51 results about "BRAF inhibitor" patented technology

The invention discloses a phosphoinositide 3-kinase (P13K) inhibitor, a pharmaceutical composition containing the P13K inhibitor, and application of the P13K inhibitor and the pharmaceutical composition. The P13K inhibitor comprises a pyrimidine compound and a stereoisomer/hydrate/pharmaceutically-acceptable salt thereof. The pyrimidine compound has a general formula I of which the structure is shown in the specification. The P13K inhibitor and the pharmaceutical composition containing the same can be used for inhibiting PI3 Ks and treating proliferative diseases on which the PI3 Ks act. According to the invention, high-effectiveness and high-selectivity inhibitors for treating proliferative diseases on which PI3Ks act can be provided.

The invention is designed to be used for the large outdoor fires such as fires on the U.S. Navy's aircraft carriers, in forests and grasslands and at airports and chemical plants. The operators of an “assist unit” should always be behind the firefighters. At long range it can blow fire suppressors into a fire and smother it. The suppressors can be water or chemicals by the firefighters. Soot, ashes, dirt or sand around a fire itself are good suppressors. The “assist unit” will blow them into the fire and it blows away the smoke and fumes as well. There are two versions of the “assist unit”: the ALL MANUAL one and the VEHICLE MOUNTED one.

Methods to treat cancer patients, especially melanoma patients, who have BRAF mutations and have become resistant to BRAF mutant kinase inhibitors employ inhibitors of multiple receptor tyrosine kinases. In addition, methods are described for identifying pharmaceutical compositions and drugs that will be successful in treating these patients.

The invention discloses a pyrimidine compound of which the structure is shown in a general formula (I), and also discloses a PI3K inhibitor which is composed of at least one of the following substances: the pyrimidine compound shown in the general formula (I), a steric isomer of the pyrimidine compound, a hydrate of the pyrimidine compound and a pharmaceutically acceptable salt of the pyrimidine compound. The invention also discloses a pharmaceutical composition comprising the PI3K inhibitor, and also discloses application of the PI3K inhibitor in preparation of a drug for treatment and/or prevention and/or auxiliary treatment of a proliferative disease of PI3K action. The pharmaceutical composition is composed of the PI3K inhibitor, at least one pharmaceutically acceptable auxiliary material, an adjuvant or a carrier. The PI3K inhibitor and the pharmaceutical composition comprising the PI3K inhibitor can be applied to inhibition of P13 kinase and the proliferative disease of P13 kinase action, and the inhibitor with better validity and selectivity can be provided for treatment of the proliferative disease of P13 kinase action.

A novel combination comprising the MEK inhibitor N-{3-[3-cyclopropyl-5-(2-fluoro-4-iodo-phenylamino)6,8-dimethyl;-2,4,7-trioxo-3,4,6,7-tetrahydro-2H-pyrido[4,3-d]pyrimidin-1-yl]phenyl}acetamide, or a pharmaceutically acceptable salt or solvate thereof, and/or a B-Raf inhibitor, particularly N-{3-[5-(2-Amino-4-pyrimidinyl)-2-(1,1-dimethylethyl)-1,3-thiazol-4-yl]-2-fluorophenyl}-2,6-difluorobenzenesulfonamide or a pharmaceutically acceptable salt thereof, and an anti-PD-L1 antibody; pharmaceutical compositions comprising the same and methods of using such combinations and compositions in the treatment of conditions in which the inhibition of MEK and/or B-Raf and/or neutralizing or inhibiting the interaction between PD-L1 and its receptor, e.g. PD-1, is beneficial, eg. cancer.

The description provides compositions and methods for treating ETBR-related cancer. In certain aspects, the description provides a delivery system for the controlled, systemic release of at least one of ETBR antagonists, caspase-8 inhibitors, or a combination thereof, optionally including an ETAR antagonist, an anti-PD-1 antibody, a bRAF inhibitor, niacinamide or a combination thereof. The compositions described are useful for the treatment of certain cancers, including, e.g., breast cancer, malignant melanoma, squamous cell carcinoma, glioblastoma, as well as others. In addition, the description provides a delivery system for the controlled release of at least one of ETBR antagonists, caspase-8 inhibitors or a combination thereof, optionally including at least one of an ETAR antagonist, an anti-PD-1 antibody, a bRAF inhibitor, niacinamide, or a combination thereof, to the central nervous system that are useful for treating cancers that have spread to the brain.

The invention discloses a compound preparation for treating BRAF inhibitor-resistant melanoma. Medicinal ingredients in the compound preparation include vemurafenib and propranolol, wherein the weightratio of the vemurafenib to the propranolol is at (5-15) to 1. The compound preparation provided by the invention is more economic and effective, so that family burdens of patients can be reduced.

