PTAB

PGR2019-00053

LAsSen Therapeutics I Inc v. Singapore Health Services Pte Ltd

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Key Events
Petition
petition

1. Case Identification

2. Patent Overview

  • Title: Treatment of Fibrosis
  • Brief Description: The ’603 patent is directed to a method of treating fibrosis in a human subject. The method comprises administering a therapeutically effective amount of an Interleukin 11 receptor α (IL-11Rα) antibody that is capable of inhibiting Interleukin 11 (IL-11) mediated signaling, wherein the fibrosis is in the heart, liver, kidney, or eye.

3. Grounds for Unpatentability

Ground 1: Lack of Written Description and Enablement - Claims 1-10 are unpatentable under 35 U.S.C. §112

  • Prior Art Relied Upon: Not applicable for this ground.
  • Core Argument for this Ground:
    • Lack of Written Description: Petitioner argued that the ’603 patent fails to provide an adequate written description because the claims define the required anti-IL-11Rα antibody purely by its function—binding to IL-11Rα and inhibiting IL-11 signaling. The specification allegedly provides no structural identification (e.g., amino acid sequences, binding epitopes, or common structural features) for any species falling within the vast claimed genus of antibodies. Petitioner asserted that this lack of structural detail fails to demonstrate that the inventors were in possession of the full scope of the claimed invention, particularly given the high unpredictability of antibody structure-function relationships. The specification allegedly lacks working examples of treating fibrosis and fails to identify the sequences of antibodies used in its in vitro experiments.
    • Lack of Enablement: Petitioner further argued that the patent fails to enable a person of ordinary skill in the art (POSITA) to make and use the full scope of the invention without undue experimentation. The claims encompass an enormous genus of potential antibodies (monoclonal, polyclonal, fragments, derivatives of any species), but the specification provides no guidance on how to identify or create antibodies with the claimed therapeutic effects beyond routine screening. Given the unpredictability of antibody development, Petitioner contended that a POSITA would need to engage in an extensive, unguided screening process to identify antibodies that both inhibit IL-11 signaling and effectively treat fibrosis in the specified organs.

Ground 2: Anticipation over Edwards - Claims 1-4, 6, and 8-10 are anticipated by Edwards

  • Prior Art Relied Upon: Edwards (Application # 2014/0219919).
  • Core Argument for this Ground:
    • Prior Art Mapping: Petitioner argued that Edwards disclosed all limitations of the challenged claims. Edwards taught using anti-IL-11Rα antibodies that neutralize IL-11 signaling to treat IL-11 mediated conditions in human subjects. While Edwards did not explicitly mention treating "fibrosis," Petitioner asserted that this limitation was inherently disclosed. Edwards specifically identified treating cachexia associated with cardiac disease and chronic kidney disease. Petitioner contended, supported by other references like Wynn, that these conditions were well-known fibroproliferative diseases. Therefore, treating the underlying cardiac or kidney disease as taught by Edwards would inherently treat the associated fibrosis in those organs. Edwards also taught methods for detecting upregulated IL-11Rα expression and administering the antibody to subjects with abnormal levels, allegedly anticipating claims 8-10.

Ground 3: Obviousness over Edwards, Wynn, and Chegini - Claims 1-10 are obvious over Edwards in view of Wynn and Chegini

  • Prior Art Relied Upon: Edwards (Application # 2014/0219919), Wynn (a 2004 Nature Reviews Immunology article), and Chegini (Application # 2008/0300147).
  • Core Argument for this Ground:
    • Prior Art Mapping: Petitioner argued that Edwards provided the primary teaching of using anti-IL-11Rα antibodies to treat IL-11 mediated conditions. To the extent Edwards did not explicitly teach treating fibrosis in the claimed organs, Wynn and Chegini supplied the missing link. Wynn, a review article, described major-organ fibrosis in the heart, liver, kidney, and eye, and established the clinical relationship between fibrosis and conditions like cardiac and kidney disease. Chegini taught that elevated IL-11 expression is indicative of fibrotic disorders and that blocking IL-11 could be useful for treating conditions including renal failure, liver cirrhosis, and heart disease.
    • Motivation to Combine: A POSITA would combine these references because Edwards taught a therapy for IL-11 mediated conditions, and both Wynn and Chegini established that fibrosis is an IL-11 mediated condition. A POSITA reading Edwards’s disclosure on treating cardiac and kidney disease would have been motivated by the knowledge in Wynn and Chegini to apply the anti-IL-11Rα antibody to treat the known associated fibrosis.
    • Expectation of Success: A POSITA would have had a reasonable expectation of success because Edwards demonstrated the therapeutic benefit of neutralizing IL-11 signaling. Since Chegini taught that fibrosis is caused or exacerbated by IL-11, a POSITA would expect that an antibody neutralizing IL-11 signaling, like the one in Edwards, would be effective in treating fibrosis.

4. Key Claim Construction Positions

  • Petitioner argued for a broad construction of the term "Interleukin 11 receptor α (IL-11Rα) antibody" to mean "any natural or synthetic, monoclonal or polyclonal antibody made using any animal system including phage, or fragment or derivative thereof, that binds to IL-11Rα of any species." This broad, purely functional construction was central to Petitioner’s arguments that the claims were invalid under §112 for lacking written description and enablement for such a vast and structurally undefined genus.

5. Key Technical Contentions (Beyond Claim Construction)

  • Unpredictability of Antibody Function: A core technical contention underpinning the §112 grounds was the inherent unpredictability of the art. Petitioner argued that antibody function is dictated by highly diverse and variable sequences (e.g., CDRs) that form complex three-dimensional structures. It is not possible to predict a priori which antibody sequences will bind a target, let alone inhibit its function and produce a therapeutic effect. Therefore, claiming a genus of antibodies by function alone, without providing representative structural information, amounts to claiming a mere research plan rather than an enabled invention.

6. Relief Requested

  • Petitioner requested institution of a Post Grant Review and cancellation of claims 1-10 of the ’603 patent as unpatentable under 35 U.S.C. §§ 112, 102, and 103.