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Use of DNA Stabilizers to Extend Plasmid Biological Activity
Jonathan De la Vega, Gabriel A. Monteiro and Duarte Miguel F. Prazeres
*
iBB- Institute for Bioengineering and Biosciences, Department of Bioengineering, Instituto Superior
Técnico, Universidade de Lisboa, Av. Rovisco Pais, 1049-001 Lisboa, Portugal
Abstract: Background: Storage stability of plasmid biopharmaceuticals is a critical issue that needs
to be addressed during clinical and process development.
Objectives: The goal of this work was to evaluate the ability of stabilizers to prolong the stability of
plasmid DNA solutions and extend the duration of transgene expression of transfected cells.
Methods: A plasmid harboring the GFP gene and Chinese Hamster Ovary (CHO) cells were used as
models. Plasmid solutions were formulated with the stabilizer DNAstablePlus
TM
, 300 mM trehalose
and 300 mM cellobiose. The biological activity was monitored by transfecting CHO cells with the preparations using
Lipofectamine.
Results: Protection against denaturation conferred by DNAstablePlus
TM
at 60 °C was outstanding, with 94% of the activ-
ity preserved after 7 days compared to 76% with trehalose, 70% with cellobiose and <10% without stabilizers. While
plasmid DNA stored at room temperature lost 95% of its ability to express GFP in the first month, trehalose, cellobiose
and DNAstablePlus
TM
were able to preserve it for 6, 8 and at least 12 months, respectively. The incorporation of trehalose,
cellobiose and DNAstablePlus
TM
in lipoplexes also contributed to extend the expression of GFP in transfected cells. While
a significant loss of GFP-expressing cells (~10%) was observed after 7days with no stabilizers, formulation with DNAsta-
blePlus
TM
, cellobiose and trehalose increased the number of cells GFP-expressing cells to more than 50%.
Conclusions: The biological activity of plasmid DNA solutions stored at room temperature was extended several fold by
incorporating cellobiose, trehalose and DNAstablePlus
TM
in the formulations.
Keywords: DNA vaccines, gene therapy, lipoplexes, non-viral gene delivery, plasmid DNA, stability.
INTRODUCTION
The safe and effective delivery of genes remains a critical
bottleneck in the development of clinical applications of
gene therapy and DNA vaccination [1]. Currently, the major-
ity of human gene transfer protocols in clinical trials employ
viral delivery systems. While very effective in many circum-
stances, safety problems and concerns are often associated
with the use of such systems [2, 3]. Plasmid-based, non-viral
systems, on the other hand, offer a number of potential ad-
vantages, including straightforward manufacturing, high
shelf stability, low immunogenicity and toxicity, and ability
to deliver larger and unrestricted genetic loads, at least in
theory [1, 4]. As a result, plasmids carrying medically-
relevant genes have emerged during the last 20 years as a
new class of biopharmaceuticals.
Storage stability is a critical issue that needs to be ad-
dressed during the development of plasmid biopharmaceuti-
cals. Ensuring that plasmids have a substantial shelf-life and
maintain biological activity (i.e. the ability to transfect cells)
*Address correspondence to this author at the iBB- Institute for Bioengi-
neering and Biosciences, Instituto Superior Técnico, Av. RoviscoPais, 1049-
001 Lisboa, Portugal; Tel: +351-218419133; +351-218419062; E-mail:
miguelprazeres@tecnico.ulisboa.pt
can be crucial both during the early stages of clinical and
process development, and once manufacturing for commer-
cialization becomes a reality [5-10]. Furthermore, the ability
to maintain biological activity at room temperature, without
the need for a cold chain, could be particularly relevant when
considering the deployment of plasmid-based DNA vaccines
in tropical countries [4].
The loss of activity of purified plasmid preparations is
essentially linked to the chemical degradation of the plasmid
molecule [11]. In aqueous solutions, the chemical degrada-
tion of plasmids and of nucleic acids in general, typically
proceeds via hydrolytic cleavage reactions (e.g. depurination,
depyrimidination, deamination, cleavage of the phosphodi-
ester bond) and oxidative damage to DNA bases [6, 12].
These processes are a function of both endogenous (e.g. pri-
mary structure, chemical modifications in bases, sugars and
phosphate residues) and exogenous (e.g. pH, buffer concen-
tration, presence of transition metal ions, oxygen presence)
factors and will typically originate degraded plasmid mole-
cules with apurinic sites, oxidized bases and strand breaks [6,
12-14]. The presence of residual nuclease impurities in
poorly purified plasmid batches can also be partially respon-
sible for strand cleavage, even if preparations are kept at low
temperatures (e.g. +4 ºC) [7, 15]. These chemical or enzy-
matic alterations in the primary structure of DNA together
Jonathan De la Vega