BusinessArea
We will keep the competitiveness of the global market based on advanced technology.
Home
Business Areas
New drug development
ARS and STR, next-generation anticancer drugs of the latest cancer immunotherapy technology.NeoTX Overview
The best experts in each field lead NeoTX.-
Robert Kramer, PhDChairman
J&J (Johnson & Johnson) Vice President, New Anticancer Drug Discovery Division
BMS (Bristol Myers Squibb) Vice President, New Anticancer Drug Discovery Division
Vice President, Princeton Research Site
Research Director, Dana-Farber Cancer Institute
-
Dr. Marcel RozencweigCMO
BMS（Bristol Myers Squibb）Global
Global Clinical Chief Manger of Blockbuster Immuno-anticancer drug Carboplatin and Anti-cancer drug Taxol
-
Asher NathanCEO
Co-founder of NeoTX
Co-founder of Zoticon Bioventure Company
Senior Executive of Paramount Biocapital
-
Ramona Lloyd, PhDCRO
Senior Executive, Sanofi, BMS (Bristol Myers Squibb), J&J (Johnson & Johnson) Pharmaceutical Industry Consulting Department
-
Dr. Roger KornbergCSO
2006 Nobel Prize in Chemistry (Announcement of 'A Study of the Process by which Genetic Information from DNA is Copied into RNA, the Molecular Basis of Eukaryotic Bio-transcription')
Current Professor of Structural Biology, Stanford University School of Medicine Current Executive Director, Teva
Bachelor's Degree in Chemistry, Harvard University
Ph.D. in Chemical Physics, Stanford University
STR platform technology
Selective activation of specific T-Cells
STR platform selectively activates specific T-cells, ignoring normal cells and inducing death by reacting specifically only to cancer cellsSelective activation of T-Cell through Activation Key
Reduced drug resistance through activation of the immune system,
Removal of the need for additional drugs
Recognizes cancer cells as bacteria and induces death
T-Cell recognizes cancer cells as bacteria and induces death by coding bacteria (Staphylococus Aureus) recognized as pathogens and killed into cancer cells.
By coding STR to recognize cancer cells as bacteria, T-Cell recognizes cancer cells as pathogens (bacteria) and kills them.
(Anticancer drugs that kill cancer cells by activating T-cells such as CAR-T and immune checkpoint inhibitors was known for its safety issue as it can recognize normal cells as cancer cells
and kill them)
T-Cell reacts specifically only to cancer cells recognized as bacteria and does not attack normal cells
This cancer cell can only be recognized by STR specific T cell.
Repeated overstimulation does not kill “good” T cell.
Able to develop various solid cancer treatments
Various solid cancer treatments can be developed by coding various solid cancer antibodies including 5T4 antibody on the STR platform.CAR-T(Cancer Immunotherapy) attacks the cancer cell by injecting CAR(Chimeric Antigen Receptor) into T-cell, and Bi-Specifics(Bi-Specific Antibody Anticancer Medicine) attacks the cancer cell while it disturbs the immune checkpoint molecule with bi-specific antibody, PD-L1/CD3 of T-cell. Both of them attack the cancer cell by manipulating T-cell.
STR does not create safety issue on attacking normal cell as it makes T-cell to attack cancer cell by coding the cancer cell to recognize as pathogenic bacteria (Bacteria) known for T-cell to attack specifically the cancer cell. In addition, it has advantage of pipeline expandability by coding the cancer cell through combining the antigen present at cancer cell to STR including 5T4 existing at solid cancer.
-
1.Car T. TCR Replacement
-
2.Bi-specifics. Nonselective Adapter
-
3.STR. Selective Adapter
Pipeline
Preclinical (NeoTx data)
NAP +CPI data
Decide to administer Clinical1b/2 phase jointly as Astrazeneca/Medimmune showed interest
-
01
At the joint administering STR + immune checkpoint inhibitor(Anti-PD1)** to cancer cell injected mice, T-Cell were found to attack the cancer cell.
-
02
No effect at anti-PD1 administered < Effect at STR administered << Joint administered STR + anti-PD1
showed 3-4 time fold effect than STR administered only. -
03
The cancer-free mice after treatment with STR alone: No grow in cancer cell when the cancer cell was injected again (memorizing effect).
Clinical Plan
Preclinical (joint research with CureBio: renal cell carcinoma)
-
01
Neopep GT, CureBio’s anticancer drug candidate substance, induces cancer cell death through cancer cell proliferation inhibitory signals by binding the CDH6 receptor on the surface of cancer cells through GRS protein secreted from macrophages. -
02
Neopep GT acts selectively on cancer cells overexpressing CDH6S and does not accompany normal cell death. -
03
Particularly in renal cell carcinoma, it efficiently induce death of cancer cells without attacking normal cells, so it is combined with NeoTx's STR technology to maximize anticancer activity based on such safety and efficiency.
Collaboration
Collaboration with advanced global research groups
-
Astrazeneca
NAP + imfinzi (durvalumab**)
Phase 1 b/2 clinical trial with a total of 13 indications such as liver cancer, melanoma, non-small cell lung cancer, pancreatic cancer, prostate cancer
-
Sanofi
NAP + docetaxel
Phase 2 clinical trial in combination with Sanofi's immune checkpoint inhibitor Docetaxel (Non-Small Cell Lung Cancer)
-
Dana-Farber Cancer Institute
STR for GBM
Joint research with Harvard University's Dana Faber Cancer Center to develop glioblastoma treatment
Technology Collaboration
-
STR + CAR-T therapy
Combination with CAR-T cell therapy technology, a next-generation anticancer drug
* Test results of all immune checkpoint inhibitors such as Keytruda: Same effect (Eli Lily and other companies showed interest)
**
Immune checkpoint inhibitors are usually effective only in 20% of patients.
When co-administered with STR leading substance NAP, the remaining 80% of cancer patients can be treated (expected to double the existing immune checkpoint inhibitor market)
