Company: INMB
Filing Date: 2025-10-30
Form Type: 10-Q
Source: 0001213900-25-104141
Chunk: 29

Company: Inmune Bio, Inc.
Filing Date: 2025-10-30
Form: 10-Q
Item: Part I, Item 1
Chunk 29
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 with
the highest dose (1mg/kg/week dose) having the greatest reduction in neuroinflammation. A broad analysis of proteomic changes following
treatment of XPro revealed significant changes in CSF proteins related to CNS neuronal function, immune/inflammatory response, Cytoskeletal,
metabolic processes, and dendritic spine morphogenesis and synaptic plasticity. Of note, XPro reduced neuronal injury markers Visinin-like
protein-1 (91%) and Neurofilament light (84%), improved measures of synaptic function as evinced by a 222% increase in Contactin 2 and
a 56% decrease neurogranin. Finally, XPro significantly reduced CSL levels of p-Tau217 (43%) and pTau181 (2%) after 3 months of therapy
(Figure 1c).

    A
    B
    C

Figure 1: (A) XPro gets into the brain
at therapeutically relevant concentrations. XPro neutralizes 99.9% of soluble TNF when drug levels exceed two logs. (B) XPro dose dependently
reduces CSF inflammation in the brain. CSF composite – a composite score of change of all cytokines measured in the OLINK Target
48 Cytokine panel. (C) XPro (at 1 mg/kg dose) reduces CSF pTau217 and pTau181 as measure by proteomics.

18

The Phase II study, also known
as AD-02 and MINDFuL, was a multicenter, randomized, double-blind, placebo-controlled clinical trial evaluating the safety, tolerability,
and efficacy of XPro1595 in individuals with early Alzheimer’s disease with biomarkers of inflammation (ADi). The primary goal of
AD02 was to determine if XPro could affect cognition following 6 months of treatment. Participants with a diagnosis of early AD (mild
cognitive impairment or mild AD) were randomized in a 2:1 (XPro:Placebo) ratio to receive either 1.0 mg/kg of XPro1595 or placebo via
weekly subcutaneous injections for 6 months. An enrichment strategy mirroring to the successful strategy used in the Phase I trial was
used to align the mechanism of the drug with the patients AD pathology. Eligibility required the
presence of at least one inflammatory biomarker—either high-sensitivity C-reactive protein (hsCRP > 1.5 mg/L), erythrocyte