22 results about "Gefitinib" patented technology

The application discloses a fluorescence enhancement anchor agent based on a fluoroboron dipyrrin-tetrazine dye for inflation microscopy technology, and belongs to the technical field of biochemical analysis. The fluorophore of the fluorescence enhancement anchor agent is shown in formula (I), formula (II) or formula (III): the tetrazine group carried by the fluorescence enhancement anchor agent is removed from fluorescence quenching through a biological orthogonal reaction with a drug probe, and the drug probe is shown in formula (IV): the fluorescence enhancement anchor agent can covalently and non-covalently anchor small molecules in a hydrogel network based on a tetrazine biological orthogonal reaction, and realizes inflation microscopic fluorescence imaging of a double fluorescence enhancement mechanism. In addition, the drug probe selects a non-covalent drug, gefitinib, as a probe core, is modified with a BCN click handle, and successfully realizes in-situ fluorescence inflation microscopic imaging of an EGFR drug-target, thereby providing a new tool for research and clinical research on non-covalent drug target co-localization information of exosomes.

Disclosed are methods of treating cancer with a tri-agent therapy. The methods include a cancer treatment regimen with two or three different antineoplastic medications, including tamoxifen, gefitinib, and vinorelbine (TGV). The cancer treatment regimen can include sequential and / or concurrent administration of tamoxifen, gefitinib, and vinorelbine. The cancer treatment regimen can include sequential and / or concurrent administration of tamoxifen and gefitinib as adjuvants to a prescribed treatment. The cancer treatment regimen can be cyclical or can be a continuous metronomic treatment with metronomic dosing. The cancer treatment regimen can be cyclical and then can be followed by a continuous metronomic treatment with metronomic dosing.

The invention relates to application of a combination of STM2457 and gefitinib in preparation of a medicine for preventing and treating lung cancer, and belongs to the technical field of biological medicines. The invention provides an application of an METTL3 inhibitor and gefitinib in preparation of a medicine for preventing and treating lung cancer. In a cell experiment, the expression of METTL3 is inhibited and then Gefitinib is used, so that the killing effect of the Gefitinib on lung cancer cells is promoted, and the drug resistance of the lung cancer cells on the Gefitinib is reduced. The small molecule inhibitor STM2457 of the METTL3 and the Gefitinib are combined for medication, so that the killing effect on cancer cells can be synergistically improved. In a mouse experiment, compared with a single drug, the drug combination has the advantages that the growth of tumors is more effectively inhibited, the lymph node metastasis of lung cancer cells can be effectively prevented, no obvious side effect exists, and a good treatment effect is shown. Therefore, the drug combination of the METTL3 inhibitor and the Gefitinib has a remarkable treatment effect on the NSCLC.

This invention provides hepatocellular carcinoma-derived growth factor (HDGF) as a target for resistance to tyrosine kinase inhibitors and its related applications. This invention provides the application of HDGF as a target in screening and / or preparing drugs that can improve resistance to tyrosine kinase inhibitors in patients. This invention discovers that high expression of HDGF is one of the mechanisms of resistance to molecularly targeted drugs such as gefitinib and other tyrosine kinase inhibitors. Targeting HDGF can effectively improve resistance to gefitinib in NSCLC and enhance therapeutic efficacy.

This invention relates to a small-molecule fluorescent photosensitizer containing a gefitinib backbone structure and an AIE group, its preparation, and its application, belonging to the field of fluorescent photosensitizer technology. The fluorescent photosensitizer includes an AIE group, a linking group, and a recognition group. On one hand, the AIE group backbone structure consists of a pyridine cation (electron acceptor, A), an ethylene group (π-bridge), a thiophene fragment (π-bridge and electron donor, D), and a triphenylamine segment (D), which is a typical D-π-A molecular configuration, thus exhibiting near-infrared fluorescence emission. On the other hand, by introducing heavy atoms to enhance the spin-orbit coupling of the photosensitizer, the efficiency of singlet oxygen generation is improved. The fluorescent photosensitizer can precisely target EGFR-overexpressing non-small cell lung cancer cells without illuminating normal cells. The fluorescent photosensitizer exhibits aggregation-induced emission properties, avoiding the ACQ effect during aggregation, greatly improving the ROS generation efficiency and promoting its tumor-killing effect.

