Method of preventing or reducing scarring of human skin

Abstract

Insulin or a peroxisome proliferator-activated receptor (PPAR) agonist provides reliable and effective prevention of scarring in human skin, or at least a reduction in the severity of scarring. The application of insulin or the PPAR agonist to wounds topically or by local injection is particularly advantageous since it simultaneously reduces/prevents scarring whilst enhancing re-epithelialisation of the wound and thus provides a dual action wound healing treatment. The present invention accordingly provides a highly effective prophylactic treatment for any individual suffering tissue trauma to reduce and/or prevent normal and/or pathological scarring.

1 . A method of reducing or preventing scarring in the skin of a human, which comprises administering to the skin an effective amount of an active agent selected from insulin and a peroxisome proliferator-activated receptor (PPAR) agonist.  
     
     
         2 . A method according to  claim 1 , wherein the active agent is administered in a medicament for a dual action wound treatment comprising reducing or preventing scarring whilst accelerating or promoting wound healing.  
     
     
         3 . A method according to  claim 1 , wherein the scarring is selected from scarring of human skin wounded as a result of burns, scalds, grazes, abrasions, incisional wounds, surgery and pathological skin scarring conditions.  
     
     
         4 . A method according to  claim 1 , wherein the scarring is selected from fibrotic dermal scarring, hypertrophic scarring, keloid scarring and ocular tissue scarring.  
     
     
         5 . A method according to  claim 1 , wherein the ocular tissue scarring is corneal scarring.  
     
     
         6 . A method according to  claim 1 , wherein the active agent is administered as a topical composition or an injectable composition.  
     
     
         7 . A method according to  claim 1 , wherein the active agent is administered to a skin wound or its vicinity, after the wound has been formed.  
     
     
         8 . A method according to  claim 7 , wherein the active agent is administered up to about 5 days after the wound has been formed.  
     
     
         9 . A method according to  claim 1 , wherein the active agent is insulin and is administered in a composition comprising a delivery vehicle, insulin in an amount from 50 picograms (1.25×10 −6 IU) to 1000 micrograms (25IU) per millilitre of the composition, and optional additional ingredients of the composition.  
     
     
         10 . A method according to  claim 1 , wherein the active agent is a PPAR agonist selected from: glitazones (thiazolidinediones), isoxazolidinediones, α-alkoxy-β-phenylpropanoic acids, fibrates, ureidofibrates, tyrosine-based PPARγ agonists, 2,3-disubstituted indole-5-acetic acid derivatives, phenylacetic acid derivatives, leukotriene antagonists, polyunsaturated fatty acids, eicosanoids, and derivatives and metabolites of prostaglandins.  
     
     
         11 . A method according to  claim 1 , wherein the active agent is a PPAR agonist selected from ciglitazone, troglitazone, pioglitazone, rosiglitazone, GW0207, GW1929, KRP-297, JTT-501, SB213068, GI262570, GW7845, L-796449, L-165041, bezafibrate, Wy-14643, clofibrate and its active metabolites, fenofibrate and its active metabolites, GW2433, linoleic acid, linolenic acid, arachidonic acid, EPA, 9-HODE, 13-HODE, 15-HETE, 15-deoxy-Δ 12,14 -prostaglandin J 2 , and any physiologically acceptable salt thereof.  
     
     
         12 . A method according to  claim 1 , wherein the active agent is a PPAR agonist and is administered in a composition comprising a delivery vehicle, the PPAR agonist in a concentration between 40 picomolar to 50 millimolar, and optional additional ingredients of the composition.  
     
     
         13 . A method of reducing or preventing scarring in the healed skin of a human after formation of a wound while maintaining a breaking strength of the healed skin substantially corresponding to that of healed skin which includes natural levels of scar tissue, which method comprises administering to the skin an effective amount of an active agent selected from insulin and a peroxisome proliferator-activated receptor (PPAR) agonist.