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  • Indication
    Pancreatic ductal adenocarcinoma (PDAC), myelodysplastic syndrome (MDS), acute myelogenous leukemia (AML), hepatocellular carcinoma (HCC)
  • Development stage
    • Completed Phase 2 clinical studies for PDAC patients
    • Phase 2 clinical study in progress for patients with MDS
    • AML and HCC clinical studies in development


Ivaltinostat's competitive advantage​
  1. 01

    Best-in-class (i.e., best inhibitor effect amongst similar HDAC inhibitors)

  2. 02

    Improved efficacy compared to existing treatments based on Phase 2 clinical study for PDAC
    (Disease control rate 93.8%, overall survival rate 10.8 months)

  3. 03

    Significantly improved safety compared to existing treatments in PDAC based on Phase 2 clinical study results
    (3등급 이상의 비혈액학적 부작용이 현저히 적게 나타남)

  4. 04

    FDA orphan drug designation:
    MFDS developmental orphan drug

​HDAC (Histone deacetylase)

Deacetylation of histone protein​


Regulates the expression of genes by managing the process of DNA condensation around histone proteins

The mechanism of cancer

Abnormal HDAC expression
Induction of persistent histone protein de-acetylation (promotes DNA condensation)
Decreased expression of cancer suppressor genes
Infinite growth of mutant cells
Cancer development

Ivaltinostat's mechanism of action
  • Anticancer effect, epigenetic homeostasis recovery
    • Promoting cancer suppressor gene expression by inhibiting overexpressed HDACs
    • Inhibiting tumor cell proliferation (increases P21 expression, induces P53 acetylation) or induces tumor cell suicide
    • Restoring anticancer drug efficacy (Gemcitabine, 5-Fu) - i.e., chemoresistance is removed and cancer cells are once again sensitive to chemotherapy
  • Immunomodulation effect that promotes the anti-tumor immune response of the body
    • Increasing cytotoxic T cells, promoting NK cell activity
    • Inhibiting proliferation of immunosuppressed cells (M2 macrophages, MDSC (Myeloid-Derived Suppressor Cells), Regulatory T cells)
    • Inducting synergistic effect against immune checkpoint inhibitor (anti-PD-1 antibody)
  1. 1.

    Kim, Y.D. et al. HDAC Inhibitor, CG-745, enhances the anti-cancer effect of anti-PD-1 immune checkpoint inhibitor by modulation of the immune microenvironment. J. Cancer. 11, 4059-4072 (2020).

  2. 2.

    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).

  3. 3.

    Yoon, G.E. et al. Histone deacetylase inhibitor CG200745 ameliorates high-fat diet-induced hypertension via inhibition of angiotensin II production. Naunyn-Schmiedebergs Arch. Pharmacol. 393, 491-500 (2020).

  4. 4.

    Oh, E.T. et al. Novel histone deacetylase inhibitor CG200745 induces clonogenic cell death by modulating acetylation of p53 in cancer cells.
    Invest. New Drugs 30, 435-442 (2012).

  5. 5.

    Jung, D.E. et al. CG200745, an HDAC inhibitor, induces anti-tumour effects in cholangiocarcinoma cell lines via miRNAs targeting the hippo pathway. Sci. Rep. 7, 10921 (2017).

  6. 6.

    Lee, H.S. et al. A novel HDAC inhibitor, CG200745, inhibits pancreatic cancer cell growth and overcomes gemcitabine resistance. Sci. Rep. 7, 41615 (2017).