466 results about "Combined therapy" patented technology

The disclosure provides a method of treating a human subject afflicted with lung cancer (e.g., non-small cell lung cancer (NSCLC)) with a programmed death-1 (PD-1) pathway inhibitor (e.g., an anti-PD-1 antibody) and a concurrent chemoradiotherapy (CCRT, e.g., a platinum doublet chemotherapy (PDCT) and a radiation therapy) followed by a combination of a PD-1 pathway inhibitor (e.g., an anti-PD-1 antibody) and a lymphocyte activation gene-3 (LAG-3) antagonist (e.g., an anti-LAG-3 antibody). In some aspects, the method comprises a recovery period that begins upon completion of the treatment with the PD-1 pathway inhibitor and the CCRT and ends at the start of the treatment with the combination of the PD-1 pathway inhibitor and the LAG-3 antagonist.

The present invention provides compositions comprising one or more ACAT inhibitors and one or more GLP-1 receptor agonists (GLP-1 RAs). The combination therapy reduces side effects associated with high-dose GLP-1 RA monotherapy and provides durable management of weight loss by suppressing rebound of body weight, blood glucose, and cholesterol levels after treatment.

The invention relates to a combination of a binding agent comprising (i) a first binding region which binds to PD-1, PD-L1, or both and which antagonizes the PD-1 / PD-L1 interaction; and (ii) a second binding region which binds to VEGF, VEGF receptor (VEGFR), or both and which antagonizes the VEGF / VEGFR interaction, and an antibody-drug conjugate comprising an antibody or fragment thereof that specifically binds to a target expressed on the surface of a tumour cell.

Disclosed are methods of treating cancer comprising administering to a subject a treatment regimen comprising a compound of Formula (I): Formula (I), or a pharmaceutically acceptable salt thereof, and a PD-1 or PD-L1 antagonist.

The disclosure provides method of treating cancer in a patient with ATM-deficient or ATR-deficient tumors, comprising safely and efficaciously administering to the patient PLXO38, a long lasting-PEGylated prodrug of the topoisomerase I inhibitor. The disclosure further provides combination therapies of PLXO38 with inhibitors of the DNA damage response (DDR).

The present invention is directed to the combination therapy of cancer with an allosteric EGFR inhibitor and an orthosteric EGFR inhibitor, as well as uses and pharmaceutical compositions thereof.

The present disclosure provides pharmaceutical combinations comprising MetAP2 inhibitors for the treatment of cancer.

The present invention provides a combination therapy for effectively treating and / or preventing diseases associated with cells expressing CA19-9, including cancer diseases such as pancreatic cancer and metastases thereof.

The invention relates to combination therapies employing an anti-PD1 / anti-LAG3 bispecific antibody and an HLA-G T cell-activating bispecific antibody, the use of these combination therapies for the treatment of cancer and methods of using the combination therapies.

1 BNT ref [P1819WO01] / / C&F ref. 240673WO A b s t r a c t The present invention relates to an anti-CTLA4 antibody or fragment thereof and / or a chemotherapy agent for use in a method of treating cancer in a subject in need thereof, wherein the subject is administered a combination comprising the anti-CTLA4 antibody or fragment thereof and the chemotherapy agent. The invention further provides a composition 5 and a kit of parts comprising the anti-CTLA4 antibody or fragment thereof and the chemotherapy agent. The invention further concerns a method of treating cancer in a subject in need thereof, wherein the method comprises administering to the subject the anti-CTLA4 antibody or fragment thereof and the chemotherapy agent. The invention further provides a combination of the anti-CTLA4 antibody or fragment thereof and the chemotherapy agent. 10

Provided herein are methods of treating proliferative diseases or disorders (e.g., a cancer) in a patient in need thereof using a combination therapy of Compound (I) or a pharmaceutically acceptable salt thereof and a PD-1 inhibitor (e.g., Pembrolizumab).

