Abstract: The present invention is a mitochondria-targeted antioxidant prodrug useful for the prevention or treatment of diseases or conditions associated with mitochondrial dysfunction resulting from changes in the mitochondrial redox environment. Antioxidant prodrugs of the invention are produced by modifying an antioxidant to a fatty acid so that the resulting prodrug is targeted to and activated by an enzyme of mitochondrial fatty acid beta-oxidation.

Abstract: The present invention is a mitochondria-targeted antioxidant prodrug useful for the prevention or treatment of diseases or conditions associated with mitochondrial dysfunction resulting from changes in the mitochondrial redox environment. Antioxidant prodrugs of the invention are produced by modifying an antioxidant to a fatty acid so that the resulting prodrug is targeted to and activated by an enzyme of mitochondrial fatty acid beta-oxidation.

Abstract: Methylecgonidine (MEG; anhydroecgonine methylester), is produced when cocaine base ("crack") is heated. MEG alone and in combination with cocaine was tested for action on isolated tracheal rings stimulated to contact with acetylcholine. At micromolar concentrations, cocaine sensitized tracheal rings, increasing both the potency and efficacy of acetylcholine-induced contraction. Surprisingly, MEG, at nanomolar concentrations and above, non-competitively and irreversibly antagonized acetylcholine-induced contraction independently of the actions of cocaine. MEG also displayed antihistaminic activity. Therefore, MEG and anticholinergically active derivatives or analogues thereof are useful in the prevention or treatment of a disease or disorder treatable by an antimuscarinic anticholinergic agent, an anti-histaminic agent or a spasmolytic agent, in particular bronchoconstriction in a number of pulmonary diseases such as asthma.

Abstract: Methylecgonidine (MEG; anhydroecgonine methylester), is produced when cocaine base ("crack") is heated. MEG alone and in combination with cocaine was tested for action on isolated tracheal rings stimulated to contact with acetylcholine. At micromolar concentrations, cocaine sensitized tracheal rings, increasing both the potency and efficacy of acetylcholine-induced contraction. Surprisingly, MEG, at nanomolar concentrations and above, non-competitively and irreversibly antagonized acetylcholine-induced contraction independently of the actions of cocaine. MEG also displayed antihistaminic activity. Therefore, MEG and anticholinergically active derivatives or analogues thereof are useful in the prevention or treatment of a disease or disorder treatable by an antimuscarinic anticholinergic agent, an anti-histaminic agent or a spasmolytic agent, in particular bronchoconstriction in a number of pulmonary diseases such as asthma.