Abstract: Interferon-?-inducible protein 10 (IP-10) peptides, IP-10 peptide variants and in silico designed C-X-C chemokine receptor 3 (CXCR3) peptide agonists are described. The small peptides can be used for inhibiting pathological tissue remodeling and treating fibrosis in a subject, such as a subject with fibrosis of the heart, lung, liver, kidney or skin. The peptide agonists can also be used to treat cardiovascular disease, including myocardial infarction and ischemia-reperfusion injury. Also described are in silico designed peptide antagonists that bind CXCR3 or ligands of CXCR3. These antagonist peptides block CXCR3 signaling by disrupting interaction of CXCR3 with its ligand. Antagonist peptides can be used, for example, to treat myocarditis and atherosclerosis. In additional embodiments agonists and antagonists of CXCR4 are disclosed.

Abstract: Interferon-?-inducible protein 10 (IP-10) peptides, IP-10 peptide variants and in silico designed C—X—C chemokine receptor 3 (CXCR3) peptide agonists are described. The small peptides can be used for inhibiting pathological tissue remodeling and treating fibrosis in a subject, such as a subject with fibrosis of the heart, lung, liver, kidney or skin. The peptide agonists can also be used to treat cardiovascular disease, including myocardial infarction and ischemia-reperfusion injury. Also described are in silico designed peptide antagonists that bind CXCR3 or ligands of CXCR3. These antagonist peptides block CXCR3 signaling by disrupting interaction of CXCR3 with its ligand. Antagonist peptides can be used, for example, to treat myocarditis and atherosclerosis. In additional embodiments agonists and antagonists of CXCR4 are disclosed.

Abstract: The present disclosure describes methods of treating angiogenic disorders of the eye, such as macular degeneration, restenosis following glaucoma treatment or diabetic retinopathy, by administering an activator of C-X-C chemokine receptor 3 (CXCR3). In some embodiments, the activator of CXCR3 is interferon-?-inducible 10 kDa protein (IP-10) or a fragment or variant thereof, such as a fragment comprising or consisting of the C-terminal ?-helix of IP-10. In other embodiments, the activator of CXCR3 is platelet factor 4 (PF4) or a fragment or variant thereof.

Abstract: Interferon-?-inducible protein 10 (IP-10) peptides, IP-10 peptide variants and in silico designed C-X-C chemokine receptor 3 (CXCR3) peptide agonists are described. The small peptides can be used for inhibiting pathological tissue remodeling and treating fibrosis in a subject, such as a subject with fibrosis of the heart, lung, liver, kidney or skin. The peptide agonists can also be used to treat cardiovascular disease, including myocardial infarction and ischemia-reperfusion injury. Also described are in silico designed peptide antagonists that bind CXCR3 or ligands of CXCR3. These antagonist peptides block CXCR3 signaling by disrupting interaction of CXCR3 with its ligand. Antagonist peptides can be used, for example, to treat myocarditis and atherosclerosis. In additional embodiments agonists and antagonists of CXCR4 are disclosed.

Abstract: The present disclosure describes methods of treating angiogenic disorders of the eye, such as macular degeneration, restenosis following glaucoma treatment or diabetic retinopathy, by administering an activator of C-X-C chemokine receptor 3 (CXCR3). In some embodiments, the activator of CXCR3 is interferon-?-inducible 10 kDa protein (IP-10) or a fragment or variant thereof, such as a fragment comprising or consisting of the C-terminal ?-helix of IP-10. In other embodiments, the activator of CXCR3 is platelet factor 4 (PF4) or a fragment or variant thereof.

Abstract: Described herein is the finding that activators of CXCR3, such as proteins that bind CXCR3 (e.g., IP-9, IP-10 and PF4), enhance the density of goblet cells in the eye. Goblet cells in the conjunctiva are the primary source of tear mucus. Accordingly, the present disclosure describes methods of treating dry eye syndrome by administering an activator of CXCR3. Also described are methods of increasing goblet cells density, such as goblet cell density in the conjunctiva.

Abstract: Interferon-?-inducible protein 10 (IP-10) peptides, IP-10 peptide variants and in silico designed C—X—C chemokine receptor 3 (CXCR3) peptide agonists are described. The small peptides can be used for inhibiting pathological tissue remodeling and treating fibrosis in a subject, such as a subject with fibrosis of the heart, lung, liver, kidney or skin. The peptide agonists can also be used to treat cardiovascular disease, including myocardial infarction and ischemia-reperfusion injury. Also described are in silico designed peptide antagonists that bind CXCR3 or ligands of CXCR3. These antagonist peptides block CXCR3 signaling by disrupting interaction of CXCR3 with its ligand. Antagonist peptides can be used, for example, to treat myocarditis and atherosclerosis. In additional embodiments agonists and antagonists of CXCR4 are disclosed.

Abstract: Described herein is the finding that activators of CXCR3, such as proteins that bind CXCR3 (e.g., IP-9, IP-10 and PF4), enhance the density of goblet cells in the eye. Goblet cells in the conjunctiva are the primary source of tear mucus. Accordingly, the present disclosure describes methods of treating dry eye syndrome by administering an activator of CXCR3. Also described are methods of increasing goblet cells density, such as goblet cell density in the conjunctiva.

