BridgeBio Presents Preclinical Data on Idiopathic Pulmonary Fibrosis at U.S. Conference
[Asia Economy Reporter Chunhee Lee] Bridge Biotherapeutics announced on the 31st that it presented key preclinical data of new IPF drug candidates ‘BBT-301’ and ‘BBT-209’ in poster form on the 30th (local time) at the ‘2022 Idiopathic Pulmonary Fibrosis (IPF) Summit 2022’ held in Boston, USA, from the 29th to the 1st of next month.
The company unveiled for the first time on the international stage preclinical data related to drug efficacy and effects confirmed in cell lines and animal models for two new candidates under development with different mechanisms of action for IPF. IPF is a fatal disease known to cause death in more than 50% of patients within 3 to 5 years without appropriate treatment. Interest in new drug development is increasing due to population aging and aftereffects of COVID-19.
BBT-301 is an IPF drug candidate with a mechanism that selectively regulates the potassium channel (Kca 3.1), an ion channel particularly known to be related to fibrotic diseases. Cell experiments confirmed that the ‘IC50’, the drug concentration required to reduce ion channel activity by half, reached a superior level compared to control drugs with the same mechanism. Additionally, in cell experiments derived from IPF patients, the expression of collagen, used as a pathological marker, was observed to be inhibited in a dose-dependent manner by BBT-301 treatment.
In particular, the anti-fibrotic efficacy of BBT-301 confirmed through cell line experiments was also verified through oral administration in disease-induced animal models. Oral administration of BBT-301 showed dose-dependent effects on improving lung function. In Ashcroft scores, which quantify the severity of pulmonary fibrosis, and collagen deposition, BBT-301 demonstrated efficacy equal to or greater than existing IPF treatments.
BBT-209 is an innovative drug that suppresses fibrotic diseases by activating the receptor ‘G protein-coupled receptor 19 (GPCR19)’, which regulates the occurrence of inflammation. According to preclinical data, treatment with BBT-209 in monocyte-derived macrophages significantly suppressed the expression of inflammatory cytokines, signaling molecules that can promote pulmonary fibrosis. In cell line experiments comparing the suppression of inflammatory cytokine expression, BBT-209 showed broad and excellent efficacy compared to various substances with different inflammation regulation mechanisms.
In disease-induced animal models, BBT-209 showed statistically significant high-level suppression of smooth muscle actin (α-SMA) expression compared to existing treatments, suggesting the possibility of combination therapy with existing standard antifibrotic treatments such as BBT-877. Notably, smooth muscle actin is gaining attention as a pathological marker for tissue fibrosis in fibrotic diseases like IPF. Targeting the upstream pathogenesis of IPF with BBT-209 has raised expectations for the fundamental treatment potential of the disease.
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Jungkyu Lee, CEO of Bridge Biotherapeutics, said, “This conference was meaningful as we were able to disclose preclinical data of BBT-209 and BBT-301, which are being developed with new mechanisms in the IPF field, on the global stage with many major R&D companies and clinicians participating.” He added, “Just as the initial data presentation and business development meetings at the IPF Summit were important milestones during the technology transfer of BBT-877, we will strengthen our R&D pipeline in the idiopathic pulmonary fibrosis sector and strive to accelerate the creation of global business development achievements through the successful presentation of preclinical studies on new projects this year.”
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