Treatment of hyperproliferative skin disorders with C18 to...

Drug – bio-affecting and body treating compositions – Designated organic active ingredient containing – C-o-group doai

Reexamination Certificate

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C514S863000

Reexamination Certificate

active

06313179

ABSTRACT:

FIELD OF THE INVENTION
The present invention relates to the treatment of hyperproliferative disorders of the skin by topical administration of a composition comprising one or more C18 to C26 aliphatic alcohols.
BACKGROUND OF THE INVENTION
Benign hyperproliferative disorders of the skin result from excess keratin deposition (hyperkeratosis) of the corneous layer. Such hyperproliferative disorders include epidermolytic hyperkeratosis and follicular keratosis. One common benign hyperproliferative disorder is hypertrophic scar formation (a keloid), a sharply elevated, irregularly-shaped, progressively enlarging scar due to the formation of excessive amounts of collagen in the corium during connective tissue repair following surgical and traumatic lacerations. While such hypertrophic tissue repair is most evident at sites of external wound healing, keloid-prone individuals also manifest hypertrophic scarring internally. The major consequences of external keloid scarring are mainly cosmetic, although keloids can also result in varying degrees of psychological and social trauma for the afflicted individuals. In such cases, surgical or laser intervention is indicated because there is currently no generally effective topical or systemic treatment for this condition. Other hyperproliferative disorders are corns and calluses. Current non-surgical treatments for less acute cases of hyperkeratosis include 17% salicylic acid in collodion and 40% salicylic acid plasters. A keloid is usually treated by injection of a corticosteroid into the base of the lesion. This treatment may flatten the keloid, but is often ineffective.
Malignant hyperproliferative disorders of the skin include Kaposi's sarcoma (KS) and skin cancer. KS is a neoplasm, often associated with AIDS patients, characterized by vascular skin tumors. KS lesions originate from multifocal sites in the mid-dermis and extend to the epidermis. Histopathology shows spindle cells and vascular structures admixed to various degrees. Repeated biopsies show a progressive sarcomatous-like appearance. In more advanced stages, the lesions appear as multiple purplish to brown subcutaneous nodular or plaque-like dermal lesions, often with a varicose surface. The characteristic histological features of KS include the proliferation of spindle-shaped cells (KS cells, considered the tumor element) and of endothelial cells (CDC Task Force on KS and Opportunistic Infections,
New Engl. J. Med
., 306:248, 1982). There are two types of KS: indolent and lymphadenopathic. Indolent KS is characterized by nodular or plaque-like dermal lesions. Treatment options include freezing, electrocoagulation or electron beam radiotherapy. Unresponsive lesions are treated locally with 1,000-2,000 rads of x-ray therapy.
Aliphatic alcohols are known to have various biological activities. U.S. Pat. No. 3,031,376 discloses that n-tetracosanol (C24), n-hexacosanol (C26), n-octacosanol (C28) and triacontanol (C30) and their esters improved physical performance of athletes and disclosed compositions comprising such alcohols and esters for oral ingestion. U.S. Pat. No. 4,670,471 discloses the use of triacontanol for treatment of inflammatory disorders such as herpes simplex, eczema, shingles, atopic dermatitis and psoriasis. U.S. Pat. No. 3,592,930 discloses a medicant vehicle comprising 15 to 45 parts of saturated aliphatic alcohol having from 16 to 24 carbons as a carrier for antibiotics, steroids and antihistamines. U.S. Pat. No. 3,863,633 discloses a composition for topical treatment of the eye comprising 10-80% C12 to C22 surface active alcohols such as n-docosanol, n-hexadecanol, n-octadecanol and n-eicosanol. U.S. Pat. No. 4,874,794 discloses a method of treating virus-induced and inflammatory diseases of the skin and membranes with a composition comprising one or more of the aliphatic alcohols n-docosanol (C22), n-tetracosanol and n-hexacosanol. Antiviral and anti-inflammatory activities of aliphatic alcohols having from 20 to 32 carbons are disclosed in U.S. Pat. No. 4,874,794, U.S. Pat. No. 5,071,879, U.S. Pat. No. 5,166,219, U.S. Pat. No. 5,194,451 and U.S. Pat. No. 5,534,554. Related chemical compounds and compositions having therapeutic activities are disclosed therein.
