PTAB

PGR2023-00014

Forte Biosciences Inc v. University Of Massachusetts

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1. Case Identification

2. Patent Overview

  • Title: Diagnosis and treatment of vitiligo
  • Brief Description: The ’505 patent discloses methods for treating vitiligo and other T cell-mediated autoimmune disorders by administering a therapeutically effective amount of an inhibitor of interleukin-15 (IL-15) or its receptor (IL-15R).

3. Grounds for Unpatentability

Ground 1: Claims 1-5 Lack Written Description under 35 U.S.C. §112

  • Core Argument for this Ground: Petitioner argued that the claims lack written description because their immense scope is not commensurate with the patent’s narrow disclosure. The claims are functionally defined to cover any method of treating any subject with vitiligo using any inhibitor of IL-15 or its receptor. However, the specification provided only a single working example: the use of a specific chimeric antibody (ChMBC7) targeting one receptor subunit (CD122) in an artificial mouse model where vitiligo was induced by transferring CD8+ T cells.
  • Petitioner contended this single example was not representative of the vast genera claimed. The arguments focused on three areas of overbreadth:
    • Inhibition Pathways: The working example’s inhibition of the CD122 subunit was not representative of inhibiting other targets like IL-15 itself, the IL-15Rα subunit, or the CD132 subunit (which is shared by at least six different cytokine pathways), making the results unpredictable across the claimed scope.
    • Chemical Structures: The single antibody example did not provide written description for the entirely different classes of inhibitors recited in claim 2, such as small molecules, peptide inhibitors, or inhibitory nucleic acids, for which no structure or working data was provided.
    • Subjects: Data from an induced-lesion mouse model was not representative of treating naturally occurring vitiligo in other subjects, particularly humans, due to the complexity of the human immune system and known differences between species. The nascent and unpredictable nature of the field meant a POSA could not extrapolate the results of the single experiment to the full scope of the claims.

Ground 2: Claims 1-5 Lack Enablement under 35 U.S.C. §112

  • Core Argument for this Ground: Petitioner argued the claims are not enabled because practicing their full scope would require undue experimentation. The specification provided only a starting point for research—the ChMBC7 antibody in a mouse model—but failed to provide guidance on how to make and use the full claimed invention.
  • Citing the complexity of cytokine signaling, the unpredictability of the art, and the nascent state of the field, Petitioner asserted that a POSA would have to engage in an extensive, iterative research program to practice the claims. This would involve synthesizing and screening an incalculable number of potential compounds (small molecules, antibodies, peptides, nucleic acids) against multiple distinct biological targets (IL-15, IL-15Rα, CD122, CD132) to determine if they had the claimed therapeutic effect. This process would need to be repeated across different subject types (e.g., mouse vs. human) and disease models (induced vs. spontaneous vitiligo). The specification’s lack of structural details for its exemplified antibody and its failure to describe how to identify other effective inhibitors rendered the claims non-enabling.

Ground 3: Claims 1-5 are obvious over Xing and Harris under 35 U.S.C. §103

  • Prior Art Relied Upon: Xing (a 2014 journal article in Nature Medicine) and Harris (a 2012 journal article in Journal of Investigative Dermatology).
  • Core Argument for this Ground:
    • Prior Art Mapping: Petitioner asserted that Harris disclosed the exact adoptive transfer mouse model of vitiligo later used in the ’505 patent, in which the disease is caused by autoreactive CD8+ T cells. Harris taught that preventing the accumulation of these T cells had therapeutic potential for treating vitiligo. Xing taught that systemic administration of a CD122 antibody (TM-β1), an inhibitor of the IL-15 receptor, successfully depleted autoreactive CD8+ T cells and prevented hair loss in a mouse model of alopecia areata, a closely related autoimmune skin disease also driven by CD8+ T cells. The combination of Harris and Xing therefore disclosed all elements of the claimed method.
    • Motivation to Combine: A POSA would have been motivated to apply the CD122 antibody from Xing to the vitiligo model in Harris. Harris identified both the problem (vitiligo caused by CD8+ T cells) and a clear therapeutic strategy (depleting those cells). Xing provided an explicit, proven tool (a CD122 antibody) for executing that exact strategy in a highly analogous disease.
    • Expectation of Success: A POSA would have had a reasonable expectation of success because both diseases share a common underlying pathology (CD8+ T cell-driven autoimmunity in the skin), and Xing demonstrated that a CD122 antibody was effective at targeting and depleting those specific cells to treat disease symptoms. For dependent claims 3-5, Petitioner noted that local and subcutaneous administration of inhibitors for skin lesions was also known in the art and taught by Xing for downstream JAK inhibitors.

4. Relief Requested

  • Petitioner requested the institution of post-grant review and the cancellation of claims 1-5 of Patent 11,278,505 as unpatentable.