14 results about "Strong inhibitor" patented technology

This disclosure relates to administration of a combination of: 1) about 100-110 mg, about 104-106 mg, or about 105 mg of bupropion hydrochloride, or a molar equivalent amount of the free base form or another salt form of bupropion; and 2) about 40-50 mg, about 44-46 mg, or about 45 mg of dextromethorphan hydrobromide, or a molar equivalent amount of the free base form or another salt form of dextromethorphan in certain patient populations, such as patients having moderate renal impairment, patients receiving a concomitant strong CYP2D6 inhibitor, patients who are known CYP2D6 poor metabolizers, those in need of an NMDA antagonist that does not cause dissociation, and those at risk of QT prolongation.

The application discloses an inhibitor for inhibiting KRAS phase separation to play an anti-tumor role and application, and relates to the fields of tumor molecular biology and targeted therapy.The application aims at solving the problems of limited effect, strong drug resistance and limited application range of KRAS tumor treatment methods, and the inhibitor is a statin.The KRAS protein can form a liquid condensate in cells, and the application discloses the mechanism of the KRAS protein in promoting KRAS protein processing, transportation and downstream signal activation, and further provides a technical scheme for inhibiting tumor growth and enhancing the therapeutic effect of a KRAS inhibitor by inhibiting the formation of KRAS condensates, so as to provide a new target and intervention approach for tumor treatment.

The present invention pertains to a composition, containing aripiprazole as an active ingredient, for enhancing the anticancer effect of a RAF inhibitor. More specifically, the present invention pertains to a composition for enhancing the anticancer effect of the RAF inhibitor, wherein the composition can treat cancer by acting as an agent for enhancing the anticancer effect of the RAF inhibitor when used in combination therapy with aripiprazole. Administering an effective amount of aripiprazole according to the present invention in combination with the RAF inhibitor is highly effective in enhancing the anticancer effect of the RAF inhibitor, such as by inducing cancer cell death, and thus the composition can be advantageously used as an agent for enhancing the anticancer effect of the RAF inhibitor.

The invention discloses application of an HDAC8 inhibitor in preparation of a medicine for enhancing the curative effect of a PARP inhibitor or reversing / improving the drug resistance of the PARP inhibitor, and relates to the technical field of biological medicine. According to the scheme of combining the HDAC8 inhibitor and the PARP inhibitor, the curative effect of the PARP inhibitor is remarkably enhanced, the drug resistance of the PARP inhibitor is reversed / improved, and the core problem in clinical application of the PARP inhibitor is effectively solved. Through combined inhibition of targeting HDAC8 and PARP, a new strategy capable of effectively overcoming drug resistance of a PARP inhibitor, improving treatment sensitivity and being good in safety is provided, the defects in the aspects of targeting, safety and curative effect stability in the prior art are overcome, and a new feasible path is provided for solving the technical defects existing in the field for a long time.

The present invention relates to a composition containing aripiprazole as an active ingredient for enhancing the anti-cancer effect of an ERK inhibitor. More specifically, the present invention concerns a composition for enhancing the anticancer effect of an ERK inhibitor, which acts as an enhancer for the anti-cancer effect of the ERK inhibitor when used in combination therapy with aripiprazole, thereby enabling the treatment of cancer. When used at an effective dose in combination with an ERK inhibitor, aripiprazole according to the present invention excellently enhances the anticancer effect of the ERK inhibitor by inducing cancer cell death, etc. Thus, it can be advantageously used as an enhancer for the anti-cancer effect of the ERK inhibitor.

This application discloses the use of artesunate in the preparation of drugs for enhancing the therapeutic effect of PARP inhibitors, belonging to the field of biomedical technology. The artesunate described in this application is a sesquiterpene lactone derivative extracted from the traditional Chinese medicine Artemisia annua. It has an inhibitory effect on the proliferation of BRCA wild-type ovarian cancer cells and low toxicity to normal human ovarian epithelial cells. This application's research found that artesunate can enhance the DNA damage and apoptosis induced by PARP inhibitors (such as olaparib, niraparib, and rucaparib), and improve the sensitivity of PARP inhibitors to BRCA wild-type ovarian cancer.

The invention discloses a metformin enhanced PARP inhibitor as well as a preparation method and application thereof, belongs to the technical field of biological medicines, and particularly relates to the metformin enhanced PARP inhibitor. The PARP inhibitor is prepared from metformin and olaparib; the molar ratio of the olaparib to the metformin is 1: (200-600). The energy metabolism states of different BRCA1 mutation subtype triple negative breast cancer cells are remodeled through metformin, the inhibition effect of olaparib on the cancer cells in a drug-resistant environment is remarkably enhanced, cell apoptosis is effectively promoted, cell migration is inhibited, and therefore the synergistic improvement of the curative effect of a PARP inhibitor is achieved.

