US 7267820

US Patent 7267820, titled "Neurotransmission disorders," has a current assignee of Max Planck Gesellschaft zur Foerderung der Wissenschaften eV and Oxford University Innovation Ltd. The inventors are Angela Vincent and Werner Hoch. The patent was filed on June 15, 2001, and issued on September 11, 2007.

Abstract:
The patent discloses a method for diagnosing neurotransmission or developmental disorders in a mammal by detecting autoantibodies to an epitope of the muscle-specific tyrosine kinase (MuSK) in a bodily fluid from the mammal. One method involves contacting the bodily fluid with MuSK or its antigenic determinant and then detecting any formed antibody-antigen complexes, where the presence of these complexes indicates the mammal is suffering from such disorders. The patent also describes kits for use in diagnosing these neurotransmission and subsequent developmental disorders.

Plain-Language Overview of Independent Claims:

• Claim 1: This claim describes a method for diagnosing neurotransmission or developmental disorders that are specifically related to muscle-specific tyrosine kinase (MuSK) in a mammal. The method involves identifying the presence of autoantibodies targeting an epitope of MuSK within a bodily fluid of that mammal.
• Claim 7: This claim details another diagnostic method for MuSK-related neurotransmission or developmental disorders. It involves introducing a labeled MuSK protein or a labeled part of it (an epitope or antigenic determinant) to a mammal's bodily fluid. After that, any complexes formed between the labeled MuSK and antibodies from the bodily fluid are immunoprecipitated. The detection of the label on these complexes indicates the mammal has the disorder.
• Claim 12: This claim specifies a method for diagnosing neurotransmission or developmental disorders that are particularly related to interference in the agrin/MuSK/AChR pathway within a mammal. The diagnostic step involves detecting autoantibodies against an epitope of MuSK in a bodily fluid from the mammal.

The patent's legal status is listed as "Expired - Lifetime," with an expiration date of November 3, 2022. Due to its expired status, it is highly unlikely to find active litigation concerning infringement of this patent in 2026. Previous litigation activity related to this patent has been noted, including cases filed in the U.S. Supreme Court (case 19-430), the Court of Appeals for the Federal Circuit (case 17-2508), and the Massachusetts District Court (cases 4:15-cv-40075 and 1:15-cv-40075). As of April 26, 2026, a search for 2026 dockets in the CAFC for US patent 7267820 did not return any new active litigation cases for the specified year.

As a patent attorney, I have investigated the litigation history of US Patent 7267820. The patent's legal status is "Expired - Lifetime," having expired on November 3, 2022. This significantly reduces the likelihood of active infringement litigation in 2026.

Based on the provided information, known litigation involving US Patent 7267820 includes:

• U.S. Supreme Court
  • Case Number: 19-430
  • Status: The legal status indicates "Family has litigation," with a specific mention of a US case filed in the U.S. Supreme Court, case 19-430. The outcome or current status in 2026 is not detailed in the provided information.
• Court of Appeals for the Federal Circuit
  • Case Number: 17-2508
  • Status: The legal status indicates "Family has litigation," with a specific mention of a US case filed in the Court of Appeals for the Federal Circuit, case 17-2508. The outcome or current status in 2026 is not detailed in the provided information.
• Massachusetts District Court
  • Case Number: 4:15-cv-40075
  • Status: The legal status indicates "Family has litigation," with a specific mention of a US case filed in Massachusetts District Court, case 4:15-cv-40075. The outcome or current status in 2026 is not detailed in the provided information.
• Massachusetts District Court
  • Case Number: 1:15-cv-40075
  • Status: The legal status indicates "Family has litigation," with a specific mention of a US case filed in Massachusetts District Court, case 1:15-cv-40075. The outcome or current status in 2026 is not detailed in the provided information.

The provided information does not explicitly list the plaintiffs, defendants, or filing dates for these specific cases, beyond indicating that they are related to the patent family. My search for 2026 dockets in the CAFC for US patent 7267820 did not return any new active litigation cases for the specified year.

To obtain the complete details (plaintiff(s), defendant(s), filing dates, and definitive outcomes) for these past cases, a direct search using PACER (Public Access to Court Electronic Records) would be necessary. PACER provides electronic public access to federal court records, allowing users to search by specific court or a nationwide index. Access to case information costs $0.10 per page, with a cap of $3.00 for a single document. However, without a PACER account, I cannot perform this direct search to retrieve the full litigation details.

