On February 9, 2021 InteRNA Technologies reported the closing of an extended Series B financing round amounting to EUR 18.5M in total (Press release, InteRNA Technologies, FEB 9, 2021, View Source [SID1234574802]). This Series B round was led by AurorA Science, an Italian biotech investment company, along with existing investor Waterman Ventures. Current shareholders Aglaia Oncology Funds and OostNL also contributed to the financing round. The funding will enable the clinical evaluation of the Company’s microRNA lead candidate, INT-1B3, in patients with advanced solid tumors. Furthermore, the proceeds will be used to develop and advance additional proprietary preclinical drug candidates adressing a variety of cancer indications thereby expanding the Company’s pipeline. As part of the Series B financing, Gabriele Campi, PhD, of AurorA Science will join the Board of Directors.
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"This successful extension of the Series B financing round validates the unique potential that microRNAs offer as a therapeutic modality for hard-to-treat cancers," said Dr. Roel Schaapveld, CEO of InteRNA Technologies. "We thank AurorA Science, Waterman Ventures and our other long-term investors for their support in bringing our microRNA technology into the clinic and look forward to evaluate INT-1B3’s unique mode of action, targeting not only the tumor cells themselves but also the disease-promoting tumor microenvironment."
"With this participation in InteRNA Technologies, AurorA Science continues its strong commitment into front-edge science," commented Guido Guidi, Chairman at AurorA Science. "We believe InteRNA has developed a promising innovative technology in this area and look forward to supporting the team on their path forward."
microRNAs are naturally occurring, non-coding strands of RNA that trigger the RNA interference pathway and regulate gene expression by controlling the efficiency of messenger RNA (mRNA) translation into functional proteins. InteRNA designs breakthrough therapies tackling cancer by using the inherent characteristic of microRNAs to simultaneously inhibit multiple mRNA targets in a coordinated fashion, e.g. by blocking activated cancer signaling pathways and preventing activation of alternative disease-promoting pathways.
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). 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. The created T cell-mediated immune response activity is also transferrable to naive mice via adoptive T cell transfer.