A C22 aliphatic alcohol, n-docosanol, suspended in a surfactant exhibits potent antiviral activity against a variety of lipid enveloped viruses including herpes simplex virus and respiratory syncytial virus in cell culture assays (Katz, D. H., et al.,
Proc. Natl. Acad. Sci. USA
88:10825-10829, 1991; U.S. Pat. No.5,534,554, hereby incorporated by reference). Intracellular metabolic conversions of n-docosanol may account for its antiviral activity (Pope et al.,
J. Lipid Res
., 37:2167-2178, 1996). The alcohol is not cytotoxic in concentrations up to 300 mM.
There is a need for therapeutic agents which will inhibit hyperproliferative skin lesions. The present invention addresses this need.
SUMMARY OF THE INVENTION
One embodiment of the present invention is a method of treating or inhibiting the growth of a hyperproliferative skin lesion in an individual in need thereof, comprising topically administering to the lesion an effective proliferation-inhibiting amount of one or more C18 to C26 aliphatic alcohols in a pharmaceutically acceptable carrier. Preferably, the skin lesion is benign. Advantageously, the said skin lesion is hyperkeratosis or keloid. According to another aspect of this embodiment, the skin lesion is malignant. The skin lesion may be Kaposi's sarcoma or skin cancer. Preferably, the aliphatic alcohol is present in an amount from about 0.1% to 20% by weight; more preferably, the aliphatic alcohol is present in an amount from about 5% to 15% by weight. Advantageously, the aliphatic alcohol is n-docosanol, n-tetracosanol or n-hexacosanol; more advantageously, the aliphatic alcohol is n-docosanol.
DETAILED DESCRIPTION OF THE PREFERRED EMBODIMENTS
The present invention relates to the treatment or growth inhibition of hyperproliferative skin lesions by topical administration of one or more aliphatic straight-chain saturated monohydric alcohols which have from 18-26, preferably 22-26 carbons, in a topically acceptable carrier. Compositions of this invention suitable for use in treating or inhibiting the growth of hyperproliferative skin lesions comprise an active ingredient or combination of compounds as the active ingredient, selected from a group consisting of C18 to C26 saturated aliphatic alcohols and mono-unsaturated aliphatic alcohols. The C18 to C26 alcohols usefuil in the present invention include n-eicosanol (C20), n-docosanol (C22), n-tetracosanol (C24) and n-hexacosanol (C26). The use of C22 aliphatic alcohols is particularly preferred. The corresponding low molecular weight ether or ester derivatives of these alcohols (e.g., methyl-, ethyl, propyl-) are also contemplated for use in the present invention.
Methods of synthesis of n-docosanol are known to those skilled in the art (e.g., see U.S. Pat. No. 4,186,211). Methods of synthesis of aliphatic alcohols are well known in the art (e.g., see A. Streitwieser, Jr. & C. H. Heathcock,
Introduction to Organic Chemistry
, 2nd ed., Macmillan Publishing Co., New York, N.Y., 1981, at pages 160, 243-247, 303-307, 311-312, 315-317, 401-406, 447-453, 516, 550-555, 604-605 and 670).
n-Docosanol exhibits antiproliferative activity against cultured hypertrophic fibroblasts. This inhibitory activity is specific to hyperproliferative cell populations, as the growth of normal cells was unaffected under the tissue culture conditions used. Reduction of cell proliferation by n-docosanol is favored by low cell densities and longer incubation times and is concentration-dependent. Unexpectedly, n-docosanol significantly reduced hyperproliferative keloid formation in a patient for whom other treatments had not been successful.
The hyperproliferative skin lesions for treatment with the C18 to C26 aliphatic alcohols may be either benign or malignant. Benign lesions may arise from hyperkeratosis occurring, for example, in keloid, dermatitis papi

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