Drug – bio-affecting and body treating compositions – Designated organic active ingredient containing – Peptide containing doai
Reexamination Certificate
1996-10-11
2002-01-08
Celsa, Bennett (Department: 1627)
Drug, bio-affecting and body treating compositions
Designated organic active ingredient containing
Peptide containing doai
C514S002600, C514S844000, C424S040000
Reexamination Certificate
active
06337320
ABSTRACT:
TECHNICAL FIELD OF THE INVENTION
The present invention deals with the combination of several anti-oxidants, including enzymatic co-factors and thiol compounds, and various tissue and cell growth stimulating factors in appropriate delivery vehicles employed in a topical carrier as a means of both minimizing and ameliorating and also concomitantly repairing free radical damage to the skin from ultraviolet radiation and also stimulating the growth, differentiation and maturation of epidermal cells resulting from environmental and metabolic factors.
BACKGROUND OF THE INVENTION
When cutaneous tissues are exposed to radiation such as solar ultraviolet rays (UVA and UVB radiation), damage to the skin ensues, particularly UVB which results in sunburn and tanning. Chronic UV ray exposure contributes to the skin aging process, the so-called photoaging process and in many cases to the development of cutaneous malignancies. Many common pathological factors exist as the various layers of skin are injured from local release of free radical species, emanating from cellular metabolism and enhanced by environmental UV radiation injury, while the skin is exposed to oxygen in the atmosphere as well as ozone, smog, smoke and other pollutants.
The skin repair processes are common to environmental and dermatologic conditions. Cutaneous tissues so exposed to injury, such as UV radiation with resulting “burns,” react so that water molecules contained within cells are altered as are lipids of membranes and of extracellular tissues resulting in the formation of a number of noxious free radicals. This phenomenon on the body has also been called oxidant stress and the free radicals are also known as reactive oxygen species. The latter two are known as the process of lipid peroxidation.
Ultraviolet radiation is responsible for the effects of sunburn and tanning of the skin. Moreover, both short and long wave length ultraviolet light contribute to the skin's photoaging and the development of the various types of skin cancer. Photoaging enhances the chronologic changes of skin, known as chronoaging. Ultraviolet B radiation exerts its most harmful effects when the sun is high on the horizon (high noon hours). In contrast, ultraviolet A radiation is more variable with time of day and time of the year making protection to UVA radiation a year round requirement. Sun care products should protect against both UVA and UVB radiation.
Ultraviolet radiation consists of short wave length, high energy UVB rays (290 NM to 320 NM) and longer wave length, lower energy UVA radiation (320 NM to 400 NM). The former is responsible for the range of sunburn damage from slight erythema to painful burns and blistering. These are acute phase effects. In contrast, UVA radiation penetrates the skin's deeper layers, epidermis and dermis, and is more responsible by its attack on collagen for the so-called premature aging of skin or photoaging. Both UVA and UVB by their creation of free radicals may act synergistically on the pathogenesis of skin cancers. In the laboratory, acute phototoxic reactions using the chemical psoralen and ultraviolet A rays have been used to study dermatologic pathologic responses and concomitant repair processes. Skin reactions, such as acute sunburn, includes redness (erythema) and swelling (edema), with resulting infiltration of the dermal layers by inflammatory cells (polymorphonuclear leukocytes, lymphocytes and macrophages) and pigmentation of the overlying skin by stimulation of melanocytes. Besides the aging process, the chronic UV radiation damage may lead to cutaneous malignancies, particularly squamous and basal cell carcinomas, and in many instances to malignant melanomas.
There is a worldwide epidemic of skin cancer. Announcements say “fry now, pay later.” In Australia, Sid Seagull, pictured on the beach, urges and reminds all to play it safe in the sun “Slop! Slip! Slap! Slop on the sunscreen, slip on the shirt and slap on the hat.” Although there are some variations among countries, the incidence for the three major skin cancers has risen steadily during this century. Most disturbing are the progressive high mortality rates for malignant melanomas. All three neoplasias are associated with ultraviolet radiation exposure, the culture of sun loving and a tanned skin, the diminishing ozone layer, and complicating environmental pollutants. Since World War II, in the USA and other countries, family incomes have risen with more leisure time available for outdoor activities with faster transportation to exotic tropical areas for more sun exposure. This is coupled with modern scant clothing styles for all ages and genders.
In basal cell carcinomas, epidemiologic studies suggest that exposure to the sun up to age 20 initiates a process of carcinogenesis which manifests itself as a neoplasia many years later, particularly as our generations live longer. Exposure to sunlight induces changes in the DNA of epidermal cells and suppresses the local immune system. Moreover, as we age our ability to repair DNA injury emanating from solar damage is markedly reduced. Basal cell carcinomas with an incidence rising from age 30 and a peak at age 70, develop typically in cutaneous exposed areas with strong evidence of chronic sun damage such as wrinkling, irregular pigmentation, collagenosis, telangiectasias and solar keratoses. Early clinical recognition of these lesions is imperative with subsequent complete surgical extirpation.
Squamous cell carcinoma is the second most common skin cancer with a greater morbidity (case fatality rate is 7 per 1000) due to its more aggressive features. This cancer is also on the rise with its true incidence difficult to calculate due to underreporting as lesions are often excised in doctor's offices. Higher case rates are recorded for Caucasians than for Hispanics, Japanese and African-Americans in various series published in the literature. Cutaneous lesions related to squamous cancers include intraepidermal or invasive keratinocyte dysplasias, including solar keratoses and Bowen's Disease. For squamous cell carcinoma a major constitutional risk factor is skin type, which is clinically graded by the reaction of unprotected skin to strong sunlight. The risk is highest for those individuals least able to tan; however, the incidence in Australia is 70 per 100,000 even in those who “just tan but don't burn.” Sunlight is the major environmental carcinogen for these neoplasias, particularly UVB with a wave length range of 290 to 320 NM. Although UVA may also play a role, cumulative UV dose is most important in the etiology of this cancer. Early diagnosis and prompt removal of squamous cell carcinoma is paramount. The Skin Cancer Foundation champions their excellent self examination brochure with “Skin Cancer: if you can spot it, you can stop it!”
Although the incidence of malignant melanoma is certainly lower than the two aforementioned carcinomas, the case fatality rate is much higher for melanoma. The mortality rate from the tumor is rising albeit novel therapeutic modalities. Anatomic distribution of melanomas among white populations is predominantly the trunk in males and the lower extremities in females. A strong hypothesis for etiology of melanoma states that intermittent and intense sun exposure of susceptible (untanned) subjects is more important than total lifetime solar exposure. Proximity of residence to the Equator is another risk factor. In addition, association of high sun exposure during childhood with melanoma is related to a higher appearance of numbers of common melanocytic nevi in the exposed skin. This lesion is regarded as both a marker with an elevated risk and a precursor of melanoma. Freckles in adolescents is another strong yet independent risk factor for melanoma. Intense and intermittent sun exposure leads to greater stimulation of the normal function of melanocytes resulting in their proliferation and an increase in cellular melanin production. This occurs because of an increased synthesis of melanocyte—stimulating
Hersh Theodore
Warshaw Michael A.
Celsa Bennett
Thione International, Inc.
Wittenberg Malcolm B.
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