Advancing the future of relief one signal at a time.

WHAT WE DO

Revolutionizing the treatment of autoimmune disorders, one signal at a time

Signal26 Biotherapeutics is a Biotechnology startup dedicated to advancing the development of a novel biological drug for the treatment of Psoriasis. In collaboration with our colleagues at CHUV, we are pioneering research into the role of interleukin 26 (IL-26) in
autoimmune disorders.

About us

Roadmap

Our Mission

We're commited to providing relief for thousands of patients and improving their quality of life

At Signal26, our mission is to provide effective solutions for patients suffering from conditions like Psoriasis, Inflammatory Bowel Disease, and Rheumatoid Arthritis. We're doing this based on years of research and a novel understanding of the IL-26 signalling pathway.

Palmoplantar Pustular Psoriasis (PPPP) is the most common form of Pustular Psoriasis which has a significant negative impact on quality of life for thousands of patients. There are currently no approved treatments. We aim to change that, with our unique approach built on years of research.

Targeted Therapy

The pathogenesis of PPPP differs from Plaque Psoriasis. The IL-26 signalling pathway is heavily implicated in PPPP, and the underlying mechanism has been shown to involve microbial DNA found in the skin lesions. Together with CHUV, we have developed a monoclonal antibody to IL-26.

Demonstrated Efficacy

Over the last three years, we have dedicated extensive efforts to research into the mechanisms of IL-26-driven inflammation. The antibody's efficacy in blocking IL-26 activity was demonstrated in vitro and in vivo. Following pre-clinical success, we humanized the antibody and are now carrying out the next stages of development.

A person with vitiligo on their back and arm, standing against a neutral background, with curly hair visible.

NEXT STEPS

Unlocking targeted therapy for the people who need it the most

In 2025, pre-clinical studies of anti-IL-26 will commence, in collaboration with our international partnering institutions. By 2027 we aim to begin the first study in humans. And by the end of 2028 we will begin clinical trials with Pustular Psoriasis patients.

We are working towards making our treatment commercially available at scale by 2034.

To learn more about our roadmap going forward, click below:

Our roadmap

Based on active research supported by leading institutions and partners

About Psoriasis

Psoriasis affects 125 million people globally, driven by immune system disruptions and characterized by excessive skin cell growth.

1. Global Prevalence

Psoriasis is a chronic inflammatory skin disease affecting approximately 125 million people worldwide. The pathogenesis of psoriasis involves a complex interplay between genetic, environmental, and immunological factors. The disease initiation often follows trauma, infection, or drug exposure, which disrupts the innate immune response leading to sustained inflammation and uncontrolled keratinocyte proliferation.

2. Signals

Two primary pathways are involved in psoriasis pathogenesis: the Th17 pathway and DNA methylation. Keratinocytes, the outermost skin layer cells, and dendritic cells (DCs) play crucial roles. Activation of plasmacytoid dendritic cells (pDCs) is pivotal in forming psoriatic plaques, characterized by the production of Type I interferons (IFN-a & IFN-b). These interferons promote myeloid dendritic cell (mDC) maturation and are implicated in Th1 and Th17 cell differentiation.

Activated mDCs secrete TNF-a, IL-23, and IL-12, modulating Th17 and Th1 cell differentiation. Th17 cells secrete cytokines (IL-17, IL-21, and IL-22) that drive keratinocyte proliferation. IL-23, composed of p19 and p40 subunits, expands Th17 cells into IL-17A/F expressing subtypes.

3. Key discovery: IL-26

A key insight is that IL-26, produced by Th17 cells, activates keratinocytes and forms complexes with DNA, leading to DC activation and further promoting the Th17-IL-17 pathway.Understanding these mechanisms highlights potential therapeutic targets, such as blocking IL-26, to mitigate psoriasis symptoms and progression.

About IL-26

IL-26, a cytokine with antimicrobial properties, plays a crucial role in inflammation, particularly in psoriasis, by activating immune response.

1. What is IL-26?

IL-26 is a 19 kDa cytokine part of the IL-10 cytokine family, including IL-19, IL-20, IL-22, and IL-24. It binds to a heterodimeric receptor composed of IL-10R2 and IL-20R1. Upon receptor activation, IL-26 induces Jak1 and tyrosine kinase 2 signaling, leading to the activation of STAT1 and STAT3. This signaling cascade in keratinocytes results in the production of pro-inflammatory cytokines like IL-1 and neutrophil-recruiting chemokines (CXCL1, CXCL2, and IL-8). In intestinal epithelial cells, it triggers TNF and IL-8 production.

2. How does IL-26 Impact inflammatory diseases?

IL-26 is structurally similar to antimicrobial peptides, exhibiting broad-spectrum antimicrobial activity. It is a key driver of auto-inflammation in psoriasis and pustular disease activity. Neutrophils release IL-26 more abundantly and rapidly than Th17 cells, storing it in primary granules and releasing it upon activation. IL-26-DNA complexes trigger TLR9 activation in neutrophils, particularly noted in palmoplantar pustular psoriasis (PPPP) and generalized pustular psoriasis (GPP). In plaque psoriasis, IL-26 is linked to Th17 cells, while in pustular psoriasis, it is associated with neutrophils. IL-26's presence in various body sites, including synoviocytes and myofibroblasts in rheumatoid arthritis (RA), and its role in intestinal integrity suggest its involvement in multiple inflammatory diseases, including psoriasis, inflammatory bowel disease (IBD), and RA.
Activated mDCs secrete TNF-a, IL-23, and IL-12, modulating Th17 and Th1 cell differentiation. Th17 cells secrete cytokines (IL-17, IL-21, and IL-22) that drive keratinocyte proliferation. IL-23, composed of p19 and p40 subunits, expands Th17 cells into IL-17A/F expressing subtypes.

Our Anti-IL26 Antibody

Our monoclonal antibody targets IL-26 to reduce its inflammatory effects, showing promise in preventing psoriasis in preclinical studies.

1. Anti-IL26 Antibody

The development of an anti-IL-26 antibody aims to specifically target the inflammatory activities of IL-26, offering a novel therapeutic approach for psoriasis and other related inflammatory conditions. In vitro studies have demonstrated the antibody's capability to block IL-26's binding to DNA and its ability to stimulate innate immune cells. This inhibition is crucial in preventing the downstream inflammatory responses driven by IL-26-DNA complexes.

2. Demonstrated Efficacy

In vivo experiments have shown that the monoclonal antibody (MAb) can effectively block IFN-driven inflammation and psoriasis development induced by IL-26 or skin injury in IL-26 transgenic mice. This antibody holds promise for treating various forms of psoriasis by mitigating the excessive inflammatory responses and keratinocyte proliferation associated with the disease.

3. Potential Impact

Targeting IL-26 with this antibody could also have broader implications, potentially offering therapeutic benefits for other IL-26 related inflammatory diseases, such as inflammatory bowel disease (IBD) and rheumatoid arthritis (RA). This innovative approach underscores the importance of understanding cytokine signaling pathways in developing targeted therapies for chronic inflammatory conditions.

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