Composition for the treatment of hair loss

Drug – bio-affecting and body treating compositions – Designated organic active ingredient containing – Cyclopentanohydrophenanthrene ring system doai

Reexamination Certificate

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C514S171000, C514S180000, C514S559000

Reexamination Certificate

active

06344448

ABSTRACT:

BACKGROUND OF THE INVENTION
I. Field of the Invention
The present invention relates to a compound and method of treatment for hair loss, and more particularly, to a compound and method using a compound having all-trans-retinoic acid and betamethasone dipropionate.
II. Description of the Prior Art
Restoration of human hair has been attempted for centuries. In many cases, hair loss is merely covered by wigs or toupees. Many medical treatments have been attempted over the years; however, up until now, no treatment has been found which satisfactorily stimulates hair growth for a wide variety of cases, including alopecia.
Each hair extends from a tube-like depression called a hair follicle. The hair follicle extends from the surface of the skin into the dermis and may pass into the subcutaneous layer. At the base of the follicle is a group of epidermal cells which receive nourishment from blood vessels that occur in a projection of connective tissue at the base of the follicle.
As the epidermal cells divide and grow, older cells are pushed toward the surface. The cells that move upward and away from the nutrient supply become keratinized and die. Thus, hair is dead keratin, just like scale, and is formed at a predetermined rate.
The normal rate of growth of hair is 1 cm per month. Each hair follicle goes through a cycle of a growth stage (anagen hair), and an involution or resting stage (telogen hair). The anagen stage lasts about three years, while the telogen stage lasts only about three months. Once the hair follicle reaches the end of the telogen stage, the hair falls out. Eventually, the hair follicle produces a new growing hair.
The cycle of hair activity for hair follicles is independent for each hair follicle. However, when the hair follicles fail to regenerate hair, baldness results.
Many causes of hair loss are known. Exposure to chemotherapy, X-ray therapy, exposure to toxic chemicals, and topical chemicals on the scalp can cause anagen hair loss. Hormonal imbalances, stress, nutritional deficiency, and usage of many drugs can cause telogen effluvium. The cause of alopecia areata is unknown, and male/female androgenetic alopecia is caused by genetics. There are numerous other causes of hair loss, as well.
It is known that the hair follicle is an immune-privileged organ, and it has been postulated that hair growth may be regulated by the immune system (Frusgate et al.,
Journal of Investigative Dermatology,
97: 417-420, 1991). Thus, in order to restore hair, it is necessary to treat any underlying causes of the hair loss, such as disease, stress, hormonal imbalance, or nutritional deficiency. It is known, as disclosed by Olson (Alopecia Evaluation,
Primary Care
1989: 16 (3), p. 765-787), to treat hair loss by making an evaluation of the patient, including patient history, physical exam, and lab studies, treating any treatable underlying causes of hair loss, and treating alopecia with topical minoxidil and antiandrogens. However, treatment with minoxidil has many undesirable side effects and hair growth, if it occurs, takes place only as long as the minoxidil is being used. Thus, in order to restore hair growth, it is desirable to overcome the causes of alopecia and permit hair follicles to grow hair without continuous stimulation, such as by minoxidil.
It is known to use various commercial shampoo preparations to strengthen the hair. These shampoos typically include protein and affect only dead keratin, not the hair follicle, and therefore cannot prevent hair loss.
SUMMARY OF THE INVENTION
Applicant's method and compound for hair restoration produces hair growth in all cases of hair loss arising from all of the previously-recited causes for this condition. The rate of hair growth is greater than previously known methods and compounds. The method includes first identifying the causes of the patient's hair loss. The identification step includes a complete patient history to identify dietary problems, stress, genetic factors, and drug usage. Additionally, the patient is given a physical exam for identifying hormonal imbalances and disease. Then, an external examination of the scalp and condition of the hair is made.
After the identification step, a diagnosis is made. Following the diagnosis, an application of betamethasone dipropionate and all-trans-retinoic acid is made to the patient. The betamethasone dipropionate and all-trans-retinoic acid are administered together in a compound applied topically to the scalp. The compound and method have been found to effectively restore hair growth even after discontinuance of use of the compound.


