The present disclosure provides IL12 and IL23 muteins as partial agonists comprising modified human p40 molecules that associate with human p35 (hP35) and human P19 (hP19) to form modified hIL-12 and IL23 partial agonists wherein the individual components of IL12 and IL23 muteins are linked to engineered Fc domains.

This disclosure relates to recombinant proteins comprising a GM-CSF sequence and an interleukin sequence and nucleic acids related thereto. In certain embodiments, the disclosure relates to recombinant proteins comprises N-terminal sequences that are the result of improved production techniques and uses for treating or preventing autoimmune diseases such as multiple sclerosis and cancer.

Disclosed are cysteine variants of interleukin-11 (IL-11) and methods of making and using such proteins in therapeutic applications.

Disclosed are cysteine variants of interleukin-11 (IL-11) and methods of making and using such proteins in therapeutic applications.

The present disclosure relates to targeted degradation platform technology. For example, the present disclosure relates to bispecific binding agents for degrading endogenous proteins, whether membrane-associated or soluble, using the lysosome pathway. The disclosure also provides methods useful for producing such agents, nucleic acids encoding same, host cells genetically modified with the nucleic acids, as well as methods for modulating an activity of a cell and/or for the treatment of various disorders.

Embodiments relate to peptide antagonists of -family cytokines, which is associated with important human diseases, such as leukemia, autoimmune diseases, collagen diseases, diabetes mellitus, skin diseases, degenerative neuronal diseases and graft-versus-host disease (GvHD). Thus, inhibitors of -cytokine activity are valuable therapeutic and cosmetic agents as well as research tools. Traditional approaches to inhibiting yc-cytokine activity involve raising neutralizing antibodies against each individual -cytokine family member/ receptor subunit. However, success has been limited and often multiple -cytokine family members co-operate to cause the disease state. Combinatorial use of neutralizing antibodies raised against each factor is impractical and poses an increased risk of adverse immune reactions. The present embodiments overcome these shortcomings by utilizing peptide antagonists based on the consensus -subunit binding site to inhibit -cytokine activity. Such approach allows for flexibility in antagonist design. In several embodiments, peptides exhibit Simul-Block activity, inhibiting the activity of multiple -cytokine family members.

Featured are recombinant adenoviruses and vectors thereof. In particular, the adenoviruses are simian (rhesus) adenoviruses having a low seroprevalence and high immunogenicity (when expressing, e.g., an antigenic polypeptide) relative to other adenoviruses and vectors thereof. Also featured are methods for producing the adenoviruses and methods of treatment of diseases by administering the adenoviral vector(s) to a subject (e.g., a human).

Methods are disclosed for generating antibodies and an expression vector used to express protein(s) which provoke the antibody response. The expression vector may be useful in generating an antibody directed to an antigen, comprising a gene in operable linkage with a promoter, which gene encodes upon expressing a fusion protein comprising (i) CD134L, a fragment, homologous or orthologues protein thereof as N-terminal moiety of the fusion protein; and (ii) all or part of an antigenic protein as C-terminal moiety of the fusion protein. To generate the antibodies, the vector is injected into a subject animal, which produces a fusion protein, against which antibodies are generated.

Embodiments relate to peptide antagonists of ?c-family cytokines, which is associated with important human diseases, such as leukemia, autoimmune diseases, collagen diseases, diabetes mellitus, skin diseases, degenerative neuronal diseases and graft-versus-host disease (GvHD). Thus, inhibitors of ?c-cytokine activity are valuable therapeutic and cosmetic agents as well as research tools. Traditional approaches to inhibiting ?c-cytokine activity involve raising neutralizing antibodies against each individual ?c-cytokine family member/receptor subunit. However, success has been limited and often multiple ?c-cytokine family members co-operate to cause the disease state. Combinatorial use of neutralizing antibodies raised against each factor is impractical and poses an increased risk of adverse immune reactions. The present embodiments overcome these shortcomings by utilizing peptide antagonists based on the consensus ?c-subunit binding site to inhibit ?c-cytokine activity. Such approach allows for flexibility in antagonist design. In several embodiments, peptides exhibit Simul-Block activity, inhibiting the activity of multiple ?c-cytokine family members.

Peptide antagonists of ?c-family cytokines, which is associated with important human diseases, such as leukemia, autoimmune diseases, collagen diseases, diabetes mellitus, skin diseases, degenerative neuronal diseases and graft-versus-host disease (GvHD). Thus, inhibitors of ?c-cytokine activity are valuable therapeutic and cosmetic agents as well as research tools. Traditional approaches to inhibiting ?c-cytokine activity involve raising neutralizing antibodies against each individual ?c-cytokine family member/receptor subunit. However, success has been limited and often multiple ?c-cytokine family members co-operate to cause the disease state. Combinatorial use of neutralizing antibodies raised against each factor is impractical and poses an increased risk of adverse immune reactions. The present embodiments overcome these shortcomings by utilizing peptide antagonists based on the consensus ?c-subunit binding site to inhibit ?c-cytokine activity. Such approach allows for flexibility in antagonist design. The disclosed peptides exhibit Simul-Block activity, inhibiting the activity of multiple ?c-cytokine family members.