The present invention provides compounds, compositions thereof, and methods of using the same.

The present invention relates to antibodies, or antigen-binding fragments thereof, directed against human leukocyte antigen-G (HLA-G) protein and raised against an immunogenic peptide derived from the α3 domain of HLA-G protein. The invention further relates to the immunogenic peptide, and methods for producing said anti-HLA-G specific antibodies.

The present invention relates to antibodies, or antigen-binding fragments thereof, directed against human leukocyte antigen-G (HLA-G) protein and raised against an immunogenic peptide derived from the α3 domain of HLA-G protein. The invention further relates to the immunogenic peptide, and methods for producing said anti-HLA-G specific antibodies.

The present invention relates to cyclic NTCP targeting peptides which are preS-derived peptides of hepatitis B virus (HBV). The present invention further relates to pharmaceutical compositions comprising at least one cyclic peptide. The present invention further relates to medical uses of said cyclic peptides and the pharmaceutical compositions, such as in the diagnosis, prevention and/or treatment of a liver disease or condition, and/or in the inhibition of HBV and/or HDV infection. The present invention further relates to methods of diagnosis, prevention and/or treatment of a liver disease or condition and/or the inhibition of HBV and/or HDV infection.

The present invention relates to cyclic NTCP targeting peptides which are preS-derived peptides of hepatitis B virus (HBV). The present invention further relates to pharmaceutical compositions comprising at least one cyclic peptide. The present invention further relates to medical uses of said cyclic peptides and the pharmaceutical compositions, such as in the diagnosis, prevention and/or treatment of a liver disease or condition, and/or in the inhibition of HBV and/or HDV infection. The present invention further relates to methods of diagnosis, prevention and/or treatment of a liver disease or condition and/or the inhibition of HBV and/or HDV infection.

The present invention relates to the field of genetic engineering, and provides a zipper fastener structure of promoting formation of a protein dimer and application thereof. The zipper fastener can be applied to dimerization of proteins of the same type and dimerization of proteins of different types, and can also be applied to polypeptide cycle formation, polypeptide dimerization, and polypeptide extension. A ESAT6-CFP 10 dimer having an approximately native conformation can be obtained, and the dimer has better solubility, and has a better stimulating effect on memory T cells than a ESAT6-CFP10 fusion protein capable of linear fusion expression. A dimer zipper fastener can assist the formation of a more stable cyclic polypeptide, and a CCP polypeptide added with a dimer fastener can improve the detection rate for citrullinated autoantibodies in serum of a rheumatoid arthritis patient.

The present invention relates to the field of genetic engineering, and provides a zipper fastener structure of promoting formation of a protein dimer and application thereof. The zipper fastener can be applied to dimerization of proteins of the same type and dimerization of proteins of different types, and can also be applied to polypeptide cycle formation, polypeptide dimerization, and polypeptide extension. A ESAT6-CFP 10 dimer having an approximately native conformation can be obtained, and the dimer has better solubility, and has a better stimulating effect on memory T cells than a ESAT6-CFP10 fusion protein capable of linear fusion expression. A dimer zipper fastener can assist the formation of a more stable cyclic polypeptide, and a CCP polypeptide added with a dimer fastener can improve the detection rate for citrullinated autoantibodies in serum of a rheumatoid arthritis patient.

Disclosed are compounds, compositions, and methods involving cyclic peptides that can bind to KRAS (G12D) oncogenic protein. For example, disclosed are cyclic peptides that selectively bind KRAS (G12D) oncogenic protein. Also disclosed are methods of inhibiting KRAS (G12D) oncogenic protein in a cancer cell expressing KRAS (G12D) oncogenic protein. In some forms, the method comprises incubating the cancer cell with any one or more of the disclosed cyclic peptides. In some forms, the method comprises bringing into contact the cancer cell with any one or more of the disclosed cyclic peptides.

Disclosed are compounds, compositions, and methods involving cyclic peptides that can bind to KRAS (G12D) oncogenic protein. For example, disclosed are cyclic peptides that selectively bind KRAS (G12D) oncogenic protein. Also disclosed are methods of inhibiting KRAS (G12D) oncogenic protein in a cancer cell expressing KRAS (G12D) oncogenic protein. In some forms, the method comprises incubating the cancer cell with any one or more of the disclosed cyclic peptides. In some forms, the method comprises bringing into contact the cancer cell with any one or more of the disclosed cyclic peptides.

Disclosed is a general, reversible bicyclization strategy to increase both the proteolytic stability and cell permeability of peptidyl drugs. A peptide drug is fused with a short cell-penetrating motif and converted into a conformationally constrained bicyclic structure through the formation of a pair of disulfide bonds. The resulting bicyclic peptide has greatly enhanced proteolytic stability as well as cell-permeability. Once inside the cell, the disulfide bonds are reduced to produce a linear, biologically active peptide. This strategy was applied to generate a cell-permeable bicyclic peptidyl inhibitor against the NEMO-IKK interaction.