Diseases with which we struggle
Peripheral Artery Disease & Critical Limb Ischemia (CLI)
The Problem: Severe arterial occlusion causing a critical deficit in distal limb perfusion. Annually, over 1.5 million individuals suffer from advanced vascular disease in the region, with more than 144,000 cases deteriorating into CLI. This leads to 30,000–40,000 emergency amputations due to the complete lack of safe, functional pro-angiogenic therapies
Our Solution: Angiogenocept (Dll4-Fc). An engineered truncated protein that eliminates systemic Notch toxicities to induce local, functional capillary branching and restore downstream tissue oxygenation
Solid Tumors & Colorectal Cancer (CRC)
The Problem: Colorectal cancer represents a massive global burden with over 600,000 new cases diagnosed annually. Due to late-stage diagnostics, 1-year mortality rates approach 40%. Traditional therapies are hindered by severe systemic toxicity and tumor resistance
Our Solution: PDGFRα-hFc. A highly selective protein trap that starves tumor vasculature and stalls metastasis by blocking stromal cell signaling, bypassing the severe multi-kinase toxicities of chemical inhibitors (TKIs)
Fibrotic Disorders & Autoimmune Diseases
The Problem: Chronic inflammation triggered by hyperactivation of TNFα, IL-1, and IL-6 inevitably drives irreversible organ scarring (liver cirrhosis, pulmonary fibrosis) and severe systemic degradation (rheumatoid arthritis, gout). Current biologics require frequent, painful dosing and often trigger neutralising anti-drug antibodies (ADA)
Our Solution: TNFR1-hinge-Fc, IL-1RA-hFc, and IL-6R-hFc. Ultra-safe cytokine traps featuring optimized linkers that eliminate immunogenicity risks while extending plasma half-life to enable a patient-friendly once-monthly dosing regimen
Advanced Rheumatoid Arthritis & Severe Uveitis
The Problem: Autoimmune destruction of joint cartilage and ocular tissues driven by hyperactivation of Tumor Necrosis Factor-alpha (TNFα). Existing standard-of-care monoclonal antibodies are limited by high systemic multi-dose toxicity, escalating production costs, and the rapid development of neutralizing anti-drug antibodies (ADA) that cause patient resistance
Our Solution: TNFR1-hinge-Fc. A high-affinity recombinant receptor antagonist utilizing an optimized structural hinge region. It enables the receptor and the Fc-domains to operate independently, delivering a nanomolar binding affinity (~1 nM) that safely suppresses joint inflammation during long-term therapy
Cytokine Release Syndrome (CRS) & Gouty Flares
The Problem:Acute, life-threatening hyperinflammatory responses—such as Cytokine Release Storms (CRS) induced by systemic infections and acute gouty arthritis—driven by the uncontrolled release of Interleukin-1 (IL-1α and IL-1β). Standard flexible peptide linkers (e.g., GGGGS repeats) in early-generation fusion proteins carry high structural risks of aggregate formation and severe immunogenicity
Our Solution: IL-1RA-hFc. An ultra-safe, engineered interleukin receptor antagonist configured with a proprietary, ultra-short rigid RS-linker. This architecture eliminates the risk of neo-epitope creation and cross-reactivity, ensuring high therapeutic safety and an extended plasma half-life for monthly dosing
