155 results about "Etoposide" patented technology

The present invention provides amphiphilic prodrugs comprising a therapeutic compound conjugated to an PEG-oligomer/polymer and methods for using said prodrugs to enable oral drug delivery and/or delivery of drugs across the blood brain barrier into the central nervous system.

Medical devices, and in particular implantable medical devices, may be coated to minimize or substantially eliminate a biological organism's reaction to the introduction of the medical device to the organism. The medical devices may be coated with any number of biocompatible materials. Therapeutic drugs, agents or compounds may be mixed with the biocompatible materials and affixed to at least a portion of the medical device. These therapeutic drugs, agents or compounds may also further reduce a biological organism's reaction to the introduction of the medical device to the organism. In addition, these therapeutic drugs, agents and/or compounds may be utilized to promote healing, including the formation of blood clots. Also, the devices may be modified to promote endothelialization. Various materials and coating methodologies may be utilized to maintain the drugs, agents or compounds on the medical device until delivered and positioned. In addition, the devices utilized to deliver the implantable medical devices may be modified to reduce the potential for damaging the implantable medical device during deployment. Medical devices include stents, grafts, anastomotic devices, perivascular wraps, sutures and staples. In addition, various polymer combinations may be utilized to control the elution rates of the therapeutic drugs, agents and/or compounds from the implantable medical devices.

The present invention relates to pharmaceutical compositions and methods for the mucosal and oral administration of monoterpenes and derivatives thereof. The compositions of this invention further comprise one or more surfactants and cosolvents and are in the form of self-emulsifying compositions. The compositions of the invention may further comprise water-insoluble therapeutic agents, vaccines and diagnostics. Such agents include but are not limited to taxanes, steroids, topoisomerase inhibitors such as etoposide and other water-insoluble or lipophilic drugs.

The invention relates to a medicine technical field. Etoposide has broad-spectrum anticancer activity and rather high therapeutic index, however, the etoposide hardly can be dissolved in water and the fat-soluble property is rather poor, the shortcoming of low bioavailability exists to different extent in oral preparations for present clinical use, tablet and soft capsule, for example. The invention aims at improving the hydrophilic property and the lipotropy of the etoposide, promoting the bioavailability of the etoposide and providing an etoposide preparation which has a simple preparation technique and is easily taken. Main medicine of the preparation of the invention is phospholipid compound of etoposide. The invention also provides a self-emulsifying agent and a preparation method thereof. The zooperies is a primary indication that the ACU of the self-emulsifying agent of the phospholipid compound of etoposide is 1.3 to 1.7 times of that of the soft capsules on sale.

Compositions containing epidithiodioxopiprazines and methods of their use are provided. Epidithiodioxopiprazines can be isolated from natural resources or synthesized de novo. Moreover, epidithiodioxopiprazines, including Verticillin A, are shown to effectively sensitize multiple types of tumor cells to TRAIL-induced apoptosis. In addition, epidithiodioxopiprazines, including Verticillin A, are shown to effectively overcome cancer cell resistance to existing drugs (i.e. Etoposide, Cisplatin, 5-FU and Doxorubicin). Therefore, compositions and methods are provided for use in sensitizing target cancer cells to death receptor- and other anticancer drugs-induced apoptosis. Methods of treating cancer in a subject in need thereof are also provided.

A 4'-demethylepipodophyllotoxin derivative IIIa-n is prepared by taking etoposide as raw material, reacting with sodium iodide to generate 4-bit iodine substitute and obtain intermediate II, agitating while adding into barium carbonate, regulating reactive system pH 7-8, adding into amino-compound, and reacting to room temperature for 8-10 hrs to obtain final product. It's simple and efficient, it can avoid 4-bit surface isomerization and 4-bit demethylation, it has strong inhibiting function of multiple tumor cell strain and non-toxic.

The invention provides an etoposide lipidosome used for injection or oral administration. The etoposide lipidosome is characterized in that etoposide is enveloped with phospholipid type substance, and the etoposide lipidosome with small grain size, high entrapment efficiency, good stability and low toxic side effect is prepared. The prepared etoposide lipidosome enhances the solubility and the stability of the etoposide, reduces the toxicity of the etoposide and prolongs the cycling time of the medicine in the blood, thereby improving the therapeutic effect of the medicine; and the preparation prepared by the etoposide lipidosome has the characteristics of low toxicity, low sensitivity and high efficiency on the clinical application. The invention also relates to a preparation method of the etoposide lipidosome, which has simple preparation process and low cost and is suitable for the industrial production.

