31 results about "Combination cancer therapy" patented technology

A method of treating a subject with cancer includes the step of co-administering to the subject over three to five weeks, a taxane in an amount of between about 243 μmol / m2 to 315 μmol / m2 (e.g., equivalent to paclitaxel in about 210-270 mg / m2); and a bis(thiohydrazide amide) in an amount between about 1473 μmol / m2 and about 1722 μmol / m2 (e.g., Compound (1) in about 590-690 mg / m2). The bis(thiohydrazide amide) is represented by Structural Formula (I), Y is a covalent bond or an optionally substituted straight chained hydrocarbyl group, or, Y, taken together with both >C=Z groups to which it is bonded, is an optionally substituted aromatic group. R1-R4 are independently —H, an optionally substituted aliphatic group, an optionally substituted aryl group, or R1 and R3 taken together with the carbon and nitrogen atoms to which they are bonded, and / or R2 and R4 taken together with the carbon and nitrogen atoms to which they are bonded, form a non-aromatic heterocyclic ring optionally fused to an aromatic ring. R7-R8 are independently —H, an optionally substituted aliphatic group, or an optionally substituted aryl group. Z is O or S.

Normal tissue complications limit curative broadbeam radiotherapy to tumors including lung cancer. Radiation retinitis causing blindness limits quality of life and long term survival for patients with ocular melanoma. This invention pertains to alternative, normal tissue sparing 100 to 1,000 Gy microbeam radiations with least normal tissue complications and concomitant radio-immunotherapy by innate immune response of epidermis and dermis to low dose radiation with 50 kV X-rays. Total body skin radiation with former airport passenger screening machines with 50 kV X-ray is disclosed. Microbeams are generated without contaminating scatter and neutron radiations from collinear gamma ray and electron beam produced by inverse Compton interaction with high energy laser and electron beam and from proton and carbon ion beams in tissue equivalent cylindrical collimators. Extracorporeal immunotherapy and chemotherapy and apheresis of mutated subcellular particles released into circulation in response to cancer-therapies are by clinical continuous flow ultracentrifugation combined chromatography.

A combination cancer therapy based upon catechins, the major biologically active polyphenol in plant products, including green tea extract, and one or more chemotherapeutic agents. A common complication of cancer chemotherapy is neutropenia, and in spite of advances in its prophylactic management is a major cause of risk for the development of serious microbial infections leading to increased morbidity and mortality in both humans and animals. The use of cathechins such as those found in green tea (Camellia sinensis), including but not limited to epigallocatechin gallate (EGCG) as nontoxic adjuvant to aid in the prevention of opportunistic microbial infections in patients undergoing immunosuppressive chemotherapy is a novel application. Also contemplated are methods using catechins to ameliorate the immunosuppressive effects of cancer chemotherapy by administering the compound to a patient in need thereof.

The invention provides a method of treating a subject with cancer, particularly leukemia, lymphoma, solid cancer such as colorectal cancer, gastric cancer, bladder cancer, non-small cell lung cancer, and breast cancer, comprising administering to the subject a compound of formulae (I) 40 or (Ia) in combination with an antimetabolite such as methotrexate, pemetrexed, cytarabine or nelarabine, or 5-fluorouracil, or capecitabine or their derivatives.

Methods are disclosed for preventing toxic drug-drug interactions during combination cancer therapy with a drug that is an anti-ErbB3 agent, such as an anti-ErbB3 antibody, together with a drug that is a tyrosine kinase inhibitor and / or a drug that binds to alpha-1 acid glycoprotein (e.g., erlotinib). Health care practitioners obtaining any one of the drugs are warned that when co-administering the drug that is an anti-ErbB3 agent with either or both of a drug that is a tyrosine kinase inhibitor and a drug that binds to alpha-1 acid glycoprotein, at least one of the co-administered drugs should be administered using a reduced dosage to prevent toxicity. In a reduced dosage, the amount of drug administered per unit time is reduced as compared to a dose that would be administered if the drug was administered as monotherapy. The reduced dosage can be, for example, a reduced drug dose or a reduced drug dosing frequency, or both. Compositions useful in practicing the disclosed methods are also provided.

The disclosure provides methods and compositions for treating cancer cells, including cancer cells in a subject, whereby two or more therapeutic agents are used, one being an EGFR-TKI agent and the other being a microRNA.

The disclosure provides methods and compositions for treating cancer cells, including cancer cells in a subject, whereby two or more therapeutic agents are used, one being an EGFR-TKI agent and the other being a microRNA.

