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.

Start Date01 Jun 2023

Sponsor / Collaborator

INmune Bio, Inc.

NCT05522387 / Active, not recruitingPhase 2

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.

Start Date21 Feb 2023

Sponsor / Collaborator

INmune Bio, Inc.

NCT05318976 / RecruitingPhase 2

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.

Start Date28 Feb 2022

Sponsor / Collaborator

INmune Bio, Inc.

100 Clinical Results associated with INB-03

100 Translational Medicine associated with INB-03

100 Patents (Medical) associated with INB-03

Literatures (Medical) associated with INB-03

01 Nov 2024·International Immunopharmacology

Unveiling the role of astrogliosis in Alzheimer’s disease Pathology: Insights into mechanisms and therapeutic approaches

Review

Author: Kumari, Sneha ; Paidlewar, Mohit ; Dhapola, Rishika ; Sharma, Prajjwal ; HariKrishnaReddy, Dibbanti

Alzheimer's disease (AD) is one of the most debilitating age-related disorders that affect people globally. It impacts social and cognitive behavior of the individual and is characterized by phosphorylated tau and Aβ accumulation. Astrocytesmaintain a quiescent, anti-inflammatory state on anatomical level, expressing few cytokines and exhibit phagocytic activity to remove misfolded proteins. But in AD, in response to specific stimuli, astrocytes overstimulate their phagocytic character with overexpressing cytokine gene modules. Upon interaction with generated Aβ and neurofibrillary tangle, astrocytes that are continuously activated release a large number of inflammatory cytokines. This cytokine storm leads to neuroinflammation which is also one of the recognizable features of AD. Astrogliosis eventually promotes cholinergic dysfunction, calcium imbalance, oxidative stress and excitotoxicity. Furthermore, C5aR1, Lcn2/, BDNF/TrkB and PPARα/TFEB signaling dysregulation has a major impact on the disease progression. This review clarifies numerous ways that lead to astrogliosis, which is stimulated by a variety of processes that exacerbate AD pathology and make it a suitable target for AD treatment. Drugs under clinical and preclinical investigations that target several pathways managing astrogliosis and are efficacious in ameliorating the pathology of the disease are also included in this study. D-ALA2GIP, TRAM-34, Genistein, L-serine, MW150 and XPro1595 are examples of few drugs targeting astrogliosis. Therefore, this study may aid in the development of a potent therapeutic agent for ameliorating astrogliosis mediated AD progression.

01 Jun 2024·Neurobiology of Disease

Diet-induced metabolic and immune impairments are sex-specifically modulated by soluble TNF signaling in the 5xFAD mouse model of Alzheimer's disease

Article

Author: Blackmer-Raynolds, Lisa ; Rodrigues, Maria Elizabeth De Sousa ; Chang, Jianjun ; Tansey, Malú Gámez ; Bolen, MacKenzie L ; Schwartz, Noah ; Sampson, Timothy Robert

Emerging evidence indicates that high-fat, high carbohydrate diet (HFHC) impacts central pathological features of Alzheimer's disease (AD) across both human incidences and animal models. However, the mechanisms underlying this association are poorly understood. Here, we identify compartment-specific metabolic and inflammatory dysregulations that are induced by HFHC diet in the 5xFAD mouse model of AD pathology. We observe that both male and female 5xFAD mice display exacerbated adiposity, cholesterolemia, and dysregulated insulin signaling. Independent of biological sex, HFHC diet also resulted in altered inflammatory cytokine profiles across the gastrointestinal, circulating, and central nervous systems (CNS) compartments demonstrating region-specific impacts of metabolic inflammation. Interestingly, inhibiting the inflammatory cytokine, soluble tumor necrosis factor (TNF) with the brain-permeant soluble TNF inhibitor XPro1595 was able to restore aspects of HFHC-induced metabolic inflammation, but only in male mice. Targeted transcriptomics of CNS regions revealed that inhibition of soluble TNF was sufficient to alter expression of hippocampal and cortical genes associated with beneficial immune and metabolic responses. Collectively, these results suggest that HFHC diet impairs metabolic and inflammatory pathways in an AD-relevant genotype and that soluble TNF has sex-dependent roles in modulating these pathways across anatomical compartments. Modulation of energy homeostasis and inflammation may provide new therapeutic avenues for AD.

