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Immunotherapy emerges as a future of cancer therapy, but still with limitations

FDA-approved immune checkpoint inhibitors improve survival of cancer patients over chemo and targeted therapies, but they have a very low response rate of only 10-20% in most solid tumors. Tumor metastasis to liver, but not other organs, restrains immunotherapy efficacy. A notable example is metastatic colorectal cancer, which does not respond to immunotherapy.

Liver metastasis restrains immunotherapy efficacy. The liver is the organ which cancers most commonly metastisize to. About 80% of body macrophages are in the liver, and are usually M2 type that are immune-suppressive by inducing apoptosis of cytotixic T cells. This makes liver metastasis a difficult condition for immunotherapy. Patients with liver metastasis respond poorer to immunotherapy than the same type of cancer that metastasizes to other organs. Animal study demonstrates that elimination of liver lesions may improve the efficacy of immunotherapy.

TATE is an ideal approach to debulk liver lesions with minimal side effect. Tumor necrosis induced by TATE induces M1 macrophage migration to the necrosis area for phagocytosis and tumor antigen presentation to boost anti-tumor immunity.

Teclison develops a novel, first-in-class approach to enhance immune checkpoint inhibitor drug to transform the lives of cancer patients with solid tumors. Our Phase 2 compound, TEC-001, when combined with FDA-approved immune checkpoint inhibitors, induces profound tumor necrosis and long-term remission.

Teclison has developed a first-in-class hypoxia-activating agent injected arterially that achieves a high local concentration within the tumor to kill the tumor with an excellent safety profile. Our lead compound, TEC-001, when combined with immune checkpoint inhibitors activates anti-tumor T cells to control residual disease and achieves long-term remission.

Our results are superior compared to standard chemotherapy combined with approved checkpoint inhibitors, yielding negligible immunosuppression, markedly enhanced and potent anti-tumor immunity, and a substantial reduction in tumor volume to prolong survival.

Phase 1 has demonstrated robust efficacy with 60% of liver cancer patients achieving durable complete tumor necrosis, and Phase 2 in colorectal cancer achieved 36.4% response by TEC-001 + Keytruda. Our results indicate strong applicability to all solid tumors (breast, melanoma, colorectal, lung, kidney, liver, bladder, head and neck cancers).

Well-Established Science Driven by Mechanism

TEC-001 is a hypoxia-activating agent that is converted to free radical by reductase. In the presence of oxygen, the free radical reverses back to the pro-drug. Therefore TEC-001 is not active in a normal oxygen environment. In a persistent hypoxia condition, free radical is accumulated and induces cell necrosis, which is different from programmed cell death or apoptosis by the ability to release Damage-Associated Molecular Patterns (DAMPs) from the necrotic cells. DAMPs serve as inflammatory cytokines to attract macrophage and dendritic cells to the necrotic region, which conduct phagocytosis of the tumor debris and present tumor-associated antigens to the immune system and enhance anti-tumor immunity just like a cancer vaccine. The expanded anti-tumor T cells are synergized by anti-PD-1 antibody or other immune checkpoint inhibitors.

Unique way of dosing TEC-001 to achieve maximal activity (40-60% Complete Response)
Due to the mechanism that TEC-001 is only activated in hypoxia, TEC-001 is designed to be administrated before trans-arterial embolization. The procedure is conducted by interventional radiologists, who place a catheter under X-ray guidance into the tumor-feeding hepatic artery. TEC-001 is injected via the tumor feeding artery into tumor to achieve a very high concentration (Step 1). Trans-arterial embolization was then conducted to obstruct the tumor feeding artery and induce tumor hypoxia (Step 2). TEC-001 is thus activated in tumor by the hypoxia and induce rapid tumor necrosis within 24 hours (Step 3).

Synergy between TATE and anti-PD-1

In untreated metastatic cancer, a tumor in the liver is a poor immunogen and can induce very limited production of anti-tumor T cells. In addition, even if the limited number of anti-tumor T cells are generated in the immune system, the immune checkpoint of the tumor prevents T cells from attacking the tumor. Thus, the tumor continues to systemically grow in liver.

In metastatic cancer treated with anti-PD-1 or an immune checkpoint inhibitor, anti-PD-1 antibody neutralizes the immune checkpoint, so the limited number of the existing T cells are able to attack tumor. But, there is a low response rate. The presence of liver metastasis induces T cells apoptosis and restrains the efficacy of anti-tumor T cells activated by the anti-PD-1 antibody.

In metastatic cancer treated with TATE in liver lesions, TATE induces tumor necrosis and attracts macrophages to the inflammatory tumor, which is equivalent to a therapeutic vaccine to increase the generation of anti-tumor T cells. However, these T cells are still suppressed by the immune checkpoint and unable to attack the systemic tumor to be effective.

In metastatic cancer treated with the combination of TATE and anti-PD-1, liver tumor undergoes necrosis after TATE treatment. Necrosis-induced inflammation attracts macrophages and stimulates the production of anti-tumor T cells in the immune system. The expanded anti-tumor T cells become much more active after the immune checkpoint is neutralized by the anti-PD-1 antibody. Systemic tumor outside of liver thus responds much better to anti-PD-1 antibody, which is called the “abscopal effect”.

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