42 results about "Resistant cancer" patented technology

This invention discloses a butyrolactone compound with multidrug resistance reverse transcription activity, its preparation method, and its uses. The compound's structural formula is shown in Figure I. The preparation method includes the following steps: fermenting *Aspergillus pyrolyticus* (accession number CCTCC NO: M2014086) to obtain a butyrolactone fermentation product; extracting the fermentation product with ethyl acetate to obtain a crude extract; degreasing the crude extract with hexane and dichloromethane to obtain a final extract; and purifying the final extract using normal-phase silica gel column chromatography, reversed-phase medium-pressure column chromatography, and reversed-phase semi-preparative high-performance liquid chromatography. The advantage of this butyrolactone compound is that it possesses multidrug resistance reverse transcription activity and the ability to regulate P-gp-mediated drug efflux in multidrug-resistant cell lines, making it a potential drug for treating multidrug-resistant cancers.

The present invention relates to a composition for inhibiting multidrug resistance, the composition containing an autocrine motility factor (AMF) as an active ingredient. Specifically, treating cancer cells with an AMF protein or an AMF peptide inhibits the mRNA and protein expression of P-glycoprotein or multidrug resistance related protein-1 (MRP-1), which are major causes of multidrug resistance, and administering the AMF protein or AMF peptide in combination with an anticancer agent inhibits the release of the anticancer agent from cells, thus having the effect of increasing the accumulation of the anticancer agent inside cancer cells. Therefore, the composition can be effectively used as a pharmaceutical composition for inhibiting multidrug resistance to an anticancer agent or as an anticancer adjuvant for multidrug-resistant cancer.

To provide a therapeutic agent for PARP inhibitor-resistant cancer.SOLUTION: The present invention relates to a pharmaceutical composition for treating or preventing a solid cancer patient having resistance to a PARP inhibitor, and the pharmaceutical composition according to the present invention can effectively reduce the size of a tumor in a patient having resistance to a PARP inhibitor.SELECTED DRAWING: Figure 4

Embodiments disclosed herein use forward genetics tools (e.g., ORF libraries, perturbation libraries) to study fitness advantages under immune pressure, including resistance mechanisms. Once the resistance mechanisms are identified, vulnerabilities (i.e., dependencies) in resistant cells can be identified (e.g., synthetic lethality screens in resistant cancer cells). For example, drug or CRISPR screening can be performed in cells with an identified resistant state. Embodiments disclosed herein also provide targets for resistance to IFN-y treatment.

The present invention relates to combination therapies for treating cancer, optionally chemotherapy-resistant cancers, in a subject. The combination therapies comprise (a) an antibody or antigen-binding portion thereof that specifically binds to CD40, and (b) chemotherapy. The invention also relates to pharmaceutical compositions, kits and methods of using such therapies.

The present invention relates to a pharmaceutical composition for preventing or treating anticancer drug-resistant cancer, containing rucaparib camsylate as an active ingredient. Rucaparib camsylate can function as an immune checkpoint inhibitor by blocking the binding of PD-1 and PD-L1, and thus can be effectively used in pharmaceuticals for the prevention or treatment of cancer. In addition, rucaparib camsylate according to the present invention has an excellent anticancer effect against uterine sarcoma cancer that exhibits resistance to doxorubicin, and thus can be very effectively used for the prevention or treatment of resistant cancer.

The present invention relates to a composition for the prevention or treatment of cisplatin-resistant cancer comprising an inhibitor of DUSP23 expression or activity as an active ingredient. It was found that DUSP23 expression is upregulated in cell clusters exhibiting characteristics of cancer stem cells, and that knocking down DUSP23 significantly reduces cell cluster formation as well as decreases the expression of SOX2, a major stem cell marker. Furthermore, DUSP23 expression was increased in lung cancer cells that had developed cisplatin resistance, and it was confirmed that the downregulation of DUSP23 inhibits self-renewal and invasive capabilities during the induction of cancer cell death. In addition, it was confirmed that DUSP23 plays an important role in promoting cancer stem cell characteristics through SOX2 expression. In conclusion, it has been shown that targeting DUSP23 can be a promising therapeutic strategy to overcome anticancer drug resistance in lung cancer, and the composition of the present invention is expected to be usefully utilized as a treatment for lung cancer cells with cisplatin resistance.

