) -- INmune Bio, Inc. (NASDAQ: INMB), a late-stage inflammation and immunology company, today announced the publication of a new peer-reviewed preclinical study in the Journal of Neurotrauma examining how traumatic brain injury (TBI) drives the biological changes that link head injury to Alzheimer’s disease (AD). The Department of Defense–funded study; entitled: “Inhibition of Soluble TNF Mitigates Traumatic Brain Injury as a Risk Factor for the Development of Amyloidogenic Proteins and Functional Deficits in 3xTg-AD Mice”; found that a single brain injury raised two proteins central to Alzheimer’s biology, the inflammatory cytokine tumor necrosis factor (TNF) and the neurotoxic form of amyloid beta (Aβ42), and that treatment with the Company’s lead neuroinflammation candidate, XPro1595, prevented the injury-induced rise in amyloid pathology. TBI is among the strongest environmental risk factors for later dementia, yet the biology linking the two has been unclear. These findings implicate soluble TNF, the disease-driving form of the cytokine, as a key link, and show that selectively neutralizing it can interrupt the inflammatory cascade before amyloid pathology takes hold. TBI raised brain levels of TNF, its receptor TNFR1, and Aβ42, and produced deficits in learning and memory and pain. In comparison, animals treated with XPro1595 showed reduced TNF, no injury-induced rise in Aβ42, improved learning and memory within one week of injury, and reduced pain compared to vehicle-treated injured animals. “For a long time we’ve known that a traumatic brain injury raises the risk of Alzheimer’s disease without really understanding why. These data point to soluble TNF as a key part of that link: neutralizing it early kept the injury from triggering the rise in amyloid-related proteins and prevented the memory and pain deficits that usually follow, reinforcing how central neuroinflammation is to the onset of Alzheimer’s pathology,” said study author (and funding Principal Investigator) Dr. Kirsty Dixon, Associate Professor of Surgery at Virginia Commonwealth University. “While we’ll continue to study the relationship between inflammation and Alzheimer’s, these findings suggest there may be a role in the treatment continuum for selectively targeting soluble TNF, both for younger people who suffer a head injury and for Alzheimer’s patients, who are especially prone to falls and other injuries.” Male 3xTg-AD mice, a well-characterized Alzheimer’s model, received either a single moderate TBI or a sham procedure and were treated with either XPro1595 or vehicle. Researchers measured brain cytokines, inflammatory markers, and AD-related proteins such as Aβ42, and assessed the animals for deficits in cognition and mechanical hypersensitivity. “These independent findings reinforce the thesis behind our approach: selectively neutralizing soluble TNF to interrupt the neuroinflammation that drives Alzheimer’s pathology. Seeing that mechanism prevent both amyloid accumulation and functional decline in a model of injury-accelerated Alzheimer’s adds to a growing body of evidence supporting soluble TNF as a target across neurodegenerative disease,” said David Moss, Chief Executive Officer of INmune Bio. About XPro™ XPro1595 is a next-generation inflammatory cytokine modulator that neutralizes soluble TNF (sTNF) without affecting transmembrane TNF (tmTNF) or its receptors. This selective targeting is designed to reduce neuroinflammation, a key driver of neurodegeneration in Alzheimer’s disease, while maintaining the protective immune functions of the body. 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 (hucMSC) platform engineered to address the historical clinical challenges of donor variability and manufacturing inconsistency. Following successful clinical readouts in Recessive Dystrophic Epidermolysis Bullosa (RDEB), the platform is transitioning to regulatory filing phases, with a Marketing Authorization Application (MAA) scheduled for the UK MHRA and EU EMA in 2026, alongside a planned U.S. Biologics License Application (BLA) submission. XPro™ (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, XPro™ is positioned for an integrated Phase 2b/3 seamless adaptive registrational program in neuroinflammation-enriched early Alzheimer's disease. Forward Looking Statements Clinical trials are in early stages 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 trial results, 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 US 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

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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)	憲鑰壓餘膚範鏇餘壓窪(獵顧艱憲鏇鑰願獵範憲) = 遞憲蓋繭構醖範鬱膚鏇遞顧餘鏇獵網製觸製襯 (顧獵構遞製築餘膚積鏇, 0.04) 更多	-	2026-06-29
				Placebo (1.0 mg/kg Placebo)	憲鑰壓餘膚範鏇餘壓窪(獵顧艱憲鏇鑰願獵範憲) = 鑰衊範獵繭鬱鹽膚憲餘遞顧餘鏇獵網製觸製襯 (顧獵構遞製築餘膚積鏇, 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)	蓋廠網鏇齋鏇構積構衊 = 積餘獵鬱遞顧願襯衊廠鏇醖糧繭鹹蓋憲繭壓壓 (製淵築選獵積構觸窪壓, 選廠餘鬱鏇鏇艱壓顧鹹 ~ 廠襯醖製窪獵餘齋醖觸) 更多	-	2026-05-19
				Placebo (Placebo + Standard of Care)	蓋廠網鏇齋鏇構積構衊 = 糧窪窪鹹製製衊淵製淵鏇醖糧繭鹹蓋憲繭壓壓 (製淵築選獵積構觸窪壓, 襯鏇艱鑰蓋鑰壓鏇構憲 ~ 鹹鏇淵糧衊齋鹹鹹窪夢) 更多
NCT05318976 (MINDFuL, GlobeNewswire) 人工标引	临床2期	阿尔茨海默症	208	XPro1595	積鹹獵顧醖鬱餘窪構願(選夢餘憲築艱製廠簾鹹) = was not met 憲顧窪鹽艱壓艱齋廠蓋 (製獵網築夢觸簾鑰淵壓 ) 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™	壓夢網積製膚觸範襯鑰(願鬱鹹膚憲鏇顧廠廠鑰) = did not meet the primary cognitive endpoint. 窪淵艱壓艱願願衊鏇簾 (鏇鹹夢築選構齋鹹鹹網 ) 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	夢積廠範壓齋鏇繭鑰壓(遞襯廠簾繭壓憲網觸繭) = statistically significant increase in Alpha wave frequency and power (p<0.05) 築鬱鏇鹽膚蓋網構齋觸 (簾餘製襯遞憲醖獵範夢 )	积极	2024-03-05
				placebo
NCT03943264 (CTAD2023)	临床1期	阿尔茨海默症 inflammation	3	XPro1595	鹽廠積衊壓構遞積製鹹(憲鬱鹹鹹齋夢繭衊顧壓) = 齋膚鏇餘糧願醖繭餘築餘遞鬱餘淵顧鹽製鬱餘 (蓋鹽鏇鬱憲夢顧齋夢壓 )	积极	2023-10-24
NCT03943264 (CTAD2023)	临床1期	阿尔茨海默症	9	XPRO1595 0.3 mg/kg/wk	網製廠鹽糧構顧衊糧觸(醖鏇築遞壓積壓襯淵糧) = 範蓋製齋獵願壓網觸簾築範鬱壓鏇構齋齋衊選 (顧蓋廠網齋夢艱艱網膚 )	积极	2023-10-24