Patents by Inventor Peter Carmeliet

Peter Carmeliet 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).

  • Patent number: 10106601
    Abstract: The present application relates to the field of leukemias, and more in particular to how P1 GF inhibition can help to treat Philadelphia chromosome positive (Ph+) leukemias. Methods are provided for treating Ph+ leukemias by administering P1 GF inhibitors. Also disclosed are uses of P1 GF inhibitors in the treatment of Ph+ leukemias, or for the preparation of a medicament against Ph+ leukemias.
    Type: Grant
    Filed: October 2, 2009
    Date of Patent: October 23, 2018
    Assignees: VIB VZW, Life Sciences Research Partners VZW
    Inventors: Peter Carmeliet, Sonja Loges
  • Publication number: 20170066822
    Abstract: The invention is concerned with a method of determining whether a patient is more suitably treated by a therapy with an angiogenesis inhibitor, such as bevacizumab, by determining the genotype of VEGFR-1 gene. The invention further relates to a pharmaceutical composition comprising an angiogenesis inhibitor, such as bevacizumab, for the treatment of a patient suffering from cancer based on the genotype of VEGFR-1 gene. The invention further relates to a method for improving the treatment effect of chemotherapy of a patient suffering from cancer by adding an angiogenesis inhibitor, such as bevacizumab, based on the genotype of VEGFR-1 gene.
    Type: Application
    Filed: November 17, 2016
    Publication date: March 9, 2017
    Inventors: Peter Carmeliet, Sanne Lysbet de Haas, Diether Lambrechts, Stefan Scherer
  • Publication number: 20160193192
    Abstract: The present invention relates to an extracellular binding domain for an allosteric inhibitor, whereby said binding domain is derived from a single membrane span tyrosine kinase receptor. More specifically, the invention relates to an extracellular domain derived from a Fibroblast Growth Factor Receptor (FGFR). It further relates to the use of this domain for the identification of similar domains in the extracellular part of other tyrosine kinase receptors, and to a screening method for identification of a small compound allosteric inhibitor.
    Type: Application
    Filed: November 30, 2015
    Publication date: July 7, 2016
    Inventors: Peter Carmeliet, Frederik De Smet, Joost Schymkowitz, Frédéric Rousseau, Corentin Herbert
  • Publication number: 20160166532
    Abstract: This disclosure relates to the field of angiogenesis, more particularly to the field of pathological angiogenesis. In particular, the disclosure has found that inhibitors reducing the activity of the enzyme carnitine palmitoyltransferase 1A can be used for treatment of diseases in which pathological angiogenesis is involved. In particular, the disclosure provides siRNAs directed against carnitine palmitoyltransferase 1A for the treatment of pathological angiogenesis. The disclosure also provides the use of a therapeutically effective amount of inhibitors of carnitine palmitoyltransferase 1A, or a pharmaceutically acceptable salt thereof, for the treatment of pathological angiogenesis.
    Type: Application
    Filed: July 25, 2014
    Publication date: June 16, 2016
    Applicant: Life Sciences Research Partners VZW
    Inventors: Peter Carmeliet, Sandra Schoors
  • Patent number: 9234025
    Abstract: The present invention relates to an extracellular binding domain for an allosteric inhibitor, whereby said binding domain is derived from a single membrane span tyrosine kinase receptor. More specifically, the invention relates to an extracellular domain derived from a Fibroblast Growth Factor Receptor (FGFR). It further relates to the use of this domain for the identification of similar domains in the extracellular part of other tyrosine kinase receptors, and to a screening method for identification of a small compound allosteric inhibitor.
    Type: Grant
    Filed: July 2, 2010
    Date of Patent: January 12, 2016
    Assignees: SANOFI, VIB VZW, LIFE SCIENCES RESEARCH PARTNERS VZW, VRIJE UNIVERSITEIT BRUSSEL
    Inventors: Peter Carmeliet, Frederik De Smet, Joost Schymkowitz, Frédéric Rousseau, Corentin Herbert
  • Patent number: 9085617
    Abstract: The present invention provides novel monoclonal antibodies directed to PlGF and fragments and derivatives thereof, more particularly to humanized antibodies and fragments thereof for use in the treatment and/or prevention of pathological angiogenesis.