Small molecule ERα biomodulators that kill therapy-resistant ERα positive breast, ovarian, and endometrial cancer cells are disclosed. In one embodiment, the small molecule biomodulator has increased therapeutic utility because of an increased ability to kill therapy-resistant cancer cells compared to BHPI and other conventional therapies (endocrine therapies, tamoxifen, and fulvestrant / ICI). The small molecule biomodulators not only inhibit proliferation of the cancer cells but kills them, which prevents reactivation of tumors years later. Compounds of the invention, such as ErSO-TFPy, are effective for treating ERα positive cancers such as breast cancer, ovarian cancer, uterine cancer, cervical carcinoma, endometrial cancer, and the like.

The invention represents new hybrid compounds of two natural products sclareol and doxorubicin in the form of their conjugates. These compounds are in the form of conjugates, where doxorubicin and sclareol are covalently linked by a linker in a 1:1 molar ratio. The hybrids have shown to possess anticancer properties and are effective in treating resistant cancer cells that have P-glycoprotein membrane transporter, responsible for resistance to doxorubicin. The hybrids have been tested on different types of cell lines, including human glioblastoma, non-small cell lung carcinoma, and colorectal carcinoma. Also, a method for their preparation and their use in medical products or pharmaceutical preparations has been determined. The results of the study include the cytotoxic activity of single, combined, and conjugated compounds in pairs of sensitive and resistant cancer cells, with and without P-glycoprotein expression. The selectivity towards cancer cells was determined by comparing with commercially available normal human lung fibroblast cells. The study also investigated the nanoparticle nature of hybrid compounds, their intracellular localization and toxicity in vivo.

The present invention relates to a pharmaceutical composition for the prevention or treatment of anticancer-agent-resistant cancer, containing trovafloxacin as an active ingredient. The trovafloxacin can function as an immune checkpoint inhibitor by blocking the binding between PD-1 and PD-L1, and thus can be effectively used in medicines for the prevention or treatment of cancer. In addition, the trovafloxacin according to the present invention has an excellent anticancer effect against uterine sarcoma showing resistance to doxorubicin, and thus can be very effectively used for the prevention or treatment of resistant cancer.

The invention provides an mRNA (messenger Ribonucleic Acid) medicine for inhibiting tumor stem cells and reducing the dryness of the tumor cells and a preparation method of the mRNA medicine. The mRNA medicine comprises any one or a combination of at least two of linear PTEN mRNA, self-replicating PTEN mRNA and annular PTEN mRNA; the linear PTEN mRNA comprises a 5 'UTR (Untranslated Region) sequence, a PTEN protein coding sequence and a 3' UTR sequence; the nucleotide sequence of the PTEN protein coding sequence comprises a sequence as shown in SEQ ID NO. 1. The mRNA nano-drug prepared by the invention not only has high transfection efficiency in tumor stem cells, but also can induce differentiation of the tumor stem cells and remarkably inhibit growth of the tumor stem cells; in drug-resistant tumor cells, the stemness of the drug-resistant tumor cells is inhibited, so that the sensitivity to chemotherapy, targeted antibodies, immunotherapy and the like is improved, and the killing effect of the drug is improved. The invention also shows an excellent anti-tumor effect in a human tumor cell line xenotransplantation model of the drug-resistant breast cancer in vivo, and provides a promising treatment strategy for the treatment of the drug-resistant breast cancer.

To provide safe and effective compositions and methods for enhancing the efficacy and / or reducing the side effects of cancer chemotherapy and increasing the sensitivity of chemotherapy-resistant cancer cells.SOLUTION: Nutritional supplements comprising fish oil and selenium have been found to provide various activities that are beneficial in treating cancer and related conditions. The supplement provides a synergistic effect in reducing cancer cell growth when used in combination with a chemotherapeutic agent and can reduce growth in drug resistant cancer cells when used in combination with a chemotherapeutic agent to which the cells are resistant. Effects in reducing angiogenesis, reducing metastasis, decreasing the number of circulating cancer cells, and altering AXL signaling have also been found. The use of the supplement was found to reduce the wasting associated with cachexia and decrease circulating cytokines associated with inflammation. The overall effect was found to prolong survival in a clinical study.SELECTED DRAWING: Figure 1

The present invention relates to a composition for preventing or treating cancer having resistance to anticancer agents and, more specifically, to a pharmaceutical composition for preventing or treating resistant cancer, comprising a 3-ketoacyl CoA thiolase (ACAA) inhibitor and a carnitine acylcarnitine carrier (CAC) inhibitor and inhibiting the regrowth of cancer having resistance to anticancer agents. It is has been identified that the composition comprising the 3-ketoacyl CoA thiolase (ACAA) inhibitor and the carnitine acylcarnitine carrier (CAC) inhibitor, of the present invention, effectively inhibits the regrowth of cancer cells and tumors having resistance to various anticancer agents, and thus can be effectively used for the prevention or treatment of cancer having resistance to anticancer agents.

