Conference Day Two

Thursday, February 27, 2025

7:30 am CHECK-IN & COFFEE

7:55 am Chair’s Opening Remarks

INVESTIGATING PRECLINICAL MODEL DEVELOPMENT TO DRIVE NEUROIMMUNOLOGY TRANSLATION INTO THE CLINIC

8:00 am Elucidating the Potential of Bruton’s Tyrosine Kinase Inhibitors to Modulate Microglial Inflammation using Advanced 2D/3D Human Brain Cell Systems

  • James Keaney Lab Head & Research Project, Leader, Neuroimmunology, Roche

Synopsis

  • Evaluating the functional and pharmacological properties of Fenebrutinib in blocking BTK-mediated disease-associated activation in human microglia and complex brain cell systems
  • Fenebrutinib treatment attenuated pathogenic neuroinflammation associated with FcyR activation while preserving homeostatic innate immune cell functions
  • This study increases understanding of potential BTK functions in human microglial signalling and neuroinflammation relevant to MS pathogenesis

8:30 am Reviewing Utility of Current Neuroinflammatory Models: Reviewing Stimuli, Transcriptomics, Comparative In Vitro & In Vivo Model Translatability

  • Erica Koval Principal Scientist and Research Program Lead, Biogen

Synopsis

  • Understanding if we have the right transcriptomic profile of microglia to reflect the human condition
  • Evaluating relevance of various stimuli: are iPSCs and LPS still relevant for microglia?
  • Exploring whether wild type microglia better at representing the clinical state (20yr aged microglia), or if APOE4 microglia are more relevant
  • Navigating when to use TREM2 mutant in vivo model vs disease specific models for neuroinflammatory pathology

9:00 am Session Reserved for BrainXell

9:10 am Improving In Vitro Models to Better Recapitulate Human Biology of Neurodegeneration

Synopsis

  • Covering limitations, pros and cons, of in vivo and in vitro models for drug discovery in neurodegeneration
  • Development of in vitro iPSC models for AD drug discovery. Evaluation of donor differences by RNA-seq.
  • Roadmap to scaling up production of iPSC-microglia and neurons using automation

9:40 am Sharing Insights on an Open-Access Living Inventory of Neuroinflammatory Preclinical Model & Target Data to Determine Rigor to Encourage Pre-Competitive Collaboration

Synopsis

  • Overviewing the categorization of data and preclinical models of neuroinflammation in Alzheimer’s Disease to encourage pre-competitive collaboration
  • Sharing perspectives on additional evidence generation required in day-to-day, aiming to increase model rigor, transparency and translatability in Alzheimer’s research
  • Incentivizing stakeholders developing tools to share information to help others make informed decisions, towards pre-competitive collaboration

10:10 am MORNING BREAK & NETWORKING

NOVEL TECHNOLOGY & MODALITIES FOR IMPROVED TARGETING OF NEUROINFLAMMATION

10:40 am Integrating Blood-Brain Barrier Technology for Enhanced Delivery of Therapeutic Agents to the CNS

Synopsis

  • Explaining the difference between transferrin receptor and CD98, and why they are good BBB targets
  • Exploring transferrin CD98 and fine-tuning moiety and carrier protein for delivery of different cargos to the brain
  • Unpacking use cases: enzyme replacement with GCASE

11:10 am T Cell Therapies Related to Neuroimmunological Indications & Mechanisms Are Entering Early Clinical Development & May Transform The Therapeutic Landscape

Synopsis

  • CAR-T for neuroimmune indications
  • Tregs for neuroimmune and neuroinflammatory indications
  • CAR-T for brain tumor
  • Other selected therapeutic initiatives

11:40 am Roundtable Discussion: To What Degree is Neuroinflammation the Cause of Disease vs Just Increases Susceptibility to CNS Diseases?

Synopsis

  • Evaluate to what extent does disease cause neuroinflammation vs neuroinflammation causes disease?
  • Reviewing the cause of early inflammatory response prior to disease onset and appearance of cognitive changes, as well as prevalence of neuroinflammation both before and after disease onset
  • Navigating how the cause vs susceptibility ‘weighting’ changes across Alzheimer’s, Parkinson’s, FTS, Multiple Sclerosis, etc..
  • Exploring relevance to treatment regime: should neuroinflammation-targeted therapeutics be considered as more of adjunct treatment in copathology? How does this vary between CNS diseases?
  • What are the steps to further define this cause/susceptibility relationship in clinical development?

