Abstract: An isolated peptide of up to 6 amino acids comprising an amino acid sequence which inhibits binding of an endothelial cell protein C receptor (EPCR) ligand to the EPCR is disclosed. Also disclosed is an isolated peptide comprising an amino acid sequence which inhibits binding of an endothelial cell protein C receptor (EPCR) ligand to the EPCR, wherein the peptide comprises a modification in at least one amino acid. Also disclosed is a molecule comprising an amino acid sequence which inhibits binding of an endothelial cell protein C receptor (EPCR) ligand to the EPCR attached to a heterologous moiety. Pharmaceutical compositions and methods of treatment are also disclosed.

Abstract: Ophthalmic formulations comprising a PAR1 antagonist and/or an agent that interferes with an interaction of PAR1 and a protease (e.g., thrombin), and an ophthalmically acceptable carrier, and uses thereof in treating or preventing retinal pathologies such as retinal degeneration, are provided. The agent can be, for example, a peptide conjugate represented by Formula I, as defined in the specification.

Abstract: 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.

Abstract: Provided herein are method and kits for identifying thrombus origin based on temporal thrombin activity assay, and use thereof for optimizing post-ischemic event treatment, and further preventing recurrence of secondary ischemic events.

Abstract: 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.

Abstract: An isolated peptide of up to 6 amino acids comprising an amino acid sequence which inhibits binding of an endothelial cell protein C receptor (EPCR) ligand to the EPCR is disclosed. Also disclosed is an isolated peptide comprising an amino acid sequence which inhibits binding of an endothelial cell protein C receptor (EPCR) ligand to the EPCR, wherein the peptide comprises a modification in at least one amino acid. Also disclosed is a molecule comprising an amino acid sequence which inhibits binding of an endothelial cell protein C receptor (EPCR) ligand to the EPCR attached to a heterologous moiety. Pharmaceutical compositions and methods of treatment are also disclosed.

Abstract: The present invention is directed to a peptide conjugate comprising an alpha-amino protecting moiety, a peptide comprising the amino acid sequence at least 3 amino-acid long derived from the C?-terminus of PAR-1, or an active variant thereof and a protease-disabling moiety. The present invention is further directed to pharmaceutical compositions comprising the peptide conjugate and use thereof for treating diseases and disorder associated with excessive PAR-1 activity.

Abstract: The present invention is directed to a peptide conjugate comprising an alpha-amino protecting moiety, a peptide comprising the amino acid sequence at least 3 amino-acid long derived from the C?-terminus of PAR-1, or an active variant thereof and a protease-disabling moiety. The present invention is further directed to pharmaceutical compositions comprising the peptide conjugate and use thereof for treating diseases and disorder associated with excessive PAR-1 activity.

Abstract: Disclosed are methods for treating multiple sclerosis patients that entail co-administration of effective amounts of a Ras antagonist which is farnesylthiosalicylic acid or an analog thereof, and a second active agent selected from glatiramer acetate, laquinimod and combinations thereof. Therapeutic compositions and methods of making them are also disclosed.

Abstract: Disclosed is a method for inhibiting Ras-induced or mediated proliferation of cells associated with a non-malignant disease, disorder or pathological condition. The method entails administering to a patient a Ras antagonist in an amount effective to inhibit the proliferation. The invention is particularly applicable to diseases characterized by a proliferation of T-cells such as autoimmune disease, e.g., type 1 diabetes, lupus and multiple sclerosis, and pathological states such as graft rejection induced by the presentation of a foreign antigen such as a graft in response to a disease condition (e.g., kidney failure). Other non-malignant diseases characterized by proliferations of cells include cirrhosis of the liver and restenosis. Preferred Ras antagonists are S-trans-trans farnesylthiosalicylic acid (FTS) and structurally related compounds (or analogs) thereof.

Abstract: Disclosed is a method for inhibiting Ras-induced or mediated proliferation of cells associated with a non-malignant disease, disorder or pathological condition. The method entails administering to a patient a Ras antagonist in an amount effective to inhibit the proliferation. The invention is particularly applicable to diseases characterized by a proliferation of T-cells such as autoimmune disease, e.g., type 1 diabetes, lupus and multiple sclerosis, and pathological states such as graft rejection induced by the presentation of a foreign antigen such as a graft in response to a disease condition (e.g., kidney failure). Other non-malignant diseases characterized by proliferations of cells include cirrhosis of the liver and restenosis. Preferred Ras antagonists are S-trans-trans farnesylthiosalicylic acid (FTS) and structurally related compounds (or analogs) thereof.