An anti-human ROR1 antibody, an antibody-drug conjugate comprising the anti-human ROR1 antibody, and use for treating drug-resistant cancer.

The present invention provides, inter alia, methods, pharmaceutical compositions, and kits for treating or ameliorating the effects of a cancer in a subject, which cancer is refractory or resistant to non-ERK MAPK pathway inhibitor therapy. Also provided are methods for identifying a subject having cancer who would benefit from therapy with an ERK inhibitor and methods for inhibiting phosphorylation of RSK in a cancer cell that is refractory or resistant to a non-ERK MAPK pathway inhibitor.

Provided herein, inter alia, are compositions and methods comprising combination therapies including a BRAE axis inhibitor and a COX-2 inhibitor for the treatment of cancer. In embodiments, the combination therapies further include an EGER inhibitor. The combination therapies provided herein are particularly effective for treating BRAE intrinsically resistant cancers.

The present invention relates to a pharmaceutical composition for preventing or treating anticancer drug-resistant cancer, containing teriflunomide as an active ingredient, wherein the teriflunomide can function as an immune checkpoint inhibitor by blocking the binding of PD-1 and PD-L1, and thus can be effectively used in medicines for preventing or treating cancer. In addition, the teriflunomide according to the present invention has an excellent anticancer effect against uterine sarcoma cancer that is resistant to doxorubicin, and thus can be very effectively used for preventing or treating resistant cancer.

The inventors establish a role for primary cilia in human TNBC chemotherapeutic resistance. They developed patient-derived organoids, and showed that these recapitulated the cellular heterogeneity of TNBC biopsies. They treated their TNBC organoids with chemotherapeutics and observed partial killing. The surviving cells with organoid-reconstituting capacity showed selective enrichment for the quasi-mesenchymal ciliated cell subpopulation. They developed a family of small-molecule inhibitors of ciliogenesis and show that these, or genetic ablation of primary cilia, suppress chemoresistance. In particular, the present invention relates to a method of preventing therapeutic resistance in a patient suffering from a cancer comprising administering to the patient a therapeutically effective amount of an inhibitor of ciliogenesis. The present invention also relates to a method of treating a therapy-resistant cancer in a patient suffering from a cancer comprising administering to the patient a therapeutically effective amount of an inhibitor of ciliogenesis.

The present technology provides a combination approach for treating multidrug resistant cancer. Multidrug resistant cancers have more mitochondrial networks than drug sensitive cancers. A first agent fragments mitochondrial networks, dissociates mitochondria from the endoplasmic reticulum, and lower the threshold for apoptosis. A second active agent induces the unfolded protein response, causing stress to the endoplasmic reticulum and limiting the ability of multidrug resistant cancer cells to grow and survive. A third active agent directly activates mitochondrial apoptosis, leading to death of the cancer cells. The active agents can be combined into a nanoparticle formulation for simultaneous delivery into multidrug resistant cancer cells. The formulation serves as a nanomedicine for treatment of multidrug resistant cancers such as multidrug resistant triple negative breast cancer.

The present invention relates to a reduced graphene oxide nanocomposite for targeting multiple drug-resistant cancer cells capable of simultaneously performing enhanced photothermal therapy and photodynamic therapy, and a method for manufacturing the same. The nanocomposite of the present invention comprises reduced graphene, poly(N-isopropylacrylamide)-acrylic acid, and folic acid, thereby exhibiting excellent targeting function for multiple drug-resistant cancer cells. In particular, when an anticancer agent including indocyanine green is encapsulated internally, it exhibits a synergistic effect of photothermal and photodynamic therapy against multiple drug-resistant cancer.