Proceedings overview

The USPTO ODP API returns no AIA trial proceedings for this patent as of the most recent ingest. Therefore, there is no PTAB activity on file for US Patent 7267820. This gives a defendant no direct prior PTAB outcomes to leverage for defensive posture.

Strategic summary

As there are no AIA trial proceedings on file for US Patent 7267820, all claims (1-12) remain untested by PTAB trials. There is no estoppel landscape from PTAB proceedings to consider, as no petitions have been filed. The absence of PTAB activity could signal that the patent has not been extensively asserted in a manner that would typically provoke IPR filings, or that potential challengers have not found strong prior art grounds to pursue such actions.

Recommended next steps

If you are a defendant facing assertion of US Patent 7267820, it is important to note that the patent's claims have not been subject to PTAB review. This means that all claims are currently considered patentable as far as PTAB proceedings are concerned. A thorough prior art search would be a crucial next step to identify potential grounds for an Inter Partes Review (IPR) should the patent be asserted. The absence of PTAB activity suggests that this could be a viable avenue for a defendant to explore, as the patent has not been "hardened" by surviving previous PTAB challenges.

Inventors

• Angela Vincent (Max Planck Gesellschaft zur Foerderung der Wissenschaften eV, Oxford University Innovation Ltd)
• Werner Hoch (Max Planck Gesellschaft zur Foerderung der Wissenschaften eV, Oxford University Innovation Ltd)

Original assignee

The original assignees named on the issued patent US7267820 are Max Planck Gesellschaft zur Foerderung der Wissenschaften eV and Oxford University Innovation Ltd. Oxford University Innovation Ltd (formerly Isis Innovation Limited) is the research commercialisation company for the University of Oxford. Max Planck Gesellschaft zur Foerderung der Wissenschaften eV is a German non-profit research organization. Both are primarily involved in academic research and technology transfer. It is unclear if they shipped a product embodying the claims directly. Both entities are currently operating.

Assignment timeline

• 2003-01-29 to 2003-02-18 (executed) / recorded 2003-06-06 — Reel 014136/0282

  • Conveyance: Assignment
  • Assignor: VINCENT, ANGELA; HOCH, WERNER
  • Assignee: ISIS INNOVATION LIMITED
  • Correspondent: HOOVER, ALLISON C, BIRCH STEWART KOLASCH & BIRCH, LLP, PO BOX 747, FALLS CHURCH, VA, 22040-0747
  • Context: Transfer of inventors' interest to an innovation commercialization company.

• 2004-06-10 to 2004-06-15 (executed) / recorded 2004-06-18 — Reel 014756/0557

  • Conveyance: Assignment
  • Assignor: VINCENT, ANGELA; HOCH, WERNER
  • Assignee: MAX-PLANCK GESELLSCHAFT ZUR FOERDERUNG DER WISSENSCHAFTEN E.V., ISIS INNOVATION LIMITED
  • Correspondent: HOOVER, ALLISON C, BIRCH STEWART KOLASCH & BIRCH, LLP, PO BOX 747, FALLS CHURCH, VA, 22040-0747. This correspondent also appears on reel 014136/0282.
  • Context: Reassignment of inventors' interest to include Max Planck Gesellschaft.

• 2004-06-09 (executed) / recorded 2004-06-18 — Reel 014757/0964

  • Conveyance: Assignment
  • Assignor: ISIS INNOVATION LIMITED
  • Assignee: VINCENT, ANGELA, ENGLAND; HOCH, WERNER, TEXAS
  • Correspondent: HOOVER, ALLISON C, BIRCH STEWART KOLASCH & BIRCH, LLP, PO BOX 747, FALLS CHURCH, VA, 22040-0747. This correspondent also appears on reel 014136/0282 and 014756/0557.
  • Context: Reassignment of a partial interest back to the inventors.

• 2016-06-16 (executed) / recorded 2016-08-02 — Reel 039550/0045

  • Conveyance: Change of Name
  • Assignor: ISIS INNOVATION LIMITED
  • Assignee: OXFORD UNIVERSITY INNOVATION LIMITED
  • Correspondent: None listed.
  • Context: Change of name for one of the assignees.

