Advantage and Core Benefit
- Novel therapeutic concept focusing on the expression mechanism of Meflin molecules that inhibit cardiac fibrosis
- Compound X has been shown to improve diastolic dysfunction in animal models of HFpEF
- New drug development for inducers of anti-fibrotic factors as well as repositioning.
Background and Technology
Chronic heart failure includes HFrEF, which is left ventricular systolic failure, and HFpEF, which is mainly diastolic failure with preserved left ventricular ejection fraction, and the number of patients with these conditions is reported to be almost equal. Four drugs have been developed for the treatment of heart failure: β-blockers, MRAs, ANRIs and SGLT2 inhibitors, and some SGLT2 inhibitors have been reported to improve prognosis in HFpEF. However, these effects are also limited, and no drug therapies have been developed based on a detailed understanding of the pathogenesis of HFpEF.
The inventors have previously reported that Meflin expression has an inhibitory effect on cardiac fibrosis. Loss of Meflin promotes differentiation of normal cardiac fibroblasts into myofibroblasts, and Meflin-deficient mice develop HFpEF-like heart failure. A drug screen to induce Meflin expression resulted in several compounds. Furthermore, when the effects were tested in a recently published mouse model of HFpEF, a significant improvement in left ventricular diastolic capacity was observed with compound X. The invention is expected to expand the application of Compound X and similar compounds to HFpEF and to develop new HFpEF therapeutics targeting the cardiac fibrotic mechanism.
Data
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Patent
JP 2022-073966 (Pending unpublished)
Researcher
Dr. Katsuhiro Kato and Atsushi Enomoto (Nagoya University)
Expectations
We look forward to collaborating with companies interested in developing HFpEF therapeutics based on our knowledge of Compound X and related compounds. Detailed information on the compounds is available for disclosure under the CDA.
Project No: WL-04170