01 Nov 2023·CNS & Neurological Disorders - Drug Targets

Selective Inhibition of Soluble TNF using XPro1595 Improves Hippocampal Pathology to Promote Improved Neurological Recovery Following Traumatic Brain Injury in Mice

Article

Author: Larson, Katelyn ; Nixon-Lee, Nancy ; Randhi, Rajasa ; Dixon, Kirsty J. ; Damon, Melissa

Aims:To determine the efficacy of XPro1595 to improve pathophysiological and functional outcomes in a mouse model of traumatic brain injury (TBI).Background:Symptoms associated with TBI can be debilitating, and treatment without off-target side effects remains a challenge. This study aimed to investigate the efficacy of selectively inhibiting the soluble form of TNF (solTNF) using the biologic XPro1595 in a mouse model of TBI.Objectives:Use XPro1595 to determine whether injury-induced solTNF promotes hippocampal inflammation and dendritic plasticity and associated functional impairments.Methods:Mild-to-moderate traumatic brain injury (CCI model) was induced in adult male C57Bl/6J WT and Thy1-YFPH mice, with XPro1595 (10 mg/kg, S.C.) or vehicle being administered in a clinically relevant window (60 minutes post-injury). The animals were assessed for differences in neurological function, and hippocampal tissue was analyzed for inflammation and glial reactivity, as well as neuronal degeneration and plasticity.Results:We report that unilateral CCI over the right parietal cortex in mice promoted deficits in learning and memory, depressive-like behavior, and neuropathic pain. Using immunohistochemical and Western blotting techniques, we observed the cortical injury promoted a set of expected pathophysiology’s within the hippocampus consistent with the observed neurological outcomes, including glial reactivity, enhanced neuronal dendritic degeneration (dendritic beading), and reduced synaptic plasticity (spine density and PSD-95 expression) within the DG and CA1 region of the hippocampus, that were prevented in mice treated with XPro1595.Conclusion:Overall, we observed that selectively inhibiting solTNF using XPro1595 improved the pathophysiological and neurological sequelae of brain-injured mice, which provides support for its use in patients with TBI.

102

News (Medical) associated with INB-03

28 Oct 2024

·www.globenewswire.com

INmune Bio Inc. to Host Webinar on Cognitive Testing Using EMACC and CDR-SB

“Why EMACC is the Optimal Tool for Measuring Cognitive Change in Early Alzheimer’s Trials” Webinar to be Held on November 7, 2024, at 1 PM ET. Poster on EMACC Sensitivity and Performance in Phase II Alzheimer’s Trial to be Presented at CTAD2024 Boca Raton, Florida, Oct. 28, 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 is hosting a Webinar on November 7, 2024 at 1 PM ET. The webinar, titled "Why EMACC is the Optimal Tool for Measuring Cognitive Change in Early Alzheimer’s Trials," will explore the development of EMACC and its advantages in assessing cognitive changes over time in early Alzheimer’s Disease (AD) patients. It will also cover the regulatory landscape for Alzheimer’s disease drug development and the role of the CDR-SB clinical scale. Speakers include Dr. Judith Jaeger, President of CognitionMetrics and leader of the team that developed and validated EMACC, Dr. Sarah Barnum, and CJ Barnum, VP of CNS Drug Development at INmune Bio. The Webinar builds on data being presented this week in a poster at the 7th annual Clinical Trial in Alzheimer’s Disease (CTAD) conference being held in Madrid, Spain, October 28-November 1. CTAD, the largest medical meeting focused on clinical trials in AD, is a preferred venue for release of important clinical data. The poster titled Validation of a precision measure of cognitive change in a phase II clinical trial in early AD: The Early and Mild Alzheimer’s Cognitive Composite (EMACC) will be presented by lead authors Sarah Barnum, PhD, Judith Jaeger, PhD, and Lisle Kingery, PhD on Friday, November 1. “The CDR was developed as a diagnostic interview to determine if the patient had AD, and if so, to determine their stage of disease,” said Dr. Jaeger. “Clinical trials don’t measure disease stage, they measure change in cognition. In this case, we are measuring the extent to which cognitive change differs between patients treated with XPro™ vs patients treated with placebo. For early AD trials, the assessments that make up the EMACC objectively and quantitatively capture cognitive change.” “We believe that the EMACC has incredible potential to improve AD clinical development,” stated CJ Barnum, VP of CNS Drug Development at INmune Bio. “Improving assessment of cognitive change will lead to smaller, shorter clinical trials, which means less burden on both patients and investors in terms of time and money. We look forward to sharing a more detailed discussion of the EMACC in this webinar.” Registration Details: Date: November 7, 2024 Time: 1:00pm Eastern Time Webcast: Click Here to Register INmune Bio is currently conducting a global, blinded, randomized Phase II trial in patients with Early AD using XPro™. The trial uses enrichment criteria to focus on patients with neuroinflammation. This unique enrollment strategy focuses the trial on patients with neuroinflammation as a cause of their cognitive decline. XPro™ targets glial cells that drive neuroinflammation in the brain to allow decreased neurodegeneration and demyelination with improved synaptic function and remyelination. The primary endpoint is change from baseline cognitive function after 6 months of XPro™ therapy, measured using EMACC and CDR-SB. About EMACC: EMACC is an empirically validated cognitive measure composed of standardized and widely used neuropsychological tests that are ideally suited for use in clinical trials in Early Alzheimer’s Disease (AD). Compared to CDR-SB and ADAS-Cog for example, the EMACC is an objective measure of cognitive function that accurately captures cognitive changes that occur during early AD. The performance characteristics of the EMACC in early AD were first reported by Biogen at CTAD in 2021 (LBR05) where it was successfully applied to measure cognitive decline in the Biogen Tango Study of the gosenuremab program (BIIB092). Notably, EMACC was also found to be strongly associated with biological markers of inflammation in the Alzheimer’s Disease Neuroimaging Initiative (ADNI) AD study; which was used to compute the statistical power for AD02. 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. DN-TNF product candidates are in clinical trials to determine if they can treat cancer (INB03™), Mild Alzheimer’s disease, Mild Cognitive Impairment and treatment-resistant depression (XPro™). The Natural Killer Cell Priming Platform includes INKmune™ developed to prime a patient’s NK cells to eliminate minimal residual disease in patients with cancer. INmune Bio’s product platforms utilize a precision medicine approach for the treatment of a wide variety of hematologic and solid tumor malignancies, and chronic inflammation. 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 (XPro™), 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. David MossCo-founder and Chief Financial Officer(858) 964-3720info@inmunebio.comDaniel CarlsonHead of Investor Relations(415) 509-4590dcarlson@inmunebio.com Investor Contact:Mike MoyerManaging Director – LifeSci Advisorsmmoyer@lifesciadvisors.com

