Provided are methods for and compounds for modulating the complement system. In particular, compounds are provided that inhibit complement activation and compounds are provided that promote complement activation. The compounds are therapeutics by virtue of their effects on the complement system. Hence, the compounds that inhibit complement activation can be used for treatment of ischemic and reperfusion disorders, including myocardial infarction and stroke, sepsis, autoimmune diseases, inflammatory diseases and diseases with an inflammatory component, including Alzheimer's Disease and other neurodegenerative disorders.

Methods of using an ET.sub.B receptor agonist, such as IRL-1620, for the treatment of stroke or cerebrovascular accidents are disclosed. The ET.sub.B receptor agonist is used alone or in combination with a second agent useful in the treatment of stroke or other cerebrovascular accident.

Methods of using an ET.sub.B receptor agonist, such as IRL-1620, for the treatment of stroke or cerebrovascular accidents are disclosed. The ET.sub.B receptor agonist is used alone or in combination with a second agent useful in the treatment of stroke or other cerebrovascular accident.

Methods of using an ET.sub.B receptor agonist, such as IRL-1620, for the treatment of stroke or cerebrovascular accidents are disclosed. The ET.sub.B receptor agonist is used alone or in combination with a second agent useful in the treatment of stroke or other cerebrovascular accident.

Methods are described for the isolation and selection of a heterogeneous bone marrow cell population, called NCS-01, that is effective at treating neurodegeneration. For example, NCS-01 cells are shown to treat neurodegeneration caused by ischemia. In vivo studies demonstrate that selected NCS-01 cell populations treat neurodegeneration in a standard rat middle cerebral artery occlusion (MCAO) animal model under conditions of transient or permanent total arterial occlusion. These studies also disclose that when the neurodegeneration is caused by ischemic stroke, combining the administration of a selected NCS-01 cell population with thrombolytic agents and/or mechanical methods of clot removal leads to a decrease in the volume of infarction caused by acute onset neurodegeneration. The disclosed cell therapy promises to make a significant clinical impact on patient survival after stroke.

Methods are described for the isolation and selection of a heterogeneous bone marrow cell population, called NCS-01, that is effective at treating neurodegeneration. For example, NCS-01 cells are shown to treat neurodegeneration caused by ischemia. In vivo studies demonstrate that selected NCS-01 cell populations treat neurodegeneration in a standard rat middle cerebral artery occlusion (MCAO) animal model under conditions of transient or permanent total arterial occlusion. These studies also disclose that when the neurodegeneration is caused by ischemic stroke, combining the administration of a selected NCS-01 cell population with thrombolytic agents and/or mechanical methods of clot removal leads to a decrease in the volume of infarction caused by acute onset neurodegeneration. The disclosed cell therapy promises to make a significant clinical impact on patient survival after stroke.

Methods are described for the isolation and selection of a heterogeneous bone marrow cell population, called NCS-01, that is effective at treating neurodegeneration. For example, NCS-01 cells are shown to treat neurodegeneration caused by ischemia. In vivo studies demonstrate that selected NCS-01 cell populations treat neurodegeneration in a standard rat middle cerebral artery occlusion (MCAO) animal model under conditions of transient or permanent total arterial occlusion. These studies also disclose that when the neurodegeneration is caused by ischemic stroke, combining the administration of a selected NCS-01 cell population with thrombolytic agents and/or mechanical methods of clot removal leads to a decrease in the volume of infarction caused by acute onset neurodegeneration. The disclosed cell therapy promises to make a significant clinical impact on patient survival after stroke.

The present invention relates to methods and agents useful for the treatment of stroke, including ischemic stroke and hemorrhagic stroke. In particular, methods and agents for treating stroke in a subject are provided, wherein the agent is administered prior to diagnosis of the stroke as an ischemic stroke or a hemorrhagic stroke.

The present invention relates to methods and agents useful for the treatment of stroke, including ischemic stroke and hemorrhagic stroke. In particular, methods and agents for treating stroke in a subject are provided, wherein the agent is administered prior to diagnosis of the stroke as an ischemic stroke or a hemorrhagic stroke.

The present invention relates to methods and agents useful for the treatment of stroke, including ischemic stroke and hemorrhagic stroke. In particular, methods and agents for treating stroke in a subject are provided, wherein the agent is administered prior to diagnosis of the stroke as an ischemic stroke or a hemorrhagic stroke.