Disclosed herein is an agent that modulates a cis interaction between Repulsive Guidance Molecule A (RGMa) and Neogenin or lipid rafts. Modulation by the agent may include blocking the cis interaction between RGMa and Neogenin and/or disrupting lipid rafts. In turn, this promotes neuronal cell survival and axon growth and/or regeneration. Also disclosed herein is a method of treating a disease in a subject in need thereof. The method may include administering the agent to the subject. Further disclosed herein is a method of identifying an agent that modulates the cis interaction between RGMa and Neogenin.

Disclosed herein is an agent that modulates a cis interaction between Repulsive Guidance Molecule A (RGMa) and Neogenin or lipid rafts. Modulation by the agent may include blocking the cis interaction between RGMa and Neogenin and/or disrupting lipid rafts. In turn, this promotes neuronal cell survival and axon growth and/or regeneration. Also disclosed herein is a method of treating a disease in a subject in need thereof. The method may include administering the agent to the subject. Further disclosed herein is a method of identifying an agent that modulates the cis interaction between RGMa and Neogenin.

Compositions and methods for treating malignant gliomas such as glioblastoma are provided, comprising a combination of a peptide conjugate comprising an amino acid sequence derived from the N-terminus of the receptor PAR-1, and the chemotherapeutic agent temozolomide.

Compositions and methods for treating malignant gliomas such as glioblastoma are provided, comprising a combination of a peptide conjugate comprising an amino acid sequence derived from the N-terminus of the receptor PAR-1, and the chemotherapeutic agent temozolomide.

Compositions and methods for treating malignant gliomas such as glioblastoma are provided, comprising a combination of a peptide conjugate comprising an amino acid sequence derived from the N-terminus of the receptor PAR-1, and the chemotherapeutic agent temozolomide.

Disclosed is use of NK3R antagonists for the therapeutic treatment leptin-related disease.

Disclosed is use of NK3R antagonists for the therapeutic treatment leptin-related disease.

This invention relates to agents that are inhibitors or activators of variant forms of endogenous proteins and novel methods of identifying such variants. Of particular interest are inhibitors and activators of endogenous protein variants, encoded by genes which have mutated, which variants often arise or are at least first identified as having arisen following exposure to a chemical agent which is known to be an inhibitor or activator of the corresponding unmutated endogenous protein.

This invention relates to agents that are inhibitors or activators of variant forms of endogenous proteins and novel methods of identifying such variants. Of particular interest are inhibitors and activators of endogenous protein variants, encoded by genes which have mutated, which variants often arise or are at least first identified as having arisen following exposure to a chemical agent which is known to be an inhibitor or activator of the corresponding unmutated endogenous protein.

Antibody molecules that bind to CD73 are disclosed. The anti-CD73 antibody molecules can be used to treat, prevent and/or diagnose cancer.