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Updated: Jan 10, 2026

Intravitreal Injections in the Ovine Eye
Published on: July 5, 2022
Novel Needle for Intravitreal Injections Does Not Affect Biological Activity of Anti-VEGF Drugs
Lyubomyr Lytvynchuk1,2,3, Kai L Nolte1, Isabell Fuezy1
1Department of Ophthalmology, Justus Liebig University Giessen, Giessen, Hessen, Germany.
Purpose:
In this in vitro study, we investigated if the biological activity of commonly used VEGF antagonists might be affected by their passage through a newly designed 30 G needle (NDN) for intravitreal injection (IVI). To reduce the risk of intraocular inflammation compared to conventional injection with a standard hypodermic 30 G needle (SHN), the NDN contains an occluded front orifice and a side port for drug delivery, resulting in an altered direction of the injection stream.
Methods:
Anti-VEGF drugs, such as ranibizumab, faricimab, and aflibercept, were passed twice through one of the two needle types to imitate IVI. To evaluate the VEGF-A-binding capacity of the un- or pretreated antagonists, VEGF-A165 was incubated with a 1-10fold molar excess of them for 15 min at 37°C, and unbound VEGF-A was determined by ELISA. As the capture antibody and antagonists bind to the same region of the growth factor, only the non-complexed VEGF-A was measured. Biological activity of pretreated antagonists was studied by assessing their capacity to prevent VEGF-A165-induced impairment of the barrier formed by retinal endothelial cells: VEGF-A165 plus antagonists were added to the cells and, as a measure of permeability, the cell index was continuously monitored by electric cell-substrate impedance measurements for three days.
Results:
Only a marginal amount of free VEGF-A, if any, was detected after incubation of the growth factor with a fourfold molar excess of any of the antagonists, independent of the drugs' pretreatment. VEGF-A165-induced low cell index values, indicative of a dysfunctional barrier, were similarly prevented by different pretreated antagonists.
Conclusion:
The passage of the proteins through NDN or SHN did neither affect efficient binding to their target, nor their capacity to prevent VEGF-A165-induced barrier dysfunction. Overall, regarding the stability of therapeutic proteins, the NDN was not inferior to the SHN, and can now be considered for evaluation in clinical studies.

