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> Insights > World Ankylosing Spondylitis Day | ACRO Stands with You in Safeguarding Spinal Health 
Each year, the first Saturday in May marks World Ankylosing Spondylitis (AS) Day, raising awareness for the 54 million patients worldwide living with a "folded existence"– spinal rigidity, bone spur proliferation, morning stiffness and pain, and even irreversible disability. Statistics reveal that 65% of AS patients who do not receive standardized treatment will develop disabilities within 10 years, while early diagnosis and treatment can control 80% of disease progression.
Progression of AS
AS is a chronic inflammatory autoimmune disorder primarily characterized by inflammation of the sacroiliac joints and axial spine. As the disease progresses, patients may develop severe complications such as spinal fusion (manifesting as "bamboo spine" structural changes), restricted thoracic mobility, and hip joint destruction. While the introduction of biologic therapies has revolutionized AS management, a subset of patients still exhibits suboptimal responses to current treatments or encounter drug tolerance challenges. This unmet medical need has propelled global research institutions and pharmaceutical companies to prioritize the development of novel targeted therapies and precision medicine approaches addressing distinct pathogenic mechanisms.
We have developed a comprehensive product portfolio including highly active recombinant proteins, stable cell lines, and inhibitor screening kits. Our solutions span the entire drug development continuum – from target discovery and validation, candidate drug screening and development to CMC manufacturing and quality control – accelerating the efficient translation of AS innovative therapies from foundational research to clinical implementation.
AS develops through a complex interplay of genetic, immune, infectious, and environmental factors. While not the sole determinant, the HLA-B27 gene acts as a molecular "trigger," priming the immune system of carriers to hyperreact to specific antigens. When pathogens like Klebsiella invade the gut, the immune system mistakenly identifies HLA-B27-associated joint tissues as foreign threats, unleashing a storm of inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α)) and interleukin-17 (IL-17). This immune dysregulation initiates a domino effect: TNF-α hyperactivates osteoclasts, accelerating bone resorption; IL-17 drives fibroblast proliferation, narrowing joint spaces; and an imbalance in Th17/Treg cell ratios amplifies inflammatory cascades. Collectively, these mechanisms shift the disease trajectory from transient inflammatory pain to irreversible structural bone damage, culminating in spinal fusion and rigidity.
AS and its pathogenic mechanisms
The approved therapies for AS primarily function by targeting key molecules in inflammatory pathways, including TNF-α, IL-17, and IL-23. TNF-α inhibitors (e.g., adalimumab, infliximab), as the earliest approved biologics, alleviate joint inflammation by blocking the pro-inflammatory cytokine TNF-α. Adalimumab (Humira) once dominated as the global "blockbuster drug" with annual sales exceeding $20 billion, though its market position faced significant erosion from biosimilars following patent expiration in 2023. IL-17/IL-23 pathway inhibitors, targeting upstream inflammatory mediators, have emerged as mainstream options due to superior clinical response rates: Novartis' secukinumab (IL-17A inhibitor) achieved $4.788 billion in 2022 sales, while Eli Lilly's ixekizumab reached $2.894 billion. UCB's bimekizumab rapidly gained market traction through its unique dual-targeting mechanism targeted IL-17A/F. IL-23 inhibitors like risankizumab and tildrakizumab demonstrate enhanced safety profiles via precise p19 subunit inhibition, with risankizumab surpassing $7.9 billion in global sales by 2023. Among emerging therapies, Hengrui Pharmaceuticals' self-developed fully humanized frexizumab (approved 2024) reduces immunogenicity as China's first domestically developed IL-17A inhibitor, marking a breakthrough for domestic pharmaceutical companies in the AS field.
Approved originator biologics for AS (Source: Pharmacodia)
Cutting-edge research is exploring regenerative therapeutic strategies that transcend traditional immunosuppression. Drug development leveraging the gut-joint axis theory has emerged as a disruptive frontier, with oral sphingosine-1-phosphate receptor modulators demonstrating dual mechanisms of action—simultaneously regulating lymphocyte migration and restoring intestinal barrier function. Early-phase clinical data indicate significant reductions in C-reactive protein levels. In cellular therapy, Treg cell expansion technologies and CAR-Treg therapies aim to reestablish immune equilibrium, while CRISPR-Cas9 gene-editing tools targeting HLA-B27 conformational abnormalities have successfully rectified antigen-presentation defects in preclinical models. These groundbreaking advances are propelling the transition of AS treatment paradigms from symptomatic management to disease-modifying interventions.
Immune regulation of the joint-gut-microbiome axis in AS
As our understanding of AS heterogeneity deepens and technological innovations accelerate, AS is poised to transition from a chronic debilitating disease to a controllable and treatable chronic condition, delivering transformative improvements in quality of life for patients globally. We have developed a comprehensive product portfolio including highly active recombinant proteins, stable cell lines, and inhibitor screening kits. Our solutions span the entire drug development continuum – from target discovery and validation, candidate drug screening and development to CMC manufacturing and quality control – accelerating the efficient translation of AS innovative therapies from foundational research to clinical implementation.
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1. Kim, Se Hee, and Sang-Hoon Lee. "Updates on ankylosing spondylitis: pathogenesis and therapeutic agents." Journal of rheumatic diseases 30.4 (2023): 220-233.
2. Garrido-Mesa, Jose, and Matthew A. Brown. "T cell repertoire profiling and the mechanism by which HLA-B27 causes ankylosing spondylitis." Current rheumatology reports 24.12 (2022): 398-410.
3. Perrotta, Fabio Massimo, et al. "Therapeutic targets for ankylosing spondylitis–recent insights and future prospects." Open Access Rheumatology: Research and Reviews (2022): 57-66.
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