Page 15 - M. Immunology

Nuclear Import Inhibition of SRTFs With Nuclear Importin Binding Peptide

Suppresses Expression of Pro-Inflammatory Cytokines
Dongho Kim, Gyunam Kim, Danbi Lee, Sanghyeon Yu, Misuk Baek, Jieun Kim, Mingu Kang, Hakyoung Park, Jaewook Lee,
Seokwon Lee, Hyemin Yu, Hyewon Lee, Dasom Shin, Bo-ram Kim, Youngsil Choi, and Daewoong Jo
Drug Development Team, Cellivery R&D Institute, Cellivery Therapeutics, Inc., Seoul 03929, Korea.
BACKGROUND AIM
Various stress responsive transcription factors (SRTFs), NF-κB, This study suggest that iCP-NI has potential as a novel therapeutic
NFAT, STAT1 and AP-1 are activated to trigger innate immunity agent for various uncontrolled inflammation mediated disease such
against to SARS-CoV-2 Infection. Excessive expression of cytokine as sepsis and COVID-19. By suppressing the excessive secretion of
results severe inflammation in organs and leading death, eventually. inflammatory cytokines, iCP-NI may save patients from death.
METHODS
To regulate the excessive expression and secretion of inflammatory cytokines, namely cytokine-storm, improved cell-permeable nuclear import
inhibitor (iCP-NI) peptide has been developed by fusing sequence-optimized hydrophobic cell-penetrating peptide (CPP) with nuclear localization
signal (NLS) and demonstrated its improved therapeutic applicability preventing apoptosis by reducing secretion of pro-inflammatory
cytokines in various inflammatory disease animals.
RESULTS

CONCLUSION REFERENCES Contact information
Chung et al. (2020) Science Advances, 6: eaba 1193
Cell-permeable iCP-NI regulates pro- & anti- Minyong Jung
inflammatory cytokines by inhibiting the nuclear Lim et al. (2013) Clinical Cancer Research, 19: 680-690 New Drug & Business Development
translocation inflammatory transcription factor. Lim et al. (2013) Biomaterials, 34: 6261-6271
Cellivery Therapeutics, Inc.
Therefore, iCP-NI showed therapeutic efficacy Lim et al. (2012) Molecular Therapy, 20: 1540-1549
in severe inflammatory animal models and jungmy@cellivery.com
Jo et al. (2005) Nature Medicine, 11: 892-898
SARS-CoV-2 infected COVID-19 monkeys.
Jo et al. (2001) Nature Biotechnology, 19: 929-933 +82-2-3151-8900