Ocular iontophoretic device and method for inhibiting...

Surgery – Means for introducing or removing material from body for... – Treating material introduced into or removed from body...

Reexamination Certificate

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C604S501000, C604S020000, C424S427000

Reexamination Certificate

active

06579276

ABSTRACT:

BACKGROUND OF THE INVENTION
1. Field of the Invention
The present invention relates in general to an ocular iontophoretic device, and more particularly, to an ocular iontophoretic device which, upon association with the eye of a living being, and application of an electrical potential difference, iontophoretically delivers an aptamer into the living being's eye, thereby inhibiting VEGF function therewithin.
2. Background Art
Vascular Endothelial Growth Factor (VEGF) is a protein that stimulates the growth of new blood vessels in the body of a living being, which has been identified in the art as angiogenesis and/or neovasculation. VEGF is presently believed to comprise four isoforms, including VEGF-121, VEGF-165, VEGF-189, and VEGF-206, which are believed to be the result of alternative splicing of mRNA. Of these isoforms, VEGF-165 is the most abundant, amounting to approximately 90% of the total VEGF.
VEGF was originally identified as a factor which increased the permeability of vascular tissues; consequently it is also known as Vascular Permeability Factor (VPF). VEGF is, therefore, a factor in causation of edema as well as neovascularization.
While normal blood vessel growth within a living being's eye is desirous for healthy tissues and surrounding structures, abnormal blood vessel growth and edema facilitated, at least in part by VEGF, can contribute to numerous eye diseases, including vision impairment, blindness, and the growth of malignant tumors—just to name a few. For example, Age-Related Macular Degeneration (AMD) is a leading cause of blindness in people aged 65 and older. The disease is characterized by the abnormal growth of new blood vessels into the macula of the retina. These new vessels are generally leaky and edematous. When the blood vessel leaks, scars form on the retina, leading to vision impairment, and sometimes, complete loss of vision.
One solution to the problems associated with VEGF and the undesirable, abnormal formation of new blood vessels, is to bind or attach an aptamer to VEGF—thus inactivating it by rendering it incapable of binding to its receptor in the vascular tissue. Recent studies have indicated that when an aptamer binds to VEGF, the VEGF function is slowed or stopped, thereby slowing or stopping the undesirable, abnormal growth of blood vessels.
While binding an aptamer to VEGF has been identified as a mechanism to inhibit the formation of new blood vessels, heretofore, problems associated with delivery of an aptamer to an affected area of a living being's eye has remained problematic. Indeed, known prior art devices and associated methods of delivering an aptamer, identified hereinbelow, are replete with drawbacks and disadvantages.
For example, delivering an aptamer to an affected, local area of a living being's eye using a systemic delivery method is problematic because of the many conventional side effects associated with systemic delivery, including unnecessary medicament exposure to unaffected areas, toxicity buildup, concentration control—just to name a few.
Local delivery of an aptamer via interocular injection is problematic, because of the opportunity for, among other things, retinal detachment, bleeding into the interior of the eye, increased interocular pressure, and increased risk of secondary infection. Although perhaps justifiable for occasional acute conditions, these risk factors render interocular injection undesirable as a delivery mode for chronic administration. Furthermore, interocular injections can be scary, unpleasant, and painful for the patient.
In addition to the above-identified problems associated with interocular injection, peribular or subconjuctival injection of an aptamer is problematic, because such injections may not deliver sufficient quantities to the interior of the eye. Moreover, peribular or subconjuctival injections are demanding of the physician inasmuch as placement of the needle requires an extremely high level of precision.
Topical administration of an aptamer to an affected, local area of a living being's eye is problematic due to its ineffectiveness for many applications, including affected areas in the back of the eye.
SUMMARY OF THE INVENTION
The present invention is directed to an ocular iontophoretic device for delivering an aptamer to an affected area of a living being's eye for inhibiting VEGF function therein, comprising an active electrode assembly associated with a matrix, wherein the matrix includes an aptamer capable of inhibiting VEGF function.
In a preferred embodiment of the invention, the matrix includes an aptamer capable of inhibiting at least one VEGF selected from the group consisting of VEGF-121, VEGF-165, VEGF-189, and VEGF-206, such as NX-1838.
In another preferred embodiment of the invention, the matrix also includes a PEGylating agent, reversibly attached to an aptamer, which slows enzymatic tissue digestion of the aptamer upon delivery of the same to the affected area of the living being's eye.
In yet another preferred embodiment of the invention, the aptamer is present in a concentration between approximately 0.1 milligrams (mg) and approximately 10 mg of aptamer per milliliter (ml) of water, and the water is buffered to a pH ranging between approximately 6.5 and approximately 8.5.
Preferably, the affected area of the eye is selected from at least one of the group consisting of the vitreous humor, retina, choroid, circulation of the retina, circulation of the choroid, and sclera.
It is also contemplated that the above-identified ocular iontophoretic device further comprises: (a) a counter electrode assembly, wherein the counter electrode assembly is configured for completing an electrical circuit between the active electrode assembly and an energy source; and (b) an energy source for generating an electrical potential difference.
The present invention is also directed to an ocular iontophoretic device for delivering an aptamer to an affected area of a living being's eye for inhibiting VEGF function therein, comprising: (a) a reservoir, wherein the reservoir includes an aptamer capable of inhibiting VEGF function; (b) a matrix, wherein the matrix is capable of temporarily retaining a solution having an aptamer; (c) an active electrode assembly associated with the matrix, wherein the active electrode assembly is configured for iontophoretically delivering the aptamer to the affected area of the living being's eye; (d) a counter electrode assembly, wherein the counter electrode assembly is configured for completing an electrical circuit between the active electrode assembly and an energy source; and (e) an energy source for generating an electrical potential difference.
In accordance with the present invention a method for treating an affected area of a living being's eye is disclosed comprising the steps of: (a) associating an aptamer with an ocular iontophoretic device; (b) positioning at least a portion of the ocular iontophoretic device on the eye of the living being; and (c) iontophoretically delivering the aptamer to an affected area of the living being's eye.
The present invention further discloses a method for inhibiting VEGF function within an affected area of a living being's eye comprising the steps of: (a) associating an aptamer with a matrix of an ocular iontophoretic device; (b) associating the ocular iontophoretic device having an active electrode assembly with the eye of the living being; (c) iontophorectically delivering an effective amount of the aptamer to an affected area of the living beings' eye having an amount of VEGF; (d) binding the effective amount of aptamer to the amount of VEGF; and (e) inhibiting function of the amount of VEGF.


REFERENCES:
patent: 5676648 (1997-10-01), Henley
patent: 6319240 (2001-11-01), Beck

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