CA2064509A1 - Treatment for acne - Google Patents
Treatment for acneInfo
- Publication number
- CA2064509A1 CA2064509A1 CA 2064509 CA2064509A CA2064509A1 CA 2064509 A1 CA2064509 A1 CA 2064509A1 CA 2064509 CA2064509 CA 2064509 CA 2064509 A CA2064509 A CA 2064509A CA 2064509 A1 CA2064509 A1 CA 2064509A1
- Authority
- CA
- Canada
- Prior art keywords
- glucose
- compound
- stilbesterol
- hydroxyphenyl
- sebum
- Prior art date
- Legal status (The legal status is an assumption and is not a legal conclusion. Google has not performed a legal analysis and makes no representation as to the accuracy of the status listed.)
- Abandoned
Links
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- Acyclic And Carbocyclic Compounds In Medicinal Compositions (AREA)
- Cosmetics (AREA)
Abstract
ABSTRACT OF THE DISCLOSURE
Acne is treated by administering to the subject a substance which is effective in blocking glucose entry into sebaceous cells, thereby inhibiting the production of sebum by these cells. Typically, the substance is administered topically and is dissolved or suspended in an appropriate solvent. The preferred substance is phloretin, which can for example, be dissolved in propylene glycol.
Acne is treated by administering to the subject a substance which is effective in blocking glucose entry into sebaceous cells, thereby inhibiting the production of sebum by these cells. Typically, the substance is administered topically and is dissolved or suspended in an appropriate solvent. The preferred substance is phloretin, which can for example, be dissolved in propylene glycol.
Description
BACKGROUND OF THE INVENTION
Acne is a skin disease with usual onset at adolescence. It is characterized by the overproduction of sebum. One principle in treating acne has been to reduce the secretion of sebum. At the time of puberty, the sebaceous glands responding to hormonal influences increase the production of sebvm e~cessively. Prior to the present invention, sebum secretion could only be suppressed by estrogen administration which is satisfactory for the treatment of females, but the side effects contraindicate the use of systemic estrogen in males. Labeled studies indicate that sebaceous cells form sebum from glucose.
Glycogen is first synthesized and is then converted to grease and extruded into the duct as sebum.
~ n understanding of the roll of glucose in the synthesis of sebum is important. Factors governing glucose entry into the sebaceous cell are similar to those found in other cells where insulin plays a prominent role. The utilization of glucose by the skin of diabetics is diminished, but is enhanced by insulin in both normals and diabetics. The pathways to the synthesis of fatty acid are enhanced by insulin. (Can.~.Biochem. 44:801 1966). The stimulating effect of insulin on acne vulgaris has been demonstrated, (Zeit of Haut & Geschects Krank. 41:429 1966) and this investigation proved that lipids were synthesized by the skin under the influence of insulin. Wheatly presented a simple method for testing the formation of lipids in thin tissue slices. His data indicated that C-14 labeled glucose was the best precursor for the synthesis of cutaneous lipids. (~.Clin. Invest. Derm. 54:288 1970). It has also been found that drugs that interfere with sterol synthesis do not influence sebum formation. (Brit, J. Derm.
81:280 1969).
The normal se~aceous gland contains immature cells at the periphery of the sebaceous acini. These cells contain large nuclei which are usually larger than the cytoplasm. As the peripheral cells mature, large quantities of glycogen accumulate in the cytoplasm. This accumulation of glycogen results from the entrance of glucose into the cell and its conversion to glycogen. This anabolism appears to be stimulated by androgens. As cells undergo sebaceous transformation glycogen decreases concomitantly with the increase of lipid globules. (J.Invest.Dermatol. 17:147 1951; Anat. Rec. 114:231 1952). The concentration of glycogen in the cell is inversely related to the lipid concentration since it is decreased by the conversion of glycogen to lipid. As the concentration of lipid increases, the entire cell becomes converted to a mass of lipid. The entire lipid rich cell is destroyed and extruded into the duct of the gland. New cells at the periphery grow and replace the extruded cell.