Abstract: The present disclosure describes methods of treating angiogenic disorders of the eye, such as macular degeneration, restenosis following glaucoma treatment or diabetic retinopathy, by administering an activator of C-X-C chemokine receptor 3 (CXCR3). In some embodiments, the activator of CXCR3 is interferon-?-inducible 10 kDa protein (IP-10) or a fragment or variant thereof, such as a fragment comprising or consisting of the C-terminal ?-helix of IP-10. In other embodiments, the activator of CXCR3 is platelet factor 4 (PF4) or a fragment or variant thereof.

Abstract: Described herein is the finding that activators of CXCR3, such as proteins that bind CXCR3 (e.g., IP-9, IP-10 and PF4), enhance the density of goblet cells in the eye. Goblet cells in the conjunctiva are the primary source of tear mucus. Accordingly, the present disclosure describes methods of treating dry eye syndrome by administering an activator of CXCR3. Also described are methods of increasing goblet cells density, such as goblet cell density in the conjunctiva.

Abstract: The present disclosure describes methods of treating angiogenic disorders of the eye, such as macular degeneration, restenosis following glaucoma treatment or diabetic retinopathy, by administering an activator of C-X-C chemokine receptor 3 (CXCR3). In some embodiments, the activator of CXCR3 is interferon-?-inducible 10 kDa protein (IP-10) or a fragment or variant thereof, such as a fragment comprising or consisting of the C-terminal ?-helix of IP-10. In other embodiments, the activator of CXCR3 is platelet factor 4 (PF4) or a fragment or variant thereof.

Abstract: Described herein is the finding that activators of CXCR3, such as proteins that bind CXCR3 (e.g., IP-9, IP-10 and PF4), enhance the density of goblet cells in the eye. Goblet cells in the conjunctiva are the primary source of tear mucus. Accordingly, the present disclosure describes methods of treating dry eye syndrome by administering an activator of CXCR3. Also described are methods of increasing goblet cells density, such as goblet cell density in the conjunctiva.

Abstract: The present disclosure describes methods of treating angiogenic disorders of the eye, such as macular degeneration, restenosis following glaucoma treatment or diabetic retinopathy, by administering an activator of C-X-C chemokine receptor 3 (CXCR3). In some embodiments, the activator of CXCR3 is interferon-?-inducible 10 kDa protein (IP-10) or a fragment or variant thereof, such as a fragment comprising or consisting of the C-terminal ?-helix of IP-10. In other embodiments, the activator of CXCR3 is platelet factor 4 (PF4) or a fragment or variant thereof.

Abstract: The present disclosure describes methods of treating angiogenic disorders of the eye, such as macular degeneration, restenosis following glaucoma treatment or diabetic retinopathy, by administering an activator of C-X-C chemokine receptor 3 (CXCR3). In some embodiments, the activator of CXCR3 is interferon-?-inducible 10 kDa protein (IP-10) or a fragment or variant thereof, such as a fragment comprising or consisting of the C-terminal ?-helix of IP-10. In other embodiments, the activator of CXCR3 is platelet factor 4 (PF4) or a fragment or variant thereof.

Abstract: The present disclosure describes methods of treating angiogenic disorders of the eye, such as macular degeneration, restenosis following glaucoma treatment or diabetic retinopathy, by administering an activator of C-X-C chemokine receptor 3 (CXCR3). In some embodiments, the activator of CXCR3 is interferon-?-inducible 10 kDa protein (IP-10) or a fragment or variant thereof, such as a fragment comprising or consisting of the C-terminal ?-helix of IP-10. In other embodiments, the activator of CXCR3 is platelet factor 4 (PF4) or a fragment or variant thereof.

Abstract: The present disclosure describes methods of treating angiogenic disorders of the eye, such as macular degeneration, restenosis following glaucoma treatment or diabetic retinopathy, by administering an activator of C-X-C chemokine receptor 3(CXCR3). In some embodiments, the activator of CXCR3 is interferon-?-inducible 10 kDa protein (IP-10), or a fragment or variant thereof, such as a fragment comprising or consisting of the C-terminal ?-helix of IP-10. In other embodiments, the activator of CXCR3 is platelet factor 4 (PF4) or a fragment or variant thereof.

Abstract: The present disclosure describes methods of treating angiogenic disorders of the eye, such as macular degeneration, restenosis following glaucoma treatment or diabetic retinopathy, by administering an activator of CXCR3. In some embodiments, the activator of CXCR3 is IP-10 or a fragment or variant thereof, such as a fragment comprising or consisting of the C-terminal ?-helix of IP-10. In other embodiments, the activator of CXCR3 is PF4 or a fragment or variant thereof.

Abstract: Disclosed are peptides having activity against receptor CXCR3 are disclosed that exhibit activity in preventing the formation of new vessels and activity in mediating the dissociation of newly-formed vessels and resolving of wounds in the later stages of wound healing. Preferred peptides are derived from the ?-helix portion IP-10 (CXCL10) or from IP-9 (CXCL11), are nontoxic, and smaller than naturally occurring peptides, making them useful in therapies against diseases or disease states marked by unwanted angiogenesis, including tumorogenic diseases such as cancers, and in healing of chronic wounds.

Abstract: Disclosed are peptides having activity against receptor CXCR3 are disclosed that exhibit activity in preventing the formation of new vessels and activity in mediating the dissociation of newly-formed vessels and resolving of wounds in the later stages of wound healing. Preferred peptides are derived from the ?-helix portion IP-10 (CXCL10) or from IP-9 (CXCL11), are nontoxic, and smaller than naturally occurring peptides, making them useful in therapies against diseases or disease states marked by unwanted angiogenesis, including tumorogenic diseases such as cancers, and in healing of chronic wounds.