A combination comprising tasquinimod, or a pharmaceutically acceptable salt thereof, and at least one further compound selected from a proteasome inhibitor, an immunomodulatory imide, and an antibody, for use as a in the treatment of multiple myeloma. A kit comprising tasquinimod and a package insert with instructions for using tasquinimod in combination with at least one further compound selected from a proteasome inhibitor, an immunomodulatory imide, and an antibody, to treat multiple myeloma in an individual. Tasquinimod for use in the treatment of multiple myeloma, in combination with a further compound selected from a proteasome inhibitor, an immunomodulatory imide, and an antibody.

A combination comprising tasquinimod, or a pharmaceutically acceptable salt thereof, and at least one further compound selected from a proteasome inhibitor, an immunomodulatory imide, and an antibody, for use as a in the treatment of multiple myeloma. A kit comprising tasquinimod and a package insert with instructions for using tasquinimod in combination with at least one further compound selected from a proteasome inhibitor, an immunomodulatory imide, and an antibody, to treat multiple myeloma in an individual. Tasquinimod for use in the treatment of multiple myeloma, in combination with a further compound selected from a proteasome inhibitor, an immunomodulatory imide, and an antibody.

Compositions and methods for promoting skin restoration of aging skin are provided herein. Compositions and methods described herein may result in elastin and/or collagen stimulation, extracellular matrix (ECM) recycling, anti-inflammatory effects, or combinations thereof.

Compositions and methods for promoting skin restoration of aging skin are provided herein. Compositions and methods described herein may result in elastin and/or collagen stimulation, extracellular matrix (ECM) recycling, anti-inflammatory effects, or combinations thereof.

The present invention relates in a first aspect to a method for the treatment of chronic fatigue syndrome (CFS) comprising administering to a patient in need thereof a therapeutically effective amount of inhibitory or cytotoxic agent against plasma cells. In a further aspect, the present invention relates to a combination of the inhibitory or cytotoxic agent against plasma cells with a B-cell depleting agent or an inhibitor of B-cell activation in the treatment of chron-ic fatigue syndrome. In addition, a combination of an inhibitory or cytotoxic agent against plasma cells and B-Cell depleting agent or an inhibitor of B-cell activation are described. Said combination may be provided in form of a kit comprising suitably effective dosages of said compounds. Further, the use of the compounds or the combination in the treatment of CFS is described.

The present invention relates in a first aspect to a method for the treatment of chronic fatigue syndrome (CFS) comprising administering to a patient in need thereof a therapeutically effective amount of inhibitory or cytotoxic agent against plasma cells. In a further aspect, the present invention relates to a combination of the inhibitory or cytotoxic agent against plasma cells with a B-cell depleting agent or an inhibitor of B-cell activation in the treatment of chron-ic fatigue syndrome. In addition, a combination of an inhibitory or cytotoxic agent against plasma cells and B-Cell depleting agent or an inhibitor of B-cell activation are described. Said combination may be provided in form of a kit comprising suitably effective dosages of said compounds. Further, the use of the compounds or the combination in the treatment of CFS is described.

Methods and compositions to deplete deleterious mitochondrial genomes (ΔmtDNAs), resulting in a compensatory increase in WT mtDNAs, by inhibition of LONP1, e.g., by inhibitory nucleic acids (including RNAi); inducing mutations that prevent the protease from binding mtDNA; or administering an inhibitor, e.g., the clinically relevant compound CDDO-Me (Bardoxolone), all of which result in the preferential loss of ΔmtDNAs.

Methods and compositions to deplete deleterious mitochondrial genomes (ΔmtDNAs), resulting in a compensatory increase in WT mtDNAs, by inhibition of LONP1, e.g., by inhibitory nucleic acids (including RNAi); inducing mutations that prevent the protease from binding mtDNA; or administering an inhibitor, e.g., the clinically relevant compound CDDO-Me (Bardoxolone), all of which result in the preferential loss of ΔmtDNAs.

Disclosed herein are methods of treating Rett syndrome comprising administering trofinetide to a subject in need thereof in which a dosage is provided that may reduce or avoid underexposure, e.g., in low body weight subjects, and/or provide other benefits.

A method of treating a patient who has hepatocellular carcinoma (HCC), colorectal carcinoma (CRC), glioblastoma (GB), gastric cancer (GC), esophageal cancer, NSCLC, pancreatic cancer (PC), renal cell carcinoma (RCC), benign prostate hyperplasia (BPH), prostate cancer (PCA), ovarian cancer (OC), melanoma, breast cancer (BRCA), CLL, Merkel cell carcinoma (MCC), SCLC, Non-Hodgkin lymphoma (NHL), AML, gallbladder cancer and cholangiocarcinoma (GBC, CCC), urinary bladder cancer (UBC), and uterine cancer (UEC) includes administering to said patient a composition containing a population of activated T cells that selectively recognize cells in the patient that aberrantly express a peptide. A pharmaceutical composition contains activated T cells that selectively recognize cells in a patient that aberrantly express a peptide, and a pharmaceutically acceptable carrier, in which the T cells bind to the peptide in a complex with an MHC class I molecule, and the composition is for treating the patient who has HCC, CRC, GB, GC, esophageal cancer, NSCLC, PC, RCC, BPH, PCA, OC, melanoma, BRCA, CLL, MCC, SCLC, NHL, AML, GBC, CCC, UBC, and/or UEC. A method of treating a patient who has HCC, CRC, GB, GC, esophageal cancer, NSCLC, PC, RCC, BPH, PCA, OC, melanoma, BRCA, CLL, MCC, SCLC, NHL, AML, GBC, CCC, UBC, and/or UEC includes administering to said patient a composition comprising a peptide in the form of a pharmaceutically acceptable salt, thereby inducing a T-cell response to the HCC, CRC, GB, GC, esophageal cancer, NSCLC, PC, RCC, BPH, PCA, OC, melanoma, BRCA, CLL, MCC, SCLC, NHL, AML, GBC, CCC, UBC, and/or UEC.