INmune Bio Inc. Announces Publication in Cell Reports Demonstrating XPro™ Promotes Remyelination
INmune Bio (NASDAQ: INMB) announces publication in Cell Reports demonstrating XPro™'s ability to promote remyelination in demyelinating disease animal models. The study, led by Dr. Leslie Probert at Hellenic Pasteur Institute, shows that XPro1595 converts microglia from damaging to reparative cells by blocking soluble TNF. This research has implications for treating various CNS diseases, including Alzheimer's Disease, where myelin loss compromises neuron function. The company expects to report top-line cognitive results from its Phase II Early AD patients trial in first half of 2025.
INmune Bio (NASDAQ: INMB) annuncia la pubblicazione su Cell Reports che dimostra la capacità di XPro™ di promuovere la remielinizzazione in modelli animali di malattie demielinizzanti. Lo studio, condotto dal Dr. Leslie Probert presso l'Istituto Pasteur Ellenico, mostra che XPro1595 converte le microglia da cellule dannose a cellule riparative bloccando il TNF solubile. Questa ricerca ha implicazioni per il trattamento di varie malattie del SNC, inclusa la Malattia di Alzheimer, dove la perdita di mielina compromette la funzione neuronale. L'azienda prevede di riportare i risultati cognitivi principali dal suo studio di Fase II sui pazienti con Malattia di Alzheimer precoce nella prima metà del 2025.
INmune Bio (NASDAQ: INMB) anuncia la publicación en Cell Reports que demuestra la capacidad de XPro™ para promover la remielinización en modelos animales de enfermedades desmielinizantes. El estudio, dirigido por el Dr. Leslie Probert en el Instituto Pasteur Helénico, muestra que XPro1595 convierte la microglía de células dañinas a células reparativas al bloquear el TNF soluble. Esta investigación tiene implicaciones para el tratamiento de diversas enfermedades del SNC, incluida la Enfermedad de Alzheimer, donde la pérdida de mielina compromete la función neuronal. La empresa espera informar los resultados cognitivos principales de su ensayo de Fase II en pacientes con Alzheimer temprano en la primera mitad de 2025.
INmune Bio (NASDAQ: INMB)는 Cell Reports에 발표하여 XPro™가 탈수초질환 동물 모델에서 재탈수초를 촉진할 수 있음을 보여줍니다. 헬레닉 파스퇴르 연구소의 Leslie Probert 박사가 이끄는 이 연구는 XPro1595가 용해성 TNF를 차단함으로써 미세 아교 세포를 해로운 세포에서 재생 세포로 전환시킨다는 것을 보여줍니다. 이 연구는 알츠하이머 병을 포함한 다양한 CNS 질환 치료에 대한 함의를 가지고 있습니다. 왜냐하면 미엘린 손실이 신경 세포 기능을 손상시키기 때문입니다. 이 회사는 2025년 상반기에 조기 알츠하이머 환자 시험의 주요 인지 결과를 보고할 것으로 예상하고 있습니다.
INmune Bio (NASDAQ: INMB) annonce la publication dans Cell Reports démontrant la capacité de XPro™ à promouvoir la remyélinisation dans des modèles animaux de maladies démyélinisantes. L'étude, dirigée par le Dr. Leslie Probert à l'Institut Pasteur Hellénique, montre que XPro1595 convertit les microglies de cellules nuisibles en cellules réparatrices en bloquant le TNF soluble. Cette recherche a des implications pour le traitement de diverses maladies du SNC, y compris la Maladie d'Alzheimer, où la perte de myéline compromet la fonction neuronale. L'entreprise prévoit de présenter les résultats cognitifs principaux de son essai de Phase II sur des patients atteints de la Maladie d'Alzheimer précoce dans la première moitié de 2025.
INmune Bio (NASDAQ: INMB) gibt die Veröffentlichung in Cell Reports bekannt, die die Fähigkeit von XPro™ zeigt, die Remyelinisierung in Tiermodellen von demyelinisierenden Krankheiten zu fördern. Die von Dr. Leslie Probert am Hellenischen Pasteur-Institut geleitete Studie zeigt, dass XPro1595 Mikroglia von schädlichen in reparative Zellen umwandelt, indem es lösliches TNF blockiert. Diese Forschung hat Auswirkungen auf die Behandlung verschiedener Erkrankungen des ZNS, einschließlich Alzheimer-Krankheit, bei denen der Verlust von Myelin die Funktion der Neuronen beeinträchtigt. Das Unternehmen plant, in der ersten Hälfte von 2025 die kognitiven Top-Ergebnisse aus seiner Phase-II-Studie bei Patienten mit früher Alzheimer-Krankheit zu berichten.
- Publication in prestigious Cell Reports journal validates XPro™ technology
- Successful demonstration of XPro™'s ability to promote remyelination in animal models
- Phase II trial for Early AD patients progressing with results expected H1 2025
- None.
Insights
The publication in Cell Reports marks a significant scientific advancement for XPro1595, demonstrating its ability to promote remyelination through microglial regulation. The study reveals a critical mechanism where XPro™ can convert harmful microglia into beneficial, repair-promoting cells. This has profound implications for treating Alzheimer's Disease (AD) and other neurodegenerative conditions.
