10 results about "PI3K signaling" patented technology

The application provides an oxazinane compound, a preparation method, a pharmaceutical composition and application, and a general formula of the oxazinane compound or a pharmaceutically acceptable salt thereof is shown as formula (I). The oxazinane compound has obvious proliferation inhibition effect on cancer cells, especially human head and neck squamous cell carcinoma cell strains HSC4, HSC3, HSC2, CAL33, SCC4 and human glioma cell strain U251, can block the cell cycle, effectively inhibit the phosphorylation level of key proteins in the PI3K / AKT / mTOR pathway at the molecular level, has the potential to be prepared into a new antitumor drug, and has a good market prospect.

The application provides a peptide lipid nanoparticle, a preparation method, an application and a cancer combined treatment drug combination, and belongs to the technical field of biological medicines.The application proposes a novel synergistic anti-tumor strategy based on the combination of a peptide lipid nanoparticle and a low-dose mTOR inhibitor, synergistically inhibits a PI3K / AKT / mTOR signal pathway, co-applies the peptide lipid nanoparticle loaded with p53 circular RNA and the mTOR inhibitor to cancer cells, restores p53 function, reactivates PTEN, blocks the feedback activation of PI3K / AKT, and directly inhibits mTOR by the mTOR inhibitor, thereby producing a persistent cascade double blocking. Moreover, p53 inhibits the evirolimus-induced pro-survival autophagy, converts it into a stress-induced process, and realizes the double inhibition and persistent blocking of the PI3K / AKT / mTOR pathway.

The invention provides an application of metformin in preparation of a medicine for preventing or treating immune checkpoint inhibitor related colitis. It is found through experiments that when the immune checkpoint inhibitor causes colitis, change of metabolic level represented by glycolysis caused by change of a PI3K / AKT / mTOR pathway in the colon is obviously accompanied, then Treg / Th17 steady state in the colon is affected, and a high inflammatory state is shown in the colon. According to the present invention, the influence on glycolysis and other metabolic pathways is achieved through the targeted interference of the metformin on the PI3K / AKT / mTOR pathway, the colitis caused by the immune checkpoint inhibitor can be significantly improved, the anti-tumor drug effect of the immune checkpoint inhibitor is not affected, and the method is generally superior to the original clinical methylprednisolone intervention scheme.

This invention discloses a pharmaceutical composition with preventive or therapeutic effects on liver injury. The pharmaceutical composition consists of turmeric dione and atractylodes lactone II. Through the synergistic effect of turmeric dione and atractylodes lactone II, it is used to treat liver injury caused by various reasons. Cell experiments show that this invention can effectively inhibit the proliferation activity of hepatic stellate cells (LX-2 cells) and inhibit the phosphorylation activation of the PI3K / AKT / mTOR pathway. Animal experiments show that this invention can improve liver function indicators and liver tissue pathological damage in animals with liver injury, regulate blood rheological indicators and related factor levels, and has broad application prospects. The preparation method and application of this invention are also disclosed.

The application discloses application of a SUCNR1 gene expression inhibitor in preparation of a product for preventing or treating a dairy cow dystocia. The application provides application of a substance taking a SUCNR1 protein as an inhibition target and / or a substance taking a SUCNR1 gene as an inhibition target in preparation of a product. The application of the product is as follows: promoting trophoblast cell apoptosis; inhibiting macrophage M2 type polarization; promoting trophoblast cell apoptosis by inhibiting macrophage M2 type polarization. The inventors of the application find that silencing the SUCNR1 gene can inhibit a PI3K signal pathway, thereby inhibiting macrophage M2 type polarization, thereby promoting trophoblast cell apoptosis, thereby helping to solve the problem of dystocia.

