Societe Des Produits Nestle S.a.

Baylor College of Medicine

Pepgen Corporation

Stephen Kirnon

Rajagopal V Sekhar

Eric Freedland

Chih-Ping Liu

Lorelie H Villarete

A method of neutralizing or mitigating a drug-induced mitochondrial dysfunction or impairment for an individual, the method including providing to the individual an effective amount of a composition containing glycine or a functional derivative thereof and N-acetylcysteine or a functional derivative thereof. The drug-induced mitochondrial dysfunction or impairment is from at least one drug consumed by the individual selected from the group consisting of an anticonvulsant; a psychotropic other than an antipsychotic drug; an analgesic/anti-inflammatory drug other than acetaminophen; an antibiotic; an anti-arrhythmic drug; a steroid; a beta-blocker; and an immunization.

Benefits of supplementation with n-acetylcysteine and glycine to improve glutathione levels

Compositions and methods are related to utilizing glycine and N-acetylcysteine for a variety of medical conditions related to reduced levels of glycine, N-acetylcysteine, and/or glutathione, for example, muscle loss such as sarcopenia, HIV infection and other infections, organ damage such as those from diabetes and insulin resistance and diabetic nephropathy, cardiac function and failure such as preventing or improving heart failure, fatty liver, cancer prevention, and other conditions.

The present invention concerns compositions and methods related to utilizing glycine and N-acetylcysteine for a variety of medical conditions (e.g., muscle loss such as sarcopenia, HIV infection and others, organ damage such as those from diabetes and insulin resistance and diabetic nephropathy, cardiac function and failure such as preventing or improving heart failure, fatty liver, cancer prevention, and others) related to reduced levels of glycine, N-acetylcysteine, and/or glutathione.

Benefits of supplementation with N-acetylcysteine and glycine to improve glutathione levels

A method for treating an IL-10 deficiency in a human subject is described, where a person having an IL-10 deficiency is identified and treated with interferon-tau (IFN&#x3c4;) at a dose sufficient to increase the IL-10 level.

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San Ramon, CA, United States of America

Stephen Kirnon