摘要:
The subject invention provides materials and methods for inhibiting the biofouling of surfaces exposed to aquatic environments. In one embodiment, the subject invention provides additives for marine paints and surface treatments. The subject invention further provides repellents and selective inhibitors for aquatic and/or terrestrial crustacean pests.
摘要:
Embodiments of the present disclosure provide for compounds such as those shown in FIG. 1.1 (compounds A, B, C, and D), 2′substituted nicotine compounds, azetidine compounds, ether linked nicotine compounds (FIG. 1.2, compounds E, F, G, and H), methods of synthesis of the compounds, methods of treatment of a condition using compounds A, B, C, D, 2′substituted nicotine compounds, azetidine compounds, or ether linked nicotine compounds, methods of selectively stimulating alpha7 nAChR and/or alpha4beta2 receptors, and the like.
摘要:
The subject invention pertains to controlled-release dosage forms of anabaseine compounds, such as 3-(2,4-dimethoxybenzylidene)-anabaseine (also known as DMXBA or GTS-21) or a pharmaceutically acceptable salt thereof, methods of use, and methods for producing controlled-release dosage forms.
摘要:
The invention relates to the design and synthesis of 3-arylidene-anabaseine compounds that exhibit enhanced selectivity toward alpha7 nicotinic receptors. The compounds are expected to be useful in treating a wide variety of conditions, including neurodegenerative conditions such as Alzheimer's Disease, neurodevelopmental diseases such as schizophrenia, and certain peripherally located inflammations mediated by macrophage infiltration.
摘要:
The invention relates to the design and synthesis of 3-arylidene-anabaseine compounds that exhibit enhanced selectivity toward alpha7 nicotinic receptors. The compounds are expected to be useful in treating a wide variety of conditions, including neurodegenerative conditions such as Alzheimer's Disease, neurodevelopmental diseases such as schizophrenia, and certain peripherally located inflammations mediated by macrophage infiltration.