12 results about "Focal adhesion" patented technology

The formation of scars at a wound site is reduced by contacting the wound site with an effective dose of an inhibitor of focal adhesion kinase (FAK) formulated in a pullulan hydrogel. The release profile of the FAK inhibitor can be adjusted according to the nature of the wound, e.g., excisional wounds, burn wounds, etc.

A pyrrolopyrimidine or pyrrolopyridine derivative and its medical use. Specifically, the compound has the structure shown in formula I, has good inhibitory effect on focal adhesion kinase (FAK), and can inhibit its related signal pathways, and can be prepared for treating or preventing diseases related to cancer, pulmonary arterial hypertension, pathological angiogenesis, etc., and can be particularly used for treating diseases caused by excessive or abnormal cell proliferation, such as tumors or cancers.

The invention relates to application of an HOXB9 inhibitor in a medicine for reversing oxaliplatin resistance of gastric cancer, and belongs to the field of biological medicine. The invention discloses for the first time: HOXB9 is remarkably high in expression and is positively correlated with poor prognosis in tissues of patients with gastric cancer, which are poor in curative effect after chemotherapy containing oxaliplatin; by constructing an oxaliplatin drug-resistant gastric cancer cell strain and a patient-derived organ model, the HOXB9 is proved to specifically mediate the survival of the drug-resistant cell strain by activating a focal adhesion signaling pathway (p-FAK / AKT), and the HOXB9 is irrelevant to cell proliferation. Aiming at the mechanism, shRNA nucleic acid molecules (SEQ ID NO: 1-2) targeting HOXB9 are provided, and drug-resistant cell strains can be selectively killed through lentiviral vector delivery, so that the drug-resistant cell IC50 is reduced by more than 50%, the apoptosis rate is increased by 3 times, and the chemotherapy resistance of organoids is reversed. The invention provides a brand-new target spot and a treatment scheme for overcoming the drug resistance of oxaliplatin for gastric cancer.

The invention provides a compound of formula (I): or a salt thereof, wherein R1-R7 and X have any of the values described in the specification, as well as compositions comprising a compound of formula (I) or a salt thereof. The compounds and salts are useful for activating a focal adhesion kinase (FAK) and for treating epithelial disease or damage. The invention also provides methods to treat bladder disease and damage, interstitial cystitis and transplant corneas with compounds discussed in herein.

The invention provides coke and a preparation method thereof, a negative electrode material and a battery. The coke comprises a matrix structure and a sphere-like structure embedded in the matrix structure, in a polarizing microscope image obtained after a single focal particle is subjected to tangent plane treatment and is amplified by 50 times, the area ratio of the spheroidic tissue is greater than or equal to 85%; the average diameter of the spheroidic structure is R [mu] m, the average thickness of the matrix structure is L [mu] m, and the coke satisfies 5 < = R / L < = 30. The coke provided by the invention has high isotropy, rate capability reduction caused by directional arrangement of graphite can be reduced, and the negative electrode material prepared from the coke can have relatively high capacity and excellent rate capability.

The invention relates to the technical field of angiogenesis and healing of diabetic wounds, and discloses a method for promoting angiogenesis and healing of diabetic wounds based on HSP90-CD93 interaction, which comprises the following steps: applying one of an HSP90 agonist, delivering a CD93 overexpression vector or applying a CD93 glycosylation agonist, locally enhancing the HSP90-CD93 interaction on the wound, and promoting the angiogenesis and healing of the diabetic wounds based on the HSP90-CD93 interaction. According to the present invention, with the application of the CD93 in the treatment of diabetes mellitus, the level of the O-linked N-acetyl glucosamine (O-GlcNAc) modification (O-GlcNAc) of the CD93 is maintained so as to activate the downstream FAK signal channel, such that the migration, the adhesion and the angiogenesis of endothelial cells can be effectively promoted, and the wound healing under the diabetes mellitus condition can be ultimately accelerated;

A method to activate or enhance phosphorylation of focal adhesion kinase (FAK) are provided herein. Methods to treat musculoskeletal disease in a mammal, comprising the administration of one or more small molecules having FAK activation properties are also provided.

A combined drug combination, drug composition or combination product of a pan-RAS (ON) inhibitor compound and a FAK (focal adhesion kinase) inhibitor, and a method for using the combined drug combination, drug composition or combination product to prepare a drug for preventing or treating a related pathological condition.

The present invention relates to a new focal adhesion kinase (FAK) inhibitor, and particularly to a compound as represented by formula (I) or a stereoisomer, tautomer or isotopic variant thereof, or a pharmaceutically acceptable salt thereof. The present invention further relates to a pharmaceutical composition containing the FAK inhibitor, and the use thereof in the treatment of FAK-mediated diseases.

The present invention provides novel adamantane derivatives as inhibitors of a focal adhesion kinase, pharmaceutically acceptable salts thereof, stereoisomers thereof, hydrates or solvates thereof, and a pharmaceutical composition comprising same.

Cerebral small vessel disease (SVD) is a leading cause of stroke and a major contributor to cognitive decline and dementia in the population. Evidences indicate that blood brain barrier dysfunction may play a significant role in VD pathogenesis. Recently, an inverse association of TRIM47 expression in brain and vascular tissues with extensive-SVD severity was reported in a human genome wide association study combined with summary-based Mendelian randomization studies and profiling of human loss-of-function allele carriers. Now, the inventors demonstrate TRIM47 is a key regulator of actin cytoskeleton organization through KEAP1 / NRF2 signalling pathway and might be protective from oxidative stress in brain EC. In particular, the in vitro TRIM47 knockdown decreases directed EC migration and delays EC adhesion process with loss of actin cortical reorganization and focal adhesion contacts. Furthermore, RNA sequencing and BioID results indicate that TRIM47 knockdown in brain EC, represses the expression of genes associated with cytoskeleton and NRF2 antioxidant pathway through a potential interaction with KEAP1. Accordingly, the present invention relates to the use of Nrf2 activators for the treatment of SVD.

The present invention relates to a β-1 integrin subunit agonist peptide and, more specifically, to a β-1 integrin subunit agonist peptide that binds to a β-1 integrin subunit to increase focal adhesion kinase (FAK) and AKT, which are intracellular downstream signals. The peptide then increases a regeneration signal to enhance the differentiation of tight junction proteins required for regeneration, thereby exhibiting the effect of preventing or treating diseases caused by fibrosis. The peptide according to the present invention can be used as a preventive or therapeutic agent for diseases caused by fibrosis, and can be used in combination with existing therapeutic agents.