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U.S. Food and Drug Administration (FDA) provides feedback necessary to proceed into a phase 2 proof of concept (PoC)/dose ranging study of cudetaxestat in patients with idiopathic pulmonary fibrosis (IPF)
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Company plans to advance cudetaxestat, a non-competitive inhibitor of autotaxin, into a 26-week phase 2 clinical trial in the second quarter of 2022
Blade Therapeutics, Inc. (“Blade” or “Company”), a biopharmaceutical company focused on developing cutting-edge treatments for debilitating fibrotic and neurodegenerative diseases, announced receipt of feedback from the FDA regarding the company’s end-of-phase 1 data package for cudetaxestat, an investigational non-competitive autotaxin inhibitor in clinical development for treatment of IPF and other fibrotic diseases. The FDA response letter outlined requirements for a proposed phase 2 PoC/dose ranging study for use of cudetaxestat in patients with IPF. Based on the FDA feedback, Blade plans to advance cudetaxestat into a 26-week global phase 2 trial in patients with IPF in the second quarter of 2022, pending completion of preclinical toxicology studies.
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Blade Therapeutics announces receipt of FDA feedback on company’s end-of-phase 1 data package for cudetaxestat. Blade plans to advance cudetaxestat into 26wk global phase 2 trial in IPF in 2Q-2022, pending completion of preclinical toxicology studies
“We are pleased with the guidance provided by the FDA,” said Wendye Robbins, M.D., president and CEO of Blade. “Taking a stepwise approach through multiple phase 1 trials provided significant new knowledge and confidence in the safety profile of cudetaxestat. We are now ready to advance cudetaxestat into a phase 2 clinical study that reflects the clinical treatment needs of patients with IPF.”
The randomized, double-blinded, placebo-controlled phase 2 trial will evaluate the safety and efficacy of cudetaxestat (250mg once daily, 500mg once daily, and 500mg twice daily) dosed as monotherapy or co-administered with an approved IPF therapy (pirfenidone or nintedanib) in patients with IPF. The primary study endpoint is change from baseline to week 26 in forced vital capacity lung volume measured in milliliters (mL) and assessed by clinic spirometry throughout the study duration. A blinded interim analysis will be conducted at 13 weeks after completion of enrollment to assess biomarkers (lysophosphatidic acid target engagement, PRO-C3, and PRO-C6). The study is expected to enroll approximately 200 patients across approximately 90 sites in the United States, Europe, and Asia-Pacific.
Cudetaxestat
Cudetaxestat (BLD-0409), a non-competitive, reversible inhibitor of autotaxin, has demonstrated direct anti-fibrotic activity and differentiating preclinical and biochemical characteristics which support the potential for a treatment profile in lung and liver fibrosis. Available data from completed phase 1 studies in healthy volunteers showed that cudetaxestat was well tolerated with a demonstrated pharmacokinetic/pharmacodynamic correlation and biomarker activity. Cudetaxestat has been granted orphan drug designations in the treatment of IPF and systemic sclerosis. Cudetaxestat is an investigational medicine that is not approved for commercial use by the FDA or any other regulatory authority.
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Autotaxin
Pro-fibrotic processes are stimulated by autotaxin, a key enzyme responsible for generating the potent signaling lipid lysophosphatidic acid (LPA). Excessive autotaxin levels and activity play a central role in various fibrotic diseases and occur in response to epithelial cell/tissue damage, leading to elevated levels of LPA. LPA binds to LPA receptors on myofibroblasts, thereby triggering a signaling cascade that leads to myofibroblast activation/differentiation. Activated myofibroblasts produce extracellular matrix proteins that make up the fibrotic lesion (organ/tissue scarring). Increased autotaxin levels and activity are associated with liver, lung, kidney, and skin fibrosis. In addition, autotaxin levels correlate with fibrosis severity in various liver diseases (e.g., nonalcoholic fatty liver disease/nonalcoholic steatohepatitis (NASH)). Inhibition of the autotaxin pathway has been clinically validated in IPF.
Fibrosis
Fibrosis is a complex, pathologic process involving the development of organ/tissue scarring characterized by deposition of extracellular matrix proteins that develop in response to aberrant cell/tissue damage. Excessive fibrosis disrupts normal architecture and function of organs/tissues. Later-stage fibrotic disease is marked by poor outcomes and high morbidity and mortality. Diseases characterized by uncontrolled, progressive fibrosis include IPF, interstitial lung disease, and NASH. New well-tolerated therapies that provide robust attenuation of disease progression are needed to address the high burden of fibrotic diseases.
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