On March 11, 2021 InteRNA Technologies, a clinical-stage biotech company developing microRNA (miRNA)-based therapeutics with a focus on cancer, reported that it was awarded a Clinical Innovation Credit of € 2.7 Million from the Dutch government (Press release, InteRNA Technologies, MAR 11, 2021, View Source [SID1234576532]). This award will support the clinical validation of the Company’s lead candidate, INT-1B3, for the treatment of solid tumors. The funding is granted by the ‘Rijksdienst voor Ondernemend Nederland’/The Netherlands Enterprise Agency (RVO), an agency of the Dutch Ministry of Economic Affairs and Climate Policy.
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The Clinical Innovation Credit aims to fund Dutch clinical development projects that have a highly innovative character and strong commercial potential. The projects have to be focused on the development of new products, processes or services.
"The support we receive from our government through this funding recognizes the innovative character and commercial outlook of our lead program, both key prerequisites to qualify for the awarded credit," said Roel Schaapveld, CEO of InteRNA Technologies. "The Clinical Innovation Credit complements our recently closed Series B round, enabling us to execute our clinical development plan for INT-1B3 towards the treatment of more advanced stages of solid tumors for which there currently are no adequate treatments available."
Recently, InteRNA announced the dosing of the first patient in the first-in-human trial for INT-1B3, which is conducted in several clinical study centers located in the Netherlands and Belgium. Topline results from the dose escalation part of the study are expected by the end of 2021.
About INT-1B3
INT-1B3’s unique mechanism of action addresses multiple hallmarks of cancer simultaneously. It directly targets tumor cells and the tumor microenvironment by specific modulation of multiple signaling pathway components across the PTEN tumor suppressor pathway and the oncogenic PI3K/Akt and Ras/MAPK pathways resulting in inhibition of proliferation and migration and induction of cell cycle arrest and apoptosis. The triggering of the immunogenic tumor cell death (ICD) process as well as downregulation of the adenosine-A2A receptor pathway through inhibition of CD39/CD73 leads to a decrease in immunosuppressive FoxP3/Lag3 regulatory T cells and monocytic myeloid-derived suppressor cells (mMDSCs), and maturation of dendritic cells. As a result, the immune system is activated, and long-term immunity is triggered by recruitment of CD8+ effector T cells leading to decreased metastasis development and improved animal survival compared to anti-PD1 treatment in preclinical models.