Company: INMB
Filing Date: 2025-03-07
Form Type: 424B5
Source: 0001213900-25-021719
Chunk: 32

Company: Inmune Bio, Inc.
Filing Date: 2025-03-07
Form: 424B5
Chunk 32
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Likewise, we believe the DN-TNF
platform can be used to treat selected neurodegenerative diseases by modifying the brain microenvironment (“BME”). The Company
believes the core pathology of cognitive decline is a combination of neurodegeneration and synaptic dysfunction. Neurodegeneration is
nerve cell death that may include demyelination. Synaptic dysfunction means the connections between nerve cells stop working efficiently
and may decrease in number. The combination of neurodegeneration and synaptic dysfunction causes cognitive decline and behavioral changes
associated with Alzheimer’s disease (“AD”). XPro completed a Phase I trial treating patients with Alzheimer’s
disease that was partially funded by a Part-the-Clouds Award from the Alzheimer’s Association. We believe XPro targets activated
microglia and astrocytes of the brain that produce sTNF that promotes nerve cell loss, synaptic dysfunction and prevents myelin repair
- key elements in the development of dementia. In animal models, elimination of sTNF prevents nerve cell dysfunction, reverses synaptic
pruning and promotes myelin repair. The Phase I trial in patients with biomarkers of inflammation with AD has been completed. The open
label, dose escalation trial was designed to demonstrate that XPro can safely decrease neuroinflammation in patients with ADi. ADi is
the term used to delineate patients with AD with biomarkers of inflammation. The endpoints of the trial were measures of neuroinflammation
and neurodegeneration in blood and cerebral spinal fluid by measuring changes in inflammatory cytokine levels in the CNS and using MRI-DTI
to measure brain microstructural changes. XPro, at the 1mg/kg/week dose, decreased inflammatory cytokines in the CSF in the brain demonstrating
that XPro can decrease neuroinflammation in patients with AD. We also studied downstream benefits of decreasing neuroinflammation by measuring
changes in the CSF proteome and quantifying changes in novel white matter MRI biomarkers. XPro significantly decreases biomarkers of neurodegeneration as
measured by changes in the CSF proteome including neurofilament light chain, phospho Tau 217 and VILIP-1; decreases of 84%, 46% and 91%
respectively after 3 months of therapy. Three months of XPro therapy improved measures of synaptic function, as measured in the CSF proteome
including a 222% increase in Contactin 2 and a 56% decrease neurogranin