Abstract: Disclosed are methods for treating or preventing or delaying outset of Alzheimer's disease (AD) in a subject by targeting the novel pathway STAT1-CH25H in AD pathogenesis, specifically by administering to the subject a pharmaceutically effective amount of a STAT1 inhibitor, a CH25H inhibitor, or a 25-OHC inhibitor, for example, a 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitor such as simvastatin.

Abstract: Disclosed are methods and compositions for treating ore preventing a STAT5-mediated medical condition, e.g., rheumatoid arthritis, in a subject by administering to the subject a therapeutically effective amount of a compound, the compound being a STAT5 inhibitor, or a pharmaceutically acceptable salt of the STATS inhibitor, or a solvate of the STATS inhibitor, or a prodrug of the STAT5 inhibitor. In one example, the compound used in the methods and compositions is pimozide. In another example, the compound used in the methods and compositions is nicotinohydrazide.

Abstract: The disclosure provides a method of inhibiting proliferation of a cell, inhibiting m3C formation in a cell, inhibiting activity of Mettl8 in a cell, or activating ATM and p53 in a cell, the method comprising contacting the cell with a Mettl8 inhibitor. The disclosure also provides a composition comprising a cell with a reduced expression or activity of Mettl8. In another aspect, the disclosure provides methods of rendering a tumor cell sensitive to a cancer therapy.

Abstract: This disclosure provides methods of treating cytokine storm syndrome and related diseases, including infectious diseases such as COVID-19. In particular, this disclosure provides a method of treating cytokine storm syndrome (CSS) in a subject in need thereof comprising administering a therapeutically effective amount of a compound selected from the group consisting of pimozide, artemisinin and its derivatives, or a pharmaceutically acceptable salt, or a solvate thereof, to a subject in need thereof.

Abstract: A heterocyclic compound represented by formula XI, a pharmaceutically acceptable salt, a solvate, or a solvate of a pharmaceutically acceptable salt thereof, use thereof, and a composition containing the same. The compound is novel in structure and has good STAT5 inhibitory activity.

Abstract: Disclosed are methods and compositions for treating ore preventing a STAT5-mediated medical condition, e.g., rheumatoid arthritis, in a subject by administering to the subject a therapeutically effective amount of a compound, the compound being a STAT5 inhibitor, or a pharmaceutically acceptable salt of the STAT5 inhibitor, or a solvate of the STAT5 inhibitor, or a prodrug of the STAT5 inhibitor. In one example, the compound used in the methods and compositions is pimozide. In another example, the compound used in the methods and compositions is nicotinohydrazide.

Abstract: Disclosed are a pharmaceutical combination of pimozide and methotrexate and use thereof. The pharmaceutical combination comprises methotrexate, a pharmaceutically acceptable salt thereof, a solvate thereof, or a solvate of pharmaceutically acceptable salt thereof, and pimozide, a pharmaceutically acceptable salt thereof, a solvate thereof, or a solvate of pharmaceutically acceptable salt thereof. The pharmaceutical combination can be used for the treatment of rheumatoid arthritis.

Abstract: Disclosed is a compound, a medicament, and a pharmaceutical composition for treating inflammation induced autoimmune skin diseases, for example psoriasis. The compound is Nib1, a pharmaceutically acceptable salt thereof, a solvate thereof, a solvate of a pharmaceutically acceptable salt thereof, or a crystal form thereof. the compound Nib1 has a chemical formula of C28H29F2N3O. It represents a new treatment mechanism and can effectively treat inflammation induced autoimmune skin diseases, for example, non-specific dermatitis such as psoriasis, with less side effects and convenient route of administration, achieving a balance between safety and effectiveness. The compounds can be used for a long time and improve the quality of life of patients.

