Pipeline

CU106

CU106

Expanded indication of CU06 for Immuno-Oncology Combination Therapy

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CU106 Expanded indication of CU06 for Immuno-Oncology Combination Therapy
Indication Immuno-Oncology Combination Therapy
Unmet Needs

• Immune checkpoint inhibitors have been shown to be only effective against certain types of cancer such as melanoma, lung cancer, colorectal cancer, and liver cancer.

• Immuno-suppression created by the abnormal TME (tumor microenvironment) vasculature cannot be modified by anti-PD-1 therapy.

• Vascular stabilization may increase the efficacy of immunotherapy by normalizing blood vessel perfusion.

Mechanism of Action

• Improves anti-PD1 delivery through normalized tumor vessels and promotes tumor apoptosis.

• Reduces hypoxia and increases CD8+ T-cell infiltration that kills tumor cells within the central region of the tumor.

• Improves tumor vascular normalization and decreases uncontrolled tumor angiogenesis.

Efficacy & Safety

• Improvement in tumor vascular normalization and hypoxia

• Enhancing the function of tumor infiltration CD8+ T cells decreases uncontrolled tumor angiogenesis

Market

• By 2025, Immuno-Oncology drugs are expected to account for $56 billion, or 25% of the total oncology drug market.

Indication

Cause

  • TME (tumor microenvironment) is a major cause of tumor progression and treatment resistance.
  • TME changes are strongly associated with abnormalities in tumor vessels, including reduced vascular density and structurally disordered expansion.

Unmet Needs

  • Immune checkpoint inhibitors have been shown to be only effective against certain types of cancer such as melanoma, lung cancer, colorectal cancer, and liver cancer.
  • Immuno-suppression created by the abnormal TME vasculature cannot be modified by anti-PD-1 therapy.
  • Vascular stabilization may increase the efficacy of immunotherapy by normalizing blood vessel perfusion.

Mechanism of Action

  • Improves tumor vascular normalization and decreases hypoxia and vascular leakage by maintaining vessel structure.
  • Enhances the trafficking of anti-PD1 into tumor central region via normalized tumor vessels leading to the expansion of tumor infiltrated lymphocytes within central tumor region.
  • Improved TME maximizes T-cell recruitment and activation, which increases anti-tumor response.

  • The impaired drug delivery due to abnormal and leaky tumor vessels can be improved by CU106
  • Vessel normalization by CU106 can reprogram the immunosuppressive TME (tumor microenvironment) to an immuno-supportive one

Efficacy

Inhibition of tumor growth and extension of survival

‘CU106 + αPD-1’ inhibits tumor growth (colon cancer) and extends mouse survival

Tumor vascular normalization

‘CU106 + αPD-1’ improved tumor vascular normalization and decreased hypoxia & abnormal vessel density

Promotion of CD8+ T cells and apoptosis

‘CU106 + αPD-1’ promotes accumulation of CD8+ T cells and apoptosis in tumors

Improvement of tumor specific CT8+ T cell response

‘CU106 + αPD-1’ improves tumor specific CD8+ T cell response in spleen and tumor tissue (secretion of IFNγ -> upregulation of PD-L1 expression by regulating STAT1)

Development

Ongoing Study : IL-2 agonist and CU106 combination mouse model

  • Purpose: To investigate whether CU106 is effective in improving the side-effects of IL-2-induced vascular leak syndrome (VLS)
  • Expected results: CU106 decreases the side effects by IL-2 agonist treatment and enhances the IL-2 induced anti-tumor