FreshPatents.com Logo
stats FreshPatents Stats
3 views for this patent on FreshPatents.com
2013: 1 views
2012: 1 views
2011: 1 views
Updated: April 14 2014
newTOP 200 Companies filing patents this week


    Free Services  

  • MONITOR KEYWORDS
  • Enter keywords & we'll notify you when a new patent matches your request (weekly update).

  • ORGANIZER
  • Save & organize patents so you can view them later.

  • RSS rss
  • Create custom RSS feeds. Track keywords without receiving email.

  • ARCHIVE
  • View the last few months of your Keyword emails.

  • COMPANY DIRECTORY
  • Patents sorted by company.

AdPromo(14K)

Follow us on Twitter
twitter icon@FreshPatents

Cell repair and regeneration by suramin and related polysulfonated naphthylureas

last patentdownload pdfimage previewnext patent


Title: Cell repair and regeneration by suramin and related polysulfonated naphthylureas.
Abstract: Disclosed herein are compositions and methods for promoting the repair and regeneration of injured tissues, such as injuries resulting from ischemic damage. Also disclosed are compositions and methods for accelerating wound healing in diabetic and elderly patients and inhibiting allograft failure. ...


Browse recent Ballard Spahr LLP patents - Atlanta, GA, US
Inventor: Rick G. Schnellmann
USPTO Applicaton #: #20110034559 - Class: 514577 (USPTO) - 02/10/11 - Class 514 
Drug, Bio-affecting And Body Treating Compositions > Designated Organic Active Ingredient Containing (doai) >Radical -xh Acid, Or Anhydride, Acid Halide Or Salt Thereof (x Is Chalcogen) Doai >Benzene Ring Containing >Polycyclo Ring System

view organizer monitor keywords


The Patent Description & Claims data below is from USPTO Patent Application 20110034559, Cell repair and regeneration by suramin and related polysulfonated naphthylureas.

last patentpdficondownload pdfimage previewnext patent

CROSS-REFERENCE TO RELATED APPLICATIONS

This application is a continuation-in-part and claims priority to U.S. application Ser. No. 11/622,285, filed on Jan. 11, 2007 which claims benefit of U.S. Provisional Application No. 60/759,118, filed Jan. 12, 2006, which are hereby incorporated herein by reference in their entirety.

STATEMENT REGARDING FEDERALLY SPONSORED RESEARCH

This invention was made with government support under Grant ES-04410 awarded by The National Institutes of Health. The government has certain rights in the invention.

BACKGROUND

The complex process of wound healing is comprised of hemostasis, inflammation, cellular proliferation, and dermal remodeling, and any interruption in the normal progression of this process can give rise to wounds that are slow to heal or wounds which do not heal at all, potentially leading to amputations. In fact, chronic and acute wounds represent a major health burden with significant costs, morbidity, and mortality, in addition to the pain and potential infection often associated with wounds. These concerns are most significant for the diabetic or elderly patient who has increased risk of wounding due to peripheral neuropathies, injuries that go undetected, and disease- or aged-dependent diminished healing ability. Wounds in diabetic persons are also unique in that the presence of current ulcers predicts future episodes, and each additional episode increases cost and risk of mortality. Current wound therapies have not met the existing needs of diabetic patients and cannot fulfill the exclusive need of diabetics who have ulcers that are molecularly and physiologically atypical.

Recent advances in local, and molecular factors underlying wound healing have given rise to new treatments such as allogeneic skin grafting and bioengineered skin equivalents. These represent advances in wound management but none address accelerating wound healing. The best topical agent is efficacious at low doses and be effective in a single dose regimen. Furthermore, non-healing chronic diabetic ulcers are often treated with extracellular matrix replacement therapy and trends in this type of wound management include moist wound therapy, bio-engineered tissues, growth factors, and negative pressure wound therapy, and many of these have significant disadvantages such as not being feasible for all wound or patient types. Thus, new drug therapies are warranted to address the current gaps in the technology of wound healing. In particular, what is needed is a compound that promotes acute or chronic wound healing which in turn can decrease morbidity, health care utilization, and costs.

