James Noh, CEO
Seoul, South Korea
Oncobix Oncology Biosciences Website
Mutation in the kinase region of the epidermal growth factor receptor (EGFR) is found in some non-small cell lung cancer patients as a cause of cancer.
Mutation in the kinase region of the epidermal growth factor receptor (EGFR) is found in some non-small cell lung cancer patients as a cause of cancer. The epidermal cell growth factor receptor kinase inhibitors for treating these EGFR mutations include 1st generation gefitinib, erlotinib, 2nd generation afatinib, dacomitinib, and 3rd generation osimertinib and Tagrisso.
However, using these inhibitors, most patients develop resistance to the previous generation of drugs within a year.
Among these resistances, the T790M variation in the epidermal growth factor receptor is observed up to 60%, and subsequent resistance to third-generation drugs reveals the mechanisms of C797S and c-MET.
Therefore, it is necessary to develop drugs to treat patients who are unable to use third-generation drugs due to C797S mutation and c-MET amplification.
We have confirmed that OBX02-011 is not only effective in del19/T790M/C797S variation but also has an excellent inhibitory effect on L858R/T790M/C797S through analysis at the level of kinase assay and cells. Comparing the inhibitory effect on mutated cells to the IC50 value, it was confirmed that they were superior to brigatinib and osimertinib, which are already used as third and fourth-generation drugs. In addition, OBX02-011 inhibitors were found to have high selectivity that worked little on normal cells and only on mutated cells. Therefore, it is expected to be quite competitive when it is newly launched in the existing anti-cancer drug market, which is struggling with side effects from low selectivity for cancer cells. Based on the upper data, we will provide a fourth-generation drug that is less resistant and displays more selectivity.
Description of Technology
Multikinase inhibitor after the failure of Tagrisso®
The OBX02-011 compound is found to be effective in patients who have developed resistance to the third-generation treatment of non-small cell lung cancer.
The effect of inhibiting representative mutations (del19/T790M/C797S, L858R/T790M/C797S) that are expressed after treatment of previous generation therapeutic agents has been verified through numerical results and tissue experiments.
Above all, the OBX02-011 compound is a small molecule that easily melts in water and has little effect on normal wild-type cells other than cancer cells, so it is expected to overcome the problems experienced in the use of existing anticancer drugs.
PREVENTION INHIBITOR OF IPF, RIPF
We were confirmed that salt-containing OBX02-011 compounds have therapeutic effects on idiopathic pulmonary fibrosis (IPF).
IPF remains a major clinical challenge in cancer therapy due to the lack of clear treatment around the world.
When using the salt-containing OBX02-011 compounds in mouse that pulmonary fibrosis occurred, it was confirmed that fibrosis progress and EMT signals were inhibited.
These experimental results show the potential for use as a fourth-generation treatment of NSCLC and as a treatment for IPF.
The 3 months chronic oral toxicity study in dogs showed no particular alteration in the major organs with DEA and AMIO, only in the lungs signs of moderate fibrosis were observed which was less severe with DEA comparing it with AMIO. Blood chemistry showed no alteration with DEA but significant leukocytopenia was observed with AMIO. It was concluded that equal doses of DEA and AMIO administrations caused similar antiarrhythmic effects and cellular mechanisms but less drug accumulation in various organs with DEA than with AMIO treatments. This also associated with favourable pharmacokinetics and less toxicity of DEA comparing it to its parent compound AMIO.
Type of Business Relationship Sought
Out license, Partnership
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