Yonsei Cancer Center and the Korea Research Institute of Chemical Technology (KRICT) have signed a technology transfer agreement for its Traf2- and Nck-interacting kinase (TNIK) inhibitor, a colon cancer drug candidate, with FutuRx, an Israeli firm.
|From left, Professors Shin Sang-joon, Lee Hyuk and TNIK Therapeutics CEO Keren Weiser hold up the transfer agreement at Yonsei University Health System in Sinchon, Seoul, Tuesday.|
The team, led by Professors Shin Sang-joon of the oncology department at Yonsei University Health System and Lee Hyuk at the KRICT, developed the TNIK inhibitor.
FutuRx is an incubator firm that helps companies to find a source compound for new drug development worldwide and commercialize it. The company supports technology development from initial technology discovery to experimental proofs to treatments that have the potential of becoming a first-in-class or best-in-class therapy.
TNIK is a kinase protein that interacts with Beta-catenin and transcription factor 4 at the bottom of the Wnt signal.
In addition to the technology transfer, the research team, together with FutuRx, will jointly establish TNIK Therapeutics, a startup company for evaluating the usefulness of TNIK inhibitors.
FutuRx, OrbiMed, J&J, Takeda, Yonsei University Health System and KRICT will share a joint stake in the newly developed company.
Colon cancer-targeting drug market is worth 7 trillion won ($6.22 billion) globally, and about 500 billion won locally. Recently, with the patent expiration of Avastin and Erbitux, multinational pharmaceutical companies have been trying to find a new cancer treatment drug.
In the case of colorectal cancer, however, it is difficult to find a candidate and apply it as a therapeutic agent.
TNIK binds to β-catenin, formed through the Wnt signaling pathway, enters the nucleus to promote cell growth, proliferation, and metastasis.
Under normal circumstances, intracellular β-catenin-degrading complexes inhibit β-catenin degradation in the absence of Wnt signaling. However, when activating the Wnt signal, the β-catenin-destroying complex does not form, and β-catenin binds to the nucleus to enter the nucleus and enable cell growth.
In the case of cancer cells, it binds to β-catenin, which does not degrade TNIK and continuously expresses it. This complex then moves to the nucleus and induces cell growth.
TNIK inhibitors, developed by the team, inhibit the growth of colorectal cancer by inhibiting the transfer of β-catenin to the nucleus by reducing TNIK.
The researchers used the TNIK inhibitor in colorectal cancer cells to identify new biomarkers that inhibit cancer stem cell growth and have also confirmed that it reduces the growth of colorectal cancer.
“The team anticipates that this leading substance, which inhibits TNIK activity, will be developed into a drug that can produce synergistic effects when administered alone or in combination with other anticancer drugs,” Professor Shin said.
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