This invention discloses the application of fruquintinib combined with PD-1 monoclonal antibody in maintenance therapy for HER-2 negative advanced gastric cancer / geoesophageal junction adenocarcinoma, belonging to the field of tumor treatment technology. This invention targets HER2-negative advanced gastric cancer or gastroesophageal junction adenocarcinoma, specifically patients who achieve disease control after 3 months of first-line induction therapy with PD-1 monoclonal antibody combined with oxaliplatin, followed by maintenance therapy with fruquintinib combined with PD-1 monoclonal antibody without chemotherapy. The maintenance therapy regimen provided by this invention improves patients' quality of life and prolongs overall survival while delaying disease progression, and has significant clinical implications.

The invention provides an SLC16A3 inhibitor based on ferroptosis regulation and application of the SLC16A3 inhibitor in lung adenocarcinoma, and relates to the technical field of biological treatment drugs. The SLC16A3 inhibitor is a drug MSC-4381, the drug MSC-4381 is an effective SLC16A3 inhibitor, the SLC16A3 inhibitor can be used for inhibiting lactic acid transporter SLC16A3, breaking the redox steady state of tumor cells, inducing ferroptosis and remarkably enhancing the curative effect of the drug gefitinib, and in an in-vivo and in-vitro model, cell proliferation, migration and invasion can be inhibited through SLC16A3 knock-down or pharmacological inhibition, so that the SLC16A3 inhibitor can be used for preventing and treating the tumor cells. The MSC-4381 and the gefitinib are combined to promote lipid peroxidation and iron ion accumulation, the tumor growth can be obviously delayed through drug combination of the MSC-4381 and the gefitinib, the effect can be partially reversed through the Ferrostatin-1, the ferroptosis-dependent mechanism of the MSC-4381 and the gefitinib is verified, and transcriptional regulation and control of the SLC16A3 by the HIF1A and influence on ferroptosis resistance are clear. The invention provides a feasible combined medication strategy, verifies the significant tumor inhibition effect of the HIF1A-SLC16A3 axis in cell and animal models, reveals the key effect of the HIF1A-SLC16A3 axis in lung adenocarcinoma drug resistance formation, and provides a new combined treatment strategy and a new molecular target.

The present invention provides a drug for treating non-small cell lung cancer, belonging to the field of medicine. The drug's raw materials include gefitinib and andrographolide, wherein the concentration of gefitinib is 12-20 μM and the concentration of andrographolide is 200-250 μM. The drug is in the form of an oral liquid preparation or an oral tablet. Experimental results show that the drug provided by the present invention has a significant inhibitory effect on the expression of apoptosis-related proteins and genes in PC9 / G cells, with a greater inhibitory effect than gefitinib or andrographolide alone, indicating a certain synergistic relationship between the two.

The application discloses a composite nano-silicon ball drug delivery system and a preparation method and application thereof. The system takes mesoporous silica nanoparticles as a carrier, loads gefitinib, and is coated with a PD-L1 antibody modified platelet membrane on the surface. The application prepares a composite multifunctional mesoporous silica nanoparticle which loads gefitinib and is coated with a PD-L1 antibody modified platelet membrane on the surface, so that the composite multifunctional mesoporous silica nanoparticle can be directed to reach a tumor surgery blood vessel damage site, kill residual tumor cells, reduce matrix hardness in the microenvironment, enhance the permeability and toxicity of immune cells, the two effects are interdependent and mutually enhanced, and the application overcomes the invalidity of colorectal tumor immunotherapy and prolongs the survival period of patients.

The invention discloses a macrocyclic cytochalasin derivative as well as a preparation method and application thereof. The macrocyclic cytochalasin derivative comprises the macrocyclic cytochalasin derivative disclosed by the invention, and the macrocyclic cytochalasin derivative can obviously inhibit the proliferation of non-small cell lung cancer (H1975), and the inhibitory activity of part of compounds obviously exceeds that of positive control gefitinib. Wherein the efficacy of the compound 8 is equivalent to that of cis-platinum in H1975 cells, the efficacy of the compound 8 is better in HCC827 cells, and the toxicity of the compound 8 to normal cells is lower than that of the cis-platinum.

