HAROLD BREM, M.D.
Radiology at Johnson Ave, Bronx, NY

2008023, Sep 25, 2008

Mar 20, 2008

12/052672

Harold Brem - Bronx NY, US
Marjana Tomic - Hillsdale NJ, US

A61K 38/18, A61P 17/02

514 12

It has been discovered that vascular endothelial growth factor (“VEGF”) promotes migration of activated (but not differentiating) keratinocytes to skin. This growth factor specifically increases migration of keratinocytes of the “wounded skin” phenotype but does not have significant effects upon differentiated keratinocytes. It also increases collagen deposition and reduces wrinkles, enhances skin quality, and increases skin thickness to normal levels in individuals where skin has thinned due to age or disorder such as diabetes. It is particularly well suited for use as cosmeceuticals when applied in purified form and in known amounts. The data presented in the examples demonstrate efficacy and specificity of VEGF in enhancing migration of normal human keratinocytes as well as formation of new granulation tissue including collagen formation. VEGF induces keratinocyte and fibroblast migration, formation of new tissue, and not only induces deposition of collagen but improves alignment of the collagen fibers. Accordingly, this growth factor is highly suitable for use as a cosmeceutical, especially for skin resurfacing and reduction in wrinkles.

2009019, Jul 30, 2009

Mar 20, 2008

12/052670

Harold Brem - Bronx NY, US
Marjana Tomic - Hillsdale NJ, US

A61K 35/76, A61K 38/18, A61K 31/7088, A61P 17/00

424 932, 514 12, 514 44

It has been discovered that granulocyte macrophage colony stimulating factor (“GM-CSF”) promotes migration of activated (but not differentiating) keratinocytes to wound sites. It was also discovered that GM-CSF increases the quantity and improves the quality of collagen. This growth factor specifically increases migration of keratinocytes of the “wound” phenotype but does not have significant effects upon differentiated keratinocytes. Examples demonstrate reversal of skin impairment in multiple animal models of diabetic skin imparment when provided in an effective amount over an effective time period. The examples also demonstrate the efficacy of the formulations in cosmetic applications. A preferred formulation is a sustained release formulation that delivers sufficient growth factor to the skin and the underlying tissue thereof to increase the rate of keratinocyte migration, as well as collagen deposition and fibroblast proliferation, in the skin to promote rejuvenation of skin injuries resistant to repair due to underlying disease, such as diabetes, or aging.

2010031, Dec 9, 2010

Aug 18, 2010

12/858828

Harold Brem - Bronx NY, US
Marjana Tomic-Canic - Hillsdale NJ, US

A61K 8/99, A61K 8/64, A61K 8/73, A61Q 19/08

424 932, 514 81, 514 44 R

It has been discovered that vascular endothelial growth factor (“VEGF”) promotes migration of activated (but not differentiating) keratinocytes to skin. This growth factor specifically increases migration of keratinocytes of the “wounded skin” phenotype but does not have significant effects upon differentiated keratinocytes. It also increases collagen deposition and reduces wrinkles, enhances skin quality, and increases skin thickness to normal levels in individuals where skin has thinned due to age or disorder such as diabetes. It is particularly well suited for use as cosmeceuticals when applied in purified form and in known amounts. The data presented in the examples demonstrate efficacy and specificity of VEGF in enhancing migration of normal human keratinocytes as well as formation of new granulation tissue including collagen formation. VEGF induces keratinocyte and fibroblast migration, formation of new tissue, and not only induces deposition of collagen but improves alignment of the collagen fibers. Accordingly, this growth factor is highly suitable for use as a cosmeceutical, especially for skin resurfacing and reduction in wrinkles.

7919478, Apr 5, 2011

Jan 22, 2008

12/017688

Harold Brem - Bronx NY, US

New York University - New York NY

A61K 48/00, A01N 63/00, C07H 21/04

514 44R, 424 932, 536 235

A method and means have been developed to deliver a therapeutic dose or dosages of the angiogenic molecule, Vascular Endothelial Growth Factor (VEGF) that results in a statically significant decrease in the time to achieve 100% wound closure and accelerates the rate of healing in experimental diabetic ulcers. Toxicity is evaluated by measuring any local inflammatory response at the wound site, the systemic absorption of VEGF, and the effect on distant organs that may be particularly susceptible to VEGF therapy (e. g. , retinopathy and hepatitis) The angiogenic response is quantified by measuring the change in collagen deposition, epithelialization, and the closure rates of diabetic ulcers after therapeutic dosing with ADV-VEGF. Sustained administration of VEGF, stimulates and accelerates the healing process as evidenced by a reduced time to complete healing (defined by 100% epithelialization and no drainage) in experimental diabetic ulcers, with minimal to no toxicity. Important features of the method and reagents for use therein are that the VEGF is released into the ulcer in a sufficient quantity over a period of time for at least two to six weeks, or to closure of the wound.

