Blade Therapeutics Expands Anti-Fibrotic Pipeline With Acquisition of ATXCo and Its Autotaxin Inhibitor (PAT-409)

Link to full release from Blade

Blade Therapeutics, a biopharmaceutical company advancing novel anti-fibrotic therapies, today announced the acquisition of ATXCo, Inc., including its core asset, PAT-409, a Phase I ready autotaxin inhibitor for patients with fibrotic diseases.

“With the addition of this IND enabled program to our pipeline, we advance our agenda to bring innovative treatments to patients with fibrotic disorders,” stated Wendye Robbins, M.D., Blade’s President and Chief Executive Officer. “Autotaxin inhibition offers a distinct but complementary anti-fibrotic mechanism to our lead program, BLD-2660, a calpain inhibitor. We believe our two anti-fibrosis programs will each succeed as standalone therapies and potentially serve as elements for combination treatment.”

PAT-409 inhibits all the autotaxin isoforms, which are the enzymes responsible for generating most extracellular lysophosphatidic acid (LPA), and thereby attenuates the fibrosis process. In addition, PAT-409 reveals key gene expression differences relative to other clinical autotaxin inhibitors that we expect to drive a differentiated profile for this drug. The autotaxin/LPA receptor pathway has been clinically validated in patients with idiopathic pulmonary fibrosis. In multiple preclinical models, and across various tissues and organs, PAT-409 demonstrated robust ability to reduce tissue damage and fibrosis.

“As ATXCo evaluated opportunities for PAT-409, it became clear that Blade’s commitment to patients with fibrosis and best-in-class team provide an excellent vehicle for its future development,” said Robert Williamson, ATXCo’s President and Chief Executive Officer.

“With the addition of PAT-409, Blade anticipates having three active clinical programs in the near-term, including two orthogonal approaches aimed at fibrosis,” added Dr. Felix Karim, Blade’s Executive Vice President of Business Development. “We look forward to generating both single agent and combination data in a variety of disease settings.”

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