The research strengthens XPro's therapeutic potential by addressing a fundamental aspect of neurodegeneration - myelin loss. The data suggests XPro could offer a multi-modal approach to treating AD by:
- Promoting remyelination
- Restoring synaptic function
- Preventing neuronal loss
Data from Animal Model Study Demonstrate XPro™ converts microglia from a demyelinating cell to a remyelinating cell
Multi-year study published has implications for many CNS diseases including Alzheimer’s
Boca Raton, Florida, Oct. 24, 2024 (GLOBE NEWSWIRE) -- INmune Bio, Inc. (NASDAQ: INMB) (the “Company”), a clinical-stage inflammation and immunology company focused on developing treatments that harness the patient’s innate immune system to fight disease, announces the publication of a seminal paper in the journal Cell Reports that demonstrates XPro1595 promotes remyelination in an animal model of demyelinating disease. The study, Microglia Regulate Cortical Remyelination via ΤNFR1-Dependent Phenotypic Polarization, was performed under the direction of Leslie Probert PhD, Head of Immunology at the Hellenic Pasteur Institute in Athens Greece, and is the culmination of several years of work supported by EU research grants.
Myelin is necessary for fast and efficient communication between neurons. Loss of myelin compromises neuron function and communication and is a key step in the neurodegenerative process of many CNS diseases, including Alzheimer’s Disease.
“Activated microglia play a central role in both demyelination and remyelination,” said Dr. Probert, senior author of the publication. “Our data identify solTNF as a critical cytokine checkpoint that converts microglia from a reparative, remyelinating cell to a damaging, demyelinating cell. These data suggest that blocking soluble TNF is a promising strategy for treating demyelinating diseases.”
“Demyelination is a core mechanism of neurodegeneration that has been overlooked in Alzheimer's disease, despite the evidence that it’s a critical element of the disease's pathology,” said RJ Tesi MD, CEO of INmune Bio. “These new data further support the potential for XPro1595 in neurodegenerative diseases by restoring glia function to improve key components of neurodegeneration at multiple levels, including restoration of synaptic function, remyelination, and ceasing cell loss.”
INmune anticipates reporting top-line cognitive results of an ongoing blinded randomized Phase II in Early AD patients in the first half of 2025.
About Demyelination in Alzheimer's Disease
Research shows that demyelination occurs in various brain regions critical for cognition in AD patients. This damage is often associated with the presence of amyloid-beta (Aβ) plaques, suggesting that myelin loss may precede or accompany the classic pathological changes seen in AD. Changes in myelin structure can be detected even before the onset of typical AD symptoms. Advanced imaging techniques have revealed alterations in myelin density and integrity in individuals at risk for AD, indicating that demyelination might serve as an early biomarker for the disease. The mechanisms underlying myelin damage in AD involve oligodendrocyte dysfunction, which can lead to the breakdown of myelin sheaths. This breakdown not only affects neuronal health but may also contribute to the accumulation of Aβ, creating a feedback loop that exacerbates both myelin loss and neurodegeneration. Studies utilizing techniques like myelin water fraction imaging have shown significant reductions in myelin integrity among individuals with mild cognitive impairment and dementia, reinforcing the notion that demyelination is prevalent in AD.
About INmune Bio Inc.
INmune Bio, Inc. is a publicly traded (NASDAQ: INMB), clinical-stage biotechnology company focused on developing treatments that target the innate immune system to fight disease. INmune Bio has two product platforms that are both in clinical trials: The Dominant-Negative Tumor Necrosis Factor (DN-TNF) product platform utilizes dominant-negative technology to selectively neutralize soluble TNF, a key driver of innate immune dysfunction and a mechanistic driver of many diseases. XPRO, the first of several DN-TNF products, is in clinical trials to determine if it can treat patients with Mild Alzheimer’s disease. Additional therapeutic indications including d treatment-resistant depression and oncology will be pursued when resources allow. The Natural Killer Cell Priming Platform includes INKmune™, a therapy developed to prime a patient’s NK cells to treat patients with cancer. INKmune uses a precision medicine approach for the treatment of a wide variety of hematologic and solid tumor malignancies. The INKmune trial is enrolling patients into a US Phase I/II trial in men with metastatic castrate resistant prostate cancer. To learn more, 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 that do not describe historical facts may constitute forward-looking statements as that term is defined in the Private Securities Litigation Reform Act of 1995. Any statements contained in this press release that do not describe historical facts 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 a number of risks and uncertainties. Actual results and the timing of certain events and circumstances may differ materially from those described by the forward-looking statements as a result of these risks and uncertainties. INB03™, XPro1595, and INKmune™ are still in clinical trials or preparing to start clinical trials and have not been approved by the US Food and Drug Administration (FDA) or any regulatory body and there cannot be any assurance that they will be approved by the FDA 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 in order to reflect any event or circumstance that may arise after the date of this release.
INmune Bio Contact:
David Moss, CFO (858) 964-3720
info@inmunebio.com
Daniel Carlson
Head of Investor Relations
(415) 509-4590
dcarlson@inmunebio.com
Investor Contact:
Mike Moyer
Managing Director – LifeSci Advisors
mmoyer@lifesciadvisors.com
FAQ
What did INmune Bio's (INMB) Cell Reports publication reveal about XPro™?
When will INmune Bio (INMB) report Phase II trial results for Early AD patients?
How does XPro1595 affect microglia according to INmune Bio's (INMB) research?