    Type: Grant
    Filed: February 3, 2014
    Date of Patent: July 21, 2015
    Assignees: THROMBOGENICS N.V., VLAAMS INTERUNIVERSITAIR INSTITUUT VOOR BIOTECHNOLOGIE VZW, LIFE SCIENCES RESEARCH PARTNERS VZW
    Inventors: Jean-Marie Stassen, Peter Carmeliet, Desire Collen
  • Publication number: 20150004136
    Abstract: The invention is concerned with a method of determining whether a patient is more suitably treated by a therapy with an angiogenesis inhibitor, such as bevacizumab, by determining the genotype of VEGFR-1 gene. The invention further relates to a pharmaceutical composition comprising an angiogenesis inhibitor, such as bevacizumab, for the treatment of a patient suffering from cancer based on the genotype of VEGFR-1 gene. The invention further relates to a method for improving the treatment effect of chemotherapy of a patient suffering from cancer by adding an angiogenesis inhibitor, such as bevacizumab, based on the genotype of VEGFR-1 gene.
    Type: Application
    Filed: May 22, 2014
    Publication date: January 1, 2015
    Applicants: Hoffmann-La Roche Inc., VIB vzw
    Inventors: Peter Carmeliet, Sanne Lysbet de Haas, Diether Lambrechts, Stefan Scherer
  • Publication number: 20140178397
    Abstract: The present invention provides novel monoclonal antibodies directed to P1GF and fragments and derivatives thereof, more particularly to humanized antibodies and fragments thereof for use in the treatment and/or prevention of pathological angiogenesis.
    Type: Application
    Filed: February 3, 2014
    Publication date: June 26, 2014
    Inventors: Jean-Marie STASSEN, Peter CARMELIET, Desire COLLEN
  • Patent number: 8758748
    Abstract: The present invention provides novel monoclonal antibodies directed to PlGF and fragments and derivatives thereof, more particularly to humanized antibodies and fragments thereof for use in the treatment and/or prevention of pathological angiogenesis.
    Type: Grant
    Filed: December 20, 2010
    Date of Patent: June 24, 2014
    Assignees: Thrombogenics N.V., VLAAMS Interuniversitair Instituut voor Biotechnologie VZW, Life Sciences Research Partners VZW
    Inventors: Jean-Marie Stassen, Peter Carmeliet, Désiré Collen
  • Patent number: 8741862
    Abstract: A key function of blood vessels, to supply oxygen, is impaired in tumors because of abnormalities in their endothelial lining. PHD proteins serve as oxygen sensors and may regulate oxygen delivery. Therefore the role of endothelial PHD2 in vessel shaping by implanting tumors in PHD2+/? mice was studied. Haplodeficiency of PHD2 did not affect tumor vessel density or lumen size, but normalized the endothelial lining and vessel maturation. This resulted in improved tumor perfusion and oxygenation, and inhibited tumor cell invasion, intravasation and metastasis. Haplodeficiency of PHD2 redirected the specification of endothelial tip cells to a more quiescent phenotype of a filopodia-lacking “phalanx” cell type. Without being bound to a particular mechanism, this transition could at least in part be explained by upregulation of (soluble) VEGFR-1 and VE-cadherin.
    Type: Grant
    Filed: January 20, 2010
    Date of Patent: June 3, 2014
    Assignees: VIB VZW, Life Science Research Partners VZW
    Inventors: Peter Carmeliet, Massimiliano Mazzone
  • Publication number: 20130183310
    Abstract: The present invention relates to the field of pathological angiogenesis and arteriogenesis and, in particular, to a stress-induced phenotype in a transgenic mouse (PIGF?/?) that does not produce Placental Growth Factor (PIGF) and that demonstrates an impaired vascular endothelial growth factor (VEGF)-dependent response. PIGF deficiency has a negative influence on diverse pathological processes of angiogenesis, arteriogenesis and vascular leakage comprising ischemic retinopathy, tumor formation, pulmonary hypertension, vascular leakage (edema formation) and inflammatory disorders. The invention thus relates to molecules that can inhibit the binding of PIGF to its receptor (VEGFR-1), such as monocloncal antibodies and tetrameric peptides, and to the use of these molecules to treat the above-mentioned pathological processes.