Disclosed herein are methods of diagnosing tyrosine kinase inhibitor (TKI) resistant cancer and predicting response to TKI therapy in treatment. Also disclosed is a method of treating a TKI resistant cancer by administering a voltage gated potassium channel (VGKC) inhibitor. The disclosure also provides composition comprising a TKI and a VGKC inhibitor.

A novel treatment method for a drug-resistant cancer, particularly an acquired drug-resistant cancer. Said method comprises administering an anti-LIV-1 antibody-drug conjugate to a subject in need thereof.

Aspects of the disclosure relate to the discovery that galectin-1 is increased in thermal-resistant cancers, including hepatocellular carcinoma. Certain aspects relate to methods of measuring galectin-1 levels to determine a patient's responsiveness to therapies, such as thermal ablation therapy. Certain aspects relate to inhibiting galectin-1 to improve responsiveness to a therapy, such as a thermal ablation therapy.

Stapled BAD BH3 peptides and compositions comprising the same that are useful in overcoming venetoclax resistance are provided. Also provided are methods of using the stapled BAD BH3 peptides for treating a BCL-2 expressing and / or dependent cancer (e.g., a hematologic cancer or a solid tumor) in a human subject in need thereof. In some cases, the cancer is a venetoclax-resistant cancer due to acquired mutations in the BCL-2 protein. The methods involve administering to the human subject a stapled BAD BH3 peptide or pharmaceutical composition or delivery vehicle comprising the stapled BAD BH3 peptide disclosed herein.

The invention discloses a protein degradation targeting chimera targeting AKR1C3 and an application of the protein degradation targeting chimera. The invention discloses a series of compounds with a structure of a general formula (I) and application of the compounds in treatment of cancers. In-vitro cell experiments are used as carriers to evaluate the efficacy of the compound represented by the general formula (I) in degradation of aldoketoreductase 1C3 and treatment of drug-resistant cancers, and the compound represented by the general formula (I) is found to have good in-vitro activity and can be further developed into candidate molecules for treating cancers.

Methods and compositions for the treatment of cancer are disclosed herein. More specifically, disclosed herein are methods and compositions for the treatment of KRASi resistant cancers using NFAT5 inhibitors.

The present invention provides antibodies that bind to human Anx-A1 for use in the treatment of cancer, including drug-resistant cancer. Kits and products for this use are also provided.

The present invention provides an H3S28 phosphorylation inhibitor or a composition containing the same. [Solution] A histone H3 phosphorylation inhibitor comprising a benzaldehyde compound or a pharmaceutically acceptable salt thereof is provided. The inhibitor or a composition comprising the same can be used to prevent, treat, or treat various cancers involving the H3S28ph protein (e.g., hepatic cancer, pancreatic cancer, lung cancer, ovarian cancer, colon adenocarcinoma, chronic myeloid leukemia, pancreatic ductal adenocarcinoma, malignant kidney tumor, breast cancer, melanoma, etc.), radiation-resistant cancers of these cancers, heart failure, and their complications, or to treat poor prognoses, by inhibiting the expression of the H3S28ph protein. Preferably, the benzaldehyde compound is benzaldehyde, 5,6-O-benzylidene-L-ascorbic acid, monosodium 5,6-O-benzylidene-L-ascorbic acid, 4,6-O-benzylidene-D-glucopyranose, or N-benzylideneethylamine.

This invention relates to the field of biomedical technology, and more particularly to the use of a combination of RVX208 and temozolomide for the treatment of glioblastoma. It also relates to the use of RVX208 to resensitize temozolomide-resistant cancers to temozolomide treatment. The use of at least one of RVX208, a pharmaceutically acceptable salt of RVX208, a solvate of RVX208, a hydrate of RVX208, a polymorph of RVX208, an isomer of RVX208, a prodrug form of RVX208, and temozolomide in the preparation of a glioblastoma therapeutic agent. RVX208 inhibits the transcriptional activity of various genes related to cell cycle progression and proliferation maintenance by inhibiting BET family proteins or other target molecules, leading to cell cycle arrest, inhibition of cell proliferation, and induction of programmed cell death. RVX208 also interferes with the transcriptional expression of genes related to mitochondrial homeostasis regulation, resulting in a decrease in mitochondrial membrane potential and reduced ATP production, thus enabling RVX208 to disrupt mitochondrial function in GBM cells and produce a synergistic antitumor effect with temozolomide.