Provided are an shRNA for reversing EGFR-TKI drug resistance in non-small cell lung cancer and use thereof, belonging to the fields of molecular biology and biomedicine. By using the designed shRNA, the expression of the KLHL22 gene is targeted and inhibited, and the nucleotide sequence of the shRNA is set forth in SEQ ID No. 1-SEQ ID No. 2. It is found by means of in vivo experiments that targeted inhibition of KLHL22 expression can effectively reverse the drug resistance of NSCLC cells to EGFR-TKI. In in vitro cell experiments, inhibition of KLHL22 expression significantly improves the sensitivity of drug-resistant NSCLC cells to gefitinib, thereby restoring the anti-tumor effect of the drug. This innovative strategy provides a new direction for overcoming EGFR-TKI drug resistance, and has important clinical application prospects.

The invention belongs to the technical field of biological medicine, and particularly relates to application of tasilimus in preparation of a product for overcoming drug resistance of non-small cell lung cancer. The invention finds that the combined use of the first generation (gefitinib) and the third generation (osimertinib) EGFR-TKI can significantly reduce the tolerance degree of EGFR-TKI drug-resistant cells to the two drugs. In a nude mouse model experiment, the curative effect of the combination of the tasilisib and the osimertinib is obviously superior to that of the single use of the osimertinib or the combination of the osimertinib and the LY294002, the obvious tumor growth inhibition effect is shown, and the drug-resistant relapse of tumors can be effectively delayed. Different from other PI3KCA inhibitors, the enhancement of the EGFR-TKI targeted therapy effect of the tasilimus does not depend on the inhibition of a PI3K / AKT pathway, but recovers the sensitivity of the drug-resistant cells to the EGFR-TKI by awakening the dormant state of the tumor, thereby providing a new thought for a therapeutic scheme.

The invention discloses a polypeptide for inhibiting lung adenocarcinoma metastasis and application thereof, belongs to the technical field of biology, and aims to solve the problems that lung adenocarcinoma cells in the prior art have very strong invasion and migration ability, and non-small cell lung cancer patients with high expression of NSUN2 easily generate drug resistance to gefitinib drugs. The amino acid sequence of the polypeptide for inhibiting lung adenocarcinoma metastasis is as shown in a general formula X-RHTQIRPTMFPPY; x at the N terminal in the general formula represents a modification group, and Y at the tail represents a cell-penetrating peptide; the invention is suitable for preparing a therapeutic reagent for lung cancer, and can achieve the effect of inhibiting the methylation modification of NSUN2 so as to inhibit the metastasis of lung adenocarcinoma.

The application discloses a kind of biotinylated gefitinib probe and its preparation method and application, the probe described in the application is better in stability, sensitivity and accuracy are high, can be long-term preserved, can be used in the experiment needing long time preservation and multiple analysis;It can also be used to detect the binding condition of gefitinib and EGFR in various situations, treat or diagnose cancer;Determine the EGFR mutation type in combination with gene sequencing, the feasibility and effectiveness of the treatment of gefitinib to the EGFR mutation type can also be evaluated, guide drug use.Therefore, biotinylated gefitinib probe is expected to become indispensable tool in precision medicine, so that more patients benefit from gefitinib treatment.

The present invention relates to the treatment of cancer and particularly of lung cancer. In the present study, the inventors analyzed the role of the Notch pathway in EGFR-driven lung adenocarcinoma (LUAD) using complex genetic mouse models and patient derived xenografts. They found that, similarly to KRAS-driven LUAD, EGFR-driven LUAD shows both Notch pathway hyperactivation and addiction to its activity. Importantly, combination of EGFR tyrosine Kinase Inhibitors (TKIs) with Notch inhibition re-sensitizes LUAD cells harboring gatekeeper mutations EGFRT790M or EGFRC797S to gefitinib and osimertinib, respectively. Moreover, they show that pSTAT3, which is known to increase upon EGFR TKI treatment, directly binds to the HES1 promoter and represses HES1 expression. Finally, high HES1 expression levels correlate with shorter progression free survival and its expression increases upon progression in EGFR mutated patients under TKI treatment. Thus, the present invention relates to a combination of a tyrosine-kinase inhibitor (TKI) against epidermal growth factor receptor (EGFR) and an inhibitor of the Notch signalling pathway for use in the treatment of a cancer in a subject in need thereof.

The present invention relates to a novel oxazole derivative and a composition for preventing or treating cancer, comprising same. The oxazole derivative compound according to the present invention has MDH1 and MDH2 enzyme inhibitory activities, exhibits proliferation inhibitory and tumor inhibitory activities against cancer cells, exhibits an effective proliferation inhibitory effect on KRAS-LKB1 co-mutation cancer cells, and exhibits a better anticancer effect when co-administered with an anticancer agent such as an anti-PD-1 inhibitor or gefitinib. Therefore, the oxazole derivative compound according to the present invention is expected to be effectively used as a therapeutic agent for various cancers.