    Type: Application
    Filed: March 5, 2013
    Publication date: July 18, 2013
    Inventors: Peter Carmeliet, Desire Collen, Sandro De Falco, Ruvo Menotti
  • Publication number: 20130177564
    Abstract: The present invention relates to the field of pathological angiogenesis and arteriogenesis and, in particular, to a stress-induced phenotype in a transgenic mouse (PIGF?/?) that does not produce Placental Growth Factor (PIGF) and that demonstrates an impaired vascular endothelial growth factor (VEGF)-dependent response. PIGF deficiency has a negative influence on diverse pathological processes of angiogenesis, arteriogenesis and vascular leakage comprising ischemic retinopathy, tumor formation, pulmonary hypertension, vascular leakage (edema formation) and inflammatory disorders. The invention thus relates to molecules that can inhibit the binding of PIGF to its receptor (VEGFR-1), such as monocloncal antibodies and tetrameric peptides, and to the use of these molecules to treat the above-mentioned pathological processes.
    Type: Application
    Filed: March 5, 2013
    Publication date: July 11, 2013
    Inventors: Peter CARMELIET, Desire Collen, Sandro De Falco, Ruvo Menotti
  • Publication number: 20130177565
    Abstract: The present invention relates to the field of pathological angiogenesis and arteriogenesis and, in particular, to a stress-induced phenotype in a transgenic mouse (PIGF?/?) that does not produce Placental Growth Factor (PIGF) and that demonstrates an impaired vascular endothelial growth factor (VEGF)-dependent response. PIGF deficiency has a negative influence on diverse pathological processes of angiogenesis, arteriogenesis and vascular leakage comprising ischemic retinopathy, tumor formation, pulmonary hypertension, vascular leakage (edema formation) and inflammatory disorders. The invention thus relates to molecules that can inhibit the binding of PIGF to its receptor (VEGFR-1), such as monocloncal antibodies and tetrameric peptides, and to the use of these molecules to treat the above-mentioned pathological processes.
    Type: Application
    Filed: March 5, 2013
    Publication date: July 11, 2013
    Applicants: LIFE SCIENCES RESEARCH PARTNERS VZW (LSRP), VLAAMS INTERUNIVERSITAIR INSTITUUT VOOR BIOTECHNOLOGIE VZW (VIB)
    Inventors: Peter CARMELIET, Desire Collen, Sandro De Falco, Ruvo Menotti
  • Publication number: 20130078224
    Abstract: The disclosure relates to the field of ischemia and how to increase tissue perfusion in ischemic tissue by cellular therapy. Specifically, the beneficial effects of myeloid (bone marrow-derived) cells with a particular arteriogenic gene expression profile are shown, and it is shown that increased arteriogenesis and perfusion is specifically due to the effects of combined PDGFB and SDF-1. The arteriogenic gene profile of the myeloid cells used for therapy can, for instance, be obtained by inhibition of PHD2.
    Type: Application
    Filed: March 30, 2011
    Publication date: March 28, 2013
    Applicants: LIFE SCIENCES RESEARCH PARTNERS VZW, VIB VZW
    Inventors: Massimiliano Mazzone, Peter Carmeliet
  • Publication number: 20120263710
    Abstract: The present invention relates to the field of pathological angiogenesis and arteriogenesis and, in particular, to a stress-induced phenotype in a transgenic mouse (PIGF?/?) that does not produce Placental Growth Factor (PIGF) and that demonstrates an impaired vascular endothelial growth factor (VEGF)-dependent response. PIGF deficiency has a negative influence on diverse pathological processes of angiogenesis, arteriogenesis and vascular leakage comprising ischemic retinopathy, tumor formation, pulmonary hypertension, vascular leakage (edema formation) and inflammatory disorders. The invention thus relates to molecules that can inhibit the binding of PIGF to its receptor (VEGFR-1), such as monocloncal antibodies and tetrameric peptides, and to the use of these molecules to treat the above-mentioned pathological processes.
    Type: Application
    Filed: May 14, 2012
    Publication date: October 18, 2012
    Applicants: LIFE SCIENCES RESEARCH PARTNERS VZW (LSRP), VLAAMS INTERUNIVERSITAIR INSTITUUT VOOR BIOTECHNOLOGIE VZW (VIB)
    Inventors: Peter CARMELIET, Désiré Collen, Sandro De Falco, Ruvo Menotti
  • Publication number: 20120195858
    Abstract: The present invention relates to methods for improving the overall survival of a patient suffering from a malignant disease or a disease involving physiological and pathological angiogenesis by treatment with an angiogenesis inhibitor, such as bevacizumab, by determining the presence of one or more variant alleles of the vascular endothelial growth factor receptor 1 (VEGFR-1) gene. The present invention further provides methods for improving the progression-free survival of a patient suffering from a malignant disease or a disease involving physiological and pathological angiogenesis by treatment with an angiogenesis inhibitor, such as bevacizumab, by determining the presence of one or more variant alleles of the VEGFR-1 gene. The present invention also provides for methods for assessing the responsiveness of a patient to an angiogenesis inhibitor by determining the presence of one or more variant alleles of the VEGFR-1 gene.
