Abstract: The present invention provides novel cell-permeable succinates and cell permeable precursors of succinate aimed at increasing ATP-production in mitochondria. The main part of ATP produced and utilized in the eukaryotic cell originates from mitochondrial oxidative phosphorylation, a process to which high-energy electrons are provided by the Kreb's cycle. Not all Kreb's cycle intermediates are readily permeable to the cellular membrane, one of them being succinate. The provision of the novel cell permeable succinates is envisaged to allow passage over the cellular membrane and thus the cell permeable succinates can be used to enhance mitochondrial ATP-output.

Abstract: The present invention provides a novel isolated succinate prodrug as the free compound or a salt, hydrate, solvate or complex thereof being cell permeable and aimed for increasing the ATP-production in mitochondria. The compound is useful in the medical treatment of a range of diseases, in nutritional supplements, nutricosmetics and in cosmetics.

Abstract: The present invention provides a novel isolated succinate prodrug as the free compound or a salt, hydrate, solvate or complex thereof being cell permeable and aimed for increasing the ATP-production in mitochondria. The compound is useful in the medical treatment of a range of diseases, in nutritional supplements, nutricosmetics and in cosmetics.

Abstract: The present invention provides a novel isolated succinate prodrug as the free com-pound or a salt, hydrate, solvate or complex thereof being cell permeable and aimed for increasing the ATP-production in mitochondria. The compound is useful in the medical treatment of a range of diseases, in nutritional supplements, nutricosmetics and in cosmetics.

Abstract: The present invention provides a novel isolated succinate prodrug as the free com-pound or a salt, hydrate, solvate or complex thereof being cell permeable and aimed for increasing the ATP-production in mitochondria. The compound is useful in the medical treatment of a range of diseases, in nutritional supplements, nutricosmetics and in cosmetics.

Abstract: The present invention provides novel cell-permeable succinates and cell permeable precursors of succinate aimed at increasing ATP-production in mitochondria. The main part of ATP produced and utilized in the eukaryotic cell originates from mitochondrial oxidative phosphorylation, a process to which high-energy electrons are provided by the Kreb's cycle. Not all Kreb's cycle intermediates are readily permeable to the cellular membrane, one of them being succinate. The provision of the novel cell permeable succinates is envisaged to allow passage over the cellular membrane and thus the cell permeable succinates can be used to enhance mitochondrial ATP-output.

Abstract: The present invention provides novel cell-permeable succinates and cell permeable precursors of succinateaimed at increasing ATP-production in mitochondria. The main part of ATP produced and utilized in the eukaryotic cell originates from mitochondrial oxidative phosphorylation, a process to which high-energy electrons are provided by the Kreb's cycle. Not all Kreb's cycle intermediates are readily permeable to the cellular membrane, one of them being succinate. The provision of the novel cell permeable succinates is envisaged to allow passage over the cellular membrane and thus the cell permeable succinates can be used to enhance mitochondrial ATP-output.

Abstract: The present invention provides novel liver-targeted prodrugs of mitochondrial proton ionophores. These compounds have utility in medicine including their use in treatment of diseases such as NASH and NAFLD.

Abstract: The present invention relates to a succinate prodrug for use in the treatment or prevention of lactic acidosis.

Abstract: Disclosed herein are mono or di-succinate compounds where one or both of the acid groups in the succinate core are protected in the form of biologically labile moieties, and the use of said compounds to enhance mitochondrial function. The compounds may be of formula (I) wherein R1 is H or an optionally substituted alkyl group or a group of formula (II) and R2 is independently a group according to formula (II) where formula (II) is as defined 10 herein.

Abstract: The present invention provides novel cell-permeable succinates and cell permeable precursors of succinateaimed at increasing ATP-production in mitochondria. The main part of ATP produced and utilized in the eukaryotic cell originates from mitochondrial oxidative phosphorylation, a process to which high-energy electrons are provided by the Kreb's cycle. Not all Kreb's cycle intermediates are readily permeable to the cellular membrane, one of them being succinate. The provision of the novel cell permeable succinates is envisaged to allow passage over the cellular membrane and thus the cell permeable succinates can be used to enhance mitochondrial ATP-output.

