OUR PIPELINE
Medicines that reach the source of immune-mediated diseases
We develop powerful and precisely-designed therapeutics that have the potential to transform the treatment of immune-mediated diseases — and improve the lives of people suffering from them.
Our lead asset is solrikitug, a highly potent monoclonal antibody targeting thymic stromal lymphopoietin (TSLP), which was in-licensed from Merck & Co., Inc. (known as MSD outside of the U.S. and Canada). Solrikitug has the potential to be a life-changing medication for a significant group of patients who currently have minimal treatment options.
Solrikitug Program
Indication
Preclinical
Phase I
Phase II
Phase III
Approval
COPD
Asthma
EoE
Bispecific Program
Indication
Preclinical
Phase I
Phase II
Phase III
Approval
Undisclosed
Solrikitug-Based Bispecific 1
Undisclosed
Solrikitug-Based Bispecific 2
Given TSLP's position as the "master switch" cytokine sitting at the top of the inflammatory cascade, solrikitug could have potential utility in a wide array of immunology and inflammation programs. Our research suggests that the ceiling of efficacy for the TSLP class has not yet been reached in existing therapeutics, and we aim to deliver best-in-class efficacy across multiple respiratory and gastrointestinal (GI) indications through appropriate dose optimization.
Solrikitug is undergoing Phase 2 clinical trials in chronic obstructive pulmonary disease (COPD), asthma and EoE (NCT06496620, NCT06496607, and NCT06598462, respectively). Patients interested in participating in the EoE clinical trial can learn more at www.alamerestudy.com. We have already established a robust manufacturing process to optimize development and enable rapid progression into late-stage development.
expressed in response to allergens, infection, and/or cell damage
Epithelium
Barrier Impairment
Epithelial Mesenchymal Transition
Mucus Production
TSLP IS AN UPSTREAM MEDIATOR OF INFLAMMATION
Airway Mucosa
TH17 T Cell
ILC2
triggering downstream inflammation including expression of type 2 cytokines
Activated Eosinophil
Neutrophil
Elastase
TSLP ACTIVATES INNATE IMMUNE CELLS
Dendritic Cell
Naïve T Cell
B Cell
IgE
TH2 T Cell
Fibrosis
TSLP-induced inflammation may also contribute to fibrosis and tissue remodeling
TYPE 2 CYTOKINES CONTRIBUTE TO LOCAL INFLAMMATION AND TISSUE DAMAGE
Fibroblast
Hyperresponsiveness
Tissue Remodeling
Smooth
Muscle
Leukotrienes
Mast Cell
About COPD
COPD is a common and long-term lung condition that often results in restricted or blocked airflow, chronic cough and breathing problems due to significant lung damage. COPD encompasses a group of diseases, including emphysema and chronic bronchitis, and is a progressive disease that gets worse over time. There are currently no biologics approved for COPD, which affects 400 million people worldwide and 16 million in the United States. It’s the third-leading cause of death around the world and a major cause of disability.
About Asthma
Asthma is a chronic disease that causes inflammation in the airways, making it harder to breathe. It’s estimated to affect more than 260 million people across the globe and over 27 million people in the United States, including 4.5 million children. While it ranges in severity, symptoms include breathlessness, chest tightness, wheezing and coughing. An estimated 5-10% of people with asthma in the U.S. have severe asthma, which means their asthma remains uncontrolled despite high medicine doses (typically inhaled corticosteroids along with a second controller medication). This patient population continues to have significant unmet needs despite the variety of therapeutics available for asthma.
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About EoE
Eosinophilic esophagitis (EoE) is a condition of chronic inflammation in the esophagus, which is triggered by an allergic immune response. The condition can lead to symptoms such as chest pain, difficulty swallowing and eating, vomiting and abdominal pain. Previously considered a rare disease, EoE is increasing in incidence and affects more than 150,000 people in the United States. Treatment options remain extremely limited for this disease which may progress to esophageal fibrosis and strictures.
We are actively expanding our immunology and inflammation pipeline, with a laser focus on therapeutics for indications with limited or no available treatments.