Phloridzin is a glucoside which is a natural plant hormone present in apple root bark (Merk Index 1983 10:7211) and the seeds of young apple fruit (Nature 158:663 1946).
r. 7 The aglucone portion of phloridzin is a phenolic compound called phloretin. (Merk Index 10:7210 1983). Phloretin is insoluble in water and soluble in acetone and alcohols and sparingly soluble in the fat solvents benzene and chloroform, but phlorizin is soluble in hot water and alcohol, but insoluble in chloroform and benzene. Both phloridzin and phloretin are known generally to prevent the entrance of glucose into cells by blocking the glucose transfer sites on the cell membrane (Physiol. Rev. 25:255 1945; Harvey Lect. 56:63 1961). These compounds therefore prevent glycogen formation in cells and lead to glycogen depletion. They are relatively non-toxic and have been systematically administered to humans and animals.
(Physiol~Rev. 7:385 1927) (Physiol.Rev. 25:255 1945;
Am.J.Physiol. 219:1080 1970). Animals and humans respond to systemic administration with glucosuria since these drugs prevent tubular reabsorbtion of glucose from the glomerular filtrate. tSmith, H.S. The Kidney, Oxfor Univ. Press 1951, p. 97). Althou~h phloridzin and phloretin have been extensively studied, they have remained medical curiosities with no previously known medicinal use.
SUMMARY OF TE~E INVENTION
The present invention relates to a method for treating acne by administering compositions such as phloridzin, phloretin, and stilbesterol compounds which inhibit the production of sebum by denying the sebaceous cells the necessary building blocks for the synthesis of sebum.
DETAILED DESCRIPTION OF THE INVENTION
In accordance with the present invention, acne vulgaris is treated by suppressing the production of sebum in sebaceous cells by topically administering medications which block the glucose receptor sites on the surface of sebaceous cells to thus prevent glucose entry into the cell thereby preventing synthesis of glycogen or sebum. Various compositions have been found to be effective for use in the treatment of acne according to this invention, however, the preferred compositions are phloretin and its lipid soluble analogs as well as stilbesterol compounds.
Although both phloridzin and phloretin inhibit glucose entry into the cell by blocking the receptor site for glucose transfer, phloretin is preferred since it is lipid soluble. The skin is a perfect lipid barrier and water soluble compounds do not penetrate to the depths of the skin surface and cannot reach the surfaces of the sebaceous cells if topically applied. Only non polar compounds penetrate the skin. Therefore, a non polar solution of topical phloretin does inhibit glucose entry in the cell when applied to the~ skin. Phloretin has a structural formula as indicated below.
~o ~
PuLoR~n~
O- ~3- D- ql~cPse Pl~Lo~2lDz~
LeFerve who studied ylucose transport in the red blood cell found that many other diphenolic compounds such as stilbesterol also inhibited sugar transport across the red cell membrane. He compared the various compounds to one another and rated phlorizin as having a potency of 1.9 while phloretin has a potency of 160 which was the same as stilbesterol. However, 3.3'- di(chlorallyl) stilbesterol had a potency of 1600 and 3-3' diallyl stilbesterol had a potency of 1000. (Phamacol. Rev. 13:39 1961) Phlorizin is more active than phloretin in blocking ~lucose transport by renal tubular epithelium and intestinal mucosa where glucose transport is dependent on sodium transport. (Biochemica et Biphysica ~cta 288:145 1972; Am. J. Physiol 203:975 1963) Other cells act like red blood cells where phloretin is more active.
