Splice-blocking therapy for cardiovascular diseases and preeclampsia

Splice-blocking therapy for cardiovascular diseases and preeclampsia

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Partnership opportunities

We are seeking partners for:

-Collaborative development

-Technology can be licensed or assigned

 

For Contact:

Technology Transfer:
INNOVECTIS GmbH
Altenhöferallee 5
60438 Frankfurt am Main, Germany
 Phone: +49 15161153058
 juliane.mueller@innovectis.de

Technology

Researchers at Goethe University Frankfurt have developed a new splice-blocking morpholino oligonucleotide that selectively reduces sFLT1, a key anti-angiogenic factor and biomarker involved in several cardiovascular diseases and preeclampsia. The morpholino binds to a defined splice site in FLT1 pre-mRNA and prevents formation of the soluble isoform while preserving membrane-bound FLT1 and thereby maintaining physiological pro-angiogenic signaling.

In primary human umbilical vein endothelial cells, the morpholino reduced more than 95 % of sFLT1 mRNA after 24 hours and markedly lowered sFLT1 protein levels. At the same time, membrane-bound FLT1 remained unchanged, demonstrating a highly isoform-selective mode of action.

Functional assays further showed that morpholino-mediated sFLT1 knockdown increased VEGF-A-mediated sprout length and sprout number, indicating improved angiogenic capacity and suggesting the potential to restore endothelial function.

Applications

-The technology is relevant for the treatment of cardiovascular diseases in which elevated sFLT1 contributes to endothelial dysfunction and disease progression, including forms of heart failure and cardiomyopathy. The offer highlights a substantial medical need, noting that heart failure affects around 55 million patients worldwide and that the global heart-failure drug market is projected to reach 33.7 billion USD by 2032.

-Preeclampsia represents another  application area, as elevated sFLT1 is a key driver of the disease.

Technology stage

-New splice-blocking morpholino established.

-Selective targeting of sFLT1 demonstrated while preserving physiological pro-angiogenic signaling through membrane-bound FLT1.

-Strong in vitro efficacy shown in endothelial cells, including marked reduction of sFLT1 and improved angiogenic readouts.

-Next development step: establishment of a mouse model to evaluate the morpholino in vivo.

Patents

-EP patent application EP25218896.6 was filed on 27 November 2025

The technology is supported by the publication Lam et al., 2026, “LINC00607 facilitates endothelial VEGF-A receptor FLT1 splicing.”