Severe autoantibody-mediated autoimmune disease: a new treatment approach

The National Institute of Allergy and Infectious Diseases awarded Astero Erado Inc. $306,449 on August 11, 2026, to develop a novel therapeutic for bullous pemphigoid, an autoimmune disease characterized by severe blistering at the dermal-epidermal junction. The award funds work under the Allergy and Infectious Diseases Research program (CFDA 93.855).

Astero Erado is developing an engineered antibody-based therapeutic called SELDEG designed to selectively target and deplete pathogenic autoantibodies against BP180 and BP230 implicated in bullous pemphigoid pathogenesis. The approach addresses an unmet clinical need for therapies with rapid onset, deep autoantibody depletion, and minimal immunosuppression, as current treatments using corticosteroids and general immunosuppressants carry severe side effects particularly concerning in elderly patients, who are the primary population affected by the disease.

Work will be performed in Houston, Texas, with a period of performance from August 11, 2026, through July 31, 2028. This is a Phase I Small Business Innovation Research (SBIR) award, a competitive assistance type for domestic small businesses developing novel biomedical innovation. The award is the sole obligated amount; no sub-recipients or pass-through arrangements are identified in the source.

Abstract

The overall goal of this project is to develop a novel therapeutic for the treatment of bullous pemphigoid (BP). BP is characterized by tense, pruritic skin blisters that form at the dermal-epidermal junction, typically on the extremities and trunk. Oral lesions are observed in about 15% of cases. This chronic, severe disease primarily affects the elderly, and is frequently associated with neurological conditions such as parkinson's disease and dementia. The annual incidence of BP in the general population is about 10 per million, but increases to 200-300 per million in people over 80 years of age. Autoantibodies specific for the keratinocyte protein, BP180, are causal agents of disease. Autoantibodies that bind to BP230 have also been implicated in the pathogenesis of BP and are detected in up to 80% of patients. BP is associated with poor quality of life and a significant risk in mortality with, for example, a mortality rate of ~20% during the first year of disease in patients undergoing current treatments. Current treatments for BP typically involve corticosteroids that, in more severe cases, are combined with general immunosuppressants such as mycophenolate mofetil or azathioprine. However, these agents are associated with severe side effects that are of particular concern in the elderly, and frequently frail, patients that BP affects. Other treatment options for patients include plasma exchange, intravenous immunoglobulin (ivig) and b cell depletion (rituximab). These approaches can also lead to undesirable side effects, such as increased risk of infection following rituximab which additionally has a relatively slow onset of action. Consequently, for BP there is an unmet need to develop therapies that have rapid onset, lead to deep depletion of autoantibodies and are not generally immunosuppressive. This application seeks to address the need for new and improved therapies for BP by generating engineered, antibody-based reagents that rapidly induce a deep depletion of BP180- and BP230- specific antibodies. Importantly, these depleting agents are highly selective and do not affect the levels of other antibodies that have a protective role against infection. This first-in-class, novel technology has been named seldeg technology (for selective degradation). The specific aims of the study are: 1. To express seldegs to target BP180- and BP230-specific antibodies. 2. To analyze the stability, binding activity and pharmacokinetics of the seldegs. The proposed approach could be transformative for the management of BP, and also has relevance to the use of seldeg-based strategies for multiple other clinical settings where pathogenic antibodies cause disease.