12:10 pm LUNCH & NETWORKING

INNOVATIVE TARGETS & MECHANISMS IN NEUROIMMUNOLOGY TO TARGET THE BREADTH OF NEUROINFLAMMATORY PATHOLOGY

1:00 pm Exploring In Vitro & In Vivo Tools to Model Inflammasome Activation in the Context of Neurodegeneration: Highlighting the NORP3 Inflammasome Program

Synopsis

  • Addressing the limitations of demyelination models in immunodeficient mice and optimizing the use of chimeric microglial mice to better replicate human immune responses
  • Investigating alternative immunodeficient mouse strains to enhance the demonstration of demyelination in preclinical studies, with a focus on improving translational relevance to human MS
  • Developing and refining rodent models that more accurately mimic the progressive stages of MS, ensuring closer alignment with human disease pathology and progression for more effective therapeutic evaluation

1:30 pm Modulating Aberrant Activation of the cGAS Pathway to Treat Neurodegeneration in the Clinic

2:00 pm Non-selective Inhibition of Inflammasomes: Preclinical Data & Clinical Observations

  • Paul Ashton President & Chief Executive Officer, Inflammasome Therapeutics

Synopsis

  • In vivo inhibition of inflammasomes in macular degeneration
  • Preliminary clinical data
  • In vitro and in vivo inhibition of inflammasomes in ALS, MS and AD models

2:30 pm Harnessing Inflammasome Activation to Decrease Activity in Neurodegeneration

Synopsis

  • Uncovering the challenges in utilizing cytokines as surrogate markers for inflammasome activity at the individual level
  • Explore cutting-edge technologies and methodologies for studying the molecular intricacies of inflammasome activation pathways for detection at the individual level
  • Discuss the potential of these technologies to provide deeper insights into the molecular details of individual inflammasomes and their activation patterns

3:00 pm AFTERNOON BREAK & NETWORKING

3:30 pm Investigating Aβ Immunotherapy-Induced Vascular Inflammation & Cerebrovascular Damage

Synopsis

  • Examining the connections between vascular integrity, blood-brain barrier permeability, and smooth muscle health in neurodegenerative disease
  • Leveraging spatial omics to investigate cellular and molecular changes around specific vascular sites associated with disease progression
  • Highlighting the involvement of immune cells, particularly a subset of macrophages, in maintaining vascular health and their relevance to disease-related changes

4:00 pm Vidofludimus Calcium (IMU-838) Combines the Best of Two Worlds: Neuroprotection & Relapse Prevention in Multiple Sclerosis

Synopsis

  • Positive phase 2 data in relapsing-remitting multiple sclerosis (EMPHASIS)
  • Hints to slowing down disability worsening
  • Positive biomarker data from phase 2 trial in progressive multiple sclerosis (CALLIPER)
  • Unique dual mode of action addressing relapsing and progressive disease by targeting Nurr1 and DHODH
  • First-in-class Nurr1 activation going beyond inflammation

4:30 pm Panel Discussion: Bridging the Divide: Navigating Mechanistic Interplay Between the CNS & PNS for Target Discovery in Neuroimmunology

  • Vladimir Litvak Director - Global Clinical & Translational Sciences, Takeda Pharmaceutical Co. Ltd.
  • Dimitry Ofengeim Head of Precision Neurology & Neuroinflammation Cluster, Sanofi
  • Thomas Tamsett Director of Neuroscience, EMD Serono

Synopsis

  • Reviewing how immune signalling pathways in the PNS influence CNS inflammation and degeneration, and how this crosstalk can inform the identification of novel therapeutic targets
  • Debate the utility of existing models that integrate both CNS and PNS components and evaluate their potential for accelerating target discovery
  • Discuss the shared immune mechanisms underlying neuroinflammatory pathology in both the CNS and PNS, such as microglial activation and T cell infiltration and the unique features of each system

5:15 pm Chair’s Closing Remarks

5:20 pm END OF CONFERENCE