Data from completed Phase 1b study of ELA026 highlights results in patients with the poorest prognosis, those with malignancy-associated HLH
SOUTH SAN FRANCISCO, CA, November 5, 2024 – Electra Therapeutics, Inc., a clinical stage biotechnology company developing antibody therapies against novel targets for immunological diseases and cancer, announced today that clinical data for its lead drug candidate, ELA026, has been selected for presentation in an oral session at the American Society of Hematology (ASH) annual meeting being held in San Diego on December 7-10, 2024.
The oral presentation will describe clinical data from a completed Phase 1b study of ELA026 for the treatment of secondary hemophagocytic lymphohistiocytosis (sHLH), a rare, life-threatening hyperinflammatory disease for which there is no approved treatment. Specifically, data will highlight results from treatment of malignancy-associated HLH (mHLH), the deadliest type of sHLH, in frontline settings. ELA026 is a first-in-class monoclonal antibody that targets signal regulatory protein (SIRP)-α/β1/γ on the cell surface of myeloid cells and T lymphocytes, the pathological immune cells that induce hyperinflammation in sHLH. The Phase 1b study is an open-label, single-arm, multi-center study designed to evaluate the safety and efficacy of ELA026, assess biomarkers, and identify a dose regimen for further evaluation in a Phase 2/3 study (NCT05416307). The abstract is published on the ASH website.
“We are delighted to share the latest results of our clinical study of ELA026 in sHLH with the clinical and research community,” said Kim‑Hien Dao, DO, PhD, Chief Medical Officer of Electra Therapeutics. “As we engage with physicians and researchers familiar with sHLH, we are gratified to hear that ELA026 has the potential to address high unmet needs in patients with sHLH who lack effective treatment options. We hypothesize that the selective depletion of pathogenic immune cells may offer a more definitive approach to address the cytokine storm and improve survival in this highly deadly disease and are very encouraged by the data with ELA026.”
Details of the oral presentation are as follows:
Title: ELA026, a monoclonal antibody targeting signal regulatory protein (SIRP)-α/β1/γ rapidly controls inflammation and improves 2-month survival in treatment-naïve malignancy-associated hemophagocytic lymphohistiocytosis
Presenter: Abhishek Maiti, MD, Assistant Professor, Department of Leukemia, The University of Texas MD Anderson Cancer Center
Session Name: 201. Granulocytes, Monocytes, and Macrophages: From Inflammation to Hemophagocytic Lymphohistiocytosis
Session Date and Time: Monday, December 9, 2024, 2:45 p.m. PT
Location: San Diego Convention Center, Room 6DE
Publication Number: 805
About Secondary Hemophagocytic Lymphohistiocytosis
Secondary hemophagocytic lymphohistiocytosis (sHLH) is a rare, life-threatening hyperinflammatory disease for which there is no approved treatment. It can be triggered by cancer, infection, autoimmune disease, or immunotherapy. sHLH is associated with a severe inflammatory response for which patients require immediate intervention. Without effective treatment, patients may experience multiple organ failure and death. sHLH has a high mortality rate during the first months of diagnosis, with malignancy-associated HLH (mHLH) patients having the poorest outcomes.
About Electra Therapeutics
Electra Therapeutics is a clinical stage biotechnology company developing therapies against novel targets for immunological diseases and cancer. The company’s lead product candidate, ELA026, is a first-in-class monoclonal antibody that targets SIRP on the cell surface of myeloid cells and T lymphocytes, and selectively depletes pathological immune cells. ELA026 is in clinical development for secondary hemophagocytic lymphohistiocytosis (sHLH), a rare, life-threatening hyperinflammatory condition for which there is no approved treatment, as well as additional disease indications. For more information, please visit www.electra-therapeutics.com and follow us on LinkedIn.
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