The present invention relates to a peptide and its use as a medicament, in particular in the treatment of metabolic syndrome, non-alcoholic fatty liver disease (NAFLD), cardiovascular disease (CVD) or cholestatic liver disease.

Methods of culturing embryonic stem cells, induced pluripotent stem cells and/or differentiated cells in culture medium comprising activin are described. In one aspect, the disclosure features a pluripotent human stem cell, wherein the stem cell comprises: (i) a genomic edit that results in loss of function of Cytokine Inducible SH2 Containing Protein (CISH) and (ii) a genomic edit that results in a loss of function of an agonist of the TGF beta signaling pathway, or a genomic edit that results in a loss of function of adenosine Ata receptor.

Disclosed are an amphiphysin-I mutant having anti-senescence activity and the use thereof. More particularly, disclosed are an amphiphysin-I mutant (AMPH-I) wherein valine (V), which is the 392nd amino acid in the amino acid sequence of amphiphysin-I (AMPH-I) represented by SEQ ID NO: 1, is substituted with glycine (G), a composition for suppressing aging and cellular senescence containing the amphiphysin-I mutant as an active ingredient, a pharmaceutical composition for preventing or treating senescence or a senescence-associated disease, a method for suppressing aging and cellular senescence, and a method for screening an inhibitor for aging and cellular senescence. The amphiphysin-I mutant is capable of suppressing both promotion of aging and cellular senescence and reduction of endocytosis caused by suppression of expression of βPIX (PAK1-interacting exchange factor beta), of preventing cleavage of the amphiphysin-I protein caused by calpain, a protease involved in aging and cellular senescence caused by suppressed βPIX expression, and of suppressing the expression of aging and cellular senescence indicators. Thus, the amphiphysin-I mutant is effectively used as a novel therapeutic agent for senescence or senescence-associated diseases.

An isolated Methyl-CpG binding domain (MBD) variant may include an MBD core domain having at least 60% sequence homology relative to any one of SEQ ID Nos. 1-45 and comprising at least one amino acid substitution relative to the corresponding wildtype MBD in various positions. The isolated MBD variant or the conjugate may be used for determining the methylation state of cytosine residues and/or oxidation state of 5-methylated cytosine residues in a CpG dinucleotide of interest and its complement in a DNA molecule or for the enrichment of DNA molecules comprising a CpG dinucleotide of interest and its complement. At least one cytosine nucleobase in the CpG dinucleotide may be modified to be 5-methylcytosine (mC), 5-hydroxymethylcytosine (hmC), 5-formylcytosine (fC), or 5-carboxylcytosine (caC).

Provided is an improved cell-permeable nuclear import inhibitor (iCP-NI) for inhibition of cytokine storm or an inflammatory disease, in which solubility and stability are improved by introducing an advanced macromolecule transduction domain (aMTD)-based therapeuticmolecule systemic delivery technology (TSDT) into a cell-permeable nuclear import inhibitor (CP-NI, cSN50.1 peptide). The improved cell-permeable nuclear import inhibitor synthetic peptide according to the present disclosure more efficiently blocks signal transduction mediated by stress-responsive transcription factors (SRTFs) including NF-κB, based on remarkable cell permeability, and thus it may be used as an excellent prophylactic or therapeutic agent for cytokine storm or inflammatory diseases.

Provided are a bifunctional fusion protein and pharmaceutical use thereof. Specifically, provided are a bifunctional fusion protein comprising an SIRPγ peptide variant and an anti-human PD-L1 antibody, an SIRPγ peptide variant, and pharmaceutical use thereof. The bifunctional fusion protein can specifically bind PD-L1 and CD47 to block the binding of PD-L1 or CD47 to a receptor or ligand thereof. In addition, also provided are preparation and application of the bifunctional fusion protein, and treatment of cancers and immune-related diseases.

Described herein are peptides and variants and mutants thereof capable of interacting with TEAD, disrupting the HIPPO pathway, or modulating the activity or function of TEAD interactions in a cell. Pharmaceutical compositions and uses of peptides, as well as methods of designing and manufacturing such peptides, to treat cancer, tumor, or any other disease/condition associated with a dysregulated HIPPO pathway or uncontrolled cell growth are also described herein.

The present invention provides a peptide having anti-inflammatory activity. The present invention also provides the method of preparation of the peptide and compositions, and kits comprising the peptide. The invention further provides the method of treating inflammatory diseases employing the peptide of the present invention.

In certain aspects, the present invention provides compositions and methods for altering iron metabolism to increase red blood cell and/or hemoglobin levels in vertebrates, including rodents and primates, and particularly in humans.

Fusion peptide, and pharmaceutical composition containing the same, for use in treating, preventing and/or delaying the onset of a fibroproliferative vascular disease, wherein the fusion peptide comprises: (a) an amino acid sequence as defined in SEQ ID No.: 1 or a related homolog having at least 85% similarity with SEQ ID No.: 1 and having the ability of the sequence SEQ ID No.: 1 to inhibit the kinase-independent function of PI3Kγ, and (b) a peptide having the ability to penetrate a cell.