The use of the maximum tolerated dose (MTD) of individual drugs to determine appropriate administration ratios of drugs for combination therapy, wherein the ratios of drugs are fixed based on the same percentage of the MTD for each drug. Furthermore, antineoplastic compositions comprising liposomal encapsulated gemcitabine alone or in combination with free or liposomal encapsulated antineoplastic agents, such as idarubicin, irinotecan, etopside, cisplatin, cyclophosphamide, doxorubicin, or vincristine are diclosed.

The present invention describes selective cell growth inhibition of myeloma cells by ellipticine derivatives, 9-methoxy ellipticine and 9-dimethyl amino-ethoxy ellipticine. The cell growth inhibition efficacy was highest for 9-dimethyl amino-ethoxy ellipticine among the ellipcitine derivatives tested. The cell toxicity of 9-dimethyl amino-ethoxy ellipticine was selective for myeloma cells and did not kill normal cells in the effective antineoplastic dose range. 9-dimethyl amino-ethoxy ellipticine was superior to existing antimyeloma drugs, Adriamycin® and Etoposide in eliciting early and better cell growth inhibition response.

The invention provides a breast cancer multidrug-resistant cell strain constructed by virtue of epirubicin induction, wherein the breast cancer multidrug-resistant cell strain has a collection number of CCTCC C201439. The invention further provides a method for constructing the breast cancer multidrug-resistant cell strain. According to the invention, an MDA-MB-231/EPI drug-resistant strain is successfully established, wherein a drug-resistant index is 26.27 times, and obvious cross resistance is produced for taxol, etoposide and cis-platinum. A drug-resistant tumor cell model is provided for the following related researches so as to research drug-resistant tumor cell morphology and biological characteristics, research a tumor multidrug resistance mechanism, analyze sensitivity to chemotherapeutic drugs as well as screen chemotherapeutic drugs, develop tumor drug resistant reverse drugs and research and develop a more effective tumor therapeutic method, and the like.

The invention relates to a multidrug resistant cell strain for oophoroma, which is characterized in that a human oophoroma SKOV3 cell strain is selected as a parental cell; the action concentration of chemotherapeutics of etoposide (VP16) is gradually increased from 0.1 mu g/ml to 3 mu g/ml; and drug resistant SKOV3/VP16 cell strain is established. The SKOV3/VP16 cell can stably grow, transfer and reanimate in 3 mu g/ml VP16, makes the VP16 generate drug resistant index (RI) of 21.548, and performs intersect drug on MTX, DOX, DDP, VCR, 5-Fu and MMC except the VP16. The invention aims to provide a drug resistant tumor cell model for relative study on the tumor.

The invention discloses a preparation method of etoposide, which includes the following steps: preparation of beta-glucoside, coupling reaction and preparation of etoposide. In the step of the preparation of the beta-glucoside, methoxybenzylidene is protected to increase the content of the beta-glucoside; in the step of the coupling reaction, TiCl4 is used as a Lewis acid catalyst to enable the reaction to have better selectivity, so as to improve the conversion rate of a target product, reduce the generation of impurities accordingly, reduce the difficulty of purification for the etoposide, improve the yield and reduce the cost; and in the step of the preparation of the etoposide, diluted hydrochloric acid is used for being stirred at room temperature to obtain a target compound with higher purity, and the purity of obtained etoposide coarse product can reach about 90%, so as to avoid column purification, and also reduce the number of times of recrystallization. The preparation method is simple in operation, also very easy in post-treatment, and high in yield.

Etoposide analogs with improved water-solubility such as 4′-O-Demethyl-4′-(N′,N′-dimethyl-glycyl)-4β-(4″-nitroanilino)-4-desoxy-podophyllotoxin (8) and 4′-O-Demethyl-4′-(N′,N′-dimethyl-glycyl)-4β-(4″-fluoroanilino)-4-desoxy-podophyllotoxin (9) are described, along with pharmaceutical formulations containing the same, methods of use thereof, and intermediates and methods of making the same.

The invention discloses a new application of brusatol serving as a chemotherapeutic drug synergist, which is combined with a chemotherapeutic drug when in use. The chemotherapeutic drug comprises cis-platinum, carboplatin, oxaliplatin, 5-fluorouracil, paclitaxel, adriamycin or adriamycin. The brusatol provided by the invention can be prepared into an oral preparation or a non-oral preparation accepted pharmaceutically. The beneficial effects of the brusatol applied in preparing the chemotherapeutic drug synergist are as follows: (1) the brusatol can be used in an Nrf2 path, and the killing effect of various chemotherapeutic drugs on the cancer cells can be enhanced; (2) the growth inhibition of low-dose cis-platinum on transplantable tumor of a naked mouse can be increased by the brusatol, thus having clinical application prospects; (3) the cis-platinum content in non-small cell lung cancer cell strains can be increased by the combined use of the brusatol and the cis-platinum; and (4)the toxicity is not discovered when the brusatol and the cis-platinum are together used in the cellular level and in the mouse test work concentration.

