What is precision immunotherapy?
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Precision immunotherapy tailors immune modulating treatments to the biology of each patient. By integrating genetics and molecular signatures, we can predict which therapy is most likely to benefit an individual—and when to intervene—to change the course of disease.
By decoding the immune drivers behind neuroinflammatory and autoimmune disorders and applying advanced technologies such as multiomics profiling and AI driven analytics, Elixiron is advancing the real-world application of precision medicine. Multiomics approaches: spanning genomics, transcriptomics, proteomics, metabolomics enable a deep, systems level understanding of immune networks. AI powered knowledge graphs integrate these diverse data layers with clinical and biomarker information to reveal causal relationships, uncover new targets, and refine patient stratification in real time.
Together with partners across biotech, academia, and clinical networks, we aim to deliver better outcomes for patients and a more sustainable future for healthcare systems.
Our approach to precision immunotherapy
We harness large, well annotated scientific and clinical datasets, enriched by multiomics profiling, to uncover disease mechanisms and translate them into smarter trials and smarter medicines that:
- Identify high probability targets rooted in human biology and immune pathways, informed by multi-layered omics data.
- Define biomarker based subgroups most likely to using patient segmentation models.
- Design better clinical trials that enrich for the right patients and endpoints.
- Co-develop diagnostics that guide treatment selection and monitor response in practice, with algorithms refined by continuous data integration.
Across our pipeline, we aim to match the precise immune target to the right patient at the right time, and intervene earlier to prevent progression.
Disease Spotlights
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In vitiligo, our lead candidate Indemakitug, an anti-IFN-γ monoclonal antibody, targets the IFN-γ driven chemokine axis (CXCL9/CXCL10) that recruits cytotoxic T cells to melanocytes, sustaining depigmentation. By neutralizing IFN-γ, this approach disrupts the feed-forward immune loop and enables repigmentation. Evaluation includes standardized endpoints such as VASI and F-VASI scores, complemented by high-resolution dermal imaging for objective lesion quantification. Pharmacodynamic biomarkers, including reductions in IFN-γ signatures, CXCL9/CXCL10 levels, are used to assess biological response. A near-term goal is the development of a minimally invasive biomarker panel combining blood and skin readouts to guide initiation, optimize combination strategies, and monitor treatment effects in clinical practice.
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In Alzheimer’s disease, our lead candidate Enrupatinib, a selective CSF-1R inhibitor, targets microglial activation, a key driver of neuroinflammation, synaptic dysfunction, and neurodegeneration. The program combines multi-omics biomarkers (YKL-40, sTREM2, GFAP, cytokines, transcriptomic signatures, NfL, p-tau) with MRI and PET imaging to evaluate neuroinflammation and therapeutic impact. Clinical assessments include composite cognitive measures to capture functional change. In the near term, we aim to establish a blood-based biomarker panel integrating inflammatory and neurodegeneration markers, validated against imaging and clinical outcomes, to enable precise patient selection and ongoing monitoring.
