Patents by Inventor Harold Brem
Harold Brem has filed for patents to protect the following inventions. This listing includes patent applications that are pending as well as patents that have already been granted by the United States Patent and Trademark Office (USPTO).
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Patent number: 9168214Abstract: 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.Type: GrantFiled: August 18, 2010Date of Patent: October 27, 2015Assignee: New York UniversityInventors: Harold Brem, Marjana Tomic-Canic
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Patent number: 8889615Abstract: Compositions for antagonizing phosphorylation and subsequent degradation of glycogen synthase kinase 3 beta (GSK3?) in epidermal cells are disclosed. GSK3? phosphorylation antagonists include molecules that function to inhibit or reduce the binding activity or enzymatic activity of an upstream signaling molecule leading to GSK3? phosphorylation, or by downregulating the expression of one or more upstream signaling molecules involved in regulating GSK3? phosphorylation. Methods of using the GSK3? phosphorylation antagonists to inhibit or reduce the phosphorylation and degradation of GSK3? in epidermal cells are provided. The methods are useful to promote epithelialization and closure of wounds, such as chronic non-healing wounds.Type: GrantFiled: December 29, 2010Date of Patent: November 18, 2014Assignee: New York UniversityInventors: Marjana Tomic-Canic, Harold Brem
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Patent number: 8802660Abstract: 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.Type: GrantFiled: March 12, 2008Date of Patent: August 12, 2014Assignee: New York UniversityInventors: Marjana Tomic-Canic, Harold Brem, Herbert H. Samuels
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Patent number: 8673859Abstract: 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.Type: GrantFiled: March 20, 2008Date of Patent: March 18, 2014Assignee: New York UniversityInventors: Harold Brem, Marjana Tomic
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Publication number: 20120289463Abstract: Compositions for antagonizing phosphorylation and subsequent degradation of glycogen synthase kinase 3 beta (GSK3?) in epidermal cells are disclosed. GSK3? phosphorylation antagonists include molecules that function to inhibit or reduce the binding activity or enzymatic activity of an upstream signaling molecule leading to GSK3? phosphorylation, or by downregulating the expression of one or more upstream signaling molecules involved in regulating GSK3? phosphorylation. Methods of using the GSK3? phosphorylation antagonists to inhibit or reduce the phosphorylation and degradation of GSK3? in epidermal cells are provided. The methods are useful to promote epithelialization and closure of wounds, such as chronic non-healing wounds.Type: ApplicationFiled: December 29, 2010Publication date: November 15, 2012Applicant: New York UniversityInventors: Marjana Tomic-Canic, Harold Brem
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Publication number: 20110190372Abstract: 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.Type: ApplicationFiled: August 9, 2010Publication date: August 4, 2011Applicant: NEW YORK UNIVERSITYInventors: Marjana Tomic-Canic, Harold Brem
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Patent number: 7919478Abstract: 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.Type: GrantFiled: January 22, 2008Date of Patent: April 5, 2011Assignee: New York UniversityInventor: Harold Brem
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Publication number: 20100310517Abstract: 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.Type: ApplicationFiled: August 18, 2010Publication date: December 9, 2010Inventors: Harold Brem, Marjana Tomic-Canic
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BIOLOGICAL MARKERS OF CHRONIC WOUND TISSUE AND METHODS OF USING FOR CRITERIA IN SURGICAL DEBRIDEMENT
Publication number: 20090203006Abstract: 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.Type: ApplicationFiled: May 1, 2007Publication date: August 13, 2009Applicant: New York Society for the Ruptured and Crippled Maintaining the Hospital for Special SurgeryInventors: Harold Brem, Marjana Tomic-Canic -
Publication number: 20090191156Abstract: 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.Type: ApplicationFiled: March 20, 2008Publication date: July 30, 2009Inventors: Harold Brem, Marjana Tomic
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Publication number: 20080274079Abstract: 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.Type: ApplicationFiled: March 12, 2008Publication date: November 6, 2008Applicant: New York Society for the Ruptured and Crippled Maintaining the Hospital for Special SurgeryInventors: Marjana Tomic-Canic, Harold Brem
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Publication number: 20080234194Abstract: 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.Type: ApplicationFiled: March 20, 2008Publication date: September 25, 2008Inventors: Harold Brem, Marjana Tomic
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Publication number: 20080175820Abstract: 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.Type: ApplicationFiled: January 22, 2008Publication date: July 24, 2008Inventor: Harold Brem
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Publication number: 20060116904Abstract: 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.Type: ApplicationFiled: September 30, 2005Publication date: June 1, 2006Inventor: Harold Brem
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Patent number: 6638949Abstract: A method and compositions for inhibiting excessive scar formation and adhesions by administering to a patient in need thereof an effective amount of an angiogenesis inhibitor. In the preferred embodiment, the angiogenesis inhibitor is selective, such as a fumagillol derivative like 0-chloroacetylcarbamoyl-Fumagillol (TNP-470, TAP Pharmaceuticals), thalidomide, or a selective drug having more than one activity, such as minocycline or penicilliamine which also have antibiotic activity. Less selective compounds can also be used, such as the cytokine IL12. Patients to be treated include those having experienced trauma, surgical intervention, burns, and other types of injuries. The inhibitor is administered in an amount effective to decrease excessive scarring, defined as formation of high density tissue including cells and connective tissue, without preventing normal wound closure. The inhibitors can be administered systemically and/or locally or topically, as needed.Type: GrantFiled: August 25, 1998Date of Patent: October 28, 2003Inventors: Judah Folkman, Harold Brem, H. Paul Ehrlich
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Publication number: 20030180259Abstract: 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.Type: ApplicationFiled: March 12, 2003Publication date: September 25, 2003Inventor: Harold Brem
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Patent number: 6086865Abstract: The present invention provides for the use of fumagillin or an O-substituted fumagillol derivative in conjunction with interferon which increases the angiogenic inhibitory action as compared with the agents administered alone. It has also been discovered that in the treatment of certain angiogenesis-induced diseases, the combination of the present invention is synergistic in angiogenesis inhibitory effect. The invention further provides a method for treatment of angiogenesis-induced diseases.Type: GrantFiled: May 31, 1995Date of Patent: July 11, 2000Assignee: Children's Medical Center CorporationInventors: Moses Judah Folkman, Harold Brem