Prior art — US Patent 11014982

To identify the most relevant prior art for US Patent 11014982, I need to access the patent's citations from the USPTO database. Since I cannot directly browse the USPTO database in real-time, I will rely on the information provided in the patent text itself regarding cited prior art. The patent text lists several references, particularly in the "Prior art keywords" and "Prior art date" sections of the Google Patents page, and within the detailed description where various techniques and existing knowledge are cited.

Based on the provided patent text, here's an analysis of potentially relevant prior art mentioned, focusing on those directly cited rather than general knowledge. The patent refers to several general techniques and publications, but for specific prior art that could anticipate claims under 35 U.S.C. § 102, we look for previously issued patents or publications disclosing similar inventions.

The Google Patents page itself lists "Prior art keywords" and a "Prior art date" of 2017-02-07. This suggests that any prior art published or filed before this date could be relevant.

The patent text extensively discusses the background of TNF-alpha and its role in various diseases, and mentions previous work with anti-TNF antibodies. For example, it references "beneficial effects in open-label trials with a chimeric monoclonal antibody to TNF alpha (cA2)" and "Beneficial results in a randomized, double-blind, placebo-controlled trial with cA2" in rheumatoid arthritis and Crohn's disease. The patent also describes methods for producing antibodies, including humanized antibodies and transgenic animals, citing various U.S. patents for these techniques.

Without direct access to the "Examiner Citations" and "Applicant Citations" sections typically found in a USPTO patent document, I will identify the most relevant prior art mentioned or implied by the provided text that could potentially anticipate claims.

Most Relevant Prior Art (based on explicit mentions in the provided text):

The patent details a new use for an anti-TNF antibody with specific heavy and light chain sequences (SEQ ID NO:36 and SEQ ID NO:37) for treating active Ankylosing Spondylitis (AS) via IV infusion to achieve specific clinical outcomes. Therefore, the most relevant prior art would likely involve:

Prior art disclosing the specific anti-TNF antibody (SEQ ID NO:36 and SEQ ID NO:37) itself.
Prior art disclosing the use of any anti-TNF antibody for treating AS with similar outcomes, especially via IV infusion.
Prior art disclosing the specific anti-TNF antibody for treating other TNF-related conditions.

The patent mentions "cA2" extensively as a previously studied chimeric monoclonal antibody to TNF alpha. While not a direct citation with patent number, it is discussed as a known anti-TNF therapy and therefore represents relevant prior art in the field of TNF-alpha inhibition.

Reference: Chimeric monoclonal antibody to TNF alpha (cA2)
- Publication/Filing Date: Implied to be prior to the patent's priority date of 2017-02-07, as its effects in rheumatoid arthritis and Crohn's disease are discussed as established.
- Brief Description: cA2 is a chimeric monoclonal antibody to TNF alpha that has shown beneficial effects in treating rheumatoid arthritis and Crohn's disease. The patent notes its use in open-label trials and randomized, double-blind, placebo-controlled trials. The figures and examples further detail its use as a comparative control in mouse models (e.g., FIGS. 11A-C, 13A-C, 15, 17).
- Potential Anticipation (35 U.S.C. § 102):
  - If cA2 (or an antibody structurally identical or substantially similar to SEQ ID NOs:36 and 37) was previously disclosed for treating AS, it could anticipate claims related to the method of treatment for active AS (e.g., claims generally covering the method of administering an anti-TNF antibody for AS).
  - If cA2's mechanism of action and general therapeutic properties, including the ability to achieve similar clinical outcomes (like ASAS20 or ASDAS inactive disease) in other inflammatory conditions, were known, it could potentially anticipate the broader concept of anti-TNF therapy for AS, especially if the differences in the claimed antibody (SEQ ID NOs:36 and 37) are not sufficiently distinct or provide unexpected results compared to cA2 for AS. The patent specifically differentiates TNV148 from cA2 in animal models (e.g., "the 1 mg/kg TNV148 showed a significantly lower AI than 1 mg/kg cA2 at 3, 4 and 7 weeks"), suggesting the inventors believe their antibody has improved efficacy.

The patent also references several general scientific techniques and older patents, but these are generally for methods of making antibodies or genetic engineering techniques, rather than specific compositions or methods of treatment that would directly anticipate the core claims of this patent. Examples include:

Ausubel, et al., ed., Current Protocols in Molecular Biology, John Wiley & Sons, Inc., NY, N.Y. (1987-2001); Sambrook, et al., Molecular Cloning: A Laboratory Manual, 2nd Edition, Cold Spring Harbor, N.Y.
- These are general textbooks on molecular biology and cloning, providing foundational knowledge for antibody production. They would not anticipate specific antibody sequences or therapeutic uses.
Milstein and Cuello, Nature 305:537 (1983)
- Cited for methods of making bispecific antibodies. This is a methodological reference, not directly anticipating the specific antibody or its use in AS.
Elliott et al., Lancet 344:1125-1127 (1994)
- Cited in the context of defining "low immunogenicity" for antibodies (HAHA, HACA, HAMA responses). This defines a characteristic, but doesn't disclose the invention.
U.S. Pat. Nos. 5,770,428, 5,569,825, 5,545,806, 5,625,126, 5,625,825, 5,633,425, 5,661,016 and 5,789,650 issued to Lonberg et al.
- These patents are cited for methods of producing transgenic mice capable of producing human antibodies. They cover the method of making such antibodies, not the specific anti-TNF antibody of the present invention or its use in AS.
U.S. Pat. Nos. 5,827,690; 5,849,992; 4,873,316; 5,849,992; 5,994,616; 5,565,362; 5,304,489
- These patents are cited for methods of producing transgenic animals (e.g., goats, cows) that produce antibodies in their milk. Again, these are manufacturing methods, not directly anticipatory of the specific antibody or its therapeutic use for AS.

Without the actual "References Cited" section from the USPTO patent document for US11014982, it is difficult to provide a comprehensive list of all prior art considered by the examiner. However, based on the narrative in the patent, the existence and efficacy of other anti-TNF antibodies (like cA2) for inflammatory conditions would be a primary area of prior art to consider when evaluating the novelty and non-obviousness of using a specific anti-TNF antibody (with SEQ ID NO:36 and SEQ ID NO:37) for treating active Ankylosing Spondylitis with specified outcomes.

A thorough prior art analysis would require examining each patent and non-patent literature cited in the official USPTO record for US11014982, specifically focusing on disclosures of:

The exact antibody sequences (SEQ ID NOs:36 and 37).
Anti-TNF therapy for Ankylosing Spondylitis.
Specific dosing regimens and administration routes (IV infusion).
Achieving ASDAS inactive disease or ASAS20 in AS patients.

Given the current information, cA2, as a known anti-TNF antibody for inflammatory conditions, serves as a significant conceptual prior art mentioned within the patent text itself. The patent then describes its specific anti-TNF antibody (e.g., TNV148) and differentiates its efficacy from cA2 in certain models, suggesting that the novelty lies in the specific antibody's structure and/or its specific efficacy profile in AS.