Global Patent Index - EP 1242107 A4

EP 1242107 A4 20041006 - METHOD FOR PR-39 PEPTIDE MEDIATED SELECTIVE INHIBITION OF IKAPPABALPHA DEGRADATION

Title (en)

METHOD FOR PR-39 PEPTIDE MEDIATED SELECTIVE INHIBITION OF IKAPPABALPHA DEGRADATION

Title (de)

VERFAHREN ZUR HERSTELLUNG VON DURCH PR-39 PEPTID VERMITTELTE SELEKTIVER HEMMUNG VON IKAPPABALOHA ABBAU

Title (fr)

PROCEDE D'INHIBITION SELECTIVE DE LA DEGRADATION DE LA PROTEINE IKAPPABALPHA INDUITE PAR LE PEPTIDE PR-39

Publication

EP 1242107 A4 20041006 (EN)

Application

EP 00989492 A 20001227

Priority

  • US 0035293 W 20001227
  • US 47496799 A 19991229

Abstract (en)

[origin: WO0147540A1] The present invention provides both a method and means for regulating I kappa B alpha degradation, NF kappa B activity, and NF kappa B-dependent gene expression within living cells, tissues, and organs in-situ. The selective regulation is performed using native PR-39 peptide or one of its shorter-length homologs, for interaction with such I kappa B alpha and proteasomes as are present in the cytoplasm of viable cells. The result of PR-39 peptide interaction with I kappa B alpha is a selective alteration in the intracellular proteolytic activity of proteasomes, which in turn, causes a reduction of I kappa B alpha , a decrease of NF kappa B activity, and a down-regulation of NF kappa B-dependent gene expression.

IPC 1-7

A61K 38/00; A61K 38/16; C07K 7/00; C07K 7/04; C07K 7/06; C07K 14/47

IPC 8 full level

C07K 14/47 (2006.01); A61K 38/00 (2006.01)

CPC (source: EP)

C07K 14/4705 (2013.01); C07K 14/4723 (2013.01); A61K 38/00 (2013.01)

Citation (search report)

  • [X] WO 9632129 A1 19961017 - UNIV KANSAS STATE [US], et al
  • [X] WO 9835690 A1 19980820 - UNIV KANSAS STATE [US]
  • [X] US 5489575 A 19960206 - LEE JONG-YOUN [SE], et al
  • [PXL] WO 0057895 A1 20001005 - BETH ISRAEL HOSPITAL [US]
  • [EL] WO 0130368 A1 20010503 - BETH ISRAEL HOSPITAL [US]
  • [X] LI J ET AL: "CARDIAC-SPECIFIC OVEREXPRESSION OF PR-39 INDUCES ANGIOGENESIS, MYOCARDIAL HYPERTROPHY AND INCREASED MICROVASCULAR REACTIVITY", CIRCULATION, AMERICAN HEART ASSOCIATION, DALLAS, TX, US, vol. 98, no. 17, October 1998 (1998-10-01), pages 1794, XP002929855, ISSN: 0009-7322
  • [PX] GAO Y ET AL: "Inhibition of ubiquitin-proteasome pathway-mediated I-kappaBalpha degradation by a naturally occuring antibacterial peptide", JOURNAL OF CLINICAL INVESTIGATION, NEW YORK, NY, US, vol. 106, no. 3, August 2000 (2000-08-01), pages 439 - 448, XP002180614, ISSN: 0021-9738
  • [PX] HOFFMEYER M R ET AL: "PR-39, a potent neutrophil inhibitor, attenuates myocardial ischemia-reperfusion injury in mice.", AMERICAN JOURNAL OF PHYSIOLOGY. HEART AND CIRCULATORY PHYSIOLOGY. DEC 2000, vol. 279, no. 6, December 2000 (2000-12-01), pages H2824 - H2828, XP002292143, ISSN: 0363-6135
  • [PA] LI J ET AL: "PR39, a peptide regulator of angiogenesis", NATURE MEDICINE, NATURE AMERICA, NEW YORK, US, vol. 6, no. 1, January 2000 (2000-01-01), pages 49 - 55, XP002968105, ISSN: 1078-8956
  • [A] LI J ET AL: "Macrophage-dependent regulation of syndecan gene expression", CIRCULATION RESEARCH 1997 UNITED STATES, vol. 81, no. 5, 1997, pages 785 - 796, XP008033955, ISSN: 0009-7330
  • [A] GAO YOUHE ET AL: "PR39 interacts with proteasome and modulates HIF-1alpha level in ECV cells", MOLECULAR BIOLOGY OF THE CELL, vol. 9, no. SUPPL., November 1998 (1998-11-01), & 38TH ANNUAL MEETING OF THE AMERICAN SOCIETY FOR CELL BIOLOGY; SAN FRANCISCO, CALIFORNIA, USA; DECEMBER 12-16, 1998, pages 123A, XP008033931, ISSN: 1059-1524
  • See references of WO 0147540A1

Designated contracting state (EPC)

AT BE CH CY DE DK ES FI FR GB GR IE IT LI LU MC NL PT SE TR

DOCDB simple family (publication)

WO 0147540 A1 20010705; AU 2599001 A 20010709; CA 2397955 A1 20010705; EP 1242107 A1 20020925; EP 1242107 A4 20041006

DOCDB simple family (application)

US 0035293 W 20001227; AU 2599001 A 20001227; CA 2397955 A 20001227; EP 00989492 A 20001227