12 results about "PKM2" patented technology

The invention discloses application of eupatolide in preparation of a medicine for preventing and treating inflammatory bowel disease, application of eupatolide in preparation of a medicine for preventing and treating inflammatory bowel disease and application of a medicine preparation containing eupatolide in preparation of a medicine for preventing and treating inflammatory bowel disease, and researches that eupatolide (EPT) can be used for preparing the medicine for preventing and treating inflammatory bowel disease through targeting pyruvate kinase isoenzyme 2 (PKM2, Gene ID: 5135). The inflammatory response, glycolysis metabolism and mitochondrial homeostasis are synergistically regulated and controlled, so that the inhibition effect on the inflammatory bowel disease is exerted. Meanwhile, EPT has the advantages of being low in dosage, feasible in oral administration, free of obvious toxic and side effects and the like, and a solid experimental basis is provided for further developing EPT into candidate drugs for preventing and treating inflammatory bowel diseases.

The invention relates to the technical field of biological medicines, in particular to application of tetramer-form pyruvate kinase type 2 (PKM2) in preparation of a medicine for treating obesity. Pyruvate kinase type 2 is a key enzyme in a glycolytic pathway and has two conformations of dimer and tetramer, and the tetramer-form enzyme has high activity. The invention discovers that the PKM2 tetramer stabilizer TEPP-46 can stabilize PKM2 in a high-activity tetramer state and improve obesity-related metabolic disorder induced by high fat diet. The invention discloses a new way for regulating and controlling energy metabolism by stabilizing the form of the PKM2 tetramer, and provides a new medicine application direction for treating obesity and related metabolic diseases.

The invention relates to the technical field of medicines, and particularly discloses an application of artemether in preparation of an esophageal cancer radiotherapy sensitization medicine. The invention provides the application of artemether in preparation of esophageal cancer radiotherapy sensitization drugs for the first time, and researches find that the artemether can reduce glycolytic activity of esophageal cancer cells by down-regulating expression of key proteins and genes HK2, PKM2 and LDHA in a glycolytic pathway so as to enhance esophageal squamous cell carcinoma radiotherapy sensitization. The invasion ability is inhibited, and cell apoptosis is induced, so that the radiotherapy sensitivity of esophageal cancer cells is enhanced. The artemether and radiotherapy combined treatment provided by the invention is expected to provide a promising treatment scheme for ESCC patients, and has great significance in breaking through the bottleneck of esophageal cancer radiotherapy.

Provided is a chiral cannabidiol (CBD) derivative drug, comprising four chiral derivatives, i.e., (7S)-(-)-CIAC001, (7R)-(-)-CIAC001, (7S)-(+)-CIAC001, and (7R)-(+)-CIAC001; and a use of the four chiral derivatives of CBD in the treatment of neuroinflammation and opioid addiction. Also disclosed are anti-neuroinflammation effects and the ability to regulate the activity of pyruvate kinase M2 (PKM2) of CBD analogs.

A method for treating brain injury in a subject comprises administering a therapeutically effective amount of a PKM2 (pyruvate kinase M2) protein variant. The protein variant is delivered systemically and can reduce tissue damage after ischemic brain tissue reperfusion. The methods specifically involve the use of G415R mutants of PKM2 protein variants. The treatment is suitable for brain injury caused by hemorrhagic stroke and ischemic stroke. The PKM2 protein variants are ideally administered intravenously within one hour of reperfusion to maximize their therapeutic efficacy.

The invention relates to the technical field of biological medicines, and particularly discloses a novel target MFN2 protein, a targeted small-molecule compound salvianolic acid B thereof and application. The technical key points are as follows: the diagnosis and treatment effect of the MFN2 protein as a novel target in rheumatoid arthritis (RA) and the application of the MFN2-targeted small molecular compound salvianolic acid B in preparation of drugs, food or health care products for treating RA. The medicine, food or health care product comprises a medicine which takes MFN2 protein as a target spot and mainly inhibits MFN2 mediated M1 polarization in mononuclear / macrophages. It is found for the first time that MFN2 protein in peripheral blood mononuclear cells of an RA patient participates in M1 polarization of mononuclear / macrophages, and a natural small molecule compound Sal-B can inhibit the MFN2-mediated M1 polarization tendency of the mononuclear / macrophages by inhibiting interaction of the MFN2 protein and PKM2 protein, so that inflammation and bone destruction are relieved, and the effect of treating RA is achieved.

