Our Partners
At InxMed, we are strongly committed to driving groundbreaking scientific and technology advances and to transform the future of oncology treatment.
For ifebemtinib, we actively seek co-development and strategic business development opportunities, especially inhibitors of RAS pathway and tumor targeting ADCs. We aim to invent revolutionary, breakthrough therapies and to unleash the full synergy of combination regimens based on deep insights of underlying disease biology.
For novel first in class ADCs, we are looking for out-license partners.
Partner with Us
We are currently seeking strategic partners in the following areas
● Clinical co-development of Ifebemtinib combo with inhibitors of RAS pathway or RAS/IO regimens
● Clinical co-development of Ifebemtinib with ADC or ADC/IO regimens
● Co-discover new molecules leveraging innovative technologies
Contact:BD@InxMed.com
Combo with Inhibitors of RAS Pathway to Amplify the Clinical Responses
We identified Ifebemtinib is synergistic with multiple Inhibitors of RAS Pathway, including but not limited to KRAS G12C, G12D, NRAS,HRAS,pan-RAS,MEK inhibitors.
We demonstrated Ifebemtinib + RASi, smartly designed on our robust understanding of RAS biology, is potentially an ideal combo, differentiated with superior efficacy, good safety and convenient oral dosing. Ifebemtinib is proposed to brings transformative solution against tumors with any RAS mutations.
We look for partners to further explore clinical combination of ifebemtinib with any RAS pathway inhibitors.
Combo with ADCs to Improve the Tumor Penetration and Boost Efficacy
Hard-to treat cancer such as pancreatic cancers are rich in stroma, the higher stroma is, the more resistant to treatment. The efficacy of tumor cell targeting ADC is limited by its poor access to tumor cells as a result of high stroma. The high stroma is predominantly due to cancer associated fibroblasts. InxMed believes reduction of fibroblast stroma will boost ADC efficacy.
The cancer cells can transform the normal fibrotic cells into cancer-associated fibroblasts (CAFs) which are featured by the hyperactivated FAK signaling. The fast-growing CAFs would form a barrier which decreases the tumor uptake of the big molecules, conferring drug resistance of ADCs to the cancer cells.
We discovered that targeting FAK with ifebemtinib is capable to reduce CAFs associated tumor barrier, enhanced the tissue penetration of different types of ADCs regardless their respective targets. The combination regimen comprising ifebemtinib boosted efficacy of ADC in multiple pre-clinical studies.
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