Abstract: The present invention relates to the use of a peptide, or derivative thereof of general formula X1—X2—X3-Thr-X4-Lys-X5-Arg-X6 for promoting accelerated wound healing with reduced scarring. X1 is Ala or Gly; X2 is Tyr or Phe; X3, X4 and X5 are independently selected from the group comprising Met, Ile, Leu and Val; and X6 is selected from the group comprising Asp, Gln and Glu.

Abstract: There is provided the use of mannose-6-phosphate, or a salt, precursor or analogue thereof, for providing and/or maintaining a consistent skin colour, particularly to reducing redness of skin. There is also provided the use of mannose-6-phosphate, or a salt, precursor or analogue thereof, as a skin improvement agent for providing a cosmetic effect and mannose-6-phosphate, or a salt, precursor or analogue thereof, for use in treating normal or damaged skin, wherein damaged skin is skin that has been subject to epidermal and/or dermal damage.

Abstract: Provided is WNT3A, or a therapeutically effective fragment or derivative thereof, for use as a medicament for the prevention, reduction or inhibition of scarring. Also provided is a method of preventing, reducing or inhibiting scarring, the method comprising administering a therapeutically effective amount of WNT3A, or a therapeutically effective fragment or derivative thereof, to a patient in need of such prevention, reduction or inhibition. The methods and medicaments of the invention are suitable for use in the prevention, reduction or inhibition of scarring arising as a result of healing of a wound, or scarring associated with a fibrotic disorder. The methods and medicaments disclosed are of particular use in preventing, reducing or inhibiting scarring of the skin.

Abstract: The invention provides new methods of treatment using TGF-?3 to inhibit scarring in humans, and TGF-?3 for new uses in the inhibition of scarring in humans. In a first incidence of treatment TGF-?3 is provided to each centimetre of a wound margin or each centimetre of a site at which a wound is to be formed in a first therapeutically effective amount; and in a subsequent incidence of treatment TGF-?3 is provided to each centimetre of wound margin in a larger therapeutically effective amount of TGF-?3. The incidences of treatment occur between 8 hours and 48 hours apart from one another. The TGF-?3 may be provided by intradermal injection. Also provided are kits and methods of selecting an appropriate treatment regime for inhibiting scarring associated with the healing of a human wound.

Abstract: The invention provides new methods of treatment using TGF-?3 to inhibit scarring in humans, and TGF-?3 for new uses in the inhibition of scarring in humans. In a first incidence of treatment each centimetre of wound margin, or each centimetre of a site at which a wound is to be formed, is provided with between approximately 350 ng and 1000 ng of TGF-?3; and in a second incidence of treatment, occurring after a wound is formed, and between 8 and 48 hours after the first incidence of treatment, the wound is provided with an amount of between approximately 350 ng and 1000 ng of TGF-?3 per centimetre of wound margin in which scarring is to be inhibited. The amount of TGF-?3 provided may be the same in each incidence of treatment. The amount of TGF-?3 provided per centimetre in each incidence of treatment may preferably be approximately 500 ng. The TGF-?3 may be provided by intradermal injection.

Abstract: The invention provides TGF-?3s, or fragments or derivatives thereof, wherein the alpha-helix-forming domain between amino acid residues (58) and (67) of full-length wild type TGF-?3 comprises at least one alpha-helix-stabilizing substitution. The invention also provides TGF-?3s, or fragments or derivatives thereof, wherein the Glycine residue at position (63) of full-length wild type TGF-?3 is replaced with Proline. Further still, the invention provides TGF-?3s, or fragments or derivatives thereof, comprising a substitution of the Glutamic acid residue at position (12) of full-length wild type TGF-?3 and/or the Arginine residue at position (52) of full-length wild type TGF-?3. The invention also provides medicaments and methods of treatment using such TGF-?3s.

Abstract: A method and apparatus for determining the efficacy of a medicament for the treatment of wounds or scars. The method comprises selecting first and second scarring site portions wherein said first scarring site portion has been treated with said medicament. A pair of images comprising a first image of said first scarring site portion and a second image of said second scarring site portion is generated, and the pair of images is displayed. A recording element comprising first and second recording portions is provided, wherein said first recording portion comprises a plurality of first points indicating that scarring in said first image is less severe than scarring in said second image, and said second recording portion comprises a plurality of second points indicating that scarring in said second image is less severe than scarring in said first image, each of said first and second points having different associated values.

Abstract: The invention provides TGF-?3s, or fragments or derivatives thereof, wherein the alpha-helix-forming domain between amino acid residues (58) and (67) of full-length wild type TGF-?3 comprises at least one alpha-helix-stabilising substitution. The invention also provides TGF-?3s, or fragments or derivatives thereof, wherein the Glycine residue at position (63) of full-length wild type TGF-?3 is replaced with Proline. Further still, the invention provides TGF-?3s, or fragments or derivatives thereof, comprising a substitution of the Glutamic acid residue at position (12) of full-length wild type TGF-?3 and/or the Arginine residue at position (52) of full-length wild type TGF-?3. The invention also provides medicaments and methods of treatment using such TGF-?3s.