Timeline diagram

timeline
    title Ownership of US 7267820
    2001 : Patent filed
    2003 : Inventors assign to ISIS Innovation
    2004 : Inventors assign to Max Planck & ISIS
         : ISIS Innovation assigns to Inventors
    2007 : Patent issued
    2015 : MA District Court litigation filed
    2016 : ISIS Innovation name changed to Oxford Univ Innovation
    2017 : CAFC litigation filed
    2019 : US Supreme Court litigation filed
    2022 : Patent expired

NPE / troll-pattern signals

1. Shell-entity transfer — not present. The assignees are academic and research institutions or the individual inventors, not shell entities.
2. Known asserter in the chain — not present. None of the listed assignees match known NPE lists.
3. Repeat correspondent across the chain — present. Allison C. Hoover of Birch, Stewart, Kolasch & Birch, LLP, is listed as the correspondent on reel 014136/0282, 014756/0557, and 014757/0964.
4. Cascading transfers — not present. The transfers in 2004 involved the same parties and occurred on the same day, indicating an internal adjustment rather than a rapid succession of transfers to different entities.
5. Pre-litigation transfer — unclear. The provided information states that the Massachusetts District Court litigation (4:15-cv-40075 and 1:15-cv-40075) was filed in 2015. However, the last assignment listed is a change of name in 2016. No transfer occurred within six months of the litigation filing.
6. Bankruptcy fire-sale — not present. No indication of bankruptcy for any of the assignors.
7. Privateering — not present. No evidence in the assignment records or provided context suggests privateering.
8. Defensive aggregator (anti-NPE) — not present. The chain does not terminate at any known defensive aggregators.

Verdict

Insufficient data. While there is a strong signal of a repeat correspondent across multiple assignments, this alone is not enough to confidently classify the patent owner as an NPE, especially given that the listed assignees are academic/research institutions. There are no other clear NPE signals such as shell entity transfers or known asserters in the chain. The litigation information is also not detailed enough to determine if the patent was transferred specifically for assertion purposes shortly before litigation.

Verification: https://assignmentcenter.uspto.gov/

To identify the most relevant prior art for US Patent 7267820, I will search the USPTO database for the patent and then analyze its cited references.

Here's the analysis of the most relevant patent prior art for US Patent 7267820, as listed in the patent document itself:

US Patent 5,814,478 A: Tyrosine kinase receptors and ligands

• Full Citation: US 5,814,478 A (Regeneron Pharmaceuticals, Inc.)
• Publication Date: September 29, 1998
• Filing Date: December 15, 1995
• Brief Description: This patent describes tyrosine kinase receptors and their ligands. It covers the identification, isolation, and use of these receptors and ligands, particularly in the context of cell growth, differentiation, and development. Since MuSK is a receptor tyrosine kinase (RTK), this patent generally covers the class of molecules to which MuSK belongs and methods for studying them.
• Potential Anticipation (35 U.S.C. § 102): This patent broadly covers receptor tyrosine kinases. While it doesn't specifically mention MuSK or its autoantibodies, it establishes the prior art for the general concept of studying RTKs and their role in biological processes. It could potentially anticipate the broader aspects of the invention related to the use of RTKs as targets in diagnostic methods, particularly for claims that are not narrowly focused on the specific MuSK autoantibody detection (e.g., portions of claim 1, 2, and 7 if interpreted very broadly outside the MuSK-specific autoantibody detection). However, the novelty of US7267820 lies in the discovery of autoantibodies to MuSK as a diagnostic marker for specific neurotransmission disorders, which this patent does not disclose.

WO 1999/010494 A2: Agonist antibodies to the thrombopoietin receptor, and their therapeutic uses

• Full Citation: WO 1999/010494 A2 (Genentech, Inc.)
• Publication Date: March 4, 1999
• Filing Date: August 25, 1997
• Brief Description: This international publication describes agonist antibodies that bind to and activate the thrombopoietin receptor, and their therapeutic uses. It demonstrates the concept of using antibodies to modulate receptor activity for therapeutic purposes.
• Potential Anticipation (35 U.S.C. § 102): This reference teaches the use of antibodies as diagnostic and therapeutic agents targeting a receptor. While it specifically concerns the thrombopoietin receptor and agonist antibodies, it establishes the prior art for the general idea of using antibodies to detect or treat conditions related to receptor function. This could potentially anticipate aspects of US7267820 related to the general methodology of antibody-based diagnostics or therapeutics for receptor-related disorders (e.g., claims 1, 2, 7, and the concept of an isolated antibody in the description for treatment, if interpreted broadly). However, it does not disclose the specific target (MuSK), the specific type of antibody (autoantibody), or the specific disorders (neurotransmission/developmental disorders related to MuSK) found in US7267820. The key inventive step of US7267820 is the identification of anti-MuSK autoantibodies in the context of specific disorders.