Since phloritin and diallyl stilbesterol are relatively non polar compounds they are effective topically when dissolved in suitable skin penetrants. It can be diluted to a 0.5 to 2 percent by weight solution in a 6 '" . 'i J
solvent such as propylene glycol. A lesser concentration is required for the stilbesterol compounds. Upon inunction, they penetrate the skin and those glucose transfer sites on the surface of the skin are blocked. The sebaceous cells become impermeable to glucose for a prolonged period and sebum synthesis ceases. Since excessive sebum secretion is thought by some to be the cause of acne, and since the disease responds favorably to inhibition of sebum secretion with phloretin, the skin clears and sebum production drops to a minimum when the glucose blockers are rubbed into the skin.
Phloretin and diallyl stilbersterol are the preferred materials of the invention. Phloretin is the aglucone portion of phlorizin and is a polyphenolic compound. It is split from phlorizen by acid hydrolysis.
Alternatively, phloretin can be totally synthesized directly by known procedures. A number of different total synthesis have been described in the literature. Diallyl stillbesterol is similarly a poly phenolic compound as is phloretin.
Surface active compounds which may have additive advantages with respect to skin penetration can be synthesized and added to the lotion~
In addition to phloretin and its derivatives other compositions are also effective in preventing glucose entry into cells and can be used in accordance with the present invention.
. . .
Some of these compounds combine with enæymes involved in the transport process while other have a phloridzin-like action and occlude the receptor sites.
Cytochalsin B is a complex polyphenolic compound which adheres to the receptor site. A radioactive form of cytochalasin B has been used to determine the number of receptor sites for glucose transport on the cell surface.
Like phloridzin, it remains on the surface of the cell. It is very effective and the blockage of glucose entry is nearly complete.
Two Japanese chemists have found that some phenylglucosides inhibit uptake of d-glucose by monkey kidney cells. (J.Biochem 88:1399 1980). Lipid soluble derivatives o p-~sec-butyl)phenyl-6-chloro-6-deoxy-B-D-glucopyranoside could provide inexpensive substances could prevent glucose uptake by sebaceous cells.
Some non-metabolizable glucose analogues prevent glucose entry into the cell as well. They do this by competition for the receptor sites on the enzymes. While this attachment to the enzymes is usually temporary, in some cases it is irreversible. D-Xylose is an effective blocker of hexokinase and prevents glucose entry into the cell.
(Febs Letter 98:88 1979). Other modifications of glucose also render it non metabolizable and effectively compete with glucose for the receptor site on enzymes. 2-deoxy-d-glucose is such a compound which effectively inhibits hexokinase and prevents entry of gluco~e cells (Cancer Res.
8 ."~' "' ` i .J
18:518 1958). The problem with these substances is that they are too polar to pen~txate deeply into the skin.
Other analoyues oE glucose which act similarly are fluroglucose and ylucosamine. Fluroglucose (2-deoxy-2 fluro-D-glucose) and glucosamine both inhibit intracellular enzyme systems and interfere with glucose metabolism within the cell. (Eur. J. Biochem. 1~1:469 1982).
Other compounds unrelated to glucose also inhibit enzyme systems relating to glucose entry into the cell.
Oxamic acid, which is a relatively toxic substance, has been shown to inhibit glucose entry into the cell in vitro and suppresses glucose utilization and lactic acid formation.
It also prevents cellular multiplication as the result of non availability of glucose. (Jour. Biol. Chem. 236:278 1961). Esters of oxamic acid might be satisfactor~ for topical applicationO
Some diphenolic compounds have an even greater inhibitory ac-tion then phloretin at lower concentrations.
Of special interest in this respect are stilbesterol compounds which are diphenolic compounds. The most familiar of these compounds is diethyl stilbesterol with a structural formula as follows:
~ C2~ls~
Stilbesterol blocks glucose receptors in the cells as well as does phloretin. Dodds & Lawson ~Proc.Roy.Soc.ser.B 1938, 125:222) have described a number of diphenolics compounds which have estrogenic activity.
Many of these compounds have been tested by LeFerve for their ability to block glucose receptors. On a molecular basis 3,3'-Diallyl stilbesterol and 3,3' -Di ( ~chloroallyl) stilbesterol are the most potent.
