SEONGNAM, South Korea, July 30, 2024 /PRNewswire/ -- Bridge Biotherapeutics (KQ288330), a clinical-stage biotech company based in South Korea developing novel drugs for fibrosis and cancer, today announced that patient participant enrollment has been completed in the Phase 2 clinical study of BBT-877, a novel autotoxin (ATX) inhibitor for the treatment of idiopathic pulmonary fibrosis (IPF).

The Phase 2, multi-center, randomized, double-blind, placebo-controlled study (NCT05483907) aims to evaluate the efficacy, safety, and tolerability of BBT-877 in patients with IPF, with or without anti-fibrotic (AF) approved background therapies (pirfenidone or nintedanib). The primary objective is the evaluation of the efficacy of BBT-877 in IPF patients by measuring the reduction in forced vital capacity (FVC) in patients treated with BBT-877 compared to those treated with a placebo at week 24 of treatment. Secondary objectives of the study include the evaluation of drug safety, pharmacokinetics (PK), diffusing capacity of lung for carbon monoxide (DLCO), and functional exercise capacity in all patients.

A total of 120 patient participants were enrolled from approximately 50 clinical trial sites located in the U.S., South Korea, Australia, Poland, and Israel, representing diversity of ethnicity and race. Patients were randomized to either the experimental drug arm or the placebo arm, following a 200mg, twice daily (BID) regimen of BBT-877 or a placebo.

James Lee, founder and CEO of Bridge Biotherapeutics, said: "The completion of enrollment in the phase 2a clinical study of BBT-877 marks an important milestone in our efforts to develop innovative treatments for patients suffering from IPF. Closely looking for business alliance opportunities in the global pharmaceutical industry, we will remain dedicated to advancing this novel drug candidate, which we believe has the potential to make clinically meaningful outcomes in IPF patients."

The Company expects topline data from this study to be announced in the first half of 2025. In parallel with advancing the study, the company pursues a global partnership to prepare for the next phase of the study to further validate the efficacy and safety of BBT-877 in a larger number of patients around the world.

BBT-877, an experimental Autotaxin (ATX) inhibitor, demonstrated its ability to inhibit lysophosphatidic acid (LPA) production by up to 90 percent in the first-in-human study. LPA is known to bind to cell receptors and induce various physiological activities, such as neovascularization, sclerosis, tumorigenesis, and tumor metastasis, leading to the development of various fibrotic diseases, including IPF. The National Institutes of Health (NIH) in the U.S. estimates that more than 30,000 new cases of IPF are diagnosed in the U.S. alone each year, and as many as 3 million patients are affected worldwide.

About Bridge Biotherapeutics, Inc.

Bridge Biotherapeutics Inc., based in the Republic of Korea and the U.S., is a publicly traded, clinical-stage biotech company founded in 2015. Bridge Biotherapeutics is engaged in the discovery and development of novel therapeutics, focusing on therapeutic areas with high unmet needs, including fibrotic diseases and cancers. The company is developing BBT-877, a novel autotaxin inhibitor for the treatment of fibrotic diseases including idiopathic pulmonary fibrosis (IPF), and BBT-207, a potent targeted cancer therapy for non-small cell lung cancer (NSCLC) with EGFR C797S mutations. Learn more at https://www.bridgebiorx.com/en/.

About BBT-877

BBT-877 is an orally administered autotaxin enzyme inhibitor which is under development as a treatment for idiopathic pulmonary fibrosis (IPF). During the Phase 1 Clinical Study, the experimental autotaxin inhibitor demonstrated lysophosphatidic acid (LPA) inhibition of up to 90 percent in multiple-ascending dose cohorts. The topline data of the Phase 2a Clinical Study are expected to be announced in the first half of 2025.

About Autotaxin

Autotaxin (ATX), a protein of approximately 900 amino acids discovered in the early 1990s, is an important enzyme for generating the lipid-signaling molecule, lysophosphatidic acid (LPA). Autotaxin's lysophospholipase D activity converts lysophosphatidylcholine (LPC) into LPA, which engages in signaling via LPA receptors. LPA signaling results in cell proliferation, migration, secretion of cytokines and chemokines, and reduction of cell apoptosis. Ultimately, autotaxin has a pathogenic role in processes of inflammation and fibrosis, making it an attractive drug target.

About idiopathic pulmonary fibrosis (IPF)

IPF is a rare, debilitating, and fatal lung disease that affects approximately 3 million people worldwide. The progression of IPF is variable and unpredictable. Over time, the lung function of an IPF patient gradually and irreversibly declines.