13 results about "Erlotinib" patented technology

Olmsted syndrome (OS) is a rare genodermatosis classically characterized by the combination of bilateral mutilating transgredient palmoplantar keratoderma (PPK) and periorificial keratotic plaques. The inventors obtained remarkable results with a treatment with a EGFR inhibitor (e.g. erlotinib) in 3 patients with Olmsted Syndrome and erythemalgia linked to different TRPV3 mutations. In less than 3 months, the drug induced a complete disappearance of the hyperkeratosis and the pain. Anorexia and insomnia disappeared with an improvement of the growth. Accordingly, the present invention relates to the use of EGFR inhibitors for the keratodermas.

The invention provides application of cedar biflavone in preparation of an EGFR (epidermal growth factor receptor) inhibitor, and belongs to the technical field of biomedicine. The cedarwood biflavone (CAS number: 3952-18-9) can obviously inhibit proliferation, migration and invasion of lung cancer cells and induce ferroptosis and epithelial-mesenchymal transition (EMT) reversion by regulating and controlling an EGFR (epidermal growth factor receptor) signal channel. In-vivo researches further prove that the cedarwood biflavone can effectively inhibit the growth of xenograft tumors in nude mice H1299, and has no obvious visceral toxicity. Mechanism research shows that the cedarwood biflavone plays an anti-tumor role by inhibiting EGFR phosphorylation, regulating and controlling a downstream signal channel and mediating lipid peroxidation, ferroptosis and EMT inhibition. In addition, the combined use of the cedarwood biflavone and the erlotinib can enhance the anti-tumor effect. Therefore, the invention provides a potential candidate compound for developing novel lung cancer treatment drugs and EGFR phosphorylation targeted drugs.

The invention relates to the technical field of chemical synthesis of medicines, and particularly discloses a production and preparation method of an erlotinib intermediate. The method comprises the following steps: taking 3, 4-dihydroxy benzaldehyde as an initial raw material, sequentially carrying out etherification, oxidation and nitration reactions to prepare 2-nitro-4, 5-bis (2-methoxyethoxy) benzoic acid, finally dissolving the 2-nitro-4, 5-bis (2-methoxyethoxy) benzoic acid, formamide, formic acid and triethylamine in gamma-valerolactone to form two material flows, and carrying out heat treatment to obtain the 2-nitro-4, 5-bis (2-methoxyethoxy) benzoic acid. And carrying out continuous cyclization reaction in a fixed bed reactor filled with a specific composite catalyst, and carrying out post-treatment to obtain the target product 6, 7-bis (2-methoxyethoxy)-4-quinazolinone. According to the method, the raw materials are easy to obtain, the reaction efficiency and the product purity are remarkably improved by optimizing the synthesis route and the reaction conditions, and a novel efficient, environment-friendly and stable method is provided for large-scale production of the erlotinib key intermediate.

This invention discloses a bio-preparation method for a key chiral intermediate of erlotinib ethyl ester. The method utilizes resting cells of *Saccharomyces cerevisiae* ZJPH1807 as a catalyst to prepare (R)-1-[4-chloro-2-(3-methyl-1H-pyrazol-1-yl)phenyl]-2,2,2-trifluoroethanol via biocatalysis of 1-[4-chloro-2-(3-methyl-1H-pyrazol-1-yl)phenyl]-2,2,2-trifluoroethanol. The product obtained using this strain exhibits high optical purity (ee value > 99.9%) and a reaction yield of 86.4%. The process is simple, environmentally friendly, and uses microbial cells as the biocatalyst, resulting in low cost.

This invention, entitled "Combined Application and Product of BAM-15 and Erlotinib," belongs to the field of combined antitumor drug application technology. The technical problem it aims to solve is the low response and limited efficacy of existing erlotinib monotherapy to EGFR wild-type lung adenocarcinoma, and the lack of effective targeted intervention options in clinical practice. The key points of the technical solution are: combining BAM-15 and erlotinib for the interventional treatment of EGFR wild-type lung adenocarcinoma; the combination produces a significant synergistic effect, with tumor suppression superior to the additive effect of using either drug alone, without antagonistic effects, effectively enhancing the inhibitory effect on EGFR wild-type lung adenocarcinoma and enriching clinical treatment options for tumors.

