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Abstract
Granulocyte colony-stimulating factor (G-CSF; a stem cell enhancer and facilitator), DETC-MeSO (a glutamate receptor partial antagonist and anti-excitotoxicity agent), and sulindac (a potent anti-oxidant and anti-inflammatory agent) each can protect brain tissue exposed to a cerebral ischemia/reperfusion injury, and minimize the size of infarcts that develop as a result of the injury. When administered in combination, these agents are effective at protecting brain tissue and minimizing the size of an infarct resulting from the injury at much lower concentrations compared to using a single agent.
Core Innovation
The invention relates to stroke treatment and brain tissue protection in a mammalian subject suffering from acute cerebral vessel occlusion. It provides methods comprising administering a N-diethylthiocarbamate sulfoxide (DETC-MeSO) agent to treat the condition and reduce brain damage associated with cerebral ischemia/reperfusion injury. The document further describes that DETC-MeSO protects against cerebral ischemia/reperfusion injury.
The invention also addresses preventing brain damage caused by ischemic stroke, including in subjects experiencing transient ischemic attacks or having a thrombosis. In these contexts, the document provides methods in which DETC-MeSO is administered to achieve prevention of brain damage associated with ischemic stroke. The document describes that repeated administration is used in these settings and can be continued until transient ischemic attacks stop or until thrombosis is cleared.
In addition, the document describes a combination approach for stroke treatment/neuroprotection by using agents including DETC-MeSO together with sulindac and optionally Granulocyte-colony stimulating factor (G-CSF). It states that each agent provides protection against cerebral ischemia/reperfusion injury and that the combination reduces infarct size at much lower doses than single agents. The document includes experimental support using a MCAO model and reports molecular marker effects consistent with brain tissue protection.
Claims Coverage
The partial content contains three independent claims that share a core inventive concept: administering a N-diethylthiocarbamate sulfoxide (DETC-MeSO) agent for treatment or prevention of brain damage associated with ischemic stroke. Across the independent claims, the main inventive features include treating acute cerebral vessel occlusion and preventing brain damage in subjects with transient ischemic attacks or thrombosis, with optional refinement via co-administration and dosing regimens described in dependent claims.
Treating acute cerebral vessel occlusion with DETC-MeSO
Administering to a mammalian subject with acute cerebral vessel occlusion a N-diethylthiocarbamate sulfoxide (DETC-MeSO) agent.
Preventing ischemic stroke brain damage in transient ischemic attacks with DETC-MeSO
Preventing brain damage caused by ischemic stroke in a mammalian subject experiencing transient ischemic attacks by administering to the subject a N-diethylthiocarbamate sulfoxide (DETC-MeSO) agent.
Preventing ischemic stroke brain damage in thrombosis with DETC-MeSO
Preventing brain damage caused by ischemic stroke in a mammalian subject having a thrombosis by administering to the subject a N-diethylthiocarbamate sulfoxide (DETC-MeSO) agent.
Across the independent claims, the coverage centers on administering a DETC-MeSO agent for treating acute cerebral vessel occlusion and preventing brain damage caused by ischemic stroke in subjects with transient ischemic attacks or thrombosis. The dependent claim refinements described in the partial content further specify timing, repeated administration regimens, and co-administration with named agents.
Stated Advantages
Protects against cerebral ischemia/reperfusion injury.
Reduces infarct size.
The combination of agents reduces infarct size at much lower doses than single agents.
Documented Applications
Stroke treatment and neuroprotection in a mammalian subject with acute cerebral vessel occlusion.
Preventing brain damage caused by ischemic stroke in a mammalian subject experiencing transient ischemic attacks.
Preventing brain damage caused by ischemic stroke in a mammalian subject having a thrombosis.
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