Patents by Inventor Roland STAAL

Roland STAAL has filed for patents to protect the following inventions. This listing includes patent applications that are pending as well as patents that have already been granted by the United States Patent and Trademark Office (USPTO).

  • Publication number: 20230045322
    Abstract: Neuroinflammation mediated by microglia and infiltrating peripheral immune cells is a major component of stroke pathophysiology. The calcium activated potassium channel KCa3.1 is expressed selectively in the injured CNS by microglia, and KCa3.1 function has been implicated in proinflammatory activation of microglia. KCa3.1 is further implicated in the pathophysiology of ischemia/reperfusion (stroke) related brain injury. Senicapoc, an investigational drug with a proven safety profile and shown to cross the blood-brain barrier, is a potent and selective KCa3.1 inhibitor that intervenes in the inflammation cascade that follows ischemia/reperfusion, and is a potential treatment for stroke.
    Type: Application
    Filed: July 18, 2022
    Publication date: February 9, 2023
    Inventors: Roland STAAL, Jonathan WEINSTEIN, Thomas MOELLER
  • Publication number: 20220347131
    Abstract: A method is disclosed of treating pain with senicapoc, a potent Ca2+-activated K+ channel, KCa3.1 antagonist in CNS-resident microglia. Senicapoc is shown to cause in a decrease of IL-1? and NO release from microglia cells vivo and in vitro. Because of contribution of KCa3.1 to neuropathological processes, senicapoc is useful in the treatment of chronic, neuropathic, visceral, and inflammatory pain and the reversal of tactile allodynia.
    Type: Application
    Filed: July 11, 2022
    Publication date: November 3, 2022
    Inventors: Roland STAAL, Thomas MOLLER
  • Patent number: 11439607
    Abstract: A method is disclosed of treating pain with senicapoc, a potent Ca2+-activated K+ channel, KCa3.1 antagonist in CNS-resident microglia. Senicapoc is shown to cause in a decrease of IL-1? and NO release from microglia cells vivo and in vitro. Because of contribution of KCa3.1 to neuropathological processes, senicapoc is useful in the treatment of chronic, neuropathic, visceral, and inflammatory pain and the reversal of tactile allodynia.
    Type: Grant
    Filed: October 23, 2017
    Date of Patent: September 13, 2022
    Assignee: Paracelsus Neuroscience I, LLC
    Inventors: Roland Staal, Thomas Möller
  • Patent number: 11395807
    Abstract: Neuroinflammation mediated by microglia and infiltrating peripheral immune cells is a major component of stroke pathophysiology. The calcium activated potassium channel KCa3.1 is expressed selectively in the injured CNS by microglia, and KCa3.1 function has been implicated in proinflammatory activation of microglia. KCa3.1 is further implicated in the pathophysiology of ischemia/reperfusion (stroke) related brain injury. Senicapoc, an investigational drug with a proven safety profile and shown to cross the blood-brain barrier, is a potent and selective KCa3.1 inhibitor that intervenes in the inflammation cascade that follows ischemia/reperfusion, and is a potential treatment for stroke.
    Type: Grant
    Filed: January 30, 2018
    Date of Patent: July 26, 2022
    Inventors: Roland Staal, Jonathan Weinstein, Thomas Moller
  • Publication number: 20200046657
    Abstract: A method is disclosed of treating pain with senicapoc, a potent Ca2+-activated K+ channel, KCa3.1 antagonist in CNS-resident microglia. Senicapoc is shown to cause in a decrease of IL-1? and NO release from microglia cells vivo and in vitro. Because of contribution of KCa3.1 to neuropathological processes, senicapoc is useful in the treatment of chronic, neuropathic, visceral, and inflammatory pain and the reversal of tactile allodynia.
    Type: Application
    Filed: October 23, 2017
    Publication date: February 13, 2020
    Inventors: Roland Staal, Thomas Möller
  • Publication number: 20200000749
    Abstract: Neuroinflammation mediated by microglia and infiltrating peripheral immune cells is a major component of stroke pathophysiology. The calcium activated potassium channel KCa3.1 is expressed selectively in the injured CNS by microglia, and KCa3.1 function has been implicated in proinflammatory activation of microglia. KCa3.1 is further implicated in the pathophysiology of ischemia/reperfusion (stroke) related brain injury. Senicapoc, an investigational drug with a proven safety profile and shown to cross the blood-brain barrier, is a potent and selective KCa3.1 inhibitor that intervenes in the inflammation cascade that follows ischemia/reperfusion, and is a potential treatment for stroke.
    Type: Application
    Filed: January 30, 2018
    Publication date: January 2, 2020
    Inventors: Roland STAAL, Jonathan WEINSTEIN, Thomas MOLLER