Abstract: The invention relates to compounds for reducing or inhibiting a biological function mediated by LIMK1 or LIMK2, wherein the compounds are selected to bind the ATP-binding site and/or the substrate-binding site of LIMK.

Abstract: Disclosed are methods of treating lung cancer by administering to a human in need thereof effective amounts of FTS, or various analogs thereof, or a pharmaceutically acceptable salt thereof, optionally, in combination with a chemotherapeutic agent. Chemotherapeutic agents, and combinations thereof, for use with FTS, its analogs, or its salts are also disclosed.

Abstract: Disclosed are methods of treating lung cancer by administering to a human in need thereof effective amounts of FTS, or various analogs thereof, or a pharmaceutically acceptable salt thereof, optionally, in combination with a chemotherapeutic agent. Chemotherapeutic agents, and combinations thereof, for use with FTS, its analogs, or its salts are also disclosed.

Abstract: Disclosed are methods of treating lung cancer by administering to a human in need thereof effective amounts of FTS, or various analogs thereof, or a pharmaceutically acceptable salt thereof, optionally, in combination with a chemotherapeutic agent. Chemotherapeutic agents, and combinations thereof, for use with FTS, its analogs, or its salts are also disclosed.

Abstract: Disclosed are methods of treating lung cancer by administering to a human in need thereof effective amounts of FTS, or various analogs thereof, or a pharmaceutically acceptable salt thereof, optionally, in combination with a chemotherapeutic agent. Chemotherapeutic agents, and combinations thereof, for use with FTS, its analogs, or its salts are also disclosed.

Abstract: Disclosed is the identity of various Ras cell membrane anchor proteins. Also disclosed are methods for identifying other anchor proteins that bind isoforms of Ras, methods of identifying drug candidates that inhibit aberrant Ras activity and methods of determining therapeutic dosages of the drugs. Further disclosed are methods for disrupting aberrant Ras activity in vivo.

Abstract: A drug screening assay for identifying compounds for their potential effects on the long chain fatty acid dependant intracellular membrane anchorage sites of lipoproteins. Membranes-anchoring-target are incubated in the presence of the compound to be tested and the proportion of the target that is released by the compound is detected and quantitated. The benchmark for this assay are the prenylated proteins such as the farnesylated and palmitoylated oncogenic ras trigger proteins which are displaced from their anchorage at the intracellular plasma membrane by derivatives of Farnesyl Thiosalicylic Acid (FTS). The assay is adaptable to flexibly assay a large variety of anchored targets using a wide range of labeling and detection techniques in test wells, tissue culture, and in animals as injected cells or transgenic, thereby directly addressing a wide range of pharmacologically relevant needs.