| Patent application number | Description | Published |
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| 20090105146 | PROTEINS, NUCLEIC ACIDS AND MEDICAMENTS - The invention provides TGF-β3s, or fragments or derivatives thereof, wherein the alpha-helix-forming domain between amino acid residues (58) and (67) of full-length wild type TGF-β3 comprises at least one alpha-helix-stabilising substitution. The invention also provides TGF-β3s, or fragments or derivatives thereof, wherein the Glycine residue at position (63) of full-length wild type TGF-β3 is replaced with Proline. Further still, the invention provides TGF-β3s, or fragments or derivatives thereof, comprising a substitution of the Glutamic acid residue at position (12) of full-length wild type TGF-β3 and/or the Arginine residue at position (52) of full-length wild type TGF-β3. The invention also provides medicaments and methods of treatment using such TGF-β3s. | 04-23-2009 |
| 20090137475 | MEDICAMENTS AND PROTEINS BASED ON TGF-BETA MONOMERS FOR THE TREATMENT OF WOUNDS - There is provided the use of monomeric TGF-βs, or there fragments or derivatives, as medicaments. These medicaments preferably comprise monomeric TGF-β3, 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. | 05-28-2009 |
| 20090181430 | PROTEIN FOLDING - 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. | 07-16-2009 |
| 20090280995 | METHOD OF DIAGNOSIS - Provided are methods, kits and arrays for use in determining whether a scar of interest is keloid or non-keloid in nature. These determine keloid or non-keloid nature based on comparison of gene expression in the scar 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 scar of interest compared to expression of the same gene (or genes) in the control sample this indicates that the scar of interest comprises a keloid. | 11-12-2009 |
| 20090305279 | METHOD OF DIAGNOSIS - Provided are methods, kits and arrays for use in determining whether a scar of interest is keloid or non-keloid in nature. These determine keloid or non-keloid nature based on comparison of gene expression in the scar 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 scar of interest compared to expression of the same gene (or genes) in the control sample this indicates that the scar of interest comprises a keloid. | 12-10-2009 |
| 20090328250 | EXPRESSION OF TGF-BETA IN PLASTIDS - Provided is a method for the expression of a TGF-β 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-β, 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-β. The nucleic acid sequence may preferably be adapted for expression in a plant chloroplast. It is preferred that the TGF-β is TGF-β3, whether full length or in the form of an active fragment. | 12-31-2009 |
| 20100004140 | METHOD OF PROGNOSIS - 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. | 01-07-2010 |
| 20100184610 | METHOD OF PROGNOSIS - 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. | 07-22-2010 |
| 20100266532 | METHODS FOR INHIBITING SCARRING - 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-β3. 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. | 10-21-2010 |
| 20110082171 | Medicaments and Methods for Inhibition of Scarring - Provided is the use of an agonist of a GABA | 04-07-2011 |
| 20110105396 | TGF-BETA3 MUTANTS - The invention provides TGF-β3s, or fragments or derivatives thereof, wherein the alpha-helix-forming domain between amino acid residues (58) and (67) of full-length wild type TGF-β3 comprises at least one alpha-helix-stabilising substitution. The invention also provides TGF-β3s, or fragments or derivatives thereof, wherein the Glycine residue at position (63) of full-length wild type TGF-β3 is replaced with Proline. Further still, the invention provides TGF-β3s, or fragments or derivatives thereof, comprising a substitution of the Glutamic acid residue at position (12) of full-length wild type TGF-β3 and/or the Arginine residue at position (52) of full-length wild type TGF-β3. The invention also provides medicaments and methods of treatment using such TGF-β3s. | 05-05-2011 |
| 20110109651 | METHODS AND SYSTEMS FOR DETERMINING EFFICACY OF MEDICAMENTS - 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. Data identifying one of said points is received and used to determine the efficacy of said medicament. | 05-12-2011 |
| 20110152189 | METHODS FOR THE INHIBITION OF SCARRING - The invention provides new methods of treatment using TGF-β3 to inhibit scarring in humans, and TGF-β3 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-β3; 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-β3 per centimetre of wound margin in which scarring is to be inhibited. The amount of TGF-β3 provided may be the same in each incidence of treatment. The amount of TGF-β3 provided per centimetre in each incidence of treatment may preferably be approximately 500 ng. The TGF-β3 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. | 06-23-2011 |
| 20110166067 | METHODS FOR INHIBITION OF SCARRING - The invention provides new methods of treatment using TGF-β3 to inhibit scarring in humans, and TGF-β3 for new uses in the inhibition of scarring in humans. In a first incidence of treatment TGF-β3 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-β3 is provided to each centimetre of wound margin in a larger therapeutically effective amount of TGF-β3. The incidences of treatment occur between 8 hours and 48 hours apart from one another. The TGF-β3 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. | 07-07-2011 |
