Abstract: Compounds comprising peptides capable of binding C3 protein and inhibiting complement activation are disclosed. The compounds comprise compstatin analogs in which the N-terminus contains an added or substituted component that improves (1) the peptide's binding affinity to C3 or its fragments, (2) the peptide's solubility in aqueous liquids, (3) the peptide's plasma stability, (4) the peptide's in vivo retention and/or (5) the peptide's bioavailability, as compared with an unmodified compstatin peptide under equivalent conditions. Pharmaceutical compositions and methods of using the compounds are also disclosed.

Abstract: The present disclosure describes methods for preventing or treating periodontitis or diseases associated with periodontitis. The present disclosure also describes methods of screening for compounds that can be used to prevent or treat periodontitis or diseases associated with periodontitis.

Abstract: A potent complement regulator is disclosed. The complement regulator comprises a complement regulatory region connected by a flexible linker to a multifunctional binding region that enables binding to C3b activation/inactivation products and/or oxidation end products, as well as to polyanionic surface markers on host cells. An embodiment of the invention utilizes factor H SCRs 1-4 as the complement regulatory region and factor H SCRs 19 and 20 as the multifunctional binding region, linked together by a poly-Gly linker at least 12 residues in length. Pharmaceutical compositions comprising the complement regulator and methods of using the complement regulator are also disclosed.

Abstract: Compounds comprising peptides capable of binding C3 protein and inhibiting complement activation are disclosed. These compounds display greatly improved complement activation-inhibitory activity as compared with currently available compounds. The compounds comprise compstatin analogs having a constrained backbone at position 8 (glycine) and, optionally, specific substitutions for threonine at position 13.

Abstract: Methods for the treatment of sepsis with complement inhibitors are disclosed. In particular, C3 inhibitors, such as Compstatin and Compstatin analogs, are administered at various times following the onset of sepsis to alleviate tissue damage and organ failure, which are hallmarks of the second, extravascular stage of sepsis. Combination therapies for comprehensive treatment of sepsis are also disclosed. Pharmaceutical compositions and kits for use in the methods are disclosed as well.

Abstract: Compounds comprising peptides and peptidomimetics capable of binding C3 protein and inhibiting complement activation are disclosed. These compounds display greatly improved complement activation-inhibitory activity as compared with currently available compounds. Methods of making and using the compounds are also disclosed.

Abstract: The present disclosure describes methods for preventing or treating periodontitis or diseases associated with periodontitis. The present disclosure also describes methods of screening for compounds that can be used to prevent or treat periodontitis or diseases associated with periodontitis.

Abstract: Methods for treating or ameliorating the damage resulting from intracerebral hemorrhage are disclosed. The methods involve administration of a complement inhibitor to inhibit C3a or C5a formation or activity in the affected tissue. Pharmaceutical compositions suitable for use in the methods of the invention are also provided.

Abstract: Compounds comprising peptides and peptidomimetics capable of binding C3 protein and inhibiting complement activation are disclosed. These compounds display greatly improved complement activation-inhibitory activity as compared with currently available compounds.

Abstract: Compounds comprising peptides capable of binding C3 protein and inhibiting complement activation are disclosed. These compounds display greatly improved complement activation-inhibitory activity as compared with currently available compounds. The compounds comprise compstatin analogs having a constrained backbone at position 8 (glycine) and, optionally, specific substitutions for threonine at position 13.

Abstract: Compounds comprising peptides capable of binding C3 protein and inhibiting complement activation are disclosed. The compounds comprise compstatin analogs in which the N-terminus contains an added or substituted component that improves (1) the peptide's binding affinity to C3 or its fragments, (2) the peptide's solubility in aqueous liquids, (3) the peptide's plasma stability, (4) the peptide's in vivo retention and/or (5) the peptide's bioavailability, as compared with an unmodified compstatin peptide under equivalent conditions. Pharmaceutical compositions and methods of using the compounds are also disclosed.

Abstract: Compounds comprising peptides and peptidomimetics capable of binding the C3 protein and inhibiting complement activation are disclosed. These compounds display improved complement activation-inhibitory activity as compared with currently available compounds. Isolated nucleic acid molecules encoding the peptides are also disclosed.

Abstract: A potent complement regulator is disclosed. The complement regulator comprises a complement regulatory region connected by a flexible linker to a multifunctional binding region that enables binding to C3b activation/inactivation products and/or oxidation end products, as well as to polyanionic surface markers on host cells. An embodiment of the invention utilizes factor H SCRs 1-4 as the complement regulatory region and factor H SCRs 19 and 20 as the multi-functional binding region, linked together by a poly-Gly linker at least 12 residues in length. Pharmaceutical compositions comprising the complement regulator and methods of using the complement regulator are also disclosed.

Abstract: Factor H-binding peptides that binds to a region of factor H that does not impede the complement-inhibitory activity of factor H are disclosed. When immobilized onto the surface of a biomaterial, these peptides recruit factor H, resulting in a substantial inhibition of biomaterial-induced complement activation in a biological substance exposed to the biomaterial.

Abstract: Compounds comprising peptides capable of binding C3 protein and inhibiting complement activation are disclosed. These compounds display greatly improved complement activation-inhibitory activity as compared with currently available compounds. The compounds comprise compstatin analogs having a constrained backbone at position 8 (glycine) and, optionally, specific substitutions for threonine at position 13.

Abstract: Compounds comprising peptides and peptidomimetics capable of binding the C3 protein and inhibiting complement activation are disclosed. These compounds display improved complement activation-inhibitory activity as compared with currently available compounds. Isolated nucleic acid molecules encoding the peptides are also disclosed.

Abstract: Methods for treating, preventing or delaying onset of polyp formation and subsequent colon cancer are disclosed. The methods involve administration of a complement inhibitor to inhibit C5a receptor signaling in the tumorigenic or pre-tumorigenic tissue.

Abstract: Compounds comprising peptides capable of binding C3 protein and inhibiting complement activation are disclosed. These cyclic compounds are modified to improve stability while maintaining substantially equivalent complement activation-inhibitory activity as compared with currently available compounds. The compounds comprise compstatin analogs in which the disulfide bond between C2 and C12 is modified via a thioether bond to form a cystathionine.

Abstract: The present disclosure describes methods for preventing or treating periodontitis or diseases associated with periodontitis. The present disclosure also describes methods of screening for compounds that can be used to prevent or treat periodontitis or diseases associated with periodontitis.

Abstract: Factor H-binding peptides that binds to a region of factor H that does not impede the complement-inhibitory activity of factor H are disclosed. When immobilized onto the surface of a biomaterial, these peptides recruit factor H, resulting in a substantial inhibition of biomaterial-induced complement activation in a biological substance exposed to the biomaterial.