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Aandeel Pharming Group AEX:PHARM.NL, NL0010391025

  • 0,898 2 mei 2024 17:35
  • +0,022 (+2,45%) Dagrange 0,879 - 0,898
  • 2.763.190 Gem. (3M) 6,7M

1/Patentje erbij en 2/ er wordt gewerkt !

9 Posts
| Omlaag ↓
  1. jurpsy 26 september 2009 11:26
    1/US Patent 7544853 - C1 inhibitor with short half-life transient treatment

    Abstract
    The present invention relates to the use of a C1 inhibitor (C1INH) with shorter half-life than plasma-derived C1INH for the preparation of a medicament for the transient treatment of an individual. It relates to both"" therapeutic and prophylactic """treatment. The method of the invention allows for the administration of C1INH at certain therapeutic levels for a concise pre-determined time span. Pharmaceutical compositions based on C1INH with shorter half-lives may be used both in situations where transient treatment is merely and advantage. The advantage of the use according to the invention is that an individual is not exposed to C1INH for longer than required, since the levels of the C1INH more rapidly subsides after administration has stopped. In contrast, levels of plasma-derived C1INH would remain elevated for a prolonged period of time

    Inventor
    Nuijens, Johannes Henricus

    Assignee
    Pharming Intellectual Property B.V.

    www.patentstorm.us/patents/7544853.html
    www.freepatentsonline.com/7544853.html

    2/Recombinant C1-inhibitor in brain ischemic injury

    Funded by:
    Pharming Technologies B.V. HV, MM and BZ

    Interpretation:
    rhC1-INH showed a surprisingly wider time-window of efficacy compared to the corresponding plasmatic protein. We propose that the superiority of rhC1-INH is due to its selective binding to MBL, which emerged as a novel target for stroke treatment. Ann Neurol 2009.

    www3.interscience.wiley.com/journal/1...

    suc6,
    jurps
  2. [verwijderd] 26 september 2009 12:20
    Annals of Neurology
    Volume 9999 Issue 999A, Page NA
    Published Online: 11 May 2009

    Received: 12 November 2008; Revised: 9 April 2009; Accepted: 17 April 2009

    Abstract

    Objective.
    C1-inhibitor(C1-INH) is an endogenous inhibitor of complement and kinin systems. We have explored the efficacy and the therapeutic window of the recently available recombinant human (rh)C1-INH on ischemic brain injury and investigated its mechanism of action in comparison with that of plasma-derived (pd)C1-INH.

    Methods.
    rhC1-INH was administered intravenously to C57Bl/6 mice undergoing transient or permanent ischemia and its protective effects were evaluated by measuring infarct volume and neurodegeneration. The binding profiles of rhC1-INH and pdC1-INH were assessed in vitro using surface plasmon resonance. Their localization in the ischemic brain tissue was determined by immunohistochemistry and confocal analysis. The functional consequences of rhC1-INH and pdC1-INH administration on complement activation were analysed by ELISA on plasma samples.

    Results.
    rhC1-INH markedly reduced cerebral damage when administered up to 18h after transient ischemia and up to 6h after permanent ischemia, thus showing a surprisingly wide therapeutic window. In vitro rhC1-INH bound mannose binding lectin (MBL), a key protein in the lectin complement pathway, with high affinity, whereas pdC1-INH, which has a different glycosylation pattern, did not. In the ischemic brain rhC1-INH was confined to cerebral vessels where it colocalized with MBL, while pdC1-INH diffused into the brain parenchyma. In addition rhC1-INH was more active than pdC1-INH in inhibiting MBL-induced complement activation.

    Interpretation.
    rhC1-INH showed a surprisingly wider time-window of efficacy compared to the corresponding plasmatic protein. We propose that the superiority of rhC1-INH is due to its selective binding to MBL, which emerged as a novel target for stroke treatment. Ann Neurol 2009.
9 Posts
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