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Precision therapies targeting the challenges of immune-mediated conditions
Our science leverages decades of progress to address significant medical needs in neurological and immunological conditions.
TYK2: A promising therapeutic approach
Tyrosine kinase 2 (TYK2) is a key enzyme that orchestrates immune and inflammatory signaling by transmitting the effects of cytokines such as IL-23, IL-12, and type I interferons (IFNs). These pathways are central to both innate and adaptive immunity, influencing the behavior of Th17 and Th1 cells as well as myeloid-derived cells like macrophages and microglia.
Dysregulated TYK2 activity is implicated in a range of autoimmune and inflammatory diseases. Inhibiting TYK2 has already demonstrated meaningful benefit in psoriasis, psoriatic arthritis, and lupus (SLE), and compelling genetic evidence points to broader potential across conditions such as multiple sclerosis, inflammatory bowel disease, ankylosing spondylitis, and others. More recently, research has linked TYK2 signaling to the neuroinflammatory processes underlying neurodegenerative disorders including Alzheimer’s disease and amyotrophic lateral sclerosis (ALS).
Historically, efforts to inhibit TYK2 and other Janus kinases (JAKs) by targeting their catalytic (JH1) domains have faced challenges with selectivity, as these domains are highly conserved across the JAK family. This limited specificity can lead to unwanted inhibition of JAK1 or JAK2, creating safety risks that constrain the therapeutic window and restrict broader use in chronic autoimmune or neurologic settings. By contrast, selective inhibition of TYK2 through its regulatory pseudokinase (JH2) domain offers a novel, allosteric approach—achieving potent TYK2 blockade while maintaining precision and minimizing off-target effects.
Sudo Biosciences is advancing a portfolio of highly potent, TYK2 pseudokinase inhibitors engineered to deliver “fit-for-purpose” therapies across a broad spectrum of autoimmune and neuroinflammatory diseases—bringing the promise of TYK2 inhibition to conditions with significant medical need.
Diseases with immune-mediated pathology
Targeting the TYK2 pseudokinase domain could drive therapeutic progress in conditions with significant medical need.
Multiple Sclerosis
TYK2 inhibition represents a transformative opportunity in multiple sclerosis (MS). By precisely modulating immune and inflammatory signaling pathways that drive both relapsing and progressive disease, SUDO-550, a fully CNS-penetrant TYK2 inhibitor, offers the potential for a safe, effective, and convenient oral therapy that addresses key limitations of existing MS treatments.
Multiple sclerosis is a chronic, immune-mediated disease of the central nervous system that affects roughly one million people in the United States. Despite advances in disease-modifying therapies (DMTs), many patients continue to experience relapses, disability progression, or treatment-related side effects.
There is a clear need for a new class of therapies that can effectively and safely target both the inflammatory and neurodegenerative components of MS. TYK2 inhibition offers precisely that promise.
Strong human genetic evidence supports TYK2 as a validated therapeutic target in MS. Specific naturally occurring variants that reduce TYK2 activity significantly lower the risk of developing MS. Individuals carrying these variants show markedly reduced immune signaling responses to IL-12, IL-23, and type I IFNs, cytokine signaling pathways that drive immune activation and inflammation in MS. These findings demonstrate that TYK2 inhibition in humans can be both protective and well tolerated.
SUDO-550 is a brain-penetrant, oral, and highly selective TYK2 pseudokinase inhibitor optimized to treat both relapsing and progressive forms of MS. By targeting TYK2 signaling in immune cells both peripherally and within the CNS, SUDO-550 aims to address the full spectrum of MS biology—from acute inflammatory relapses to chronic neuroinflammation that drives disability progression.
TYK2 Inhibition in Neurodegenerative Disease
Neurodegenerative diseases such as Alzheimer’s disease, amyotrophic lateral sclerosis (ALS), and Parkinson’s disease share a common hallmark—chronic neuroinflammation driven by Type I interferon (IFN) signaling. By selectively modulating TYK2-mediated pathways active in both neurons and glial cells, SUDO-550 offers a novel opportunity to slow or prevent neuroinflammatory processes underlying neurodegeneration.
Chronic neuroinflammation is increasingly recognized as a key driver of neurodegenerative diseases such as Alzheimer’s disease, ALS and Parkinson’s disease. Elevated activation of Type I signaling—regulated by the TYK2 enzyme—promotes glial activation, cytokine release, and neuronal injury across these conditions. SUDO-550 is designed to precisely modulate these inflammatory pathways.
By inhibiting an underlying driver of neuroinflammatory damage, SUDO-550 offers a novel therapeutic approach with potential to modify the course of multiple neurodegenerative diseases—bridging immunology and neuroscience to advance care where few disease-modifying options exist.
