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.

Disclosed are novel carboxylated psilocybin derivative compounds and pharmaceutical and recreational drug formulations containing the same. The compounds may be produced by reacting a reactant psilocybin derivative with a carboxyl or Carboxylic acid derivative containing compound.

Disclosed are novel carboxylated psilocybin derivative compounds and pharmaceutical and recreational drug formulations containing the same. The compounds may be produced by reacting a reactant psilocybin derivative with a carboxyl or Carboxylic acid derivative containing compound.

Disclosed are nanoparticles and nanogel drug compositions and the use thereof for treating age-related macular degeneration.

Disclosed are nanoparticles and nanogel drug compositions and the use thereof for treating age-related macular degeneration.

The present disclosure provides a compositions and methods of inhibiting O.sup.6-methylguanine DNA methyltransferase in human tumor cells by providing an effective amount of an agent that directly or indirectly inhibits the O.sup.6-methylguanine DNA methyltransferase in a pharmaceutically acceptable carrier, wherein the amount is effective to potentiate an anti-tumor activity of one or more alkylating agents, platinum drugs, or antimetabolites, wherein tumor cells are triggered into programmed cell death.

The present disclosure provides a compositions and methods of inhibiting O.sup.6-methylguanine DNA methyltransferase in human tumor cells by providing an effective amount of an agent that directly or indirectly inhibits the O.sup.6-methylguanine DNA methyltransferase in a pharmaceutically acceptable carrier, wherein the amount is effective to potentiate an anti-tumor activity of one or more alkylating agents, platinum drugs, or antimetabolites, wherein tumor cells are triggered into programmed cell death.

The invention provides 2-(substituted phenylhetero) aromatic formate FTO inhibitors, a preparation method thereof, and applications thereof. Specifically, disclosed in the present invention are a 2-(substituted phenylhetero) aromatic formate compound represented by the following formula (I), and a pharmaceutically acceptable salt, a hydrate or a solvate thereof, which can be used as an FTO targeting inhibitor for treating diseases associated with FTO targets, including obesity, metabolic syndrome (MS), type 2 diabetes (T2D), Alzheimer's diseases, and cancers such as breast cancers, small-cell lung cancers, human bone marrow rhabdomyosarcoma, pancreatic cancer, malignant glioblastoma and the like. ##STR00001##

The invention provides 2-(substituted phenylhetero) aromatic formate FTO inhibitors, a preparation method thereof, and applications thereof. Specifically, disclosed in the present invention are a 2-(substituted phenylhetero) aromatic formate compound represented by the following formula (I), and a pharmaceutically acceptable salt, a hydrate or a solvate thereof, which can be used as an FTO targeting inhibitor for treating diseases associated with FTO targets, including obesity, metabolic syndrome (MS), type 2 diabetes (T2D), Alzheimer's diseases, and cancers such as breast cancers, small-cell lung cancers, human bone marrow rhabdomyosarcoma, pancreatic cancer, malignant glioblastoma and the like. ##STR00001##

The present invention relates in part to the discovery that benzodiazepines can be used to reactivate latent HIV-1 virus that is integrated into human genome. In other embodiments, the benzodiazepine is used in combination with a histone deacetylase inhibitor (HDACi), such as but not limited to SAHA (also known as N-hydroxy-N-phenyl-octanediamide, Suberoylanilide hydroxamic acid, Vorinostat). In yet other embodiments, the combination of benzodiazepine and the HDACi synergistically reactivates latent HIV-1 virus that is integrated into human genome, with minimal or no significant toxicity associated with the dose of either agent.