These compounds have the added advantage that they are mildly estogenic which also favorably influences acne and makes them quite suitable for females.
The following example demonstrates the method of the present invention:
EXAMPLE
The sebum inhibitor phloretin is dissolved in aqueous propylene glycol solution (Propylene glycol 55%, ethanol la%, Polyethylene glycol ~200) 25%) so that the final concentration of phloretin is about 1 or 2%. Because pure propylene glycol is irritative to the skin its concentation is reduced by the addition of a liquid polyethylene glycol such as is manufactured by Union Carbide under the trade name carbowax 200. The skin is cleansed of oil with cotton soaked in 50-50 alcohol-acetone mixture. A
few drops of propylene glycol-phloretin mixture is put on the defatted skin and rubbed into the involved skin area with the fingers. Any excess fluid after a three to five minute rubbing is removed with a cellulose wipe. Phloretin can also be suspended in 50% ethanol containing a non ionic detergent, polyethylene glycol 48~ and 2% polyethylene oxide 1 0 i . ~ 5 ~
esters of fatty acids as emulsifying agents. The sebum inhibitor should be applied twice a day by inunction. A
reduction of sebum secretion is evident a few days after application of the medication.
The reduction in sebum secretion can easily be measured since 90-95% of skin lipids originate from the sebaceous glands. ~igarette paper is affixed to the forehead with adhesive tape. After 3-4 hours, the cigarette paper is removed and weighed. It is then extracted with acetone and reweighed. The loss of weight i5 the amount of sebum secreted. This test as done in 10 normal males showed a 90-94% reduction in sebum secretion.
While the general embodiments of the present invention have been described, it will be apparent to those of ordinary skill in the art that various alternative configurations and embodiments can readily be adapted to the present invention and are considered to fall within the scope thereof set forth in the following claims.
Acne is a skin disease with usual onset at adolescence. It is characterized by the overproduction of sebum. One principle in treating acne has been to reduce the secretion of sebum. At the time of puberty, the sebaceous glands responding to hormonal influences increase the production of sebvm e~cessively. Prior to the present invention, sebum secretion could only be suppressed by estrogen administration which is satisfactory for the treatment of females, but the side effects contraindicate the use of systemic estrogen in males. Labeled studies indicate that sebaceous cells form sebum from glucose.
Glycogen is first synthesized and is then converted to grease and extruded into the duct as sebum.
~ n understanding of the roll of glucose in the synthesis of sebum is important. Factors governing glucose entry into the sebaceous cell are similar to those found in other cells where insulin plays a prominent role. The utilization of glucose by the skin of diabetics is diminished, but is enhanced by insulin in both normals and diabetics. The pathways to the synthesis of fatty acid are enhanced by insulin. (Can.~.Biochem. 44:801 1966). The stimulating effect of insulin on acne vulgaris has been demonstrated, (Zeit of Haut & Geschects Krank. 41:429 1966) and this investigation proved that lipids were synthesized by the skin under the influence of insulin. Wheatly presented a simple method for testing the formation of lipids in thin tissue slices. His data indicated that C-14 labeled glucose was the best precursor for the synthesis of cutaneous lipids. (~.Clin. Invest. Derm. 54:288 1970). It has also been found that drugs that interfere with sterol synthesis do not influence sebum formation. (Brit, J. Derm.
81:280 1969).
The normal se~aceous gland contains immature cells at the periphery of the sebaceous acini. These cells contain large nuclei which are usually larger than the cytoplasm. As the peripheral cells mature, large quantities of glycogen accumulate in the cytoplasm. This accumulation of glycogen results from the entrance of glucose into the cell and its conversion to glycogen. This anabolism appears to be stimulated by androgens. As cells undergo sebaceous transformation glycogen decreases concomitantly with the increase of lipid globules. (J.Invest.Dermatol. 17:147 1951; Anat. Rec. 114:231 1952). The concentration of glycogen in the cell is inversely related to the lipid concentration since it is decreased by the conversion of glycogen to lipid. As the concentration of lipid increases, the entire cell becomes converted to a mass of lipid. The entire lipid rich cell is destroyed and extruded into the duct of the gland. New cells at the periphery grow and replace the extruded cell.
