Jacqueline Heiss

Technical Advisor, Boston

Biography

Overview

Jacqueline Heiss is a patent agent who focuses her practice on patent prosecution in a broad range of life sciences industries, including matters involving gene therapy, transgenic animals, antibodies, pharmaceuticals, CRISPR, biophotonics, ocular products, protein therapeutics, protein traps, and immunology.

Jacqueline helps clients navigate intellectual property portfolio management, both within the U.S. and internationally. She regularly assists with conducting due diligence for strategic transactions and freedom to operate analyses. She has also performed due diligence investigations of the intellectual property portfolios of biopharmaceutical and gene therapy companies in accordance with initial public offerings. Furthermore, Jacqueline assists with patent litigation, including claim construction, inter partes review, and post grant review proceedings.

Prior to her legal career, Jacqueline completed her doctoral training in Pharmacology from Yale University where she studied the mechanisms underlying synaptic loss in Alzheimer's disease. During her research, she helped elucidate the role of prion protein in amyloid-beta mediated dendritic spine loss and was an author on four peer reviewed publications.

Prior to joining White & Case, Jacqueline worked as a technical advisor at an international law firm.

Bars and Courts
US Patent and Trademark Office
Education
PhD
Pharmacology
Yale University
BS
Biology
University of San Francisco
Languages
English

Experience

Publications

Rescue of Transgenic Alzheimer's Pathophysiology by Polymeric Cellular Prion Protein Antagonists. Cell Rep. 2019;26(1):145-158.e8. (Co-author)

Early Activation of Experience-Independent Dendritic Spine Turnover in a Mouse Model of Alzheimer's Disease, Cerebral Cortex, 2016. (Co-author)

Metabotropic glutamate receptor 5 is a coreceptor for Alzheimer aβ oligomer bound to cellular prion protein. Neuron. 2013;79(5):887-902. (Co-author)

Alzheimer amyloid-β oligomer bound to postsynaptic prion protein activates Fyn to impair neurons. Nat Neurosci. 2012;15(9):1227-35. (Co-author)