Treating non-alcoholic steatohepatitis with cck inhibitors
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Publication Number
US-12251364-B2
Publication Date
2025-03-18
Expiration Date
Abstract
Provided herein are methods for treating nonalcoholic steatohepatitis (NASH) in a subject, comprising administering to a subject having NASH an effective amount of a CCK receptor inhibitor.
Core Innovation
A method is disclosed for treating nonalcoholic steatohepatitis (NASH) in a subject by administering an effective amount of a cholecystokinin (CCK) receptor inhibitor, where the CCK receptor inhibitor is proglumide. The disclosed approach is based on CCK receptor blockade to decrease liver fibrosis and inflammation in the subject.
The disclosure also describes treating hepatic fibrosis in a subject by administering an effective amount of a CCK receptor inhibitor, where the CCK receptor inhibitor is proglumide. Related fibrosis indications are described alongside the NASH and hepatic fibrosis therapeutic framing.
In a mouse model, administration of proglumide is described as reversing biochemical abnormalities including AST, ALT, bilirubin, and alkaline phosphatase. Histologic NASH features including inflammation, fibrosis, and steatosis/ballooning are described as being reversed, and dysplastic nodules and hepatocellular carcinoma are also described as being prevented in the same context.
Claims Coverage
The document provides two independent methods. Across these independent claims, the core inventive theme is administering an effective amount of a CCK receptor inhibitor, specifically proglumide, to a subject with the relevant condition.
Treating nonalcoholic steatohepatitis with proglumide as a CCK receptor inhibitor
A method for treating nonalcoholic steatohepatitis (NASH) in a subject comprising administering to a subject having NASH an effective amount of a CCK receptor inhibitor, wherein the CCK receptor inhibitor is proglumide.
Treating hepatic fibrosis with proglumide as a CCK receptor inhibitor
A method for treating hepatic fibrosis in a subject comprising administering to a subject having hepatic fibrosis an effective amount of a CCK receptor inhibitor, wherein the CCK receptor inhibitor is proglumide.
Both independent claims cover treatment by administering an effective amount of a CCK receptor inhibitor where the CCK receptor inhibitor is proglumide, one for NASH and the other for hepatic fibrosis. Dependent claims specify decreased liver fibrosis, decreased inflammation, prevention of hepatocellular carcinoma, and co-administration of a second therapeutic agent.
Stated Advantages
Decreases liver fibrosis.
Decreases liver inflammation.
Prevents hepatocellular carcinoma (HCC).
Reverses biochemical abnormalities including AST, ALT, bilirubin, and alkaline phosphatase.
Reverses histologic NASH features including inflammation, fibrosis, and steatosis/ballooning.
Prevents dysplastic nodules and HCC.
Documented Applications
Treating nonalcoholic steatohepatitis (NASH) in a subject by administering proglumide as a CCK receptor inhibitor.
Treating hepatic fibrosis in a subject by administering proglumide as a CCK receptor inhibitor.
Using proglumide in a mouse model to reverse biochemical abnormalities and histologic NASH features and to prevent dysplastic nodules and HCC.
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