Our Pipeline
We leverage our LYTAC platform to efficiently generate and optimize degrader programs tailored to the biology of each target and disease. Our initial focus is on autoimmune, inflammatory and allergic diseases that are characterized by large patient populations, significant unmet need and well-validated disease biology that support clear applications for our LYTAC technology.
| Target | Program | Indication(s) | Drug Discovery | IND Enabling | Phase 1 | Phase 2 | Phase 3 |
|---|---|---|---|---|---|---|---|
| lgE | LCA-0061 | Food Allergy and Other Allergic Diseases | |||||
| lgE | LCA-0062 | Food Allergy and Other Allergic Diseases | |||||
| TRAbs | LCA-0321 | Graves' Disease | |||||
| lgE | ||||
|---|---|---|---|---|
| Drug Discovery | IND Enabling | Phase 1 | Phase 2 | Phase 3 |
Program: LCA-0061 Indication(s): Food Allergy and Other Allergic Diseases | ||||
| lgE | ||||
| Drug Discovery | IND Enabling | Phase 1 | Phase 2 | Phase 3 |
Program: LCA-0062 Indication(s): Food Allergy and Other Allergic Diseases | ||||
| TRAbs | ||||
| Drug Discovery | IND Enabling | Phase 1 | Phase 2 | Phase 3 |
Program: LCA-0321 Indication(s): Graves' Disease | ||||
CataLYTAC Degrader Classic LYTAC Degrader
IgE = immunoglobulin E; TRAbs = thyroid-stimulating hormone receptor (TSHR) autoantibodies; IND = Investigational New Drug
Our IgE Portfolio: LCA-0061 and LCA-0062
We are advancing a portfolio of IgE-targeted cataLYTAC degraders to evaluate complementary approaches to achieving deep and durable elimination of IgE, a clinically validated driver of multiple allergic diseases, including food allergy, allergic asthma, allergic rhinitis, chronic spontaneous urticaria and chronic rhinosinusitis with nasal polyps. IgE-mediated food allergy alone affects more than 33 million people in the United States. We believe targeted elimination of IgE, rather than inhibition, has the potential to provide deeper and more sustained control of allergic disease biology.
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LCA-0061 is an antibody–small molecule conjugate cataLYTAC degrader designed to eliminate the IgE pool by targeting extracellular IgE for lysosomal degradation. LCA-0061 is designed to bind both IgE and an internalizing receptor and to shuttle IgE into the cell for degradation. As a cataLYTAC degrader, LCA-0061 has the potential to cycle in and out of the cell repeatedly to bind and eliminate multiple IgE molecules per LYTAC degrader. This unique mechanism can enable the deep and durable depletion of IgE, which we believe could support use in patients with high baseline IgE levels. We are conducting a Phase 1 clinical trial of LCA-0061 in participants with elevated IgE, including participants with food allergy.
In preclinical studies, LCA-0061 produced deep and durable depletion of circulating IgE, lowering total IgE and sustaining that effect well beyond that anticipated for an established IgE inhibitor. In head-to-head preclinical studies against approved and investigational IgE blockers, LCA-0061 achieved greater depth and duration of IgE reduction, and more effectively suppressed functional markers of the allergic response. These findings support our belief that eliminating IgE, rather than blocking it, can deliver deeper and more durable control of allergic disease, including in patients with high circulating IgE.
LCA-0062 is a fast-follower bispecific antibody cataLYTAC degrader designed to target and degrade IgE. Like LCA-0061, it is designed to degrade multiple copies of IgE per LYTAC degrader and has the potential to offer additional flexibility in dosing and duration of response. We are currently conducting IND-enabling activities of LCA-0062.
We believe developing a portfolio of IgE-targeted degraders can provide multiple avenues to address clinical unmet needs and enhance commercial potential across allergic diseases.
Our Graves’ Disease Program: LCA-0321
LCA-0321 is a classic LYTAC degrader designed with an aim to selectively and rapidly degrade disease-driving thyroid-stimulating hormone receptor autoantibodies (also known as thyrotropin receptor antibodies or TRAbs), directly targeting the root cause of Graves’ disease. Based on the immunopathogenesis of Graves’ disease, selective depletion of TRAbs may restore normal thyroid hormone levels and represents a novel therapeutic approach for the treatment of Graves’ disease.
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Current treatment options for Graves’ disease primarily focus on managing symptoms rather than addressing the underlying autoimmune pathology. Treatment with LCA-0321 may provide a more targeted, effective and non-immunosuppressive approach for patients relative to current therapies and investigational agents.
Preclinical data in mice showed that a single dose of LCA-0321 resulted in the rapid and deep depletion of exogenously administered monoclonal TRAbs identified from patients with Graves’ disease, and normalized thyroxine (T4) levels in a mouse model of Graves’ disease. We are currently conducting a Phase 1 clinical trial of LCA-0321 in patients with Graves’ disease.
Preclinical Programs
Our platform is designed to efficiently generate high-quality therapeutic candidates across multiple disease areas. We have multiple preclinical programs focused on developing cataLYTAC degraders to durably deplete specific drivers of autoimmune, inflammatory and allergic diseases, prioritizing targets with strong biological rationale and clear unmet need.
