Anti-miRNA Anticancer Drugs

Advantages

S-TuD shows higher inhibitory activity in miRNA inhibition than other methods. The improved S-TuD is smaller and has enhanced stability and activity. The anti-miR-200 improved S-TuD effectively inhibits the target miR200 family.

Current Stage and Key Data​​

Early preclinical research stage Anti-miR-200 improved S-TuD (3mg/kg) encapsulated in commercially available LNP was administered via the tail vein to orthotopic xenograft mice model injected with SUM149PT cells into the mammary fat pad. Tumor growth was significantly suppressed (right figure).

Partnering Model

• We are seeking an exclusive license partner for the improved anti-miR-200 S-TuD.
• Collaborative development of LNP inclusion bodies, ligand conjugates, etc. is also possible.

Background and Technology

miRNAs form gene regulatory networks by controlling a large number of target genes, and play important roles in many biological phenomena. High expression of certain miRNAs has also been confirmed in cancer, and miRNA inhibitors such as miRNA antisense (Antagomir) have been developed. S-TuD has been reported to show higher inhibitory activity than Antagomir and others. We developed S-TuD with improved stability and activity by designing artificial nucleic acids and linkers.

The miR-200 family (miR-200a, miR-200b, miR-200c, miR-141, miR-429) is known to suppress epithelial-mesenchymal transition (EMT) in tumor cells and has been considered to be a tumor suppressor. On the other hand, we have revealed that epithelial tumor cells strongly contribute to tumorigenic activity. Furthermore, we inhibited the miR-200 family using an improved S-TuD designed to target the miR-200 family. As a result, we found that the population equilibrium of tumor cells was shifted toward the mesenchymal lineage, effectively suppressing the growth of primary tumors.

Principal Investigator

Hideo IBA (Medical Mycology Research Center, Chiba University)

Patents

• Japan: Patent No. 7306653, USA: Patent No. 11479769, Europe/China: Under examination.

Project.BK-04972