RICHARD L. GUERRANT, M.D.
Osteopathic Medicine in Charlottesville, VA

7192724, Mar 20, 2007

Nov 14, 2001

10/002842

James Hunter Boone - Christiansburg VA, US
David Maxwell Lyerly - Radford VA, US
Tracy Dale Wilkins - Riner VA, US
Richard Littleton Guerrant - Charlottesville VA, US

Techlab, Inc. - Blacksburg VA

G01N 33/00

435 724, 435 71, 435 792, 435 794, 436514, 436533, 436534

A method for aiding in differentiating irritable bowel syndrome from inflammatory bowel disease by determining the level of total endogenous human lactoferrin in clinical specimens, such as feces, mucus and bile, wherein an elevated level of lactoferrin substantially precludes diagnoses of IBS and other noninflammatory etiologies, and a kit usable in such method are provided. Further provided is a method for quantitating the level of total endogenous human lactoferrin in clinical specimens, such as feces, mucus and bile, to monitor gastrointestinal inflammation in persons having inflammatory bowel disease.

2010003, Feb 11, 2010

Jul 6, 2007

12/307150

Richard L. Guerrant - Charlottesville VA, US
Alexander Y. Kots - Houston TX, US
Ferid Murad - Houston TX, US
Byung-Kwon Choi - Katy TX, US

A61K 31/5415, A61K 31/519

5142258, 514257

We disclose a method of inhibiting activity of adenylyl cyclase or guanylyl cyclase in a mammal by administering to the mammal an amount of a composition effective to inhibit the activity, wherein the composition contains at least one compound selected from the group consisting of structural formulae (Ia) and (Ib) and salts thereof, wherein R1 is —H or has the structure —C(═O)R8; R2 is ═O or has the structure —OC(═O)R9; and R3, R4, R5, R6, and R7 are each independently selected from the group consisting of —H, —NO, formula (I), -halogen, —OC(═O)R9, —OR9, —OH, —R8OH, —CH, —OC(═O)CHPh, formulae (II), (III), (IV), —OPh, —CF, —R8, —C(═O)OR9, -Ph, —R8Ph, formulae (V), (VI), (VII), (VIII), (IX), (X), (XI), (XII), (XIII), (XIV), (XV), (XVI), (XVII), (XVIII), (XIX), (XX), and (XXI), wherein each R8 is independently a linear or branched hydrocarbon group having from 1 to 4 carbon atoms and each R9 is independently a hydrocarbon group having from 1 to 2 carbon atoms. Administering the composition can be used to treat a disease in a mammal mediated by activity of adenylyl cyclase or guanylyl cyclase and effected by a toxin produced by a pathogenic organism or to reduce cyclic AMP or cyclic GMP levels in a mammal in need of reduction thereof. The composition can also be administered to mammalian cells in vitro. The above methods of inhibiting activity of adenylyl cyclase or guanylyl cyclase and treating diseases via such inhibition can be effective without prolonged treatment, have reversible effects, have low or no toxicity, are highly potent, are unlikely to have side effects, do not act on purinergic receptors, or can negate pathogenic toxins independently of whether the pathogenic organism survives.

4923801, May 8, 1990

Apr 13, 1987

7/037938

Barry J. Marshall - Charlottesville VA
Richard L. Guerrant - Charlottesville VA

The University of Virginia Alumni Patents Foundation - Charlottesville VA

C12Q 158, C12Q 104, C12Q 134, C12Q 124

435 12

A method of enrichment and isolation of urease producing organisms from a contaminated specimen by first homogenizing the contaminated specimen in water, then introducing the homogenized contaminated specimen into a solution of urea in an acid, wherein some of the organisms are killed by the acidic medium and remaining organisms are protected from acid attack by creating a protective ammonia by breaking down the urea, and plating the remaining organisms onto a medium which contains antibiotics inhibitory to some of the remaining organisms, but not inhibitory to organisms to be isolated.