A method of treating a subject with cancer includes the step of co-administering to the subject over three to five weeks, a taxane in an amount of between about 243 μmol / m2 to 315 μmol / m2 (e.g., equivalent to paclitaxel in about 210-270 mg / m2); and a bis(thiohydrazide amide) in an amount between about 1473 μmol / m2 and about 1722 μmol / m2 (e.g., Compound (1) in about 590-690 mg / m2). The bis(thiohydrazide amide) is represented by Structural Formula (I), Y is a covalent bond or an optionally substituted straight chained hydrocarbyl group, or, Y, taken together with both >C=Z groups to which it is bonded, is an optionally substituted aromatic group. R1-R4 are independently —H, an optionally substituted aliphatic group, an optionally substituted aryl group, or R1 and R3 taken together with the carbon and nitrogen atoms to which they are bonded, and / or R2 and R4 taken together with the carbon and nitrogen atoms to which they are bonded, form a non-aromatic heterocyclic ring optionally fused to an aromatic ring. R7-R8 are independently —H, an optionally substituted aliphatic group, or an optionally substituted aryl group. Z is O or S.

The present invention provides methods for conducting screens using nucleic acid elements (e.g., interfering RNAs) to confidently identify hit genetic elements. The present invention further comprises constructing vectors that contain two or more nucleic acid elements to knock down all pairwise combinations of the hit genetic elements identified from the screen. Following quantitation of the single and double-knockdown phenotypes, genetic interactions between all gene pairs can be calculated. Genes can then be clustered according to the similarity of the pattern of their interactions with all of the other genes to obtain a genetic interaction map, which can advantageously be used to predict functional associations between genes and identify drug targets for therapy such as combination cancer therapy.

The disclosure provides methods and compositions for treating cancer cells, including cancer cells in a subject, whereby two or more therapeutic agents are used, one being an EGFR-TKI agent and the other being a synthetic oligonucleotide.

The present invention relates to combination therapies of a cytarabine conjugate and one or more anti-neoplastic agents for inhibiting cancer cell growth. In particular, the present invention relates to a conjugate of cytarabine and aspartic acid (BST-236) in combination with one or more additional anti-neoplastic agents for use in the treatment of hematological cancers.

Compositions are provided including NK cells that express chimeric antigen receptors (CARs) specific to CD19 and Her2 and a plurality of cell surface-bound multilamellar liposomal vesicles loaded withone or more anti-cancer therapeutics at an effective amount for inhibiting or killing tumor cells without causing toxicity to the NK cells. Methods of using these compositions to treat a subject withtumor are also provided, including administering an effective amount of the CAR-engineered NK cells, where an effective amount of anti-tumor therapeutics are delivered in particles (e.g., crosslinkedmultilamellar liposomal vesicles) that are bound to the surface of these CAR-engineered NK cells, without causing toxicity to the carrier NK cells.

Described herein, inter alia, are anti-cancer agents, anti-cancer pharmaceutical compositions, combinations of the agents and / or pharmaceutical compositions, and methods of using the same.

Compositions are provided including NK cells that express chimeric antigen receptors (CARs) specific to CD19 and Her2 and a plurality of cell surface-bound multilamellar liposomal vesicles loaded with one or more anti-cancer therapeutics at an effective amount for inhibiting or killing tumor cells without causing toxicity to the NK cells. Methods of using these compositions to treat a subject with tumor are also provided, including administering an effective amount of the CAR-engineered NK cells, where an effective amount of anti-tumor therapeutics are delivered in particles (e.g., crosslinked multilamellar liposomal vesicles) that are bound to the surface of these CAR-engineered NK cells, without causing toxicity to the carrier NK cells.

The invention relates to combination anticancer therapy with certain Akt inhibitor and other anticancer agents such as anticancer antimetabolites, anticancer antibiotics, plant-derived anticancer agents, anticancer platinum-coordinated complex compounds, anticancer camptothecin derivatives and anticancer tyrosine kinase inhibitors.

Described herein is TRAIL receptor targeting therapy in combination with metformin for treatment of cancer in humans. Using TRAIL receptor targeting therapy such as the TRAIL molecule, agonistic human monoclonal antibodies against TRAIL receptors, or peptides targeting TRAIL receptors in combination with metformin for the treatment of all types of cancer allows to obtain an optimum therapeutical effect at any time of the progression of the disease.

The present invention relates to combination therapies for the treatment of EGFR-related diseases, particularly EGFR-related cancers. This invention also relates to a method of enhancing the efficacy of an EGFR family member antagonist and therapeutic methods for subjects who are refractory to treatment with an EGFR family member antagonist. The invention also relates to pharmaceutical compositions useful for treatment of EGFR-related diseases.

The present invention relates to combination therapies of a cytarabine conjugate and one or more anti-neoplastic agents for inhibiting cancer cell growth. In particular, the present invention relatesto a conjugate of cytarabine and aspartic acid (BST-236) in combination with one or more additional anti-neoplastic agents for use in the treatment of hematological cancers.

The present invention relates to methods for treating cancer through combination therapy with a TRP channel antagonist and standard-of-care cancer agents.