Methods are provided for treating lung cancer, and more particularly for treating pulmonary adenocarcinoma in a canine subject. The method may comprise assaying a biological sample from the canine subject, such as a tumor sample or a plasma sample, for a mutation in the HER2 gene. The mutation may include HER2 V659E, HER2 A664T, or HER2 K676E. If one or more of the mutations is present in the biological sample, the methods further include treating the canine subject by administering a therapeutically effective amount of an inhibitor of HER2. For example, a HER2 V659E may indicate increase sensitivity to a HER2 inhibitor. The HER2 inhibitor may include a small molecule HER2 inhibitor, such as trastuzumab, neratinib, lapatinib, erlotinib, and pertuzumab.

A carrier-free nanoparticle based on the self-assembly of curcumin-erlotinib conjugate (EPC) that exhibits stronger cell killing, better anti-migration effects, and anti-invasion effects for pancreatic cancer cells than the combination of free curcumin and erlotinib.

The present application relates to the field of pharmaceutical analysis, in particular to a method for detecting erlotinib related impurities and application thereof. The method adopts high performance liquid chromatography-mass spectrometry, the chromatographic column of the high performance liquid chromatography uses high-purity silica gel as the filler, and the mass spectrometry ion source is ESI source. The method provided by the present application realizes effective separation and detection of extremely low content of erlotinib related impurities. The method has the advantages of good specificity, high sensitivity and the like, realizes simultaneous detection of multiple erlotinib impurities, and has extremely low detection limit.

The utility model discloses an environment-friendly treatment system for erlotinib intermediate production wastewater. The environment-friendly treatment system comprises a triethylamine recovery kettle, a condenser and a tail gas absorber, an exhaust port of the triethylamine recovery kettle is communicated with a shell pass of the condenser, a tail gas exhaust port of the condenser is communicated with a gas inlet pipe of the tail gas absorber, a cold and hot medium coil pipe is arranged outside the triethylamine recovery kettle, and a tail gas outlet is further formed in the top end of the tail gas absorber. Preferably, a stirrer is arranged in the triethylamine recovery kettle, and the stirrer is driven by a first rotating motor to rotate. Preferably, a discharge port is formed in the bottom end of the triethylamine recovery kettle, a liquid separation observer is mounted on the discharge port, and a transparent observation window is arranged on the liquid separation observer. According to the utility model, the absorption capacity of the absorption liquid to organic gas in the tail gas is enhanced, the tail gas can be discharged after reaching the standard after being treated, and the pollution to the atmospheric environment is reduced.

The present application relates to the technical field of animal model construction method, and particularly relates to a kind of construction method of small molecule drug induced peritoneal malignant mesothelioma animal model.The method uses epidermal growth factor receptor tyrosine kinase inhibitor (Erlotinib or its salt, Erlotinib) to be injected into abdominal cavity to mammal, and peritoneal malignant mesothelioma animal model is induced to form.The technical scheme can solve the technical problem that the construction process of peritoneal malignant mesothelioma animal model in prior art is too long or needs special equipment and conditions.The method of peritoneal malignant mesothelioma animal model constructed by the technical scheme is short in time consumption, high in efficiency, and does not need asbestos exposure and virus gene operation, greatly saves time cost and economic cost, is simple and easy to operate, and is easy to popularize, and the animal model is expected to be used for further revealing malignant mesothelioma mechanism of occurrence and development and screening new therapeutic drugs, and has ideal application prospect.

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.

The present invention relates to the field of biomedicine, and specifically, the present invention relates to the use of AREG in eosinophilic inflammation of chronic sinusitis with nasal polyps. The present invention discovered for the first time that nasal epithelial cells, especially basal cells, are both the cell source of AREG and one of the important target cells of AREG. AREG promotes the proliferation of epithelial basal cells and inhibits the differentiation of basal cells into ciliated cells, resulting in structural abnormalities and functional damage to the epithelial barrier of human CRSwNP tissue. AREG chemotaxis and activation of human peripheral blood eosinophils, and its receptor EGFR antagonist Erlotinib can antagonize the effect of AREG on eosinophils. Neutralizing AREG secreted by epithelial cells or other inflammatory cells can effectively reduce the eosinophilic inflammatory response of the nasal mucosa in the CRSwNP mouse model and restore the damaged epithelial barrier function of the mouse nasal mucosa. It is proved that the use of neutralizing antibodies or shRNA against AREG or EGFR as antagonists can reduce the eosinophilic inflammatory response of CRSwNP by inhibiting the action of AREG.