The present disclosure provides immune cells comprising an exogenous T cell receptor (TCR) and T cell modulatory polypeptides (TMPs) for use in methods of treating a disease or condition. The TMPs comprise one or more immunomodulatory polypeptides that stimulate activation and / or proliferation of the immune cell. Also disclosed are methods of expanding a population of immune cells and methods of selectively delivering an immunomodulatory polypeptide using the same. Also disclosed are pharmaceutical combinations comprising the same and their use in methods of treating a disease or condition.

Provided are combination therapies that include an inhibitor of PD-1 or PD-L1 and an antibody-drug conjugate targeting claudin 18.2.

Disclosed herein are compositions and methods for treating cancer, specifically extensive-stage small-cell lung cancer (ES-SCLC), through the administration of a combination therapy. In some embodiments, the method comprises administering plinabulin, one or more immune checkpoint inhibitors, including but not limited to pembrolizumab, and a regimen of etoposide with a platinum-based agent (EP). The disclosed methods enhance tumor reduction, prolong progression-free survival, and improve overall treatment efficacy compared to traditional therapies.

The present invention relates to a combination therapy of pexidartinib and nintedanib for use in the prevention or treatment of pulmonary fibrosis, in particular to a combination therapy of pexidartinib and nintedanib for use in the prevention or treatment of pulmonary fibrosis.

The present invention relates to a composition comprising eptinezumab and LuAG09222. This composition may be used, for example, to treat or prevent headache, pain, migraine, cluster headache, or endometriosis.

Provided are methods and compositions, for treating prostate cancer by administering to a patient in need thereof a therapeutically effective amount of a PARP inhibitor, e.g., niraparib; a therapeutically effective amount of a CYP17 inhibitor, e.g., abiraterone acetate, and a therapeutically effective amount of a glucocorticoid, e.g., prednisone.

The present invention relates to a donepezil and tadalafil combination therapy for the prevention, treatment or amelioration of Alzheimer's disease or cognitive dysfunction. The combined administration of donepezil and tadalafil according to the present invention has an improvement effect on Alzheimer's disease or cognitive impairment superior to that of the individual administration of donepezil, and thus can be effectively used as a therapeutic or complexing agent or the like for Alzheimer's disease or cognitive impairment.

To provide a method of treating an inflammatory neurological disease or condition that can result in destruction or degeneration of axons or myelin.SOLUTION: Provided is a combination comprising a) a compound of formula (I) or a pharmaceutically or veterinarily acceptable salt thereof; and b) one or more drugs selected from the group consisting of I) a compound of a particular formula or a pharmaceutically or veterinarily acceptable salt thereof; ii) a sphingosine-1-phosphate receptor inhibitor (S1PR modulator); and iii) a signal transducer and activator of transcription 3 (STAT3) inhibitor.SELECTED DRAWING: None

The present invention is directed to a combination therapy involving Pioglitazone and a MEK inhibitor for the treatment of a cancer patient in need of such a therapy.

This invention provides a combination of a PARG inhibitor and a topoisomerase inhibitor. It also provides a method for treating diseases or disorders, such as cancer, using such a combination.

The present disclosure relates to methods of treating a tumor in a subject, the method comprising administering to the subject a therapeutically effective amount of a T-cell checkpoint inhibitor in combination with chemotherapy and / or radiation therapy, wherein the subject has reduced levels of CD73 protein or CD73 activity compared to a normal subject. In some embodiments, the method further comprises administering a CD73 inhibitor prior to or concurrently with the combined T-cell checkpoint inhibitor and chemotherapy and / or radiation therapy.