The present invention relates to the combination of the HDM2-p53 interaction inhibitor drug (S)-5-(5-Chloro-1-methyl-2-oxo-1,2-dihydro-pyridin-3-yl)-6-(4-chloro-phenyl)-2-(2,4-dimethoxy-pyrimidin-5-yl)-1-isopropyl-5,6-dihydro-1H-pyrrolo[3,4-d]imidazol-4-one [HDM201] and an anti-TIM-3 antibody molecule as TIM-3 inhibitor. The present invention further relates to the use of said combination in the treatment of cancer, in particular hematological tumors. The present invention further relates to dose and dosing regimen related to this combination cancer treatment.

Drug combinations of a heteroarotinoid (e.g., SHetA2), and an Azabicyclooctan-3-one derivative (e.g., PRIMA-1 or PRIMAMET) and / or, a CDK4 / 6 inhibitor (e.g., Palbociclib, Abemaciclib, or Ribociclib), which are synergistically-effective as anti-cancer treatments, and kits and methods of use of such drug combinations.

A method for pharmacological treatment of cancers and other diseases is presented which includes the novel combination of a statin (Hmg-CoA reductase inhibitor, such as lovastatin, simvastatin, atorvastatin, cerivastatin, fluvastatin, pravastatin, or newer agents), with an interferon (such as interferon alfa-2b or others) and also including concurrent administration of selenium and calcium. The method disclosed in this invention is useful because it can prove more effective than previously known therapies for certain diseases and because its use may be more tolerable, less disfiguring, and less expensive than other methods. The method here disclosed can be readily reproduced by any person skilled in the art of treating disease.

The present invention relates to the combination of the HDM2-p53 interaction inhibitor drug (S)-5-(5-Chloro-1-methyl-2-oxo-1,2-dihydro-pyridin-3-yl)-6-(4-chloro-phenyl)-2-(2,4-dimethoxy-pyrimidin-5-yl)-1-isopropyl-5,6-dihydro-1H-pyrrolo[3,4-d]imidazol-4-one [HDM201] and the BCL2 inhibitor 4-(4-{[2-(4-chlorophenyl)-4,4-dimethylcyclohex-1-en-1-yl]methyl}piperazin-1-yl)-N-[(3-nitro-4-{[(oxan-4yl)methyl]amino}phenyl)sulfonyl]-2-[(1H-pyrrolo[2,3-b]pyridin-5-yl)oxy]benzamide [venetoclax]. The present invention further relates to the use of said combination in the treatment of cancer, in particular hematological tumors. The present invention further relates to dose and dosing regimen related to this combination cancer treatment.

The present disclosure generally relates to novel methods of activating integrin signaling to overcome CD47 checkpoint inhibition and to promote the macrophage phagocytic signaling pathway. The present disclosure also provides methods and compositions for treating cancers, including solid tumors and hematological malignancies, by promoting macrophage-mediated phagocytosis of cancer cells. Also provided is the use of integrin activation in combination with adoptive metastasis of engineered macrophages for increasing phagocytosis to cancer cells.

Disclosed herein are methods relating to combination cancer treatments that include elsamitrucin and other agents.

The invention discloses a compound cancer treatment method for mammals, especially humans, which is treated by administering a therapeutically effective dose of a GST-activated anticancer compound and a therapeutically effective dose of another anticancer therapy. Pharmaceutical compositions, products and kits for use in the method are disclosed. The use of a GST-activated anticancer compound for the manufacture of a medicament for use in the method is disclosed. Disclosed is a method for enhancing anti-cancer therapy in mammals, especially humans, comprising administering a therapeutically effective amount of a GST-activated anti-cancer compound to the mammal treated with the anti-cancer therapy. The use of GST-activated anticancer compounds for the manufacture of medicaments for use in this method is disclosed. The GST-activated anticancer compound is preferably the compound of US Patent No. 5,556,942, more preferably TLK286, especially the hydrochloride.

The present disclosure relates, in general, to methods for treating cancer comprising administering to a subject in need thereof an effective amount of CXCL9, CXCL10 or the combination, in combination with an immune checkpoint inhibitor. The CXCL9, CXCL10 or combination may be administered as a polypeptide, a polynucleotide or cells comprising a polynucleotide encoding CXCL9, CXCL10 or both. In one aspect, the treatment is amenable to patients with low or high mutational burden tumors.

The present invention provides methods for conducting screens using nucleic acid elements (e.g., interfering RNAs) to confidently identify hit genetic elements. The present invention further comprises constructing vectors that contain two or more nucleic acid elements to knock down all pairwise combinations of the hit genetic elements identified from the screen. Following quantitation of the single and double-knockdown phenotypes, genetic interactions between all gene pairs can be calculated. Genes can then be clustered according to the similarity of the pattern of their interactions with all of the other genes to obtain a genetic interaction map, which can advantageously be used to predict functional associations between genes and identify drug targets for therapy such as combination cancer therapy.