BRIEF

SUMMARY

In accordance with the purpose of this invention, as embodied and broadly described herein, this invention relates to compositions and methods for promoting tissue repair and regeneration. Additional advantages of the disclosed method and compositions will be set forth in part in the description which follows, and in part will be understood from the description, or may be learned by practice of the disclosed method and compositions. The advantages of the disclosed method and compositions will be realized and attained by means of the elements and combinations particularly pointed out in the appended claims. It is to be understood that both the foregoing general description and the following detailed description are exemplary and explanatory only and are not restrictive of the invention as claimed.

The present disclosure provides for a drug for rapid wound repair is essential, especially in people with diabetes, an ever-growing, global population. Thus, in one embodiments, disclosed herein are compositions and methods to stimulate repair and regeneration of injured tissue. In another embodiment, disclosed herein are compositions and methods to accelerate wound healing in diabetic and elderly subjects. In yet another aspect, disclosed herein are compositions and methods for inhibiting allograft failure.

BRIEF DESCRIPTION OF THE DRAWINGS

The accompanying drawings, which are incorporated in and constitute a part of this specification, illustrate several embodiments of the disclosed method and compositions and together with the description, serve to explain the principles of the disclosed method and compositions.

FIG. 1 shows promotion of RPTC outgrowth and proliferation. Renal proximal tubules were plated (Aa) and after 24 hr exposed to fresh medium alone (Ab), 50 μM suramin (Ac), 10 ng/ml EGF (Ad), or suramin+EGF (Ae) for 24 hr and then photographed. RPTC were cultured for 3 days, and then incubated with the above agents (B) or varying concentrations of suramin (C) for 24 hr. After staining with propidium iodide, cell cycle was analyzed by flow cytometry and the number of cells in S-phase determined. Data are expressed as means±SEM, n=3. Bars with different superscripts are significantly from each other (p<0.05).

FIG. 2 shows suramin promotes RPTC scattering and formation of lamellipodia. RPTC were cultured for 3 days and then treated with diluent, 50 μM suramin, 10 ng/ml EGF or suramin+EGF. After 24 hr, bright field photographs were taken (40× magnification) (A) or RPTC were fixed with methanol and then stained with fluorescein conjugated phalloidin (B). Photographs at 80× magnification. Arrows show lamelliopodia.

FIG. 3 shows blockade of the EGF receptor by AG1478 inhibits EGF-induced RPTC proliferation and scattering but not suramin-induced RPTC proliferation and scattering. FIG. 3A shows RPTC cultured for 2 days and then incubated with 10 μM AG1478 in the absence or presence of 50 μM suramin for 48 hr. Cell proliferation was determined using the MTT assay. Data are expressed as means±SEM of the percentage of MTT activity compared to controls grown with diluent (N=3). FIG. 3B shows RPTC cultured for 3 days and then incubated with diluent, 50 μM suramin, or 10 ng/ml EGF in the presence and absence of 10 μM AG1478 for 24 hr. Bright field photographs were taken at edge of the cell islands (40× magnification).

FIG. 4 shows suramin does not induce EGF receptor phosphorylation. RPTC were cultured for 3 days and then treated with 50 μM suramin or 10 ng/ml EGF for 10 min (A), or pretreated with 10 μM AG1478 for 1 hr and then exposed to EGF for 10 min (B). Cell lysates were prepared and subjected to immunoblot analysis using anti-phospho-EGF receptor antibody (Tyr1068) or anti-EGF receptor antibody. Protein loading was monitored using total EGF receptor levels. Representative immunoblot from three or more experiments.

FIG. 5 shows effects of PI3K and ERK1/2 pathway inhibitors on RPTC proliferation and scattering following plating and suramin exposure. FIG. 5A shows RPTC cultured for 2 days and then incubated with 50 μM suramin for 48 hr in the presence and absence of 20 μM LY294002 (LY) and 10 μM U0126. Cell proliferation was determined using the MTT assay. Data are expressed as means±SEM of the percentage of MTT activity compared to controls grown with diluent (N=3). FIGS. 5B and 5C show RPTC cultured for 3 days and then incubated with 50 μM suramin for 24 hr in the presence and absence of 20 μM LY294002 (LY) and 10 μM U0126. Cell proliferation was determined by measuring the number of cells in S-phase of the cell cycle. Data are expressed as means±SEM, n=3. Bars with different superscripts are significantly from each other (p<0.05). Bright field photographs were taken at edges of the cell islands (40× magnification).