Phloridzin is a glucoside which is a natural plant hormone present in apple root bark (Merk Index 1983 10:7211) and the seeds of young apple fruit (Nature 158:663 1946).
r. 7 The aglucone portion of phloridzin is a phenolic compound called phloretin. (Merk Index 10:7210 1983). Phloretin is insoluble in water and soluble in acetone and alcohols and sparingly soluble in the fat solvents benzene and chloroform, but phlorizin is soluble in hot water and alcohol, but insoluble in chloroform and benzene. Both phloridzin and phloretin are known generally to prevent the entrance of glucose into cells by blocking the glucose transfer sites on the cell membrane (Physiol. Rev. 25:255 1945; Harvey Lect. 56:63 1961). These compounds therefore prevent glycogen formation in cells and lead to glycogen depletion. They are relatively non-toxic and have been systematically administered to humans and animals.
(Physiol~Rev. 7:385 1927) (Physiol.Rev. 25:255 1945;
Am.J.Physiol. 219:1080 1970). Animals and humans respond to systemic administration with glucosuria since these drugs prevent tubular reabsorbtion of glucose from the glomerular filtrate. tSmith, H.S. The Kidney, Oxfor Univ. Press 1951, p. 97). Althou~h phloridzin and phloretin have been extensively studied, they have remained medical curiosities with no previously known medicinal use.
SUMMARY OF TE~E INVENTION
The present invention relates to a method for treating acne by administering compositions such as phloridzin, phloretin, and stilbesterol compounds which inhibit the production of sebum by denying the sebaceous cells the necessary building blocks for the synthesis of sebum.
DETAILED DESCRIPTION OF THE INVENTION
In accordance with the present invention, acne vulgaris is treated by suppressing the production of sebum in sebaceous cells by topically administering medications which block the glucose receptor sites on the surface of sebaceous cells to thus prevent glucose entry into the cell thereby preventing synthesis of glycogen or sebum. Various compositions have been found to be effective for use in the treatment of acne according to this invention, however, the preferred compositions are phloretin and its lipid soluble analogs as well as stilbesterol compounds.
Although both phloridzin and phloretin inhibit glucose entry into the cell by blocking the receptor site for glucose transfer, phloretin is preferred since it is lipid soluble. The skin is a perfect lipid barrier and water soluble compounds do not penetrate to the depths of the skin surface and cannot reach the surfaces of the sebaceous cells if topically applied. Only non polar compounds penetrate the skin. Therefore, a non polar solution of topical phloretin does inhibit glucose entry in the cell when applied to the~ skin. Phloretin has a structural formula as indicated below.
~o ~
PuLoR~n~
O- ~3- D- ql~cPse Pl~Lo~2lDz~
LeFerve who studied ylucose transport in the red blood cell found that many other diphenolic compounds such as stilbesterol also inhibited sugar transport across the red cell membrane. He compared the various compounds to one another and rated phlorizin as having a potency of 1.9 while phloretin has a potency of 160 which was the same as stilbesterol. However, 3.3'- di(chlorallyl) stilbesterol had a potency of 1600 and 3-3' diallyl stilbesterol had a potency of 1000. (Phamacol. Rev. 13:39 1961) Phlorizin is more active than phloretin in blocking ~lucose transport by renal tubular epithelium and intestinal mucosa where glucose transport is dependent on sodium transport. (Biochemica et Biphysica ~cta 288:145 1972; Am. J. Physiol 203:975 1963) Other cells act like red blood cells where phloretin is more active.