REFERENCES:
patent: 3729568 (1973-04-01), Kligman
patent: 4889847 (1989-12-01), Kligman et al.
patent: 5019569 (1991-05-01), Kligman et al.
patent: 5026691 (1991-06-01), Kligman
patent: 35854/93 (1993-09-01), None
Topical Tretinoin For Hair Growth Promotion, Gail S. Bazzano, PhD, Nia Tereszkis, MD, & Wesley Galen, MD, Journal of the American Academy of Dermatology, No. 4, Part 2, Dec., 1986, pp. 880-883.
Topical All-Trans-Retinoic Acid Prevents Corticosteroid-Induced Skin Atrophy Without Abrogating The Anti-Inflammatory Effect, Robert H. Lesnik, MD, et al., Journal of the American Academy of Dermatology, vol. 21, No. 2, Part 1, Aug., 1989, pp. 186-190.
Immune Privilege in Hair Growth, Gillian E. Westgate, et al., The Journal of Investigative Dermatology, pp. 417-419, 1991.
NX3 Nutrient Booster Intensive Treatment for Thinning Hair, (Product Box & Flyer), Nioxin Research Laboratories, Inc., Atlanta, Georgia 1991.
Rogaine, Topical Solution, (Flyer), Upjohn Dermatology Division, The Upjohn Company, Kalamazoo, Michigan, May, 1993.
Human Anatomy and Physiology, John W. Hole, Jr., William C. Brown, Publishers, pp. 163-165, 904-906, 1992.
Pathophysiology, Clinical Concepts of Disease Processes, Third Edition Price & Wilson, McGraw-Hill Book Company, pp. 1006-1009, 1986.
Effect of Retinoids on Follicular Cells, Gail Bazzano, Nia Terezakis, Hala Attia, Alicia Bazzano, Robin Dover, David Fenton, Nikki Mandir, Leonardo Celleno, Maria Tamburro, Stefano Jaconi. The Journal of Investigative Dermatology, vol. 101, No. 1, Supplement, Jul. 1993, 138S-142S.
Changes in Populations of HLA−DR+CD3+Cells and CD57−CD16+ Cells in Alopecia Areata After Corticosteroid Therapy. R. Imai, K. Takamori, H. Ogawa, 1994, Dermatology 188(2): 103-7.
The Developing Organ of Corti Contains Retinoic Acid and Forms supenumerary Hair Cells in Response to Exogenous Retinoic Acid in Culture. Matthew W. Kelley, Xiao-Mei Xu, Michael A. Wagner, Mark E. Warchol, Jeffrey T. Corwin, 1993, Development 119: 1041-1053.
Retinoic Acid Stimulates Regeneration of Mammalian Auditory Hair Cells. Philippe P. Lefebvre, Brigitte Malgrange, Hinrich Staecker, Gustave Moonen, Thomas R. Van De Water, 1993, Science 260: 692-695.
The Cutaneous Safety of Topical Tretinoin. Christopher M. Papa, 1975, Acta Dermatovener 74 Suppl: 128-132.
Dermal Papilla Cells from Human Hiar Follicles Express mRNA for Retinoic Acid Receptors in Culture. Valerie A. Randall, M. Julie Thornton, Christopher P.F. Redfern, 1991, Ann NY Acade Sci. 642: 457.
Topical Retinoic Acid Does Not Alter the Vasconstrictive Properties of Topical Corticosteroids in Humans. C. Schmied, Saurat J.H., 1991, Dermatologica 182: 107-111.
Retinoic Acid and Mouse Skin Morphogenesis. I. Expression Pattern of Retinoic Acid Recepton Genes During Hair Vibrissa Follicle, Plantar, and Nasal Gland Development. Jean P. Viallet and Danielle Dhouailly, 1994, J. Invest Dermator. 103: 116-121.
Alopecia: Evaluation and Management. Elise A. Olsen, MD, Sep. 1989, Primary Care, vol. 16, No. 3, 765-787.
Immune Privilege in Hair Growth. Gillian E. Westgate, Robert I. Craggs and Walter T. Gibson, 1991, Journal Investigative Dermatology, 97:417-420.

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