Non-peptide bradykinin receptor antagonists for use in...

Drug – bio-affecting and body treating compositions – Designated organic active ingredient containing – Heterocyclic carbon compounds containing a hetero ring...

Reexamination Certificate

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C514S913000

Reexamination Certificate

active

06500831

ABSTRACT:

The present invention relates to the topical ocular use of non-peptide bradykinin receptor antagonists to treat glaucoma and ocular hypertension.
BACKGROUND OF THE INVENTION
Glaucoma is a progressive disease which leads to optic nerve damage and, ultimately, a total loss of vision. The causes of this disease have been the subject of extensive studies for many years, but are still not fully understood. The principal symptom of, and/or risk factor for, the disease is elevated intraocular pressure or ocular hypertension due to excess aqueous humor in the anterior chamber of the eye.
The reasons why aqueous humor accumulates are not fully understood. It is known that elevated intraocular pressure (“IOP”) can be at least partially controlled by administering drugs which reduce either the production of aqueous humor within the eye, such as beta-blockers and carbonic anhydrase inhibitors, or increase the flow of aqueous humor out of the eye, such as miotics and sympathomimetics.
The pharmaceutical approaches currently being pursued in the treatment of glaucoma have exhibited various side effects. Miotics such as pilocarpine can cause blurring of vision and other visual side effects, which may lead either to decreased patient compliance or to termination of therapy. Systemically administered carbonic anhydrase inhibitors can also cause serious side effects, such as nausea, dyspepsia, fatigue, and metabolic acidosis which can affect patient compliance and/or necessitate the withdrawal of treatment. Moreover, some beta-blockers have increasingly become associated with serious pulmonary side effects attributable to their effects on beta-2 receptors in pulmonary tissue. Sympathomimetics cause tachycardia, arrhythmia and hypertension. There is therefore a continuing need for therapies which control the elevated intraocular pressure associated with glaucoma.
Bradykinin or “BK,” is an endogenous peptide made up of nine amino acids (i.e., Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg). BK is found in many organs, including the eye. BK exhibits many biological effects in the body, including tissue contraction, fluid and ion secretion and pain inducement (Regoli and Barabe,
Pharmacol. Rev.,
volume 32, pages 1-46 (1980) and Hall,
Pharmacol. Ther.,
volume 56, pages 131-190 (1992)).
BK and another endogenous peptide, Lys-BK, bind to two major BK receptor-subtypes. namely B
1
and B
2
, to produce their biological effects. The B
2
-subtype is found to be expressed under normal physiological conditions, while the B
1
-subtype is induced during injury or trauma (Regoli, and Barabe,
Pharmacol. Rev.,
and Hall,
Pharmacol. Ther.
). While the B
1
-subtype has a low affinity for BK and a high affinity for Des-Arg
9
-BK and Lys-BK, the B
2
-subtype has a high affinity for BK and Lys-BK but a low affinity for Des-Arg
9
-BK.
Both receptor subtypes have been cloned and shown to be coupled to G-proteins and phospholipase C, and their activation results in the generation of the second messengers inositol trisphosphate (“IP
3
”) and diacylglycerol (“DAG”) (Hall,
Pharmacol. Ther.
). The signal transduction of BK receptor binding results in IP
3
-stimulated mobilization of intracellular Ca
2+
, followed by DAG phosphorylation of protein kinase C. Together, these events lead to the final biological response, such as tissue contraction or fluid secretion.
The majority of the physiological and pathological effects of BK are mediated by the B
2
-receptor-subtype. However, recent pharmacological evidence points to two additional BK-receptor subtypes, namely B
3
and B
4
(Hall,
Pharmacol. Ther.,
and Sharma,
Gen. Pharmacol.,
volume 24, pages 267-274, (1993)). The B
3
and B
4
receptor subtypes are actually stimulated by certain peptide BK antagonists, whereas the B
1
and B
2
subtypes are blocked by those antagonists (Sharma,
Gen. Pharmacol.
). While the presence of B
