New Drug Pipeline

Charis1000, C1K

C1K : TNBC Anticancer Drug

c1K
c1K

Cancer refers to an uncontrollable abnormal growth of cells. Treatment of cancer cells becomes more important because they ignore normal regulatory functions and continue to multiply through tissue infiltration and metastasis to destroy normal cells and organs and eventually result in death.

Existing cancer treatments include surgical tumor removal, radiation therapy, chemotherapy, and immunotherapy, and these methods are used alone or in combination. A side effect of chemotherapy to remove cancer cells includes remarkably declined quality of patient’s life and low survival rate. Because the patient dies with the attempt to kill cancer cells and it is virtually impossible to remove all cancer cells by conventional methods, we sought to develop a treatment method that effectively removes cancer cells with fewer side effects.

Triple negative breast cancer (TNBC) is a kind of breast cancer with no female hormone (estrogen • progesterone) receptor and HER2 protein, and accounts for approximately 20% of all breast cancer patients. Because existing breast cancer treatments such as hormone therapy and targeted therapy have no effect on TNBC, chemotherapy is mostly used. However, recurrence and metastasis, development of TNBC drug is necessary. However, it frequently develops into recurrence and metastasis after treatment and has poor prognosis that the development of Drug is urgently needed.

Charis1000 (C1K) is a synthetic peptide substance, which represents a mechanism that suppresses signal pathway of Smad2 by combining with TGF-β1. Although the tumor size decreases due to paclitaxel chemotherapy, the increased expression of TGF-β1 after accelerates the proliferation and metastasis of cancer cells. Therefore, more powerful chemotherapy needs to be used. Combined use of C1K inhibits the signal pathway of TGF-β1 can effectively suppress tumor growth after chemotherapy. Unlike conventional TGF-β signaling pathway inhibitors, C1K partially reduces Smad2 phosphorylation, and has low risk of side effects due to complete suppression of TGF-β signal pathway. Since it is developed based on the combined use of paclitaxel, it can be applied to various cancers in which paclitaxel is used, not limited to TNBC.