Abstract: The present disclosure relates to the use of substituted heterocycles for the inhibition of the activity of WIP1. Suitably, the present disclosure relates to the use of substituted heterocycles for the treatment of cancer.

Abstract: Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. The present disclosure describes compounds and methods that restore DNA binding affinity of p53 mutants. The compounds of the present disclosure can bind to mutant p53 and restore the ability of the p53 mutant to bind DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers that contain a p53 mutation.

Abstract: Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. The present disclosure describes compounds and methods to recover wild-type function to p53 mutants. The compounds of the present disclosure can bind to mutant p53 and restore the ability of the p53 mutant to bind DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers that contain a p53 mutation.

Abstract: Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. The present disclosure describes compounds and methods to recover wild-type function to p53 mutants. The compounds of the present invention can bind to mutant p53 and restore the ability of the p53 mutant to bind DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers that contain a p53 mutation.

Abstract: Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. The present disclosure describes compounds and methods to recover wild-type function to p53 mutants. The compounds of the present disclosure can bind to mutant p53 and restore the ability of the p53 mutant to bind DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers that contain a p53 mutation.

Abstract: Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. The present disclosure describes compounds and methods to recover wild-type function to p53 mutants. The compounds of the present invention can bind to mutant p53 and restore the ability of the p53 mutant to bind DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers that contain a p53 mutation.

Abstract: Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. The present disclosure describes compounds and methods that restore DNA binding affinity of p53 mutants. The compounds of the present disclosure can bind to mutant p53 and restore the ability of the p53 mutant to bind DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers that contain a p53 mutation.

Abstract: An unmanned aerial vehicle (UAV) base station includes a housing and a UAV fixation system. The housing includes a top-plate configured for a UAV to land on the top-plate. The UAV fixation system is configured to direct the UAV present on the top-plate to a battery-exchange zone of the top-plate.

Abstract: An optical emitting device and an optical sensor are provided. The optical emitting device includes a body, a light source, and a first light-blocking structure. The body has an emitting cavity extending in a first preset direction. The emitting cavity has an incident light port and an emergent light port that are arranged in the first preset direction. An inner wall of the emitting cavity has a first inner wall portion and a second inner wall portion. The first inner wall portion and the second inner wall portion are oppositely arranged. The light source and the body are arranged in the first preset direction. The first light-blocking structure is arranged in the first inner wall portion of the emitting cavity. A light-transmitting channel is arranged between the first light-blocking structure and the second inner wall portion. The first light-blocking structure includes a plurality of first light-blocking sheets.

Abstract: A LiDAR is provided. The LiDAR includes two laser emission modules and one laser receiving module. The two laser emission modules are located separately on opposite sides of the laser receiving module, and a combination of emission fields of view of the two laser emission modules matches a receiving field of view of the laser receiving module.

Abstract: Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. The present disclosure describes compounds and methods that restore DNA binding affinity of p53 mutants. The compounds of the present disclosure can bind to mutant p53 and restore the ability of the p53 mutant to bind DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers that contain a p53 mutation.

Abstract: Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. The present disclosure describes compounds and methods that restore DNA binding affinity of p53 mutants. The compounds of the present disclosure can bind to mutant p53 and restore the ability of the p53 mutant to bind DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers that contain a p53 mutation.

Abstract: Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. The present disclosure describes compounds and methods to recover wild-type function to p53 mutants. The compounds of the present disclosure can bind to mutant p53 and restore the ability of the p53 mutant to bind DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers that contain a p53 mutation.

Abstract: Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. The present disclosure describes compounds and methods to recover wild-type function to p53 mutants. The compounds of the present invention can bind to mutant p53 and restore the ability of the p53 mutant to bind DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers that contain a p53 mutation.

Abstract: The present invention discloses an N-alkyl-N-cyanoalkylbenzamide compound of General Formula I, an intermediate of General Formula II used to prepare the compound, wherein R1 is selected from halo or C1-C3 alkyl; R2 is selected from halo or CN; R3 is selected from halo, or C1-C3haloalkyl; R4 is selected from halo; R5 is selected from H or halo; R6 is selected from C1-C3alkyl, C1-C3 haloalkyl or C1-C5 alkoxyalkyl; R7 is selected from C1-C5 alkyl; and R8 is selected from hydrogen or C1-C5alkyl. Compared with the compounds in the prior art, the compound of General Formula I has a higher activity at a low concentration. Particularly, the compound of the present invention still has 60% or higher of the insecticidal activity at a concentration below 1 ppm. This greatly reduces the amount of the compound used and the residue of the compound in farmland, and is thus environmentally friendly.

Abstract: Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. The present disclosure describes compounds and methods to recover wild-type function to p53 mutants. The compounds of the present invention can bind to mutant p53 and restore the ability of the p53 mutant to bind DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers that contain a p53 mutation.

Abstract: Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. The present disclosure describes compounds and methods to recover wild-type function to p53 mutants. The compounds of the present invention can bind to mutant p53 and restore the ability of the p53 mutant to bind DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers that contain a p53 mutation.

Abstract: The present invention discloses an N-alkyl-N-cyanoalkylbenzamide compound of General Formula I, an intermediate of General Formula II used to prepare the compound, wherein R1 is selected from halo or C1-C3 alkyl; R2 is selected from halo or CN; R3 is selected from halo, or C1-C3haloalkyl; R4 is selected from halo; R5 is selected from H or halo; R6 is selected from C1-C3alkyl, C1-C3 haloalkyl or C1-C5 alkoxyalkyl; R7 is selected from C1-C5 alkyl; and R8 is selected from hydrogen or C1-C5alkyl. Compared with the compounds in the prior art, the compound of General Formula I has a higher activity at a low concentration. Particularly, the compound of the present invention still has 60% or higher of the insecticidal activity at a concentration below 1 ppm. This greatly reduces the amount of the compound used and the residue of the compound in farmland, and is thus environmentally friendly.

Abstract: Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. The present disclosure describes compounds and methods to recover wild-type function to p53 mutants. The compounds of the present invention can bind to mutant p53 and restore the ability of the p53 mutant to bind DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers that contain a p53 mutation.