The application belongs to the technical field of pharmaceutical chemistry, and relates to a gefitinib pharmaceutical co-crystal and a preparation method thereof. The application specifically provides a co-crystal formed by gefitinib and malonic acid in a molar ratio of 1:2. The gefitinib pharmaceutical co-crystal provided by the application has high solubility and good solubility, is helpful to improve the bioavailability, and has important value for optimization and development of gefitinib preparations.

The present invention relates to a novel oxadiazole derivative and a composition for preventing or treating cancer, comprising same. The oxadiazole derivative compound according to the present invention has the activity of inhibiting MDH1 and MDH2 enzymes, exhibits proliferation inhibitory and tumor inhibitory activities against cancer cells and effective proliferation inhibitory efficacy against KRAS-LKB1 co-mutation cancer cells, and exhibits an excellent anticancer effect when co-administered with an anticancer agent such as an anti-PD-1 inhibitor or gefitinib. Therefore, the oxadiazole derivative compound according to the present invention is expected to be effectively used as a therapeutic agent for various cancers.

The invention provides an application of Bifidobacterium animalis H22B905 in preparation of a medicine combined with gefitinib, the Bifidobacterium animalis H22B905 is preserved in Guangdong Microbiological Culture Collection Center (GDMCC) on October 23, 2024, the preservation number is GDMCC No: 65329, the preservation address is Institute of Microbiology, Guangdong Academy of Sciences, on the 5th floor, No. 59, No. 100 Courtyard, Xianlie Middle Road, Guangzhou, and the taxonomic name is Bifidobacterium animalis. The invention not only provides a new solution for alleviating the side effect of gefitinib, but also provides powerful scientific support for taking the probiotics as an auxiliary product for treating gefitinib.

The present invention discloses the use of a substance that knocks down TIM in the preparation of a product for treating non-small cell lung cancer. The present invention also discloses the use of a substance that knocks down TIM in the preparation of a product for inhibiting the proliferation of non-small cell lung cancer cells, inhibiting the migration of non-small cell lung cancer cells, increasing the responsiveness of non-small cell lung cancer cells to gefitinib, inhibiting the activation of EGFR and / or AKT and / or mTOR pathways in non-small cell lung cancer cells, downregulating the expression levels of EGFR-regulated oncogenes in non-small cell lung cancer cells, inhibiting the expression levels of SPHK1 and / or ATF3 in non-small cell lung cancer cells, and inhibiting the activation of the STAT3 pathway in non-small cell lung cancer cells. Compared with existing drugs for treating non-small cell lung cancer, the siRNA for knocking down TIM of the present invention is effective against a variety of non-small cell lung cancer tumor cells with different gene mutations, and has a more stable anti-tumor effect.

The present invention is directed to a protein kinase inhibitor for use in the treatment of tuberculosis, by direct inhibition of the growth of a Mycobacterium tuberculosis complex species, and to corresponding methods of treating tuberculosis. More specifically, the invention relates to the use of protein tyrosine kinase inhibitors such as gefitinib, erlotinib, or imatinib for use in the treatment of tuberculosis, by direct inhibition of the growth of a Mycobacterium tuberculosis complex species, rather than through use in host-directed therapy. Also provided are methods of determining the ability of a protein tyrosine kinase inhibitor to inhibit the growth of a Mycobacterium tuberculosis complex species and methods of identifying a protein tyrosine kinase inhibitor as being potentially effective in the treatment of tuberculosis by direct inhibition of a Mycobacterium tuberculosis complex species.

Disclosed are a composition comprising a TLR4 / MD2 pathway inhibitor and an EGFR inhibitor, a pharmaceutical composition comprising the composition, and the use of the composition / pharmaceutical composition in cancer treatment. The TLR4 / MD2 pathway inhibitor and the EGFR inhibitor can synergistically kill a variety of cancers, including cutaneous melanomas, and have a significant inhibitory effect on the growth of cancer cells without affecting bodyweight of mice. Moreover, compared with separate administration of the individual components, the composition according to the present disclosure can delay the occurrence of drug resistance in tumor-bearing mice and significantly inhibit the growth of Gefitinib-resistant cancer cells (e.g., non-small cell lung cancer tumors). Therefore, the composition according to the present disclosure can be used for preparing safe and effective anti-tumor medicament.