2012001, Jan 12, 2012

Mar 16, 2010

13/257707

Paul S. Hoffman - Charlottesville VA, US
Richard L. Guerrant - Charlottesville VA, US
Timothy L. Macdonald - Charlottesville VA, US

University of Virginia Patent Foundation - Charlottesville VA

A61K 31/427, C07D 417/12, C07D 417/14, C07D 409/12, C07D 333/44, A61P 31/04, A61K 31/4439, A61K 31/381, A61K 31/454, A61K 31/5377, A61P 31/00, C07D 277/58, A61K 31/426

5142102, 548192, 5462707, 548181, 549 59, 549 69, 546209, 544133, 549 60, 514371, 514342, 514444, 514447, 514326, 5142368

The invention provides FIG. novel antimicrobial chemical entities based on a nitrothiazolide backbone that exhibit antibacterial and antiparasitic action against a wide range of human pathogens. The new classes of compounds show extended action against Gram positive bacteria including MRSA drug resistant pathogens. In the Gram-positive organisms, they specifically target and functionally inhibit microbial attachment to surfaces and biofilm formation. In Gram-negative bacteria, including enteroaggregative strains, these compounds function as pilicides by inhibiting the assembly of pilin subunits into adhesive filaments. Several of these compounds show potent antimicrobial action against Gram positive bacteria, perhaps involving novel targets. Many of the benzothiophene derivatives exhibit antimicrobial activity in the low micrograms per ml range and in blocking biofilm formation in the nanomolar range; ranges considered are well within the range of utility as therapeutics.

2013025, Oct 3, 2013

May 19, 2011

13/697860

Todd R. Klaenhammer - Raleigh NC, US
Richard L. Guerrant - Charlottesville VA, US
Glynis L. Kolling - Scottsville VA, US
Evelyn Durmaz - Cary NC, US
Michael P. Timko - Charlottesville VA, US
Cirle Alcantara Warren - Waynesboro VA, US

UNIVERSITY OF VIRGINIA PATENT FOUNDATION - Charlottesville VA
NORTH CAROLINA STATE UNIVERSITY - Raleigh NC

A61K 38/16, A61K 35/74

424 932, 4352523, 435476

Methods and compositions for targeted delivery of biotherapeutics are provided. The compositions comprise bile-sensitive bacteria modified to release a biotherapeutic agent following bile exposure. Biotherapeutic agents released by the bacteria disclosed herein include AQ and AQR rich peptides. Methods of the invention comprise administering to a subject a bacterium modified to release a biotherapeutic agent following bile exposure. Administration of the bacterium promotes a desired therapeutic response. The bacterium may be modified to express and release AQ or AQR rich peptides which subsequently inhibit cellular apoptosis or reduce mucosal damage. Thus, methods of the invention find use in treating or preventing a variety of gastrointestinal disorders including infection and antibiotic-associated diarrhea.

2008031, Dec 18, 2008

Apr 9, 2008

12/100071

Richard L. Guerrant - Charlottesville VA, US
Joel M. Linden - Charlottesville VA, US
Cirle A. Warren - Waynesboro VA, US
Gail W. Sullivan - Charlottesville VA, US
Timothy L. Macdonald - Charlottesville VA, US

A61K 38/05, A61K 31/7076, A61P 31/04

514 19, 514 46

A therapeutic method for treating intestinal damage, enteritis, diarrhea, or a combination thereof caused by a is provided. The method includes administration to a patient in need thereof an effective amount of an Aadenosine receptor agonist, optionally in combination with an effective amount of a stable glutamine derivative, e.g., alanyl-glutamine.

4820714, Apr 11, 1989

May 2, 1986

6/858674

Richard L. Guerrant - Charlottesville VA
Aldo M. Lima - University Garden VA

University of Virginia Alumni Patents Foundation - Charlottesville VA

A61K 3144, A61K 31225

514297

Hemorrhagic fluid secretion and histologic damage to the intestinal mucosa by C. difficile toxin is blocked by the use of phospholipase inhibitors.

5639750, Jun 17, 1997

Jun 7, 1995

8/477313

Richard L. Guerrant - Charlottesville VA
Guodong D. Fang - Charlottesville VA
Manasses C. Fonteles - Charlottesville VA

University of Virginia Patent Foundation - Charlottesville VA

A61K 3134, A61K 3155

514219

The invention relates to the treatment fluid secretion caused by Cholera toxin that can be blocked through the administration of PAF antagonists BN 52021 and SR 27417.