Patent classifications
A61P35/04
A COMBINATION OF, OR A BISPECIFIC BINDING MOLECULE TO, AN IMMUNE CHECKPOINT MOLECULE ANTAGONIST AND A RANK-L (NF-KB LIGAND) ANTAGONIST FOR CANCER THERAPY OR PROPHYLAXIS AND USES THEREOF
Disclosed are agents for treating or preventing cancers. More particularly, the present invention discloses therapeutic combinations comprising antagonists of receptor of NF-κB (RANK) ligand and immune checkpoint molecules in methods and compositions for treating or inhibiting the development, progression or recurrence of cancers, including metastatic cancers.
A COMBINATION OF, OR A BISPECIFIC BINDING MOLECULE TO, AN IMMUNE CHECKPOINT MOLECULE ANTAGONIST AND A RANK-L (NF-KB LIGAND) ANTAGONIST FOR CANCER THERAPY OR PROPHYLAXIS AND USES THEREOF
Disclosed are agents for treating or preventing cancers. More particularly, the present invention discloses therapeutic combinations comprising antagonists of receptor of NF-κB (RANK) ligand and immune checkpoint molecules in methods and compositions for treating or inhibiting the development, progression or recurrence of cancers, including metastatic cancers.
ONCE DAILY CANCER TREATMENT REGIMEN WITH A PRMT5 INHIBITOR
A method of treating cancers, including pancreatic cancer, endometrial cancer, non-small cell lung cancer (NSCLC), endometrial cancer, cervical cancer, bladder cancer, head and neck squamous cell carcinoma (HNSCC), urothelial carcinoma, esophageal cancer, and other cancers, the method comprising once-daily administration, to a patient in need thereof, of a therapeutically effective amount of (1S,2S,3S,5R)-3-((6-(difluoromethyl)-5-fluoro-1,2,3,4-tetrahydroiso quinolin-8-yl)oxy)-5-(4-methyl-7H-pyrrolo[2,3-d]pyrimidin-7-yl) cyclopentane-1,2-diol having the structure: Formula I or a pharmaceutically acceptable salt thereof.
ONCE DAILY CANCER TREATMENT REGIMEN WITH A PRMT5 INHIBITOR
A method of treating cancers, including pancreatic cancer, endometrial cancer, non-small cell lung cancer (NSCLC), endometrial cancer, cervical cancer, bladder cancer, head and neck squamous cell carcinoma (HNSCC), urothelial carcinoma, esophageal cancer, and other cancers, the method comprising once-daily administration, to a patient in need thereof, of a therapeutically effective amount of (1S,2S,3S,5R)-3-((6-(difluoromethyl)-5-fluoro-1,2,3,4-tetrahydroiso quinolin-8-yl)oxy)-5-(4-methyl-7H-pyrrolo[2,3-d]pyrimidin-7-yl) cyclopentane-1,2-diol having the structure: Formula I or a pharmaceutically acceptable salt thereof.
CANCER IMMUNOTHERAPY
Methods, compounds, compositions and kits for the treatment and/or prevention of cancer are provided. In particular, methods for the treatment of cancer comprising the administration of a TLR2 agonist, such as a conjugate of dipalmitoyl-S-glyceryl-cysteine (Pam2Cys) and polyethylene glycol (PEG), more particularly a Pam2Cys-Ser-PEG compound, and an immunostimulant such as an anti-PD-1, anti-PDL-1, anti-PL-1, or anti-CTLA-4 immunotherapeutic, are provided.
SELECTIVE CDK 4/6 INHIBITOR CANCER THERAPEUTICS
The disclosure describes selective and potent CDK 4/6 inhibitors that show advantageous inhibition of cancer growth, even at low concentrations. A class of the CDK 4/6 inhibitors relates to substituted pyridopyrimidines compounds having a fatty acid moiety, and are namely derivatives of Palbociclib of general formula [2A], wherein R.sup.1 is hydrogen, aryl, alkyl, alkoxy, cycloalkyl, or heterocyclyl; R.sup.2 is hydrogen, halogen, alkyl, acyl, cycloalkyl, alkoxy, alkoxy alkyl, haloalkyl, hydroxy alkyl, alkenyl, alkynyl, nitrile, or nitro; R.sup.3 is hydrogen, halogen, alkyl, haloalkyl, hydroxy alkyl, or cycloalkyl; and n is an integer from 9 to 20. These compounds may be used as pharmaceutical compounds for anti-cancer therapies, and are useful for the treatment, prevention and/or amelioration of cancer.
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SELECTIVE CDK4/6 INHIBITOR CANCER THERAPEUTICS
This disclosure describes selective and potent CDK 4/6 inhibitors that show advantageous inhibition of cancer growth, even at low concentrations. This class of anti-cancer CDK 4/6 inhibitors are substituted pyrrolopyrimidine compounds of formula IA, having a fatty acid moiety. These compounds may be used as pharmaceutical compounds for anti-cancer therapies, and are useful for the treatment, prevention and/or amelioration of cancer.
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SELECTIVE CDK4/6 INHIBITOR CANCER THERAPEUTICS
This disclosure describes selective and potent CDK 4/6 inhibitors that show advantageous inhibition of cancer growth, even at low concentrations. This class of anti-cancer CDK 4/6 inhibitors are substituted pyrrolopyrimidine compounds of formula IA, having a fatty acid moiety. These compounds may be used as pharmaceutical compounds for anti-cancer therapies, and are useful for the treatment, prevention and/or amelioration of cancer.
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Tumor specific antibody conjugates and uses therefor
Provided are antibodies, and fragments, derivatives, and nanoparticle conjugates thereof, particularly humanized derivatives thereof, which bind to tumor antigens. Also provided are nucleic acid molecules encoding chimeric antigen receptors (CARs) that bind to tumor antigens, polypeptides and CARs encoded by the nucleic acid molecules, vectors and host cells that include the nucleic acid molecules, methods of making the same, and methods for using the same to generate a persisting population of genetically engineered T cells in a subject, expanding a population of genetically engineered T cells in a subject, modulating the amount of cytokine secreted by a T cell, reducing the amount of activation-induced calcium influx into a T cell, providing an anti-tumor immunity to a subject, treating a mammal having a MUC1-associated disease or disorder, stimulating a T cell-mediated immune response to a target cell population or tissue in a subject, and imaging a MUC1-associated tumor.
Genetically modified veto cells and use of same in immunotherapy
An isolated cytotoxic T-lymphocyte (CTL), said CTL being a tolerance inducing cell and substantially depleted of alloreactivity, and wherein said CTL does not comprise a central memory T-lymphocyte (Tcm) phenotype, the CTL being transduced to express a cell surface receptor comprising a T cell receptor signaling module, is disclosed. Methods of generating same and using same are also disclosed.