3
or B
4
receptor subtypes in the eye has not been investigated, it is believed they may be present since there is a robust BK-precursor and BK-generating enzyme pool in human ocular tissues and also the presence of the B
1
and B
2
receptors (Ma et al.,
Exp. Eye Res.,
volume 63, pages 19-26, (1996)).
Most of the previously described BK antagonists have been peptides of limited potency and selectivity (Regoli et al.,
Trends in Pharmacol. Sci.,
volume 11, pages 156-161, (1990) and Hall,
Pharmacol. Ther.
). Peptides are labile, highly polar and, therefore, difficult to formulate and deliver to the site of treatment (Sharma,
Gen. Pharmacol.
). Such peptides would be especially difficult to formulate for topical administration to the eye due to the relatively impenetrable thick scleral and corneal/conjunctival covering of the eye.
Nowhere in the art has it been disclosed, taught or suggested to use non-peptide BK antagonists to treat ocular hypertension and glaucoma.
SUMMARY OF THE INVENTION
The present invention is directed to compositions and methods for the treatment of glaucoma and ocular hypertension. More specifically, the present invention is directed to topical ophthalmic compositions containing one or more bradykinin antagonists and methods of treating glaucoma and ocular hypertension.
The compositions and methods of the present invention employ antagonists to bradykinin receptors which are relatively stable and bioavailable to the relevant ocular tissues. As stated above, previous BK antagonists have been peptides and thus labile and of low bioavailability. The present invention compositions and methods, in contrast, are directed to stabile, bioavailable non-peptide BK antagonists. Preferred compositions and methods are directed to bradykinin B
2
receptor antagonists.
DETAILED DESCRIPTION OF THE INVENTION
The present invention provides compositions and methods of their use in treating glaucoma and ocular hypertension. More specifically, the present invention is directed to ophthalmic compositions comprising non-peptide bradykinin antagonists and methods of use in treating glaucoma and ocular hypertension.
While applicants do not wish to be bound by any theory, it is believed that BK causes an elevation in IOP by either inhibiting outflow of aqueous humor or increasing the production of aqueous humor. Thus, the administration of BK antagonists to the eye is thought to inhibit BK's receptor action and hence stabilize or lower IOP.
It has been shown that injection of BK in the eyes of animals (e.g., rabbits) causes pupil constriction and increases IOP (Cole and Ungar,
Ophthalmol Res.,
volume 6, pages 308-314 (1974)) by inhibiting the outflow of aqueous humor (Llobet,
Invest. Ophthalmol. Vis. Sci.
(suppl) volume 37, Abstract No. 953 (1996)). As stated above, increased IOP can lead to ocular hypertension, a major risk factor in the etiology of glaucoma.
The trabecular meshwork in the anterior chamber of the eye represents the primary locus for aqueous humor drainage, which apparently regulates IOP (“conventional outflow”). Defects(s) in this filtration system may underlie the etiology of open angle glaucoma. specifically by raising IOP. While the phagocytic action of trabecular meshwork cells appears important, the muscle-like tension in the trabecular meshwork may also contribute to the drainage of the aqueous humor to provide an homeostatic control of IOP. Recently, functional BK B
2
receptors have been discovered on the surfaces of human trabecular meshwork cells (Sharif and Xu,
Exp. Eye Res.,
volume 63, pages 631-637 (1996)). Thus, it is believed that BK may aberrantly contract the ciliary muscle and/or the trabecular meshwork, in addition to activating the ciliary epithelium, to produce its IOP-elevating effects.
The actions of BK on the ciliary epithelium to stimulate the production of aqueous humor (i.e., enhance inflow) may also result in IOP elevation. Therefore, the inventors believe that pharmacological agents which block the effects of BK in the anterior chamber will lower IOP and result in ocular hypotension, which in turn would reduce the risk for development of glaucoma.
Bradykinin receptors have been classif

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