Since phloritin and diallyl stilbesterol are relatively non polar compounds they are effective topically when dissolved in suitable skin penetrants. It can be diluted to a 0.5 to 2 percent by weight solution in a 6 '" . 'i J
solvent such as propylene glycol. A lesser concentration is required for the stilbesterol compounds. Upon inunction, they penetrate the skin and those glucose transfer sites on the surface of the skin are blocked. The sebaceous cells become impermeable to glucose for a prolonged period and sebum synthesis ceases. Since excessive sebum secretion is thought by some to be the cause of acne, and since the disease responds favorably to inhibition of sebum secretion with phloretin, the skin clears and sebum production drops to a minimum when the glucose blockers are rubbed into the skin.
Phloretin and diallyl stilbersterol are the preferred materials of the invention. Phloretin is the aglucone portion of phlorizin and is a polyphenolic compound. It is split from phlorizen by acid hydrolysis.
Alternatively, phloretin can be totally synthesized directly by known procedures. A number of different total synthesis have been described in the literature. Diallyl stillbesterol is similarly a poly phenolic compound as is phloretin.
Surface active compounds which may have additive advantages with respect to skin penetration can be synthesized and added to the lotion~
In addition to phloretin and its derivatives other compositions are also effective in preventing glucose entry into cells and can be used in accordance with the present invention.
. . .
Some of these compounds combine with enæymes involved in the transport process while other have a phloridzin-like action and occlude the receptor sites.
Cytochalsin B is a complex polyphenolic compound which adheres to the receptor site. A radioactive form of cytochalasin B has been used to determine the number of receptor sites for glucose transport on the cell surface.
Like phloridzin, it remains on the surface of the cell. It is very effective and the blockage of glucose entry is nearly complete.
Two Japanese chemists have found that some phenylglucosides inhibit uptake of d-glucose by monkey kidney cells. (J.Biochem 88:1399 1980). Lipid soluble derivatives o p-~sec-butyl)phenyl-6-chloro-6-deoxy-B-D-glucopyranoside could provide inexpensive substances could prevent glucose uptake by sebaceous cells.
Some non-metabolizable glucose analogues prevent glucose entry into the cell as well. They do this by competition for the receptor sites on the enzymes. While this attachment to the enzymes is usually temporary, in some cases it is irreversible. D-Xylose is an effective blocker of hexokinase and prevents glucose entry into the cell.
(Febs Letter 98:88 1979). Other modifications of glucose also render it non metabolizable and effectively compete with glucose for the receptor site on enzymes. 2-deoxy-d-glucose is such a compound which effectively inhibits hexokinase and prevents entry of gluco~e cells (Cancer Res.
8 ."~' "' ` i .J
18:518 1958). The problem with these substances is that they are too polar to pen~txate deeply into the skin.
Other analoyues oE glucose which act similarly are fluroglucose and ylucosamine. Fluroglucose (2-deoxy-2 fluro-D-glucose) and glucosamine both inhibit intracellular enzyme systems and interfere with glucose metabolism within the cell. (Eur. J. Biochem. 1~1:469 1982).
Other compounds unrelated to glucose also inhibit enzyme systems relating to glucose entry into the cell.
Oxamic acid, which is a relatively toxic substance, has been shown to inhibit glucose entry into the cell in vitro and suppresses glucose utilization and lactic acid formation.
It also prevents cellular multiplication as the result of non availability of glucose. (Jour. Biol. Chem. 236:278 1961). Esters of oxamic acid might be satisfactor~ for topical applicationO
Some diphenolic compounds have an even greater inhibitory ac-tion then phloretin at lower concentrations.
Of special interest in this respect are stilbesterol compounds which are diphenolic compounds. The most familiar of these compounds is diethyl stilbesterol with a structural formula as follows:
~ C2~ls~
Stilbesterol blocks glucose receptors in the cells as well as does phloretin. Dodds & Lawson ~Proc.Roy.Soc.ser.B 1938, 125:222) have described a number of diphenolics compounds which have estrogenic activity.