Abstract: The present invention provides novel cell-permeable succinates and cell permeable precursors of succinate aimed at increasing ATP-production in mitochondria. The main part of ATP produced and utilized in the eukaryotic cell originates from mitochondrial oxidative phosphorylation, a process to which high-energy electrons are provided by the Kreb's cycle. Not all Kreb's cycle intermediates are readily permeable to the cellular membrane, one of them being succinate. The provision of the novel cell permeable succinates is envisaged to allow passage over the cellular membrane and thus the cell permeable succinates can be used to enhance mitochondrial ATP-output.

Abstract: The present invention relates to a succinate prodrug for use in the treatment or prevention of lactic acidosis.

Abstract: Disclosed herein are mono or di-succinate compounds where one or both of the acid groups in the succinate core are protected in the form of biologically labile moieties, and the use of said compounds to enhance mitochondrial function. The compounds may be of formula (I) wherein R1 is H or an optionally substituted alkyl group or a group of formula (II) and R2 is independently a group according to formula (II) where formula (II) is as defined 10 herein.

Abstract: A novel method useful in drug screening. The method is useful for testing effects of substances on the mitochondria, notably toxic or beneficial effects of drug substances or candidate drug substances. The method is based on measurement in live human mitochondria ex vivo, but in a setting as near the in vivo situation as possible. The method is also useful for testing substances impact on the mitochondrial respiration.

Abstract: The present invention relates to cyclosporine emulsions containing: (i) a cyclosporine, (ii) a natural oil (long chain triglyceride), (iii) a phosphatidylcholine, (iv) glycerol, (v) a pharmaceutically tolerable alkali salt of a free fatty acid, (vi) a medium chain triglyceride-oil, (vii) optionally, hydrochloric acid or sodium hydroxide for pH adjustment and (viii) water, and to therapeutic methods using them.

Abstract: The present invention relates to a cyclosporine emulsion containing: i) a cyclosporine ii) a natural oil (long chain triglyceride) iii) a phosphatidylcholine, iv) glycerol, v) a pharmaceutically tolerable alkali salt of a free fatty acid, vi) a medium chain triglyceride-oil vii) optionally, hydrochloric acid or sodium hydroxide for pH adjustment viii) water.

Abstract: The present invention relates to a cyclosporine emulsion containing: i) a cyclosporine ii) a natural oil (long chain triglyceride) iii) a phosphatidylcholine, iv) glycerol, v) a pharmaceutically tolerable alkali salt of a free fatty acid, vi) a medium chain triglyceride-oil vii) optionally, hydrochloric acid or sodium hydroxide for pH adjustment viii) water.

Abstract: A cyclosporin-containing pharmaceutical preparation for cerebrospinal or vascular application is disclosed, comprising (1) at least one cyclosporin, and (2) DMSO.

Abstract: Method for selectively reducing mammal neuron damage or death in neuroimmunophilin-rich neurons of central, peripheral, and autonomic nervous systems of a mammal while not reducing damage or death to neuroimmunophilin-poor cells and tissues selected from the group consisting of glia, glia-derived tumor cells, abnormal neuron-derived tumor cells, non-brain tumors, and non-neuron tissue of the body from ionizing radiation. The method includes preparing a dosage of a neuroimmunophilin ligand selected from the group consisting of cyclosporins and functional derivatives, metabolites, variants, and salts thereof which are able to cross the blood-brain barrier. The dosage is from an effective amount to less than 1 gr/kg of body weight of said mammal. The method includes the step of administering that dosage to the mammal before, co-incident with, or after ionizing radiation of the mammal. The dose is administered the same day as, but not later than one week after, last radiation exposure.