Restores immune tolerance
Activates Tregs to reduce harmful inflammation without broad immunosuppression.
Research & Development
Revolutionizing autoimmune and oncology treatment
Targeting the root cause: a paradigm shift in immune modulation. Unlike traditional biologics that suppress the immune system, Tregalizumab is the first and only monoclonal antibody designed to selectively activate regulatory T cells (Tregs), restoring immune balance and addressing high-unmet-need diseases more effectively.
First-in-class
Why Tregalizumab? A first-in-class breakthrough
Addresses core pathophysiology
Modulates immunity at its source rather than just managing symptoms.
Proven clinical activity
Proof-of-concept in RA & psoriasis, paving the way for broader autoimmune applications.
Biomarker-driven development
Targeted patient selection, reducing trial risk.
Mechanism of action
How it works: a differentiated mechanism
Tregalizumab binds domain 2 of the CD4 receptor. On regulatory T cells this triggers selective activation. On effector T cells the same binding event does not.
Tregalizumab targets CD4 on T cells and binds to a distinct CD4 epitope. Regulatory T cells are selectively activated; effector T cells are not.
Schematic illustration of the mechanism of action. Not to scale; not structurally representative.
Step 01
Treg activation
Enhances immune regulation in inflammatory diseases. cAMP and TGF-β signalling are increased.
Step 02
Reduces effector T cell activity
Controls harmful immune responses without activating effector T cells.
Step 03
Balances immune modulation
Avoids the immunosuppression seen in existing biologics.
What the data shows
- Binds a unique epitope on CD4 domain 2, activating a distinct signaling cascade that strengthens Tregs without triggering inflammation.
- Induces FOXP3⁺ Treg activation and a CD137⁺ CD154⁻ signature, a hallmark of stable suppressive function.
- Excellent safety: no cytokine release, no lymphocyte depletion.
- Mechanism validated in vitro, ex vivo and in vivo.
Competitive advantage. Unlike current therapies that block inflammatory cytokines
(e.g. TNF, IL-6, IL-23), Tregalizumab rebalances the immune system, creating a
first-in-class solution with high commercial defensibility.
Target indications
Our target indications: high-value, high-impact
01 · Immune-Dermatology
Oral Lichen Planus (oLP)
A game-changer with curative intent
3M+
patients suffer from chronic, pre-malignant inflammation
60,000+
progress to oral cancer annually
€5B+
market potential
- No approved therapies. Existing treatments fail to control inflammation, therefore do not prevent malignancy potential.
Why Tregalizumab?
Tregalizumab targets and controls chronic inflammation, offering the first curative therapy for oLP.
02 · Oncology
Acute Graft-versus-Host Disease (aGvHD)
A life-saving breakthrough
60%
of patients develop aGvHD post stem cell transplant
>50%
failure rate with first-line steroids
€3B+
market potential
- Severe complications, long hospitalizations, high costs.
- U.S. Orphan Drug Designation granted for aGvHD.
Why Tregalizumab?
Unlike existing treatments, Tregalizumab prevents aGvHD at its source by activating Tregs, while preserving the graft-versus-leukemia (GvL) effect.
„Tregalizumab directly addresses the core pathophysiology of aGvHD, setting it apart from current treatments."
Market opportunity
A multi-billion-euro potential
- €10B+ combined market opportunity in oLP & aGvHD
- No competing Treg-targeting therapies in these high-unmet-need areas
- Expansion into additional autoimmune indications
Investor value proposition
A de-risked, high-impact opportunity
- Clinically validated & de-risked — PoC achieved, accelerating development
- First-in-class science — no direct competition in Treg activation
- Multi-billion-euro market potential — addressing severe, underserved diseases
- Strong leadership — proven biotech entrepreneurs with successful regulatory approvals and exits
- Strategic expansion — beyond oLP & aGvHD, unlocking new high-value indications