This provides a method for treating patients suffering from diseases caused by organ / tissue fibrosis. [Solution] The method includes administering a PKM2 activator. The PKM2 activator can reduce LOX protein expression and activate PKM2.

A method of treating a patient suffering from disease that is caused by organ / tissue fibrosis includes the administration of a PKM2 activator. The PKM2 activator can reduce LOX protein expression and activate PKM2.

The invention belongs to the technical field of biological medicine, and particularly relates to application of a short peptide entrapped by lung-targeted liposome and used for blocking combination of PKM2-FOXO3A in preparation of a medicine for treating stroke-related lung injury, the amino acid sequence of the short peptide is shown as SEQ ID NO.1, the SEQ ID NO.1 RKGEDREGKR and Pe (at) P-Lipo can be used for remarkably relieving MCAO mouse lung tissue pathological injury, and can be used for preparing a medicine for treating stroke-related lung injury. According to the present invention, with the application of the cerebral ischemia injury in the lung, the total reactive oxygen species (ROS) level in the lung tissue and the mitochondrial ROS level, the reduction of the ATP content can be reversed, the level of the lung tissue inflammation-related protein can be reduced, and the enrichment of PKM2, FOXO3A and TXNIP in the mitochondria can be reduced so as to alleviate the lung tissue oxidative stress and the mitochondrial injury caused by the cerebral ischemia injury, and provide the lung protection effect;

The application belongs to the technical field of immunotherapy, and particularly relates to a method for improving the effect function of NK cells, wherein point mutation vectors PKM2-322K-R and PKM2-433K-R of a PKM2 gene are constructed, the glycolysis metabolic process is affected, the generation of lactic acid is reduced, and the lactic acidification modification level is inhibited. The application further provides a construction method of NK92MI cells of a PKM2 protein, and the steps include constructing a vector, extracting a plasmid, packaging and concentrating viruses, and transfecting target cells. The application targets lactic acidification modification, a protein modification, blocks lactic acidification modification, reverses the functional exhaustion of NK cells, makes PKM2 de-lactic acidification through point mutation, can partially reverse the function of NK cells, and restores the expression level of effect molecules of NK92MI cells.

This invention provides the application of agents that inhibit NNMT binding to FGFR1 in the prevention and treatment of tumors. Through mutation analysis and interactomics analysis, it reveals a previously unknown, non-enzyme-dependent role of NNMT in promoting aerobic glycolysis in breast cancer. It discovers that NNMT binds to FGFR1 and acts as a scaffold protein, promoting phosphorylation of PKM2 and LDHA at Y105 and Y10 sites, respectively. By positioning the FGFR1 binding interface to the 140-154 amino acid region of NNMT, this invention designs a competitive cell-penetrating peptide, NNMT-15, which can disrupt the NNMT-FGFR1 interaction, reduce the phosphorylation levels of PKM2 and LDHA, inhibit glycolysis, and suppress proliferation in NNMT-high-expressing cancer cells and cancer-associated fibroblasts. These findings reveal NNMT as a dual-function metabolic regulator and establish the NNMT-FGFR1 scaffolding effect as a targeted therapeutic axis in glycolysis-dependent tumors.

The present invention relates to prevention of congenital deformations. The invention further relates to cancer inhibition and prevention. The invention further relates to methods and compositions to modulate, antagonize, or agonize disparate signaling pathways that may converge to regulate patterning events and gene expression during prenatal development, postnatal development, and during development in the adult organism. The invention also relates to activators or deactivators of pyruvate kinase M2 (PKM2) for the treatment, prevention, or amelioration of diseases related to PKM2 function.