• Non-clinical studies explored the potent anti-fibrotic and anti-inflammatory efficacy of BBT-301 and BBT-209 for IPF treatment
• Company enhances its strategic focus on fibrotic diseases inclusive of IPF with 1 clinical asset and 2 non-clinical assets

BOSTON and SEONGNAM, South Korea, Sept. 2, 2022 /PRNewswire/ -- Bridge Biotherapeutics (KQ288330), a South Korean clinical-stage biotechnology company focused on developing novel drugs for cancer, fibrosis and inflammation, presented the non-clinical study results of 'BBT-301', a novel, small molecular inhibitor of KCa 3.1, and 'BBT-209', an endogenous GPCR19 agonist, both being developed as novel IPF treatments, at the 6^th Annual IPF Summit (August 29 - September 1, 2022), in Boston, MA.

During the poster presentation titled "BBT-301: a potent KCa3.1 modulator in development to treat idiopathic pulmonary fibrosis", the company highlighted the potent anti-fibrotic efficacy of BBT-301, observed through cell-based biochemistry assays and animal model studies. BBT-301 inhibits KCa 3.1, a calcium-activated potassium channel at an IC50 (inhibitory concentration 50%) of 6nM, which suggests a competitive channel inhibitory efficacy in the same class of candidates.

BBT-301 also improved pulmonary function, and attenuated Ashcroft and collagen deposition in bleomycin (BLM)-induced animal model. According to the in-vivo data exhibited at the poster presentation, BBT-301 inhibited the expression of collagen in a dose-dependent manner. In terms of forced vital capacity (FVC) and pressure-volume curve, BBT-301 has also shown comparable potency in lung function recovery compared to the current standard of care (SoC).

In addition to BBT-301, the company unveiled non-clinical data of BBT-209, under the title of "BBT-209: endogenous GPCR19 agonist attenuates animal model of idiopathic pulmonary fibrosis". According to the poster presentation, BBT-209 has exhibited competitive inhibitory effects against cytokine expressions such as IL-1β and TNF-α, with EC50 (effective concentration of 50%) of 0.031 and 0.36 μM each. Through the cell-based biochemistry assay and the BLM mouse model, BBT-209 also exhibited a strong anti-inflammatory effect reaching over 80%, and inhibitory efficacy of α-SMA (α-smooth muscle actin) expression, which is suggestive of combination therapies with the current standard of care and novel IPF treatments with strong anti-fibrotic drugs such as BBT-877, which is being developed as a potent best-in-class autotaxin inhibitor.

"We are excited to present the non-clinical data of BBT-301 and BBT-209, our new assets being developed for the treatment of IPF," said James Lee, founder and CEO of Bridge Biotherapeutics. "In addition to our commitment to develop novel treatment options with therapeutic benefits, we will continue to enhance our pipeline to address the significant unmet needs in IPF, a serious disease caused by various factors."

Posters presented at the conference is available at: https://bit.ly/3CPAxmS. 

About Bridge Biotherapeutics, Inc.

Bridge Biotherapeutics Inc., based in the Republic of Korea, US, and China, 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 ulcerative colitis, fibrotic diseases, and cancers. The company is developing BBT-401, a first-in-class Pellino-1 inhibitor for the treatment of ulcerative colitis, BBT-877, a novel autotaxin inhibitor for the treatment of fibrotic diseases including idiopathic pulmonary fibrosis (IPF), and BBT-176, a potent targeted cancer therapy for non-small cell lung cancer (NSCLC) with C797S triple EGFR mutations.