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  • Indication
    Fibrotic diseases including non-alcoholic steatohepatitis (NASH), idiopathic pulmonary fibrosis (IPF), chronic kidney diseases (CKD), Alport Syndrome, etc.
  • Development stage
    Phase 1 clinical study for oral formulation in progress



During the wound healing process of each organ, the connective tissue replaces the normal parenchyma extensively and continuously.
Fibrosis is, however, a disease where this process is dysfunctional and causes tissue remodeling and permanent scar formation, resulting in loss of organ-specific functions.

The mechanism of fibrosis
  • Immune cell activity to respond to organ damage caused by physical, chemical, or infection releases fibroblast-stimulating lytic factors such as PDGF, CTGF, and IL-10, including TGF-β.
  • Uncontrolled immune cell activity induces continuous fibroblast-stimulating lytic factor generation
  • Fibroblast hyperproliferation and hyperactivity
  • Fibroblast differentiation activity of myofibroblasts and increased production of fibrotic proteins (Fibronectin, Collagen, Vimentin)
  • Loss of organ function due to fibrotic protein accumulation
​Inhibition of fibrosis by ivaltinostat in animal models
    • Inhibition of immune cell lung migration
    • Inhibition of inflammatory cytokine production through inhibition of angiotensinogen expression
    • Inhibition of the production of TGF-β, a fibroblast stimulating lytic factor
    • Inhibition of myofibroblast differentiation mechanism (Epithelial to Mesenchymal Transition)
    • Inhibition of the production of fibrotic proteins (Fibronectin, Collagen, Vimentin)
Ivaltinostat's competitive advantage
  1. 01

    Efficacy has been verified in various fibrosis models (PHMG, Bleomycin, UUO, DOCA) including Alport syndrome-like animal models.

  2. 02

    Limited safety concerns based on results from a Phase 1 clinical study in healthy adults.

  3. 03

    Completed development of oral formulation of ivaltinostat.

  1. 1.

    Suh, S.H. et al. CG200745, a novel HDAC inhibitor, attenuates kidney fibrosis in a murine model of alport syndrome. Int. J. Mol. Sci. 21, 1473 (2020).

  2. 2.

    Choi, H.S. et al. Histone deacetylase inhibitor, CG200745 attenuates renal fibrosis in obstructive kidney disease. Sci. Rep. 8, 11546 (2018).

  3. 3.

    Bae, E.H. et al. Renoprotective effect of the histone deacetylase inhibitor CG200745 in DOCA-salt hypertensive rats. Int. J. Mol. Sci. 20, 508 (2019).

  4. 4.

    Kim, Y.S. et al. The anti-fibrotic effects of CG-745, an HDAC inhibitor, in bleomycin and PHMG-induced mouse models. Molecules 24, 2792 (2019).