Abstract: Provided is the use of an agonist of a GABAA receptor for use in the prevention, reduction or inhibition of scarring formed on healing of a wound. Also provided is a method of preventing, reducing or inhibiting scarring formed on healing of a wound, in which a therapeutically effective amount of an agonist of a GABAA receptor is administered to a patient in need of such prevention, reduction or inhibition. The GABAA receptor agonist used may be an agonist specific to the GABAA receptor, such as Gaboxadol (7-tetra hydroisoxazolo[5,4-c]pyridin-3-ol), or a pharmaceutically acceptable salt thereof. The scarring to be prevented, reduced or inhibited may be scarring formed on healing of a wound of the dermis.

Abstract: The present invention relates to use of convertase inhibitors for the reduction of scarring during the healing of wounds and also for reducing fibrosis in the treatment of fibrotic conditions.

Abstract: There is provided the use of monomeric TGF-?s, or there fragments or derivatives, as medicaments. These medicaments preferably comprise monomeric TGF-?3, or fragments or derivatives thereof. The medicaments provided may be used in the acceleration of wounding and/or the inhibition of scarring, in the promotion of epithelial regeneration, or in the prevention and/or treatment of fibrotic disorders.

Abstract: The present invention concerns a method for folding a Transforming Growth Factor Beta, or a functional analogue thereof, into a dimeric, biologically active form. The method involves adding solubilized, unfolded monomeric growth factor to a solution containing 2-(cyclohexylamino)-ethanesulfonic acid (CHES) or a functional analogue thereof and a low molecular weight sulfhydryl/disulfide redox system. The solution is then incubated under conditions suitable for generating dimeric biologically active Transforming Growth Factor Beta.

Abstract: The invention provides new methods of treatment using anti-scarring agents to inhibit scarring in humans, and also provides anti-scarring agents for new uses in the inhibition of scarring in humans. In a first incidence of treatment an anti-scarring agent is provided to each centimetre of a wound margin or each centimetre of a site at which a wound is to be formed in a first therapeutically effective amount; and in a subsequent incidence of treatment the anti-scarring agent is provided to each centimetre of wound margin in a larger therapeutically effective amount. The incidences of treatment occur between 8 hours and 48 hours apart from one another. The anti-scarring agent is preferably not TGF-?3. The anti-scarring agent may be provided by intradermal N injection. Also provided are kits and methods of selecting an appropriate treatment regime for inhibiting scarring associated with the healing of a human wound.

Abstract: Provided is the use of an agonist of a member of the nuclear hormone receptor NR4A subgroup in the manufacture of a medicament for the prevention, reduction or inhibition of scarring in a non-ocular tissue. Also provided is a method of preventing, reducing or inhibiting scarring in a non-ocular tissue, the method comprising administering a therapeutically effective amount of an agonist of a member of the nuclear hormone receptor NR4A subgroup to a patient in need of such prevention, reduction or inhibition. The NR4A agonist may be 6-mercaptopurine. The medicaments and methods may preferably be used to prevent, reduce or inhibit scarring in the skin. The medicaments and methods of the invention may be used to accelerate healing of wounds.

Abstract: Provided are methods, kits and arrays for use in determining susceptibility to keloid formation. These determine susceptibility based on comparison of gene expression in a patient of interest with expression in a control sample. If expression of at least one gene, selected from the group of genes set out in Table 1, is decreased in a sample representative of gene expression in the patient compared to expression of the same gene (or genes) in the control sample this is indicative of a susceptibility to keloid formation.

Abstract: A composition for use in the treatment of wounds to inhibit scar tissue formation during healing is disclosed, comprising an effective activity-inhibiting amount of a growth factor neutralising agent or agents specific against only fibrotic growth factors together with a pharmaceutically acceptable carrier. The method of preparation of said composition and method of administering the composition to a host suffering from tissue wounding is also disclosed.

Abstract: The present invention provides compositions and methods for promoting the healing of wounds or fibrotic disorders with reduced scarring, comprising inhibitors and inhibiting IFN-?, together with compositions and methods for promoting the healing of chronic wounds, comprising stimulating and stimulators of IFN-?.

Abstract: The present invention relates to use of convertase inhibitors for the reduction of scarring during the healing of wounds and also for reducing fibrosis in the treatment of fibrotic conditions.

Abstract: Provided are methods, kits and arrays for use in determining susceptibility to keloid formation. These determine susceptibility based on comparison of gene expression in a patient of interest with expression in a control sample. If expression of at least one gene, selected from the group of genes set out in Table 1, is increased in a sample representative of gene expression in the patient compared to expression of the same gene (or genes) in the control sample this is indicative of a susceptibility to keloid formation.

Abstract: Provided is a method for the expression of a TGF-? in a plant. A chimeric nucleic acid sequence comprising: (1) a first nucleic acid sequence capable of regulating the transcription in a plant cell of (2) a second nucleic acid sequence, encoding a TGF-?, and adapted for expression in the plant cell; and (3) a third nucleic acid sequence encoding a termination region functional in said plant cell is introduced into a plant cell and the plant cell grown to produce TGF-?. The nucleic acid sequence may preferably be adapted for expression in a plant chloroplast. It is preferred that the TGF-? is TGF-?3, whether full length or in the form of an active fragment.