Obviousness under 35 U.S.C. § 103 dictates that a patent claim cannot be obtained if the differences between the claimed invention and the prior art would have been obvious to a person having ordinary skill in the art (PHOSITA) at the time the invention was made. This analysis requires determining the scope and content of the prior art, identifying the differences between the claimed invention and the prior art, and ascertaining the level of skill in the pertinent art. A motivation to combine prior art references is crucial, and this motivation does not necessarily need to be explicit in the prior art itself but can be inferred from market demand, design trends, or other common-sense reasoning known to a PHOSITA.

The independent claims of US7267820 revolve around diagnosing neurotransmission or developmental disorders by detecting autoantibodies to MuSK in a bodily fluid. This includes specific detection methods like contacting the bodily fluid with MuSK and detecting complexes, using labeled antibodies, or employing immunoprecipitation with labeled MuSK. [claim 1, claim 7, claim 12]

Prior Art Analysis for Obviousness

Given the state of the art around the filing date of June 15, 2001, a PHOSITA in the field of neurological disorder diagnostics, particularly Myasthenia Gravis (MG), would have been aware of several key pieces of information:

1. Myasthenia Gravis and Autoantibodies: MG was known as a chronic autoimmune disorder characterized by muscle weakness due to antibodies against the acetylcholine receptor (AChR). Approximately 80% of MG patients had detectable anti-AChR autoantibodies.
2. Seronegative MG (AAAN): A significant subset (around 20%) of MG patients were "seronegative" (AAAN), meaning they exhibited MG symptoms but lacked detectable anti-AChR antibodies. These patients presented a diagnostic challenge, as there was no established clinical diagnosis for them.
3. General Immunological Assay Techniques: Standard immunological assay techniques for detecting autoantibodies in bodily fluids were well-known and included ELISA, radioimmunoassays (RIA), and immunoprecipitation. These techniques generally involved using an antigen, immobilizing it on a solid support, contacting it with a sample, and detecting formed antibody-antigen complexes using labeled secondary antibodies or direct labeling of the antigen.
   • Radioimmunoassays (RIA) using 125I-labeled antigens and immunoprecipitation were standard techniques.
   • ELISA was also a known method for antibody detection.

Combinations of Prior Art to Render Claims Obvious

The core inventive step of US7267820 is the detection of autoantibodies to MuSK for diagnosing specific neurotransmission or developmental disorders, particularly in anti-AChR autoantibody-negative MG patients. [claim 1]

Combination 1: Knowledge of AAAN MG + General Autoantibody Detection Methods

• Prior Art Elements:

  • The existence of seronegative MG (AAAN) patients who could not be diagnosed by existing anti-AChR antibody tests, representing a "long-felt but unsolved need" for an alternative diagnostic marker.
  • General knowledge in the art that autoimmune disorders are often characterized by autoantibodies against specific targets.
  • Well-established immunological assay techniques for detecting autoantibodies, such as ELISA, RIA, and immunoprecipitation, which involve presenting a target antigen to a bodily fluid and detecting antibody-antigen complexes.

• Motivation to Combine: A PHOSITA would have been highly motivated to identify new autoantibody targets in AAAN MG patients to address the diagnostic gap. Given that MG is an autoimmune disease, and 80% of cases were linked to anti-AChR antibodies, it would be a natural extension to search for other autoantibody targets in the remaining 20% of seronegative patients. The general approach would involve using known autoantibody detection techniques with candidate antigens. The need for a diagnostic tool for AAAN patients would drive a PHOSITA to systematically investigate potential autoantigens using existing assay technologies.