The present invention relates to a pharmaceutical composition, quasi-drug composition, or cosmetic composition for the prevention, improvement, or treatment of skin diseases, comprising as an active ingredient a tubulin inhibitor and one or more compounds selected from the group consisting of calcium, colchicine, tapinarof, fingolimod, tofacitinib, and pharmaceutically acceptable salts thereof. The combination therapy of the present invention can be used as an active ingredient that simultaneously exhibits activities such as skin moisturizing, whitening, wrinkle improvement, acne relief, skin barrier strengthening, or keratinocyte differentiation, along with the prevention, treatment, or improvement of skin diseases.

The invention relates to cancer biology, more specifically to the treatment of KRAS mutant cancers. A potent cancer therapy is provided by the combination of a farnesyl transferase inhibitor compound and a KRAS inhibitor compound.

The present invention provides a combination therapy involving bispecific binding agents comprising two binding domains binding to CLDN 18.2 and a binding domain binding to CD3 and agents stabilizing or increasing the expression of CLDN 18.2. The combination therapy is effective in treating cancer involving cancer cells expressing CLDN18.2.

The present invention provides anti-CD73 binding molecules, such as antibodies and their antigen-binding fragments. [Solution] Provided are isolated binding molecules or antigen-binding fragments thereof that contain an antibody VL and specifically bind to CD73 having a specific sequence. Furthermore, pharmaceutical formulations comprising the disclosed composition, as well as methods for diagnosing and treating diseases associated with CD73 expression, such as cancer, are also provided. Such diseases can be treated, for example, by direct therapy with the disclosed anti-CD73 binding molecule (e.g., a naked antibody or antibody-drug conjugate that binds to CD73), by adjuvant therapy with other antigen-binding anticancer agents such as immune checkpoint inhibitors (e.g., anti-CTLA-4 and anti-PD-1 monoclonal antibodies), and / or by combination therapy in which the anti-CD73 molecule is administered before, after, or concurrently with chemotherapy.

The invention relates to the application of inhibition of transcription factor 4 (TCF4 / ITF2) in the treatment of cancer. This in particular in combination therapy in conjunction with an immunotherapeutic compound (such as for treating cancers poorly responding or refractive to immunotherapy). In particular, inhibition of TCF4 / ITF2 is capable of restoring response to immunotherapy such as immune checkpoint inhibitor therapy. Expression levels of TCF4 / ITF2 as well as levels of mesenchymal-like cancer cells in a cancer lesion are predictive of future response to immunotherapy early after initiation of the immunotherapy. Further part of the invention are methods of detecting mesenchymal-like cancer cells.

The invention described herein provides gene therapy vectors, e.g., adeno-associated virus (AAV) vectors that co-express a functional protein (e.g., a micro-human micro-dystrophin gene product) and one or more additional coding sequences for RNAi sequences (e.g., siRNA, shRNA, miRNA), antisense sequences, guide sequences for gene-editing enzymes (e.g., sgRNA for CRISPR / Cas9 or crRNA for CRISPR / Cas12a), and / or microRNA, and methods of using such vectors to treat subjects with muscular dystrophy, e.g., DMD / BMD.

Disclosed herein are methods for treating a cancer in a subject in need thereof, comprising administering IL-2 conjugates in combination with an anti-EGFR antibody.

The invention belongs to the technical field of cancer treatment, and discloses a method for inhibiting castration-resistant prostate cancer proliferation and metastasis by promoting collagen degradation through targeting ADAMTS1. According to the method, ADAMTS1 is determined to be a mechanism key point for linking epigenetic reprogramming with biomechanical microenvironment destruction. The ADAMTS1 is reactivated to degrade a collagen-rich matrix, the FAK / MAPK mechanical transduction signaling pathway is inhibited, and the epithelial-mesenchymal transition (EMT) is reversed. The strategy not only achieves more than 90% of tumor inhibition effect, but also exhausts immunosuppressive macrophages and regulatory T cells to reverse immunosuppression by enhancing toxic CD8 + T cell infiltration. The research determines that epigenetic-ECM coevolution is a symbolic feature of CRPC, and provides a reasonably designed combination therapy for treating castration-resistant prostate cancer.