The invention belongs to the technical field of biomedicament, and more specifically relates to an application of compound amino acids in preparation of a medicament for improving sensitivity of bacteria to antibiotics. Experiments have shown that a combination of compound amino acids and antibiotics can improve the sensitivity of bacteria to antibiotics, promote an entry of antibiotics into bacterial cells, significantly increase an intracellular antibiotic content, and improve a bactericidal effect of antibiotics, thereby reducing a survival rate of bacteria, and treating diseases caused by bacterial infection.

Described herein are compositions of pyrvinium salts suitable for oral administration. These compositions are in the form of solutions and demonstrate bioavailability both in blood plasma and in pancreatic tissue. Also described herein are methods of treating, ameliorating, and/or preventing pancreatic cancer, including orally administering a composition comprising pyrvinium pamoate.

Provided herein is a method of treating or alleviating one or more symptoms of cancer in a subject, comprising administering to the subject ascorbic acid and a quinone compound, e.g., a compound of Formula (I).

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Provided herein is a method of treating or alleviating one or more symptoms of cancer in a subject, comprising administering to the subject ascorbic acid and a quinone compound, e.g., a compound of Formula (I).

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Disclosed are compounds inhibiting ErbBs (e.g. HER2), pharmaceutically acceptable salts, hydrates, solvates or stereoisomers thereof and pharmaceutical compositions comprising the compounds. The compound and the pharmaceutical composition can effectively treat diseases associated ErbBs (especially HER2), including cancer.

The invention relates to heterocyclic compounds consisting of a core nitrogen atom surrounded by three pendant groups, wherein two of the three pendant groups are preferably benzimidazolyl methyl and tetrahydroquinolyl, and the third pendant group contains N and optionally contains additional rings. The compounds bind to chemokine receptors, including CXCR4 and CCR5, and demonstrate protective effects against infection of target cells by a human immunodeficiency virus (HIV).

The invention relates to heterocyclic compounds consisting of a core nitrogen atom surrounded by three pendant groups, wherein two of the three pendant groups are preferably benzimidazolyl methyl and tetrahydroquinolyl, and the third pendant group contains N and optionally contains additional rings. The compounds bind to chemokine receptors, including CXCR4 and CCR5, and demonstrate protective effects against infection of target cells by a human immunodeficiency virus (HIV).

Resistance to kinase inhibitors exemplifies the greatest hindrance to effective treatment of cancer patients. Recent studies have suggested that the onset of said resistance might not only be explained by a drug selection of pre-existing resistant sub-clones as it what was generally assumed, but may also arise de novo from a small population of drug-tolerant cells (DTC) that initially resists the treatment by entering a slow cycling state. Thus, targeting these DTC should be a new promising approach to hamper the emergence of secondary resistance to kinase inhibitors. The inventors now demonstrate that farnesyltransferase (but not geranylgeranyl transferase) inhibition can prevent the emergence of said resistance in different oncogenic contexts. In particular, the inventors determined invitro the efficacy of farnesyltransferase inhibitor (i.e. Tipifarnib) in combination with erlotinib in several EGFR-mutated cell lines. They showed that the combination efficiently eliminated all drug tolerant cells, and fully prevented the emergence of resistant clones. Interestingly, similar results were observed in other oncogenic models such as ALK-translocated lung cancer cells or BRAF-mutated melanoma cells. Thus the present invention relates to use of farnesyl transferase inhibitors for the treatment of cancers that have acquired resistance to kinase inhibitors.

Resistance to kinase inhibitors exemplifies the greatest hindrance to effective treatment of cancer patients. Recent studies have suggested that the onset of said resistance might not only be explained by a drug selection of pre-existing resistant sub-clones as it what was generally assumed, but may also arise de novo from a small population of drug-tolerant cells (DTC) that initially resists the treatment by entering a slow cycling state. Thus, targeting these DTC should be a new promising approach to hamper the emergence of secondary resistance to kinase inhibitors. The inventors now demonstrate that farnesyltransferase (but not geranylgeranyl transferase) inhibition can prevent the emergence of said resistance in different oncogenic contexts. In particular, the inventors determined invitro the efficacy of farnesyltransferase inhibitor (i.e. Tipifarnib) in combination with erlotinib in several EGFR-mutated cell lines. They showed that the combination efficiently eliminated all drug tolerant cells, and fully prevented the emergence of resistant clones. Interestingly, similar results were observed in other oncogenic models such as ALK-translocated lung cancer cells or BRAF-mutated melanoma cells. Thus the present invention relates to use of farnesyl transferase inhibitors for the treatment of cancers that have acquired resistance to kinase inhibitors.

Resistance to kinase inhibitors exemplifies the greatest hindrance to effective treatment of cancer patients. Recent studies have suggested that the onset of said resistance might not only be explained by a drug selection of pre-existing resistant sub-clones as it what was generally assumed, but may also arise de novo from a small population of drug-tolerant cells (DTC) that initially resists the treatment by entering a slow cycling state. Thus, targeting these DTC should be a new promising approach to hamper the emergence of secondary resistance to kinase inhibitors. The inventors now demonstrate that farnesyltransferase (but not geranylgeranyl transferase) inhibition can prevent the emergence of said resistance in different oncogenic contexts. In particular, the inventors determined invitro the efficacy of farnesyltransferase inhibitor (i.e. Tipifarnib) in combination with erlotinib in several EGFR-mutated cell lines. They showed that the combination efficiently eliminated all drug tolerant cells, and fully prevented the emergence of resistant clones. Interestingly, similar results were observed in other oncogenic models such as ALK-translocated lung cancer cells or BRAF-mutated melanoma cells. Thus the present invention relates to use of farnesyl transferase inhibitors for the treatment of cancers that have acquired resistance to kinase inhibitors.