The present application belongs to the technical field of traditional Chinese medicine, and particularly relates to a traditional Chinese medicine composition for treating prostate cancer and a preparation method thereof. The traditional Chinese medicine composition is prepared from raw materials including the following components by weight: cassia twig 5-50 parts, poria 5-50 parts, cortex moutan 3-30 parts, red peony root 3-30 parts, persicae semen 3-30 parts, fructus psoraleae 1-20 parts, and drynaria 1-20 parts. The present application proves through experiments that the traditional Chinese medicine composition can effectively inhibit the proliferation, migration and invasion of prostate cancer cells. Through extensive transcriptome analysis, it is found that the traditional Chinese medicine composition inhibits the expression of key genes such as HSP90AA1 and CDK1, and regulates the PI3K signal pathway and AR signal transduction in the prostate cancer pathway to achieve inhibition of prostate cancer. Therefore, the traditional Chinese medicine composition has a good application prospect.

The present disclosure relates to a pharmaceutical combination comprising (1) a first agent which is a CDK inhibitor or a pharmaceutically acceptable salt thereof and (2) a second agent which is an anti-hormonal agent or a pharmaceutically acceptable salt thereof. The present disclosure also relates to a pharmaceutical combination comprising (1) a first agent which is a CDK inhibitor or a pharmaceutically acceptable salt thereof, (2) a second agent which is an anti-hormonal agent or a pharmaceutically acceptable salt thereof, and (3) a third agent which is an agent that regulates the PI3K / Akt / mTOR pathway or a pharmaceutically acceptable salt thereof.

The invention belongs to the technical field of biological medicines, and discloses an application of ACSS1 as a target in screening / preparing a medicine for treating renal clear cell carcinoma, and an application of a reagent for inhibiting expression of ACSS1 in preparing a medicine for treating renal clear cell carcinoma. The invention also discloses application of a reagent for detecting ACSS1 expression in preparation of a kit for diagnosing renal clear cell carcinoma or prognosis of renal clear cell carcinoma. Experiments prove that by knocking down ACSS1, the expression level of a tyrosine kinase receptor EphA2 can be lowered, growth of the renal clear cell carcinoma is inhibited, a new target is provided for treatment of the renal clear cell carcinoma, PI3K / AKT / mTOR pathway activation can be inhibited by inhibiting EphA2, then proliferation, migration and metabolism of cells are regulated and controlled, and therefore the purpose of relieving or treating the renal clear cell carcinoma is achieved. The invention provides a new direction and thought for the treatment of the clear cell renal carcinoma, and is expected to be applied to the research and development of new drugs for treating the clear cell renal carcinoma.

The present disclosure relates to a pharmaceutical combination comprising (1) a first agent which is a CDK inhibitor or a pharmaceutically acceptable salt thereof and (2) a second agent which is an anti-hormonal agent or a pharmaceutically acceptable salt thereof. The present disclosure also relates to a pharmaceutical combination comprising (1) a first agent which is a CDK inhibitor or a pharmaceutically acceptable salt thereof, (2) a second agent which is an anti-hormonal agent or a pharmaceutically acceptable salt thereof, and (3) a third agent which is an agent that regulates the PI3K / Akt / mTOR pathway or a pharmaceutically acceptable salt thereof.

This invention discloses an in vitro candidate screening method based on the LAPTM5 / USP10 / PTEN pathway. This method is based on the mechanism by which LAPTM5 weakens PTEN stability by promoting lysosomal degradation of USP10, thereby activating the PI3K / AKT / mTOR pathway, inhibiting autophagy, and promoting epithelial-mesenchymal transition. The screening method includes: establishing senescence-induced or LAPTM5-overexpressing cell models; after candidate treatment, detecting multi-level indicators such as LAPTM5 / USP10 / PTEN expression and modification, PI3K / AKT / mTOR phosphorylation, autophagy markers LC3 and p62, EMT markers, cell morphology, and migration ability; and comprehensively evaluating and ranking candidates based on their regulatory effects on each indicator. The screening system integrates data acquisition, processing, analysis, evaluation, storage, and visualization output modules to automate the screening process. This invention establishes a candidate screening platform based on a clear molecular mechanism, a comprehensive indicator system, and quantifiable evaluation, which can be used to screen candidates from compound libraries or natural products that have regulatory effects on the aforementioned signaling axis, and provides a technical basis for subsequent research.