2006011, Jun 1, 2006

Sep 30, 2005

11/241800

Harold Brem - Bronx NY, US

G06Q 10/00

705002000

Methods and apparatus for storing and reviewing wound data are shown using a digital datasheet, or wound electronic medical record (WEMR). The WEMR is preferably presented via a single page containing all data that should be considered by a wound healing provider, as predetermined by protocol. This includes, but is not limited to, fields for: a digital photograph of the wound; a graph of the wound healing rate (length, width, depth and area over time); wound and other treatments including current systemic medications, along with a patient identifier and review/approval indicator. This may also include hematology and chemistry laboratory data; radiology and pathology images along with their associated reports; ambulation status and other history; and microbiology data including sensitivities. The WEMR is implemented via a wound database system, which includes templates and policies for rapid report generation and tools for protocol mapping. A particular WEMR page may be designed for electronic or paper review and approval by a treating physician, thus permitting comprehensive but efficient review of all relevant wound data, whether for a personal or remote consult, real-time or otherwise. When teaching or doing studies, patient identifier information can be masked while still enabling review of large but detailed data sets for a variety of wound and patient criteria.

2008027, Nov 6, 2008

Mar 12, 2008

12/075672

Marjana Tomic-Canic - Hillsdale NJ, US
Harold Brem - Bronx NY, US

New York Society for the Ruptured and Crippled Maintaining the Hospital for Special Surgery - New York NY

A61K 38/20, A61K 31/56, A61K 33/06, A61P 17/02, A61K 31/444, A61K 38/16

424 852, 514178, 424678, 514332, 514 12

The present invention relates to methods and compositions that control, i.e., antagonize/inhibit or agonize/stimulate, de novo glucocorticoid production in the skin. Such methods and compositions can be used for the prevention and/or treatment of a variety of skin conditions, including inflammation, acute wounds, chronic non-healing wounds, keloid, fibrotic or hypertrophic scars, and epithelial-derived cancer.

2009020, Aug 13, 2009

May 1, 2007

12/298118

Harold Brem - Bronx NY, US
Marjana Tomic-Canic - Hillsdale NJ, US

New York Society for the Ruptured and Crippled Maintaining the Hospital for Special Surgery - New York NY

C12Q 1/68, C40B 40/08

435 6, 506 17

The present invention relates to methods for identifying tissue sites in a chronic wound that are suitable for debridement and whether debridement procedure has been successful using particular biological markers of the cells within the tissue sites of the chronic wounds.

2011019, Aug 4, 2011

Aug 9, 2010

12/853065

Marjana Tomic-Canic - Hillsdale NJ, US
Harold Brem - Bronx NY, US

NEW YORK UNIVERSITY - NEW YORK NY

A61K 31/7052, A61P 29/00

514 44 A

Compositions and methods for antagonizing miRNAs that are overexpressed in chronic, non-healing wounds, as compared to healthy tissue, are disclosed. The miRNA antagonists are oligonucleotides that hybridize to selected pre-miRNA or mature miRNAs and prevent the miRNAs from binding to and downregulating their target mRNAs. Methods of using the miRNA antagonists to treat inflammatory disorders, including to promote healing of chronic, non-healing wounds and acute wounds are provided.

2012028, Nov 15, 2012

Dec 29, 2010

13/519551

Marjana Tomic-Canic - Miami FL, US
Harold Brem - Bronx NY, US

New York University - New York NY

A61K 38/02, A61K 31/265, A61K 31/407, A61K 31/58, A61K 31/352, A61P 27/02, A61K 31/567, A61K 31/69, A61K 31/5365, A61K 31/24, A61P 1/02, A61P 17/02, A61K 38/12

514 75, 514 186, 514510, 514410, 514176, 514456, 514179, 514 64, 5142295, 514534, 514 11, 514 208

Compositions for antagonizing phosphorylation and subsequent degradation of glycogen synthase kinase 3 beta (GSK3β) in epidermal cells are disclosed. GSK3β phosphorylation antagonists include molecules that function to inhibit or reduce the binding activity or enzymatic activity of an upstream signaling molecule leading to GSK3β phosphorylation, or by downregulating the expression of one or more upstream signaling molecules involved in regulating GSK3β phosphorylation. Methods of using the GSK3β phosphorylation antagonists to inhibit or reduce the phosphorylation and degradation of GSK3β in epidermal cells are provided. The methods are useful to promote epithelialization and closure of wounds, such as chronic non-healing wounds.