FIG. 6 shows suramin induces phosphorylation of Akt and ERK1/2. RPTC were cultured for 3 days and then treated with 50 μM suramin for 0-120 min (A) or pretreated with 20 μM LY294002 (LY)(B) or 10 μM U0126 (C) for 1 hr and exposed to suramin for 30 min. Cell lysates were prepared and subjected to immunoblot analysis using antibodies to phospho-Akt, phospho-ERK1/2, total Akt and total ERK1/2. Representative immunoblot from three or more experiments.

FIG. 7 shows effects of Src inhibition on RPTC proliferation and scattering following plating and suramin exposure. FIG. 7A shows RPTC cultured for 2 days and then incubated with 50 μM suramin for 48 hr in the presence and absence of 10 μM PP1. Cell proliferation was determined using the MTT assay. Data are expressed as means±SEM of the percentage of MTT activity compared to controls grown with diluent (N=3). FIGS. 7B and 7C show RPTC cultured for 3 days and then incubated with 50 μM suramin for 24 hr in the presence and absence of 10 μM PP1. Cell proliferation was determined by measuring the number of cells in S-phase of the cell cycle. Data are expressed as means±SEM, n=3 Bars with different superscripts are significantly from each other (p<0.05). Bright field photographs were taken at edge of the cell islands (40× magnification).

FIG. 8 shows Src, but not the EGF receptor, is required for suramin-induced Akt phosphorylation. RPTC were cultured for 3 days and then treated with 50 μM suramin for 0-60 min (A and B), or pretreated with 10 μM PP1 (C) and then treated with 50 μM suramin for 30 min. Cell lysates were prepared and subjected to immunoblot analysis using antibodies to phospho-Src at Tyr416 (A) and Tyr527 (B), Src, phospho-Akt, and total Akt. Representative immunoblot from three or more experiments.

FIG. 9 shows serum creatinine levels increased at 24 hrs post reperfusion to approximately 2 mg/dl and remained at this level at 48 hrs in mice subjected to ischemia/reperfusion (I/R) and diluent. Suramin, added 24 hr after I/R, at doses between 0.003 and 0.03 mg/kg stimulated recovery of renal function and decreased serum creatinine levels to approximately 1 mg/dl. Doses of suramin greater than or equal to 0.1 mg/dl completely restored renal function. Finally no toxicity was observed at doses of suramin up to 10 mg/kg.



Download full PDF for full patent description/claims.

Advertise on FreshPatents.com - Rates & Info


You can also Monitor Keywords and Search for tracking patents relating to this Cell repair and regeneration by suramin and related polysulfonated naphthylureas patent application.
###
monitor keywords



Keyword Monitor How KEYWORD MONITOR works... a FREE service from FreshPatents
1. Sign up (takes 30 seconds). 2. Fill in the keywords to be monitored.
3. Each week you receive an email with patent applications related to your keywords.  
Start now! - Receive info on patent apps like Cell repair and regeneration by suramin and related polysulfonated naphthylureas or other areas of interest.
###


Previous Patent Application:
Dp2 antagonist and uses thereof
Next Patent Application:
Liquid formulations of compounds active at sulfonylurea receptors
Industry Class:
Drug, bio-affecting and body treating compositions
Thank you for viewing the Cell repair and regeneration by suramin and related polysulfonated naphthylureas patent info.
- - - Apple patents, Boeing patents, Google patents, IBM patents, Jabil patents, Coca Cola patents, Motorola patents

Results in 3.39438 seconds


Other interesting Freshpatents.com categories:
Qualcomm , Schering-Plough , Schlumberger , Texas Instruments , -g2--0.0622
     SHARE
  
           

FreshNews promo


stats Patent Info
Application #
US 20110034559 A1
Publish Date
02/10/2011
Document #
12856413
File Date
08/13/2010
USPTO Class
514577
Other USPTO Classes
International Class
/
Drawings
18


Allograft
Suramin
Wound Healing


Follow us on Twitter
twitter icon@FreshPatents