Skip to Main Content.

Biography

Nicole’s areas of practice include patent prosecution and opinion work.  Her practice is concentrated in the area of biotechnology. Nicole has represented a variety of clients including corporate clients, university researchers, and pharmaceutical companies. She is admitted to practice in Ohio and before the United States Patent and Trademark Office. Prior to joining Frost Brown Todd, Nicole worked as a consultant to the University of Cincinnati Intellectual Property Office, and as counsel to The Procter & Gamble Company.

Other Info About Nicole

Experience

Legal Work Highlights

Patent preparation and prosecution (U.S. and Global)

Provided litigation support for patent and trademark related cases

Assists in marketing of university technologies

Drafting and management of IP Strategies

Prepare Freedom to Practice, Invalidity Studies, and Patentability Opinions

Review and negotiate materials transfer agreements and confidential disclosure agreements

Developed tutorials for university employees regarding intellectual property issues

Education

Law School

University of Cincinnati College of Law, J.D., 2005

  • Dean’s Honors List
  • Lawrence Maxwell Advocacy Prize
  • Will Ziegler Scholarship
  • Intellectual Property Law Society

Doctorate

University of Cincinnati College of Medicine, Ph.D., 2000, Pharmacology and Cell Biophysics

Undergraduate School

Thomas More College, B.A., 1994, Biology

Bar Memberships

Nicole is licensed to practice in the following state(s):

Ohio

Courts

Nicole is admitted to practice before the following court(s):

United States Patent and Trademark Office

Professional Affiliations

Professional Affiliations & Memberships

Ohio State Bar

United States Patent and Trademark Office

Cincinnati Bar Association

Firm Committees

Nicole serves or has served in the following leadership role(s) at Frost Brown Todd:

Recruiting Committee, Member

Presentations

Nicole was invited to speak at the following events:

Speaker: Women’s Economic Outreach Organization (WEDO), 2006

Adjunct Lecturer: University of Cincinnati, Media Law, Fall 2005 and 2006

Major Publications

Nicole is an author or contributor to the following publications:

Contributions to PatentBaristas.com

Intellectual Property Publications:

Author: “DNA Patents:  More than Someone Owning Your Genes,” FDLI 2007

Scientific Publications:

Liggett SB, Tepe NM, Lorenz JN, Canning AM, Jantz TD, Mitarai S, Yatani A, Dorn GW 2nd.  Early and delayed consequences of b2-adrenergic receptor overexpression in mouse hearts: critical role for expression level.  Circulation. 2000 Apr 11; 101(14): 1707-14.

Tepe NM, Liggett SB.  Functional receptor coupling to Gi is a mechanism of agonist-promoted desensitization of the b2-adrenergic receptor.  Journal of Receptor Signal Transduction Research 2000 Jan. 20(1): 75-85.

Tepe NM, Lorenz JN, Yatani A, Dash R, Kranias EG, Dorn GW 2nd, Liggett SB.  Altering the receptor-effector ratio by transgenic overexpression of type V adenylyl cyclase: enhanced basal catalytic activity and function without increased cardiomyocyte beta-adrenergic signaling.

Biochemistry. 1999 Dec 14; 38(50): 16706-13.

Tepe NM, Liggett SB.  Transgenic replacement of type V adenylyl cyclase identifies a critical mechanism of b-adrenergic receptor dysfunction in the G aq overexpressing mouse.  FEBS Letters 1999 Sep 17; 458(2): 236-40.

Dorn GW 2nd, Tepe NM, Wu G, Yatani A, Liggett SB.  Mechanisms of impaired beta-adrenergic receptor signaling in Gaq-mediated cardiac hypertrophy and ventricular dysfunction.  Molecular Pharmacology. 2000 Feb; 57(2): 278-87.

Dorn GW 2nd, Tepe NM, Lorenz JN, Koch WJ, Liggett SB.  Low- and high-level transgenic expression of b2-adrenergic receptors differentially affect cardiac hypertrophy and function in Gaq-overexpressing mice.  Proceedings of the National Academy of Science U S A. 1999 May 25;96(11):6400-5.

Dash R, Kadambi V, Schmidt AG, Tepe NM, Biniakiewicz D, Gerst MJ, Canning AM, Abraham WT, Hoit BD, Liggett SB, Lorenz JN, Dorn GW 2nd, Kranias EG.  Interactions between phospholamban and b-adrenergic drive may lead to cardiomyopathy and early mortality.  Circulation. 2001 Feb 13; 103(6): 889-96.