Many of these compounds have been tested by LeFerve for their ability to block glucose receptors. On a molecular basis 3,3'-Diallyl stilbesterol and 3,3' -Di ( ~chloroallyl) stilbesterol are the most potent.
These compounds have the added advantage that they are mildly estogenic which also favorably influences acne and makes them quite suitable for females.
The following example demonstrates the method of the present invention:
EXAMPLE
The sebum inhibitor phloretin is dissolved in aqueous propylene glycol solution (Propylene glycol 55%, ethanol la%, Polyethylene glycol ~200) 25%) so that the final concentration of phloretin is about 1 or 2%. Because pure propylene glycol is irritative to the skin its concentation is reduced by the addition of a liquid polyethylene glycol such as is manufactured by Union Carbide under the trade name carbowax 200. The skin is cleansed of oil with cotton soaked in 50-50 alcohol-acetone mixture. A
few drops of propylene glycol-phloretin mixture is put on the defatted skin and rubbed into the involved skin area with the fingers. Any excess fluid after a three to five minute rubbing is removed with a cellulose wipe. Phloretin can also be suspended in 50% ethanol containing a non ionic detergent, polyethylene glycol 48~ and 2% polyethylene oxide 1 0 i . ~ 5 ~
esters of fatty acids as emulsifying agents. The sebum inhibitor should be applied twice a day by inunction. A
reduction of sebum secretion is evident a few days after application of the medication.
The reduction in sebum secretion can easily be measured since 90-95% of skin lipids originate from the sebaceous glands. ~igarette paper is affixed to the forehead with adhesive tape. After 3-4 hours, the cigarette paper is removed and weighed. It is then extracted with acetone and reweighed. The loss of weight i5 the amount of sebum secreted. This test as done in 10 normal males showed a 90-94% reduction in sebum secretion.
While the general embodiments of the present invention have been described, it will be apparent to those of ordinary skill in the art that various alternative configurations and embodiments can readily be adapted to the present invention and are considered to fall within the scope thereof set forth in the following claims.
Claims (16)
- Claim 1. The use of a compound which prevents or inhibits the entrance of glucose into sebaceous cells for the manufacture of a medicament for the treatment of acne, seborrhea or oily skin.
- Claim 2 The use of a compound as claimed in Claim 1 selected from the group comprising: a polyphenolic compound; a phenyl glucoside; a non-metabolizable glucose analogue; an oxamic acid; a stevioside; an iso-steviol and a steviol.
- Claim 3. The use of a compound as claimed in Claim 2 in which the polyphenolic compound is selected from the group comprising: phloretin; phlorizin; cytochalasin B;
5,5Di(p-hydroxyphenyl)-nonane; 1,6Di(p-hydroxyphenyl)hexane;
3,3Di(p-hydroxyphenyl)hexane; 1,1--Di(parahydroxyphenyl) hexane; 2,2-Di(p-hydroxyphenyl) -4-methylpentane; 4,4,-Di(p-hydroxyphenyl)-heptane; 2,2-Di (p-hydroxyphenyl)-octane;
5,5-Di(p-hydroxyphenyl)-nonane; 3,3-Di (p-Hydroxy,m-allylphenyl)-4-hexanone; 3,3'-Diallyl stilbesterol; 3,3'-Di(2 methylallyl) stilbesterol; 3,3'-Di(chloroallyl) stilbesterol; 3,3' Diallyl hexesterol; 3,3'-Dipropyl hexesterol; 3,3'-Di(2-methylallyl) hexesterol; 3,3'-Di(2-chloroallyl) hexesterol; 3,3'-Diallyl dienestrol. - Claim 4. The use of a compound as claimed in Claim 2 in which the phenyl glucoside is p-z(sec butyl) pheny-6-chloro-6-deoxy-B-D-glucopyranoside.