Abstract: Disclosed is use of a compound in the preparation of a medicament for treating atherosclerosis. The compound is selected from a group consisting of a compound of formula I, Nib2 and a pharmaceutically acceptable salt thereof. Based on the mechanism of atherogenesis, the invention started with the inhibition of inflammatory reaction. The research results showed that the compounds disclosed herein can significantly inhibit the macrophage foaming, reduce the deposition of lipidic necrotic substances, and reduce the formation of plaques, thus to some extent delaying or inhibiting atherosclerosis.

Abstract: Disclosed herein is a T-helper cell (“TH-GM” cell) that is regulated by IL-7/STAT5 and which secrete GM-CSF/IL-3. Also disclosed are methods and compositions for modulating TH-GM function for the treatment of, e.g., inflammatory disorders. Diagnostic and prognostic methods for specifically identifying TH-GM-mediated inflammatory disorders (e.g., rheumatoid arthritis), as distinct from and/or in addition to non-TH-GM-mediated (e.g., TNF-?-mediated) inflammatory disorders, are also provided.

Abstract: Disclosed are methods and compositions for treating ore preventing a STAT5-mediated medical condition, e.g., rheumatoid arthritis, in a subject by administering to the subject a therapeutically effective amount of a compound, the compound being a STAT5 inhibitor, or a pharmaceutically acceptable salt of the STAT5 inhibitor, or a solvate of the STAT5 inhibitor, or a prodrug of the STAT5 inhibitor. In one example, the compound used in the methods and compositions is pimozide. In another example, the compound used in the methods and compositions is nicotinohydrazide.

Abstract: The disclosure provides a method of inhibiting proliferation of a cell, inhibiting m3C formation in a cell, inhibiting activity of Mettl8 in a cell, or activating ATM and p53 in a cell, the method comprising contacting the cell with a Mettl8 inhibitor. The disclosure also provides a composition comprising a cell with a reduced expression or activity of Mettl8. In another aspect, the disclosure provides methods of rendering a tumor cell sensitive to a cancer therapy.

Abstract: Disclosed are methods for treating or preventing or delaying outset of Alzheimer's disease (AD) in a subject by targeting the novel pathway STAT1-CH25H in AD pathogenesis, specifically by administering to the subject a pharmaceutically effective amount of a STAT1 inhibitor, a CH25H inhibitor, or a 25-OHC inhibitor, for example, a 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitor such as simvastatin.

Abstract: Receptor recognition factors exist that recognizes the specific cell receptor to which a specific ligand has been bound, and that may thereby signal and/or initiate the binding of the transcription factor to the DNA site. The receptor recognition factor is in one instance, a part of a transcription factor, and also may interact with other transcription factors to cause them to activate and travel to the nucleus for DNA binding. The receptor recognition factor appears to be second-messenger-independent in its activity, as overt perturbations in second messenger concentrations are of no effect. The concept of the invention is illustrated by the results of studies conducted With interferon (IFN)-stimulated gene transcription, and particularly, the activation caused by both IFN? and IFN?. Specific DNA and amino acid sequences for various human and murine receptor recognition factors are provided, as are polypeptide fragments of two of the ISGF-3 genes, and antibodies have also been prepared and tested.

Abstract: Receptor recognition factors exist that recognizes the specific cell receptor to which a specific ligand has been bound, and that may thereby signal and/or initiate the binding of the transcription factor to the DNA site. The receptor recognition factor is in one instance, a part of a transcription factor, and also may interact with other transcription factors to cause them to activate and travel to the nucleus for DNA binding. The receptor recognition factor appears to be second-messenger-independent in its activity, as overt perturbations in second messenger concentrations are of no effect. The concept of the invention is illustrated by the results of studies conducted with interferon (IFN)-stimulated gene transcription, and particularly, the activation caused by both IFN? and IFN?. Specific DNA and amino acid sequences for various human and murine receptor recognition factors are provided, as are polypeptide fragments of two of the ISGF-3 genes, and antibodies have also been prepared and tested.