The present invention relates to a composition for enhancing the anticancer effect of a MEK inhibitor, the composition comprising aripiprazole as an active ingredient, and more specifically, to a composition for enhancing the anticancer effect of a MEK inhibitor, the composition being capable of treating cancer by acting as an anticancer effect enhancer of the MEK inhibitor when used in combination therapy with aripiprazole. An effective amount of aripiprazole according to the present invention is highly effective in improving the anticancer effect of the MEK inhibitor, such as by inducing cancer cell death, when administered in combination with the MEK inhibitor, and thus the present invention can be effectively used as an agent for improving the anticancer effect of the MEK inhibitor.

The application discloses application of TRIM33 and miR-BART8-3p as target points in preparation of a drug for advanced nasopharyngeal carcinoma. The application first discloses that in the advanced nasopharyngeal carcinoma, EBV encoded miR-BART8-3p directly targets and inhibits the expression of TRIM33, up-regulates the expression of PD-L1, and finally promotes the molecular mechanism of immune escape. This discovery is particularly aimed at patients with advanced metastatic nasopharyngeal carcinoma, and fills the blank of the mechanism research of immunotherapy drug resistance of the population. Therefore, by up-regulating TRIM33 or inhibiting miR-BART8-3p, the antitumor immunity of the patient with advanced nasopharyngeal carcinoma can be effectively regulated, and a new strategy for treating advanced nasopharyngeal carcinoma, reversing immunotherapy drug resistance and enhancing the curative effect of a PD-1 inhibitor is formed. The application provides a complete solution from mechanism research to treatment application and precise prediction for the advanced nasopharyngeal carcinoma.

The invention belongs to the field of medicines, and particularly relates to a new application of a divalent manganese ion as a sensitizer of a KRAS G12D inhibitor. According to the application, firstly, it is found that the growth of KRAS G12D mutant pancreatic cancer tumors can be remarkably inhibited by combining divalent manganese ions (Mn < 2 + >) with the KRAS G12D inhibitor Zoldonrasib, it is indicated that the divalent manganese ions can sensitize the KRAS G12D inhibitor Zoldonrasib, so that the treatment effect of the KRAS G12D inhibitor Zoldonrasib in the KRAS G12D mutant pancreatic cancer is enhanced, and the application serves as a novel synergistic treatment scheme for improving pancreatic cancer treatment response and has a good application prospect. The method has important research significance and application value.

This invention discloses a metformin-enhanced PARP inhibitor, its preparation method, and its application, belonging to the field of biomedical technology. Specifically, it relates to a metformin-enhanced PARP inhibitor comprising metformin and olaparib, with a molar ratio of olaparib to metformin of 1:200-600. This invention reshapes the energy metabolism state of different BRCA1-mutant subtypes of triple-negative breast cancer cells through metformin, significantly enhancing the inhibitory effect of olaparib on these cancer cells under drug-resistant conditions, and effectively promoting apoptosis and inhibiting cell migration, thereby achieving a synergistic enhancement of the efficacy of PARP inhibitors.

This disclosure relates to the administration of the following combinations in certain patient populations: 1) about 100–110 mg, about 104–106 mg, or about 105 mg or less of bupropion hydrochloride or a molar equivalent of the free base form or another salt form of bupropion; and 2) about 40–50 mg, about 44–46 mg, or about 45 mg or less of dextromethorphan hydrobromide or a molar equivalent of the free base form or another salt form of dextromethorphan, in patient populations such as patients with moderate renal impairment, patients receiving a concomitant strong CYP2D6 inhibitor, patients known to be poor CYP2D6 metabolizers, patients requiring an NMDA antagonist that does not cause dissociation, and patients at risk of QT prolongation.

The present disclosure relates to administering in certain patient populations a combination of: 1) bupropion hydrochloride or bupropion in a molar equivalent amount in the form of a free base or in the form of another salt in a range of about 100 to 110 mg, about 104 to 106 mg, or about 105 mg; and 2) dextromethorphan hydrobromide or a molar equivalent amount of dextromethorphan in the form of a free base or in the form of another salt, in the range of from about 40 to 50 mg, from about 44 to 46 mg, or from about 45 mg, the present invention relates to certain populations of patients, such as patients suffering from moderate renal injury, patients receiving companion strong CYP2D6 inhibitors, patients known to be CYP2D6 weak metabolites, patients in need of NMDA antagonists that do not cause dissociation, and patients at risk of QT extension.

This invention belongs to the field of pharmaceutical technology and discloses a pharmaceutical composition of a USP7 inhibitor and fenofibrate and its antitumor application. The pharmaceutical composition uses a USP7 inhibitor and fenofibrate as the core active ingredients, with a molar ratio of 0.015625 to 0.625. The USP7 inhibitor is selected from at least one of LX04-104 and LML-17-133. This invention is the first to discover that fenofibrate can significantly enhance the antitumor effect of the USP7 inhibitor, and the combination of the two has a synergistic effect. This synergistic effect is cell type specific, particularly significant for nasopharyngeal carcinoma and pancreatic cancer, and the synergistic effect of fenofibrate is independent of the PPARα pathway. This composition can be prepared as an oral or injectable formulation for the treatment of nasopharyngeal carcinoma and pancreatic cancer, and has good prospects for clinical translation.