The present invention relates to glycosyl-etoposide prodrugs, a process for the preparation thereof and the use thereof in combination with functionalized tumor-specific enzyme conjugates for treating cancers.

A therapeutic approach to prevent drug resistance and chemotherapy-related secondary cancer associated with DNA mismatch repair (MMR) deficiency is disclosed based on screening antioxidants for reducing microsatellite instability (MSI) while enhancing the cytotoxicity of chemotherapeutic agents. The work is based on experiments using antioxidants to target reactive oxygen species generated by oxaliplatin, a commonly used chemotherapeutic agent, and is applicable to other chemotherapeutic agent, and in particular 5-fluorouracil, methotrexate, CCNU, etoposide and vinblastine. In particular oxaliplatin is co-treated with an antioxidant, including CDC, CAPE, ciclopirox ethanolamine, hinokitiol, gossypol, n-Octyl caffeate, baicalein, or curcumin.

Anthracyclin-treated turn or cells are particularly effective in eliciting an anti-cancer immune response, where the rDNA-damaging agents, such as etoposide and mitomycin C do not induce immunogenic cell death. Anthracyclins induce the rapid, pre-apoptotic translocation of calreticulin (CRT) to the cell surface. Blockade or knock down of CRT suppressed the phagocytosis of anthracyclin-treated tumor cells by dendritic cells and abolished their immunogenicity in mammals, such as mice. The anthracyclin-induced CRT translocation was mimicked by inhibition of the protein phosphatase1/GADD34 complex. Administration of recombinant CRT or inhibitors of protein phosphatase1/GADD34 restored the immunogenicity of cell death elicited by etoposide and mitomycin C, and enhanced their antitumor effects in vivo. These data identify CRT as a key feature determining anti-cancer immune responses and delineate a possible strategy for immunogenic chemotherapy.

Compounds for treatment of a patient having a tumor that is metastatic and/or that reduces an organ function, wherein the compounds are of the general formula:

wherein X is O, NH and S, wherein n is 0, 1 or 2, wherein R¹ and R² are H, methyl or ethyl, or together form a group CR³R⁴, and wherein R³ and R⁴ are H, methyl or ethyl.

The invention belongs to the field of medical embolization devices, relates to a sodium alginate microsphere targeted vascular embolization agent containing an antineoplastic drug and a preparation method thereof. Alginic acid is taken as a pharmaceutical carrier, the antineoplastic drug etoposide is a pharmaceutical active ingredient, divalent metal cation or calcium ion solution is taken as a solidifying agent, and the sodium alginate encapsulates the etoposide to prepare ideal particle size-controllable sodium alginate microspheres comprising the etoposide, thus avoiding toxic side effect of traditional etoposide administration such as anaphylaxis and inconvenience. The vascular embolization agent changes the dosage form and route of administration way of the antineoplastic drug etoposide, has high efficacy and low toxicity, and is safely and effectively applied to clinical application. The vascular embolization agent has the advantages of mild preparation condition and simple and convenient operation, and is fit for large-scale production. The vascular embolization agent can be used for vascular embolization, local targeted tumor treatment, and treating small-cell carcinoma of the lung, oophoroma, carcinoma of testis, gastric cancer and liver cancer by administering the vascular embolization agent during operations.

It is an object of the present invention to find out a novel gene marker by which a drug-resistant cancer cell can be detected and provide a means of efficiently and comprehensively detecting a drug-resistant cancer cell using this marker. In the present invention, gene amplifications or deletions have been analyzed in cancer cell strains resistant to drugs, which are anticancer drugs having particularly serious side effects and being administered to cancer patients at a high frequency (namely, camptothecins, cisplatins, etoposides, adriamycins (ADM), and cytosine arabinosides), and parent cancer cell strains. As a result, it was found out that the acquisition of drug-resistance to an anticancer drug in a test cancer cell can be detected by detecting amplification of one or more genes selected from ABC transporter genes and BCL2 family genes consisting of ABCA3 gene, ABCB6 gene, ABCB8 gene, ABCB10 gene, ABCC4 gene, ABCC9 gene, ABCD3 gene, ABCD4 gene, ABCE1 gene, ABCF2 gene, BCL2L2, BCL2L10, BCL2L1, and BCL2A1 which are novel gene markers relating to the acquisition of drug resistance of cancer cells.