- BBT-877 demonstrated the best-in-class potential at the preclinical experiments in comparison with competing compounds
- US IND will be submitted by year end
SEONGNAM, South Korea and SAN FRANCISCO, Aug. 23, 2018 /PRNewswire/ — Bridge Biotherapeutics Inc., a clinical stage biotech company headquartered in Seongnam, South Korea, presented the results of the preclinical study on ‘BBT-877’, an investigational drug candidate for IPF (Idiopathic Pulmonary Fibrosis) treatment, at the IPF Summit 2018 held in San Francisco, California.
BBT-877 was discovered by LegoChem Biosciences, publicly traded Korean biotech and licensed to Bridge Biotherapeutics for the worldwide exclusive right for further development. BBT-877 targets Autotaxin (ATX), which has emerged as a promising target for various diseases such as fibrosis and cancers.
GLPG1690, an ATX inhibitor being developed by Galapagos has been approved to proceed to phase 3 clinical trial bypassing phase 2b study in the U.S. after showing promising results of phase 2a performed with 23 IPF patients.
Bridge Biotherapeutics presented the results of BBT-877 preclinical study at the poster session of the IPF Summit 2018, which demonstrated strong efficacy in the bleomycin-induced mouse model. The study indicates that BBT-877 has effectively reduced lung fibrosis as presented by reduction of Ashcroft scores and the deposition of collagen (staining), compared to the other drugs. The data implies a high potential of BBT-877 to be the ‘best-in-class’ drug for IPF treatments.
Bridge Biotherapeutics now plans to submit a US IND of BBT-877 by the end of this year.
"It is a great opportunity for Bridge Biotherapeutics to present the outstanding preclinical study results on BBT-877 at the IPF Summit 2018. Bridge Biotherapeutics aims to develop BBT-877 as the best-in-class drug for IPF as fast as possible to bring this investigational compound to patients as new treatment option," said James Lee, CEO of Bridge Biotherapeutics.
Bridge Biotherapeutics is developing BBT-401, the first anti-Pellino-1 compound in Phase I in US for the treatment of ulcerative colitis and aims to initiate the international multi-site FIP (first-in-patient) study by year end. BBT-401 was discovered by SKKU (Sungkyunkwan University) and KRICT (Korea Research Institute of Chemical Technology) and was licensed the exclusive worldwide right to Bridge Biotherapeutics in 2015.
For more information
1. Bridge Biotherapeutics, Inc.
Bridge Biotherapeutics is a virtually-operated, venture-backed clinical stage Korean biotech engaged in the development of novel therapeutics in the therapeutic areas of high unmet needs such as ulcerative colitis, fibrotic diseases and cancers. It currently licenses novel NCE (New Chemical Entities) or NME (New Molecule Entities) mainly from Korean academics or biotech/pharmas to develop them globally. The company has raised $30m from Korean local VCs from the inception.
Autotaxin (ATX) is a protein of approximately 900 amino acids discovered in the early 1990s, and an enzyme important for generating the lipid signaling molecule, lysophosphatidic acid (LPA). Autotaxin has lysophospholipase D activity that converts lysophosphatidylcholine (LPC) into LPA. LPA, the bioactive lipid catalyzed by Autotaxin, engages in signaling via LPA receptors and the LPA signaling results in cell proliferation, migration, secretion of cytokine and chemokine and reduction of cell apoptosis. Pathologically, Autotaxin has been found to be engaged in inflammation and fibrosis and it emerges as one of attractive drug targets.
3. IPF, Idiopathic Pulmonary Fibrosis
Idiopathic Pulmonary Fibrosis (IPF) is a progressive, irreversible and fatal lung disease. A number of investigational drugs are being developed while only two therapeutics, pirfenidone and nintedanib, were approved by US FDA.
4. IPF Summit 2018
2nd Idiopathic Pulmonary Fibrosis (IPF) Summit organized by Hanson Wade was held from August 20th through the 22nd, 2018 at The Marker San Francisco, San Francisco, California. With the incredible breakthrough success of drugs now in our arsenal for slowing IPF disease progression, the increasing importance of identifying genetic mechanisms, closing the translational gap between preclinical and clinical results, and developing candidates to reverse fibrosis have opened up further challenges within IPF drug development. (http://ipf-summit.com/)