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Aptamer - Gint4.T

Gint4.T, a nuclease resistant RNAaptamer, is able to specifically bind to the human PDGFR ectodomain (Kd, 9.6 nM) causing a strong inhibition of ligand-dependent receptor activation and of downstream signaling in cell lines and primary cultures of human glioblastoma cells. It drastically inhibits cell migration and proliferation, induces differentiation, and blocks tumor growth in vivo. Gint4.T aptamer prevents PDGFR heterodimerization with and resultant transactivation of epidermal growth factor receptor (EGFR).

Categorymodified RNA
Last revisionNov 25, 2014
Author(s)L. Cerchia, V. de Franciscis
NameLaura Cerchia
AddressInstitute of Experimental Endocrinology and Oncology “G. Salvatore”, CNR, via Pansini 5, 80313 Naples Italy


Figure legend:

Secondary structure of Gint4.T

Molecular Weight10.661 KDa

Molecular target

human Platelet-derived growth factor receptor (PDGFR)

Kd9.6 nmol/l
Nucleotide modification(s)2’ F Py in the entire sequence. 2’F-Py RNAs were used because of their increased resistance to degradation by seric nucleases
Description of selection strategyCell-internalization SELEX Following 14 rounds of selection performed onto U87MG cells as previously described (ref Axl), the enriched pool was incubated onto U87MG for 30 minutes (first internalization round) and 15 minutes (second internalization round) at 37°C and unbound aptamers were removed by five washes with DMEM serum free. To remove surfacebound aptamers, target cells were treated with 0.5 μg/μl proteinase K (Roche Diagnostics, Indianapolis, IN) for 30 minutes, washed with DMEM serum free and internalized RNA aptamers were then recovered by RNA extraction and RT-PCR.
Intended UseTreatment and/or the diagnosis of a tumour expressing PDGFRβ


Quality validation: Yes

Validation info

The Gint4.T aptamer has been published in a peer-reviewed journal.


Camorani S, Esposito CL, Rienzo A, Catuogno S, Iaboni M, Condorelli G, de Franciscis V, Cerchia L.. Inhibition of receptor signaling and of glioblastoma-derived tumor growth by a novel PDGFRβ aptamer. Mol Ther. 2014;22:828-841.


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