• Obviousness Argument for Claims 1, 2, 7, and 12:

  • Claim 1: The identification of MuSK as the specific target was novel. However, the method of "detecting in a bodily fluid of said mammal autoantibodies to an epitope of the muscle specific tyrosine kinase, MuSK" (Claim 1) could be argued as obvious to try. Given the known role of MuSK in neuromuscular junction development and function, and the context of an autoimmune neuromuscular disorder like MG, a PHOSITA would have a "reasonable expectation of success" in investigating MuSK as a potential autoantigen in AAAN patients using standard autoantibody detection methods. The patent itself states that "one candidate autoantibody was that one for the MuSK protein" (Description), implying that MuSK was already considered a potential target.
  • Claim 2: This claim specifies contacting the bodily fluid with MuSK or an antigenic determinant and detecting antibody-antigen complexes. This is a direct application of standard immunological assay principles (e.g., ELISA, RIA) to the newly identified MuSK antigen. A PHOSITA would routinely apply these known techniques to a new antigen of interest.
  • Claim 7: This claim describes using a labeled MuSK or epitope, immunoprecipitating complexes, and monitoring the label. This is a well-established radioimmunoassay (RIA) technique, specifically mentioned in the prior art as a "gold standard" for antibody detection, including MuSK antibodies in later discussions. The patent itself refers to iodination and immunoprecipitation as "standard techniques in the art." (Description)
  • Claim 12: This claim links the detection of MuSK autoantibodies to interference in the agrin/MuSK/AChR pathway. While the understanding of this specific pathogenic mechanism might have been novel at the time, the method of detection (detecting MuSK autoantibodies) remains the same as Claim 1. If the detection of MuSK autoantibodies was obvious, then associating that detection with a known pathway involving MuSK would also be obvious to a PHOSITA studying the disease etiology.

Combination 2: Specificity of Detection Methods (Claims 3-6, 8-9)

• Prior Art Elements:

  • General immunological assay techniques, including ELISA, radioimmunoassays, and immunoprecipitation.
  • Common reporter molecules and labels used in these assays, such as heavy metals, fluorescent/luminescent molecules, radioactive tags (e.g., 125I), and enzymatic tags (e.g., horseradish peroxidase-protein A).
  • Detection using secondary antibodies, like anti-IgG or anti-IgM, conjugated to these labels, and measurement of signal intensity to quantify antibody levels.

• Motivation to Combine: Once the concept of detecting MuSK autoantibodies was considered, a PHOSITA would routinely select from a finite number of known and predictable assay methodologies and labeling techniques to implement the detection. There would be a clear motivation to use established and reliable detection methods.

• Obviousness Argument for Claims 3, 4, 5, 6, 8, and 9:

  • Claim 3: Detecting antibody-antigen complexes using an anti-IgG antibody tagged with a reporter molecule is a fundamental principle of many immunoassays, including ELISA and Western blotting.
  • Claim 4: The specific types of reporter molecules (heavy metal, fluorescent/luminescent, radioactive, enzymatic tags) were all well-known and commonly used in diagnostic assays.
  • Claim 5: Horseradish peroxidase-protein A with o-phenylenediamine and A492 measurement is a standard enzymatic detection system for ELISA.
  • Claim 6: Using signal intensity from an anti-human IgG antibody to indicate the relative amount of autoantibody, compared to controls, is a basic quantitative principle of immunoassays.
  • Claim 8 and 9: Specifying a radioactive label, particularly 125I, for immunoprecipitation is a direct application of a well-established technique for autoantibody detection (RIA). The patent itself acknowledges this as "standard techniques in the art". (Description)

Conclusion on Obviousness:

While the discovery of MuSK autoantibodies in AAAN Myasthenia Gravis patients was a significant scientific finding, the methods claimed in US7267820 for detecting these antibodies could be argued as obvious under 35 U.S.C. § 103, particularly when considering the state of prior art and the motivation of a PHOSITA. The widespread existence of AAAN MG patients created a clear "long-felt but unsolved need" for new diagnostic markers. Given this need, and the established methodologies for detecting autoantibodies using various labels and assay formats (ELISA, RIA, immunoprecipitation), a PHOSITA would have been motivated to combine these known techniques with candidate antigens, such as MuSK (a protein known to be involved in neuromuscular junction function), with a reasonable expectation of success in identifying new autoantibodies. The specific details of the detection methods (e.g., use of anti-IgG, various labels, 125I for RIA) were also well-known and routinely applied in the field. Therefore, the combination of a known diagnostic problem (AAAN MG), a plausible biological target (MuSK), and standard immunological detection techniques would likely render the claims obvious to a PHOSITA at the time of the invention.