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Patent Eligibility of Diagnostic Gene Signature Method Claims
A claim drafting strategy assuring the patent subject matter eligibility of diagnostic gene signature method claims is discussed in light […]
Dr. Christopher Southgate is genuinely enthusiastic about cutting-edge science and finding solutions to challenging IP legal issues. He has over 18 years of experience delivering Biologics patent services and IP strategy advice.
Seasoned in working with university and corporate clients, Christopher has also worked with large pharmaceutical companies and biotech startups. He is especially skilled at providing thorough and comprehensive freedom-to-operate and patent landscape analyses.
The breadth of Christopher’s post-graduate academic research at Harvard University, Harvard Medical School, Dana Farber Cancer Institute and UMass Medical School allows him to advise on a wide range of technologies and disciplines, including antibody therapeutics, immuno-oncology therapies, neoantigen selection, T cell therapies, checkpoint inhibitors, regenerative medicine, tissue engineering, stem cell therapies (iPSCs), AAV gene therapies, and regulation of gene expression (e.g., RNA interference, microRNAs, aptamers, reporter constructs, inducible transcription; splicing).
Before JMIN
Prior to joining JMIN, Christopher was a director and patent counsel at PTC Therapeutics for four years where he was the IP subject matter expert for all of PTC’s gene therapy programs. Before that, he was a senior life sciences patent attorney at a bustling New Jersey-based IP boutique law firm.
Education
- Washington College of Law, American University, Washington, D.C., Juris Doctor
- Institute for Molecular Biology, University of Zürich, Switzerland, Ph.D. in Molecular Biology
Admissions
- U.S. Patent and Trademark Office
- Massachusetts and the District of Columbia
Published Work
- “Preclinical studies of gene replacement therapy for CDKL5 deficiency disorder” (co-author), Molecular Therapy, October 2, 2024, p3331-3345.
- “Targeted disruption of the murine erythroid band 3 gene results in spherocytosis and severe hemolytic anemia despite a normal membrane skeleton,” Southgate et al. Nature Genetics 1996, 14:227-230.
- “Delineating minimal protein domains and promoter elements for transcriptional activation by lentivirus Tat proteins,” Southgate et al. Journal of Virology 1995, 69; 2605-2610.
- “The type 1 human immunodeficiency virus Tat binding protein is a transcriptional activator belonging to an additional family of evolutionary conserved genes,” (co-author) Proc, Nat. Aca. Sci. USA 1993, 90; 138-142.
- “The HIV-1 Tat protein activates transcription from an upstream DNA-binding site: Implications for Tat function,” Southgate et al. Genes and Development 1991, 5:2496-2507.
- “Activation of transcription by HIV-1 Tat protein tethered to nascent RNA through another protein,” Southgate et al. Nature, 1990, 345:640-642.
- “In Vivo and in vitro expression of U7 snRNA genes: Cis and trans-acting elements required for RNA polymerase II-directed transcription,” Southgate et al., EMBO Journal 1989, 8:539-549.
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Sep 24 2024