Goodwin Associate Dr. Mayim Wiens, from San Francisco, focuses her practice on US and foreign patent prosecution for life sciences industry clients. Learn more.

Mayim Wiens

Associate
Mayim Wiens
San Francisco
+1 415 733 6233

Dr. Mayim Wiens concentrates her practice on US and foreign patent prosecution for clients in the life science industry with a focus on biological therapeutics. She assists clients with prior art research, patent preparation, patent prosecution, and freedom to operate analyses. Her areas of technical expertise include cell biology, molecular biology, virology, and microbiology.

Prior to joining Goodwin, Dr. Wiens was a patent agent at a leading Bay Area life sciences and technology law firm. Dr. Wiens earned her PhD from the University of Washington under the supervision of Jason Smith, where she studied the molecular mechanisms by which defensins, a class of innate immune effector proteins, inhibit Human Papillomavirus infection. She utilized classic and cutting edge virology, molecular biology, and microscopy techniques in her research. During her time at the University of Washington, Dr. Wiens was a patent intern at CoMotion, the UW center for commercialization, and performed patentability and freedom to operate searches.

Prior to attending graduate school, Dr. Wiens was an EID Research Fellow at the Centers for Disease Control and Prevention (CDC) in the Influenza Division, where she performed research on the innate immune response to influenza infection.

Credentials

Education

JD2023

University of California College of the Law, San Francisco

(magna cum laude)

PhD2016

University of Washington

BS2008

University of California, Santa Cruz

Admissions

Bars

  • California
  • U.S. Patent and Trademark Office (USPTO)

Publications

Wiens ME, Smith JG. 2017. α-Defensin HD5 Inhibits Human Papillomavirus 16 Infection via Capsid Stabilization and Redirection to the Lysosome. mBio 8 (1) e02304-16; DOI: 10.1128/mBio.02304-16

Wiens ME, Smith JG. 2015. Alpha-defensin HD5 inhibits furin cleavage of human papillomavirus 16 L2 to block infection. J Virol 89:2866–2874. doi:10.1128/JVI.02901-14.