The present invention relates to use of an aminomethylenecyclohexane-1,3-dione compound, more particularly to use of a compound shown in the following formula (I) or a pharmaceutically acceptable salt thereof alone or in combination with other drug in preparing a drug for regulating or treating a disease related to autophagy, especially mammalian ATG8 homologous proteins. ##STR00001##

Disclosed herein are methods for treating juvenile onset neurological conditions, such as autism (ASD), intellectual disability, or epilepsy, with an inhibitor of N-methyl-D-aspartate receptor (NMDAR). The inhibitor may be NitroSynapsin or a derivative thereof.

Gastric residence systems for administration of agents, such as drugs, are disclosed. Features which enhance gastric retention during the desired residence time and which allow for more precise control over residence time are disclosed, including circumferential filaments connecting the arms of a stellate gastric residence system; flexible arms for a gastric residence system; improved time-dependent and enteric disintegrating matrices (linkers); and release rate-modulating polymer coatings which are resistant to change in release rate properties during heat-assisted assembly or thermal cycling. Combinations of these features are also disclosed.

Gastric residence systems for administration of agents, such as drugs, are disclosed. Features which enhance gastric retention during the desired residence time and which allow for more precise control over residence time are disclosed, including circumferential filaments connecting the arms of a stellate gastric residence system; flexible arms for a gastric residence system; improved time-dependent and enteric disintegrating matrices (linkers); and release rate-modulating polymer coatings which are resistant to change in release rate properties during heat-assisted assembly or thermal cycling. Combinations of these features are also disclosed.

Gastric residence systems for administration of agents, such as drugs, are disclosed. Features which enhance gastric retention during the desired residence time and which allow for more precise control over residence time are disclosed, including circumferential filaments connecting the arms of a stellate gastric residence system; flexible arms for a gastric residence system; improved time-dependent and enteric disintegrating matrices (linkers); and release rate-modulating polymer coatings which are resistant to change in release rate properties during heat-assisted assembly or thermal cycling. Combinations of these features are also disclosed.

Methods of preventing or treating elevated pulmonary vascular pressure or exercise-induced pulmonary hemorrhage in mammals are provided, the methods comprise administering compositions comprising type V phosphodiesterase inhibitors and an organic base (e.g., meglumine) to the mammal. Compositions, kits and methods of making type V phosphodiesterase inhibitor are also provided. In one embodiment, the composition comprises E-4021, which is sodium 1-[6-chloro-4-(3,4-methylenedioxybenzyl)-aminoquinazolin-2-yl]piperidine-4-carboxylate sesquihydrate and meglumine.

Methods of preventing or treating elevated pulmonary vascular pressure or exercise-induced pulmonary hemorrhage in mammals are provided, the methods comprise administering compositions comprising type V phosphodiesterase inhibitors and an organic base (e.g., meglumine) to the mammal. Compositions, kits and methods of making type V phosphodiesterase inhibitor are also provided. In one embodiment, the composition comprises E-4021, which is sodium 1-[6-chloro-4-(3,4-methylenedioxybenzyl)-aminoquinazolin-2-yl]piperidine-4-carboxylate sesquihydrate and meglumine.

The present invention relates generally to methods and materials for treating synaptopathies, based on the use of Leu-co-methylthioninium acid salts, which are disclosed herein to increase synaptophysin levels in various brain regions at therapeutically relevant doses both in animal models of neurodegenerative disease, and in normal animals.

The present invention relates generally to methods and materials for treating synaptopathies, based on the use of Leu-co-methylthioninium acid salts, which are disclosed herein to increase synaptophysin levels in various brain regions at therapeutically relevant doses both in animal models of neurodegenerative disease, and in normal animals.

The present disclosure is directed to the treatment of Alzheimer's disease by administering 1′,3′-dihydro-2H-spiro[imidazo[1,2α]pyridine-3,2′-inden]-2-one orally at a daily dose of 180 mg as a single active agent or co-administered with donepezil hydrochloride and/or memantine hydrochloride.