13 results about "Trametinib" patented technology

The invention discloses an MEK / HDAC double-target inhibitor as well as a synthesis method and application thereof, and belongs to the technical field of medicines. Through molecular docking and in-vitro thermodynamic migration experiments, the applicant finds that the inhibitor not only can stabilize MEK and HDAC proteins, but also can be specifically combined with the MEK and HDAC proteins in an intracellular environment; protein immunoblotting experiments find that the inhibitor can inhibit reactivation of ERK, overcomes the limitation of a single-target inhibitor in curative effect and activity, and significantly improves the drug resistance problem of trametinib in ovarian cancer treatment and various EGFR-TKI treatment in non-small cell lung cancer treatment; furthermore, an in-vitro anti-tumor activity experiment shows that the IC50 value of the MEK / HDAC inhibitor on tumor cells from human ovarian cancer and various lung cancers is 0.07-10 mu M, and the MEK / HDAC inhibitor has a wide and remarkable proliferation inhibition effect.

The application belongs to the field of medicine, and particularly relates to application of axitinib in preparation of a medicine for treating plexiform neurofibroma. In the medicine, axitinib serves as the only effective component or one of the effective components. When axitinib serves as one of the effective components in the medicine, the effective components further include a MEK inhibitor. The MEK inhibitor is selected from one of selumetinib and trametinib. The application proves that axitinib can play a role in inhibiting plexiform neurofibroma (pNF) by targeting OTUD3, an important gene for promoting pNF progression. Moreover, axitinib is a drug that has been used for clinical treatment, and has good safety. The research result of the application shows that the combination use of axitinib and the MEK inhibitor can improve the inhibitory effect on neurofibroma.

Compounds of formula (I) [Formula 1] A pharmaceutical combination comprising: (a) a Raf inhibitor that is TIFF2026503267000030.tif4686 or a pharmaceutically acceptable salt thereof; (b) a KRAS G12C inhibitor T; and / or (c) trametinib.

The application provides a drug composition for treating non-small cell lung cancer KRAS G12C mutation and application thereof, and relates to the technical field of biological medicine. The drug composition comprises trametinib and artesunate, and the mass ratio of the two is 1:100. The drug composition of trametinib and artesunate can more significantly inhibit the growth of tumors than single drug, the drug resistance time is significantly prolonged, the side reaction of single drug is reduced, and the price is low. The drug composition can be used for preparing a novel therapeutic drug for treating non-small cell lung cancer KRAS G12C mutation, and has important clinical significance.

Described herein are methods useful for the treatment of cancers in a canine subject with a pharmaceutical compositions comprising HDAC inhibitors, Rapamycin, Dasatinib, Lapatinib, Trametinib, Vorinostat, Imatinib, Crizotinib, Sorafenib, and combinations thereof. Also described herein are methods for identification of subjects with cancers that will benefit from administration of the pharmaceutical compositions comprising HIDAC inhibitors, Rapamycin, Dasatinib, Lapatinib, Trametinib, Vorinostat, Imatinib, Crizotinib, Sorafenib, and combinations thereof. In certain aspects, the methods described herein further comprise administering a therapeutically effective amount of at least one additional anti-cancer agent.

The application belongs to the technical field of biology, and specifically discloses a method for rapidly constructing a liver fibrosis animal model, which establishes a mouse liver fibrosis model by jointly using CCl4 and a MEK1 / 2 kinase inhibitor, i.e., trametinib. The trametinib can inhibit the MEK1 / 2 kinase and the ERK1 / 2 pathway. Compared with a traditional CCl4 modeling method, the modeling method provided by the application has the advantages of rapid modeling speed, obvious liver fibrosis phenotype after two weeks of administration, and the like. After four weeks of administration, the liver fibrosis degree of the "CCl4+trametinib" group is significantly higher than that of the CCl4 group, and meanwhile, the liver damage of the mouse is also significantly aggravated, but the trametinib has no obvious influence on the kidney function. In general, the liver fibrosis model provided by the application has the advantages of high specificity, rapid modeling speed, obvious phenotype, simple and safe operation, and the like, and is a modeling method superior to the traditional CCl4 modeling method.

A method of treating and / or preventing a skin toxicity associated with the administration of a therapeutic treatment comprising trametinib, naporafenib, or a combination thereof in a subject in need thereof; the method comprising pre-emptively administering to the subject an effective amount of a rash treatment.

A pharmaceutical combination comprising: a Raf inhibitor, which is a compound of formula (I) or a pharmaceutically acceptable salt thereof, (b) a KRAS G12C inhibitor, and / or (c) trametinib.

Disclosed herein is a method of treating melanoma in a subject, the method comprising administering (a) naporafenib and (b) a MEK inhibitor such as trametinib, wherein the melanoma comprises a cell that has: 1) a wild-type NRAS genotype and 2) a wild-type BRAF or a wild-type BRAF genotype.

The invention relates to the technical field of medicine screening, and particularly discloses application of an MEK inhibitor combined with a p53 activator in preparation of a medicine for treating pancreatic cancer and a construction method of a medicine screening platform. The MEK inhibitor trametinib is combined with the p53 activator COTI-2 to treat pancreatic cancer, it is found that trametinib and COTI-2 have a synergistic interaction effect, and the treatment effect of the combination of trametinib and COTI-2 is remarkably better than that of a single drug.

The invention discloses an NUT cancer organ as well as a culture method, a culture medium and application thereof, and belongs to the technical field of biological medicines. The culture medium comprises 10 to 100 [mu] M / L of GSK269962A, 1 to 10 nM / L of trametinib and 1 to 10 [mu] M / L of BIP-135. The invention also provides a culture method of the NUT cancer organoid. The culture method comprises the following steps: obtaining a pleuroperitoneal fluid sample of an NUT cancer patient, carrying out anticoagulation treatment, and centrifuging to obtain cell precipitate; re-suspending the cell precipitate with PBS, and enriching the cells through Percoll density gradient centrifugation; and mixing the enriched cells with matrigel, inoculating the mixture to a culture plate, adding a culture medium, and culturing for 5-7 days to obtain the NUT cancer organoid. The cultured NUT cancer organoid can be used for screening drugs for treating NUT cancer and detecting the sensitivity of anti-cancer drugs to NUT cancer, is especially suitable for sensitivity detection of NHWD-870 drugs, and provides a new research tool for individualized treatment of NUT cancer.