Blade Therapeutics Announces Successful Completion of Phase 1 Clinical Study that Evaluated Co-Administration of Cudetaxestat with Either of Two Approved Therapies for Idiopathic Pulmonary Fibrosis
- Clinical study found that cudetaxestat, a non-competitive inhibitor of autotaxin, was well tolerated and showed no reports of drug-related serious adverse events or discontinuations when co-administered with either pirfenidone or nintedanib
- Submission of study data to
U.S. Food and Drug Administration(FDA) anticipated in first quarter of 2022
- Blade expects to advance cudetaxestat into phase 2 clinical study in patients with idiopathic pulmonary fibrosis (IPF) in second quarter of 2022
The phase 1 study assessed the effect of cudetaxestat 750mg on the pharmacokinetics of two approved drugs for IPF – pirfenidone and nintedanib – in 83 healthy adult volunteers (NCT04939467). In the study, co-administration of cudetaxestat with either pirfenidone or nintedanib showed that cudetaxestat was well tolerated, with no reports of drug-related serious adverse events or discontinuations due to treatment-emergent adverse events.
Blade expects to submit an end-of-phase 1 data package to the FDA in the first quarter of 2022 prior to planned discussions with regulatory authorities to further inform the clinical development program for cudetaxestat. The company plans to start a phase 2 clinical study of cudetaxestat in patients with IPF in the second quarter of 2022.
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 showed that cudetaxestat was well tolerated with a demonstrated pharmacokinetic/pharmacodynamic correlation and biomarker activity, and a supportive clinical safety profile. 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.
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 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.
About Blade Therapeutics
Blade Therapeutics, Inc. is a biopharmaceutical company focused on developing cutting-edge treatments for debilitating, incurable fibrotic and neurodegenerative diseases that impact millions of people worldwide. The company has deep expertise in novel biological pathways – including autotaxin / LPA and calpain biology – that are foundational to cell- and tissue-damage responses resulting from protein deposition or aggregation associated with fibrotic and neurodegenerative diseases. Blade expects to advance a differentiated pipeline of oral, small-molecule therapies that include a non-competitive autotaxin inhibitor and inhibitors of dimeric calpains designed for potential treatment of lung, liver and cardiac fibrosis or neurodegenerative diseases. The company’s focused approach offers the potential to produce disease-modifying, life-saving therapies. Visit www.blademed.com for more information and follow Blade on LinkedIn.
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