Abstract: Receptor recognition factors exist that recognizes the specific cell receptor to which a specific ligand has been bound, and that may thereby signal and/or initiate the binding of the transcription factor to the DNA site. The receptor recognition factor is in one instance, a part of a transcription factor, and also may interact with other transcription factors to cause them to activate and travel to the nucleus for DNA binding. The receptor recognition factor appears to be second-messenger-independent in its activity, as overt perturbations in second messenger concentrations are of no effect. The concept of the invention is illustrated by the results of studies conducted with interferon (IFN)-stimulated gene transcription, and particularly, the activation caused by both IFN? and IFN?. Specific DNA and amino acid sequences for various human and murine receptor recognition factors are provided, as are polypeptide fragments of two of the ISGF-3 genes, and antibodies have also been prepared and tested.

Abstract: Receptor recognition factors exist that recognizes the specific cell receptor to which a specific ligand has been bound, and that may thereby signal and/or initiate the binding of the transcription factor to the DNA site. The receptor recognition factor is in one instance, a part of a transcription factor, and also may interact with other transcription factors to cause them to activate and travel to the nucleus for DNA binding. The receptor recognition factor appears to be second-messenger-independent in its activity, as overt perturbations in second messenger concentrations are of no effect. The concept of the invention is illustrated by the results of studies conducted With interferon (IFN)-stimulated gene transcription, and particularly, the activation caused by both IFN&agr; and IFN&ggr;. Specific DNA and amino acid sequences for various human and murine receptor recognition factors are provided, as are polypeptide fragments of two of the ISGF-3 genes, and antibodies have also been prepared and tested.

Abstract: Receptor recognition factors exist that recognizes the specific cell receptor to which a specific ligand has been bound, and that may thereby signal and/or initiate the binding of the transcription factor to the DNA site. The receptor recognition factor is in one instance, a part of a transcription factor, and also may interact with other transcription factors to cause them to activate and travel to the nucleus for DNA binding. The receptor recognition factor appears to be second-messenger-independent in its activity, as overt perturbations in second messenger concentrations are of no effect. The concept of the invention is illustrated by the results of studies conducted with interferon (IFN)-stimulated gene transcription, and particularly, the activation caused by both IFN&agr; and IFN&ggr;. Specific DNA and amino acid sequences for various human and murine receptor recognition factors are provided, as are polypeptide fragments of two of the ISGF-3 genes, and antibodies have also been prepared and tested.

Abstract: The present invention relates generally to methods of modulating the rate and/or amount of a cellular process selected from the group consisting of cell growth, cell detachment and cell migration, and cellular apoptosis, said method comprising altering the RECEPTOR/PTK-STAT pathway of a cell. More particularly, the present invention relates to methods wherein the RECEPTOR/PTK-STAT pathway is altered by increasing or decreasing the amount of phosphorylated RECEPTOR/PTK-STAT proteins present in a cell. The present invention also relates to the identification of agents that either promote or inhibit the phosphorylation of RECEPTOR/PTK-STAT proteins, as well as to the agents themselves and to the methods which utilize such identified agents. The methods of the present invention are useful for treating mammalian diseases, including, but not limited to, cancer, autoimmune diseases, viral susceptibility, degenerative disorders, ischemic injuries, and conditions of obesity.

Abstract: Receptor recognition factors exist that recognizes the specific cell receptor to which a specific ligand has been bound, and that may thereby signal and/or initiate the binding of the transcription factor to the DNA site. The receptor recognition factor is in one instance, a part of a transcription factor, and also may interact with other transcription factors to cause them to activate and travel to the nucleus for DNA binding. The receptor recognition factor appears to be second-messenger-independent in its activity, as overt perturbations in second messenger concentrations are of no effect. The concept of the invention is illustrated by the results of studies conducted with interferon (IFN)-stimulated gene transcription, and particularly, the activation caused by both IFN&agr; and IFN&ggr;. Specific DNA and amino acid sequences for various human and murine receptor recognition factors are provided, as are polypeptide fragments of two of the ISGF-3 genes, and antibodies have also been prepared and tested.