    Type: Application
    Filed: August 3, 2010
    Publication date: August 2, 2012
    Inventors: Dorothee Foernzler, Paul Delmar, Stefan Scherer, Diether Lambrechts, Peter Carmeliet
  • Publication number: 20120094864
    Abstract: The present invention relates to an extracellular binding domain for an allosteric inhibitor, whereby said binding domain is derived from a single membrane span tyrosine kinase receptor. More specifically, the invention relates to an extracellular domain derived from a Fibroblast Growth Factor Receptor (FGFR). It further relates to the use of this domain for the identification of similar domains in the extracellular part of other tyrosine kinase receptors, and to a screening method for identification of a small compound allosteric inhibitor.
    Type: Application
    Filed: July 2, 2010
    Publication date: April 19, 2012
    Applicants: SANOFI, VRIJE UNIVERSITEIT BRUSSEL, LIFE SCIENCES RESEARCH PARTNERS VZW, VIB VZW
    Inventors: Peter Carmeliet, Frederik De Smet, Joost Schymkowitz, Frédéric Rousseau, Corentin Herbert
  • Publication number: 20120022135
    Abstract: A key function of blood vessels, to supply oxygen, is impaired in tumors because of abnormalities in their endothelial lining. PHD proteins serve as oxygen sensors and may regulate oxygen delivery. Therefore the role of endothelial PHD2 in vessel shaping by implanting tumors in PHD2+/? mice was studied. Haplodeficiency of PHD2 did not affect tumor vessel density or lumen size, but normalized the endothelial lining and vessel maturation. This resulted in improved tumor perfusion and oxygenation, and inhibited tumor cell invasion, intravasation and metastasis. Haplodeficiency of PHD2 redirected the specification of endothelial tip cells to a more quiescent phenotype of a filopodia-lacking “phalanx” cell type. Without being bound to a particular mechanism, this transition could at least in part be explained by upregulation of (soluble) VEGFR-1 and VE-cadherin.
    Type: Application
    Filed: January 20, 2010
    Publication date: January 26, 2012
    Applicants: LIFE SCIENCES RESEARCH PARTNERS VZW, VIB VZW
    Inventors: Peter Carmeliet, Massimiliano Mazzone
  • Publication number: 20110288020
    Abstract: The present invention relates to neurological and physiological dysfunction associated with neuron disorders. In particular, the invention relates to the involvement of vascular endothelial growth factor (VEGF) and homologues in the aetiology of motor neuron disorders. The invention further concerns a novel, mutant transgenic mouse (VEGFm/m) with a homozygous deletion in the hypoxia responsive element (HRE) of the VEGF promoter which alters the hypoxic upregulation of VEGF. These mice suffer severe adult onset muscle weakness due to progressive spinal motor neuron degeneration which is reminiscent of amyotrophic lateral sclerosis (ALS)—a fatal disorder with unknown aetiology. Furthermore, the neuropathy of these mice is not caused by vascular defects, but is due to defective VEGF-mediated survival signals to motor neurons.
    Type: Application
    Filed: December 3, 2010
    Publication date: November 24, 2011
    Inventors: Peter Carmeliet, Désiré Collen, Bert Oosthuyse
  • Publication number: 20110250209
    Abstract: The present application relates to the field of leukemias, and more in particular to how P1 GF inhibition can help to treat Philadelphia chromosome positive (Ph+) leukemias. Methods are provided for treating Ph+ leukemias by administering P1 GF inhibitors. Also disclosed are uses of P1 GF inhibitors in the treatment of Ph+ leukemias, or for the preparation of a medicament against Ph+ leukemias.
    Type: Application
    Filed: October 2, 2009
    Publication date: October 13, 2011
    Applicants: LIFE SCIENCES RESEARCH PARTNERS VZW, VIB VZW
    Inventors: Peter Carmeliet, Sonja Loges