The present invention relates to pharmaceutical compositions for treating cancer comprising BRAF inhibitors, (e.g. vemurafenib) and/or MEK inhibitor, (e.g. trametinib, RO5068760), in combination with anti-tubulin compounds of the invention or other known tubulin inhibitors, and using such compositions for treating cancer such as melanoma, drug-resistant cancer, and cancer metastasis.

The present invention relates to combination therapies for melanoma, and in particular, metastatic melanoma. Drugs for use in such therapies in include BRAF inhibitors such as PLX 4720 and PLX 4734 in combination with RO 31-8220, bafetinib or cardiac glycosides.

The present invention relates to combination therapies for melanoma, and in particular, metastatic melanoma. Drugs for use in such combination in include MEK inhibitors, BRAF inhibitors and cardiac glycosides.

The invention belongs to the field of biomedicine, and relates to a method for sensitizing a BRAF inhibitor. An SOX4 gene can be used to adjust the killing effect of a BRAF inhibitor on a drug resistant melanoma cell strain and can be taken as a maker of apoptosis-inducing effect of the BRAF inhibitor on the drug resistant melanoma cell strain. The SOX4 gene can be regulated, the expression of SOX4 is inhibited, the killing effect of the BRAF inhibitor on the drug resistant melanoma cell strain is enhanced, and the apoptosis-inducing effect of the BRAF inhibitor on the drug resistant melanomacell strain is also strengthened. Furthermore, the antitumor effect of the BRAF inhibitor can be enhanced by inhibiting the expression of SOX4.

The present invention relates to a pharmaceutical combination comprising a cyclin dependent kinase (CDK) inhibitor represented by a compound of formula I (as described herein) or a pharmaceutically acceptable salt thereof; and at least one anticancer agent selected from a BRAF inhibitor or a MEK inhibitor, for use in the treatment of melanoma. The present invention also relates to a method for the treatment of melanoma comprising administering to a subject in need thereof, a therapeutically effective amount of a CDK inhibitor and a therapeutically effective amount of at least one anticancer agent selected from a BRAF inhibitor or a MEK inhibitor.

The present invention discloses methods of treatment, prevention and/or amelioration of radiation dermatitis caused by radiotherapy, by administration to a subject in need thereof of a topical composition comprising a therapeutically or prophylactically effective amount of at least one BRaf inhibitor of this invention, thus treating, preventing and/or ameliorating the effects of radiation dermatitis.

The present invention discloses novel BRaf inhibitors, compositions comprising these inhibitors and uses thereof for the treatment, amelioration and/or prevention of cutaneous reactions.

The present invention relates to a method for treating a subject suffering from melanoma resistant by administering to said subject an inhibitor of NAMPT. Using a global metabolic profiling, inventors have showed that in addition to glycolysis, the BRAF inhibitor, PLX4032, promoted a complex metabolic rewiring of melanoma cells, including protein catabolism and fatty acid synthesis. Importantly, they observed that PLX4032 reduced the levels of nicotinamide adenine dinucleotide (NAD+), an important redox co-factor in numerous metabolic processes, including glycolysis, tricarboxylic acid cycle (TCA) cycle, glutamate metabolism and fatty acid betaoxidation. Pharmacological or genetic inhibition of NAMPT impaired melanoma cell growth, whereas the overexpression of NAMPT dampened the antiproliferative effect of PLX4032. In vivo, the inhibition of NAMPT also prevented the xenograft development of PLX4032-sensitive and -resistant melanoma cells, identifying NAMPT as a potential target for BRAFi-resistant melanomas.

The invention discloses application of a BRAF inhibitor to preparation of novel drugs for treating programmed necrotic diseases and a screening method of the BRAF inhibitor. The method is characterized by taking necrotic pathway sensitive cell line L929-FADD gene knockout cell strains as model cells of cell proliferation and necrosis, screening out small-molecule compounds influencing and inhibiting cell death from an FDA drug library, detecting different drug concentration of the small-molecule compounds obtained by screening, determining toxicity-effect concentration, and performing comprehensive evaluation from toxicity and recovery efficiency to obtain the BRAF inhibitor; and through inhibition of the BRAF inhibitor on cell necrosis, the BRAF inhibitor can be used for preparing novel drugs for treating the programmed necrotic diseases. The BRAF inhibitor has excellent necrosis inhibition effects on necrotic sensitive cell line L929-FADD knockout strains, human cell line HT29 and animal models; the water solubility of the BRAF inhibitor is better than that of Nec-1; the BRAF inhibitor is an FDA-approved clinical drug; the targeting property and the safety of the BRAF inhibitor are guaranteed; and the BRAF inhibitor is easy for clinical promotion.