We are developing a robust pipeline to eliminate pathogenic disease drivers across multiple indications

Graves’ disease is the most common cause of hyperthyroidism. It is driven by pathogenic autoantibodies that bind thyroid-stimulating hormone receptors (TSHR) in the thyroid gland, triggering excess thyroid hormone production and accelerating metabolic activity. These same autoantibodies also lead to Graves’ orbitopathy, or thyroid eye disease (TED), which affects approximately half of patients with Graves’ disease, and can cause ocular inflammation, pain, bulging of the eyes, and double vision.

Standard therapies for Graves’ disease have remained largely unchanged for decades and can be burdensome. Many patients ultimately require radioactive iodine treatment or thyroidectomy to shrink or remove the thyroid, resulting in loss of thyroid function and lifelong hormone replacement.

Merida is developing MER511, a precision biologic designed to selectively eliminate pathogenic autoantibodies and their B-cell sources while preserving normal immune function. By directly targeting the underlying drivers of Graves’ diseases, MER511 aims to directly target the autoantibodies that cause this difficult-to-manage disease, while sparing healthy thyroid signaling.

MER511 is being evaluated in the NEXUS Phase 1 Study for the treatment of Graves’ disease. Learn more about the NEXUS Study at ClinicalTrials.gov (NCT07305818).

For any inquiries on clinical trials at Merida, please contact clinicaltrials@meridabio.com.

In immunoglobin E (IgE)-mediated allergic diseases, the body mounts an exaggerated immune response to harmless allergens, which can lead to a variety of conditions including severe asthma, atopic dermatitis, urticaria and food allergy. In the U.S., IgE-mediated food allergy affects approximately 1 in 10 adults and this inappropriate immune reaction can lead to hives, vomiting or even anaphylaxis.

We are engineering a therapeutic antibody designed to dramatically disrupt treatment of food allergy by specifically neutralizing and eliminating IgE antibodies. Compared to standard of care, our approach has the potential to address higher levels of IgE in patients, with less frequent dosing, reduced toxicity and stronger clinical benefit.

Primary membranous nephropathy (pMN) is a chronic inflammatory kidney disease that is predominantly (70-80% of patients) caused by autoantibodies that target the phospholipase A2 receptor (PLA2R) on epithelial podocytes and damage or destroy the kidney’s blood filtration system.

Autoantibody levels have been shown to correlate with disease progression, likelihood of remission, response to treatment and risk of end-stage kidney disease. Compared to standard of care, which includes alkylating agents associated with increased cancer risk, or broad immunosuppression, our goal is to rapidly clear and eliminate the pathogenic autoantibodies that underlie this kidney-specific autoimmune disease while preserving essential immunity and preventing significant side effects.