- Claim 5. The use of a compound as claimed in Claim 2 in which the non-metabolizable glucose analogue is selected from the group comprising: glucosone; D-xylose; 2-deoxy-d-glucose; fluroglucose (2-deoxy-2-fluro-D-glucose);
and glucosamine. - Claim 6. The use of a compound as claimed in Claim 2 in which the compound is selected from the group comprising: stevioside; isosteviol; and steviol.
- Claim 7. A composition containing a compound as claimed in any of the previous claims in which said composition is in the form of a topical preparation.
- Claim 8. A composition as claimed in Claim 7 which composition comprises a pharmaceutically acceptable carrier.
- Claim 9. A composition as claimed in Claim 7 in which the compound is present in an effective amount.
- Claim 10. A cosmetic composition characterized in that it contains a compound which prevents or inhibits the entrance of glucose into sebaceous cells.
- Claim 11. A method of improving the appearance of a human comprising administering a compound which inhibits the entrance of glucose into sebaceous cells in an amount effective to achieve a cosmetically beneficial reduction in the production of sebum.
- Claim 12. A method of treating acne located on the sebaceous cells of skin of a human subject by administering topically to the skin a preparation containing
- 13 a substance selected from the group consisting of stevioside, isosteviol and steviol, which blocks glucose entry into said sebaceous cells thereby inhibiting production of same.
Claim 13. The method of Claim 12 wherein said preparation contains a carrier which is propylene glycol or glycerol. - Claim 14. A method for treating acne, seborrhea, and oily skin which comprises topically administering to a human subject in need of such treatment in an amount effective to prevent entry of glucose into sebaceous cells thereof and to inhibit production of sebum, a substance selected from the group consisting of 3,3'-Diallyl stilbesterol, 3,3'-Di(2-methylallyl) stilbesterol and 3,3'-Di(chloroallyl) stilbesterol.
- Claim 15. A method for treating acne, seborrhea, and oily skin which comprises topically administering to a human subject in need of such treatment, phloretin in an amount effective to prevent entry of glucose into sebaceous cells thereof and to inhibit production of sebum.
- Claim 16. A method for treating acne, seborrhea, and oily skin which comprises topically administering to a human subject an effective amount of a substance to prevent glucose entry into the subjects sebaceous cells, thereby inhibiting production of sebum.
Priority Applications (1)
| Application Number | Priority Date | Filing Date | Title |
|---|---|---|---|
| CA 2064509 CA2064509A1 (en) | 1992-04-02 | 1992-04-02 | Treatment for acne |
Applications Claiming Priority (1)
| Application Number | Priority Date | Filing Date | Title |
|---|---|---|---|
| CA 2064509 CA2064509A1 (en) | 1992-04-02 | 1992-04-02 | Treatment for acne |
Publications (1)
| Publication Number | Publication Date |
|---|---|
| CA2064509A1 true CA2064509A1 (en) | 1993-10-03 |
Family
ID=4149532
Family Applications (1)
| Application Number | Title | Priority Date | Filing Date |
|---|---|---|---|
| CA 2064509 Abandoned CA2064509A1 (en) | 1992-04-02 | 1992-04-02 | Treatment for acne |
Country Status (1)
| Country | Link |
|---|---|
| CA (1) | CA2064509A1 (en) |
Cited By (1)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| US7531578B2 (en) * | 2003-09-18 | 2009-05-12 | City Of Hope | Compounds and methods for treating breast cancer and other diseases |
-
1992
- 1992-04-02 CA CA 2064509 patent/CA2064509A1/en not_active Abandoned
Cited By (2)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| US7531578B2 (en) * | 2003-09-18 | 2009-05-12 | City Of Hope | Compounds and methods for treating breast cancer and other diseases |
| US8119695B2 (en) | 2003-09-18 | 2012-02-21 | City Of Hope | Compounds and methods for treating breast cancer and other diseases |
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