# US 2014/0155322 A1 · Method of Preventing Or Reducing Scarring Of Human Skin

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- Number: US 2014/0155322 A1
- Document ID: US20140155322A1
- Status: Published application
- Kind: A1
- Application number: 14/025,809
- Filed: 2013-09-12
- Published: 2014-06-05
- Earliest claimed: 2000-11-29
- Assignees: Pharmecosse Ltd.
- Inventors: Claire Linge; Ian Paul Mackie
- Web page: https://patentgrep.com/patent/US20140155322A1

## CPC

- A61K 38/28: Insulins
- A61K 45/06: Mixtures of active ingredients without chemical characterisation, e.g. antiphlogistics and cardiaca
- A61P 17/02: for treating wounds, ulcers, burns, scars, keloids, or the like
- A61K: PREPARATIONS FOR MEDICAL, DENTAL OR TOILETRY PURPOSES (devices or methods specially adapted for bringing pharmaceutical products into particular physical or administering forms A61J3/00; chemical aspects of, or use of materials for deodorisation of air, for disinfection or sterilisation, or for bandages, dressings, absorbent pads or surgical articles A61L; soap compositions C11D)
- A61P: SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS

## 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.

## Claims

### Claim 1

A method of reducing dermal scarring in a skin wound of a human, which comprises administering to the skin wound, in a period consisting of up to about 2 days after the wound is formed and before a peak myofibroblast level is reached in the wound, an effective amount of an active agent selected from insulin and a specific peroxisome proliferator-activated receptor gamma (PPARγ) agonist.

### Claim 2 (depends on 1)

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.

### Claim 3 (depends on 1)

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.

### Claim 4 (depends on 1)

A method according to claim 1, wherein the scarring is selected from fibrotic dermal scarring, hypertrophic scarring, and keloid scarring.

### Claim 5 (depends on 1)

A method according to claim 1, wherein the active agent is administered as a topical composition or an injectable composition.

### Claim 6 (depends on 1)

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.

### Claim 7 (depends on 1)

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 (25 IU) per millilitre of the composition, and optional additional ingredients of the composition.

### Claim 8 (depends on 1)

A method according to claim 1, wherein the active agent is a specific PPARγ 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.

### Claim 9 (depends on 1)

A method according to claim 1, wherein the active agent is a specific PPARγ agonist selected from ciglitazone, troglitazone, pioglitazone, rosiglitazone, GW0207, GW1929, linoleic acid, linolenic acid, arachidonic acid, EPA, 9-HODE, 13-HODE, 15-HETE, 15-deoxy-Δ12, 14-prostaglandin J2, and any physiologically acceptable salt thereof.

### Claim 10 (depends on 1)

A method according to claim 1, wherein the active agent is a specific PPARγ agonist and is administered in a composition comprising a delivery vehicle, the specific PPARγ agonist in a concentration between 40 picomolar to 50 millimolar, and optional additional ingredients of the composition.

### Claim 11

A method of reducing dermal 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, in a period consisting of up to about 2 days after the wound is formed and before a peak myofibroblast level is reached in the wound, an effective amount of an active agent selected from insulin and a specific peroxisome proliferator-activated receptor gamma (PPARγ) agonist.

### Claim 12 (depends on 1)

A method according to claim 1, wherein the active agent comprises a specific PPARγ agonist.

### Claim 13 (depends on 12)

A method according to claim 12, wherein the active agent includes insulin.

### Claim 14 (depends on 13)

A method according to claim 13, wherein the active agent includes one or more other active agents known for wound care uses.

### Claim 15 (depends on 12)

A method according to claim 12, wherein the active agent includes one or more other active agents known for wound care uses.

### Claim 16 (depends on 1)

A method according to claim 1, wherein the active agent comprises insulin.

### Claim 17 (depends on 16)

A method according to claim 16, wherein the active agent includes one or more other active agents known for wound care uses.