Phase 2

24 Oct 2024

·www.globenewswire.com

INmune Bio Inc. Announces Publication in Cell Reports Demonstrating XPro™ Promotes Remyelination

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) 964-3720info@inmunebio.com Daniel CarlsonHead of Investor Relations(415) 509-4590dcarlson@inmunebio.com Investor Contact: Mike MoyerManaging Director – LifeSci Advisorsmmoyer@lifesciadvisors.com

Phase 2Immunotherapy

24 Oct 2024

·www.globenewswire.com

INmune Bio Inc. to Report Third Quarter 2024 Financial Results and Provide Corporate Update on October 31, 2024

Management to host conference call and webcast at 4:30 pm ET on that day Boca Raton, Florida, Oct. 24, 2024 (GLOBE NEWSWIRE) -- INmune Bio Inc. (NASDAQ: INMB) (the “Company”), a clinical-stage inflammation and immunology company targeting microglial activation and neuroinflammation as a cause of Alzheimer’s Disease (AD), today announced that it will host a conference call on Thursday October 31, 2024, at 4:30pm EDT to discuss results for its quarter ended September 30, 2024 and to provide a corporate update. Conference 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 Third Quarter Conference Call when reaching the operator. Date: October 31, 2024 Time: 4:30 PM Eastern Time Participant Dial-in: 1-800-343-4136 Participant Dial-in (international): 1-203-518-9843 Conference ID: INMUNE A live audio webcast of the call can be accessed by clicking here or using this link: https://viavid.webcasts.com/starthere.jsp?ei=1692115&tp_key=9ac4a06029 A transcript will follow approximately 24 hours from the scheduled call. A replay will also be available through November 7, 2024 by dialing 1-844-512-2921 or 1-412-317-6671 (international) and entering PIN no. 11157233. 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 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 Investor Contact: Mike MoyerManaging Director – LifeSci Advisorsmmoyer@lifesciadvisors.com

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100 Deals associated with INB-03

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Indication	Highest Phase	Country/Location	Organization	Date
Mild cognitive disorder	Phase 2	PL	INmune Bio, Inc.	28 Feb 2022
Mild cognitive disorder	Phase 2	FR	INmune Bio, Inc.	28 Feb 2022
Mild cognitive disorder	Phase 2	CA	INmune Bio, Inc.	28 Feb 2022
Mild cognitive disorder	Phase 2	ES	INmune Bio, Inc.	28 Feb 2022
Mild cognitive disorder	Phase 2	DE	INmune Bio, Inc.	28 Feb 2022
Mild cognitive disorder	Phase 2	AU	INmune Bio, Inc.	28 Feb 2022
Mild cognitive disorder	Phase 2	GB	INmune Bio, Inc.	28 Feb 2022
Complication	Phase 1	US	INmune Bio, Inc.	21 Oct 2020
COVID-19	Phase 1	US	INmune Bio, Inc.	21 Oct 2020
COVID-19 respiratory infection	Phase 1	US	INmune Bio, Inc.	-

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


GlobeNewswire Manual	Phase 2	Alzheimer Disease	7	XPro1595	(ptugadkmwe) = statistically significant increase in Alpha wave frequency and power (p<0.05) pkxzykaxad (gtpvpqnohe )	Positive	05 Mar 2024
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