Devices and compounds for treating arterial restenosis

Drug – bio-affecting and body treating compositions – Preparations characterized by special physical form – Implant or insert

Reexamination Certificate

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C424S423000, C424S424000, C424S425000

Reexamination Certificate

active

06544541

ABSTRACT:

FIELD OF THE INVENTION
The present invention relates generally to the field of chemical compounds for medical treatments. More specifically, the present invention relates to compounds and devices for treating diseases or disorders associated with tissue damage due to environmental, interventional or autogenous injury.
BACKGROUND OF THE INVENTION
Diseases and disorders induced by tissue damage are a growing concern in the healthcare industry. Typically, these diseases are characterized by prolonged or unwanted response to injury, including inflammation of a tissue portion, secretion of degrading enzymes and/or compounds resulting in tissue destruction within the region and attempted tissue repair. Examples of such conditions include proliferative and/or inflammatory disorders, for example, restenosis, psoriasis, graft rejection, arthritis and multiple sclerosis.
Psoriasis is an inflammatory skin disease characterized by raised scaly lesions. Specifically, skin cells are pushed to the skin surface more quickly than the skin surface can shed dead skin cells. The end result is the formation of scaly lesions which are invaded by macrophage, lymphocytes and neutrophils, creating inflammation and soreness of the tissue region. In addition, these cells may produce growth factors which may in fact cause skin cells to be produced even more rapidly, thereby worsening the condition. While the exact cause is unknown, psoriasis is hypothesized to be an autoimmune disorder.
Multiple sclerosis is an inflammatory disease that affects the nervous system of an individual. Typically, the disease causes demyelination in the brain which in turn leads to a progressive loss of motor functions. While the cellular mechanism triggering destruction of the myelin is not understood, it is known that there is a localized increase in astrocyte proliferation and protease activity in afflicted regions. As with psoriasis, the exact cause of multiple sclerosis is unknown although it is also hypothesized to be an autoimmune disorder.
Inflammatory bowel disease includes a number of specific diseases which cause intestinal inflammation or ulceration. For example, in ulcerative colitis, an inflammatory reaction involving the colonic mucosa leads to ulcerations. Furthermore, repeated inflammatory responses lead to fibrosis and a subsequent shortening of the colon. Similarly, Crohn's disease is characterized by chronic inflammation of all layers of the intestinal wall.
Polycystic kidney disease is characterized by the formation of multiple cysts throughout the kidneys which progressively cause compression and destruction of kidney parenchyma. The disease appears to be caused by proliferation of epithelial cells in tubule segments within the kidneys, which in turn lead to fluid accumulation and enlargement of the kidneys.
Rheumatoid arthritis is a chronic inflammatory disease which causes pain, swelling and destruction of joints and can also lead to organ damage. Specifically, the disease is characterized by infiltration of the synovial membrane with white blood cells and a thickening of the synovial membrane. There is subsequent tissue growth within the joints as well as the release of degrading enzymes and compounds associated with the inflammatory response which leads to progressive destruction of the cartilage tissue. It is of note that rheumatoid arthritis is also hypothesized to be an autoimmune disorder.
Asthma is characterized by recurring airway obstruction caused by inflammatory cell infiltration, smooth muscle cell proliferation and hypertrophy in the airway and mucus secretion into the airway lumen.
Graft rejection occurs when the grafted tissue is recognized as foreign by the host's immune system. This rejection leads to inflammation and arteriosclerosis in the graft tissue and surrounding area.
Hypertrophic disease involves cell growth in the absence of increased cell number. This definition applies to a number of conditions associated with trauma, including hypertrophic gastropathy, hypertrophic burn scars, keloids, or post-operative hypertrophy affecting numerous tissues. For example, hypertension is an increase in smooth muscle cell volume within a blood vessel due to excessive pressure, lack of oxygen
utrients or enhanced production of hypertrophy-inducing factors released as a result of trauma distinct from the site of action (for example, kidney disease). Also, hypertrophic cardiac disease (for example, congestive heart failure, hypertrophic cardiomyopathy, valve replacement surgery) results from an increase in cardiomyocyte volume as a result of hypoxia, surgical intervention or genetic defect. Cellular hypertrophy and inflammation occur in the region affected by the causative factor.
Cutaneous fibrosis is an integral component of a variety of human disorders including keloids, hypertrophic scars, and most notably, scleroderma. Each has its own etiology and unique clinical characteristics, but all involve the disregulation of connective tissue metabolism, in particular, the activation of dermal fibroblasts. Atrophic scars also occur secondary to surgery, trauma, and common conditions such as acne vulgaris and varicella. Hypertrophic scars and keloids occur as the result of an exaggerated wound healing response of the skin following injury. Keloids and hypertrophic scars are benign fibrous growths that occur after trauma or wounding of the skin which are frequently pruritic, painful and occasionally form strictures. Keloid and hypertrophic scarring develops as a result of a proliferation of dermal tissue following skin injury. These proliferative scars are characterized by increased collagen and glycosaminoglycan content, as well as increased collagen turnover. Excision only of hypertrophic scars and keloids results in 45-100% recurrence. The current objective is to decrease scar height and reduce the number of post-operative recurrences.
Vascular lesions that develop in autologous saphenous vein grafts (SVG) after transplantation into the aorto-coronary circulation or the peripheral vascular circulation share elements of smooth muscle migration, proliferation,and fibrous tissue deposition in common with nibrointimal proliferation, post-operative recurrences of the fibrovascular proliferations of pterygia and keloids.
Restenosis is caused by vascular stress or injury and leads to vessel wall thickening and loss of blood flow. These stresses may be, for example, mechanical, hypoxia, injury, shear-stress, pharmacological, infectious, inflammatory, oxidative, immunogenic, diabetic or pressure. The normal arterial vessel wall consists of a regular arrangement of endothelial, smooth muscle and fibroblast cells, present in three distinct layers of endothelium, media and adventitia. A single layer of endothelial cells forms the luminal barrier to blood-borne signals that modulate vascular function. The adventitia, which forms the outer layer around the artery, consists primarily of extracellular matrix as well as some fibroblasts, nerve fibres and microvessels. The media consists of numerous layers of smooth muscle cells (SMCs) intermixed with extracellular matrix that is bound by the internal and external elastic lamina.
The response to injury or other stress stimuli varies between the different cellular components of the vessel. Endothelial cells are capable of proliferation and migration, properties that permit re-endothelialization of the vessel after denudation or injury (Reidy, 1985,
Lab Invest
53: 513-520). Medial SMCs are also able to reversibly modulate their phenotype which allows for their proliferation and/or migration into the intima at the site of injury (Schwartz et al, 1995,
Circ Res
77: 445-465). It is these characteristics that lead to the adaptive and pathogenic growth of SMCs which is key to vascular remodelling and lesion formation.
This is of particular concern for the treatment of coronary disease, wherein a common treatment for constricted, clogged or narrowed coronary arteries is balloon angioplasty. Angioplasty involves the use of a balloon-tipped catheter which is

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