DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Claim Status
Claims 3-5 are cancelled. Claims 1-2 and 6-13 as filed on 26 August 2025 are pending. Claims 9-13 are withdrawn. Claims 1-2 and 6-8 are under examination.
Rejections Withdrawn
Rejection of claims 3-5 under 35 U.S.C. 112(b) is withdrawn with cancellation of claims.
Rejection of claims 1 and 7-8 under 35 U.S.C. 102(a)(2) is withdrawn with applicant’s declaration and Lotersztajn (WO 2018/234843 A1) (IDS) is disqualified as prior art under 102(b)(2) by the Declaration filed 08/26/2025.
Applicant’s arguments, see page 4-5 of Remarks, filed 08/26/2025, with respect to the limiting definition of Metabolic Syndrome pointed to by Applicant have been fully considered and are persuasive. The rejection of 1 and 7-8 under 35 U.S.C. 102(a)(1) over Rouxel et. al. is withdrawn.
Metabolic Syndrome of the claims is limited to a subject characterized by three or more of the following symptoms: abdominal obesity, hyperglyceridemia, low HDL cholesterol, high blood pressure, and high fasting plasma glucose.
Rejection Maintained
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
Claims 1-2 and 6-8 are rejected under 35 U.S.C. 103 as being unpatentable over Kumar & Ahmad. International Reviews of Immunology. 37(2):90-110. (2018) (Of Record), Shaler et. al. PLOS Biology. 15(6):1-35. (2017) (Of Record), Rouxel et. al. Nat Immunol 18:1321–1331 (2017), as evidenced by Eckel et. al. The Lancet. 375:181-183. (2010) (Of Record), and Lantz (WO 2008087219 A1) (Of Record).
Khumar teaches MAIT cells have a role in autoimmune, inflammatory disease, infectious diseases, cancer, and a number of acute and chronic diseases in humans. Khumar further teaches exploration of MAIT cells for novel therapies (abstract).
Khumar teaches aberrant MAIT cell localization and activity in type 2 diabetes patients and the adipose tissue of obese patients. Khumar specifically teaches there are increased number of MAIT cells in the adipose tissue of obese patients and that they are secreting higher levels of cytokines (page 101 in col 1 in lines 8-23).
Khumar teaches the use of corticosteroids in the treatment of inflammatory and autoimmune disease resulting in reduction of proliferation and activity of MAIT cells (page 104 in col 1 in par 1).
Khumar teaches the barrier to further development was a lack of animal model but further teaches the recent development of multiple mouse models for use in the study of MAIT including the model used by Shaler and cites Shaler (page 104 in col 1 in par 2).
Khumar does not teach the administration of a MAIT cell inhibitor to an obese subject in a method of treatment.
These deficiencies are filled by Rouxel, Shaler, and Lantz.
Shaler teaches the use of a transgenic mouse for the purpose of studying MAIT cells (Abstract) and the use of staphylococcal enterotoxin B (SEB) as a modulator of MAIT cells (abstract and Figures 1, 3, and 8). Shaler teaches SEB is considered a category B priority bioterrorism agent by the CDC (page 3 in lines 1-2). Shaler further teaches the administration of SEB to a mouse model resulting in weight loss in the mouse and loss of MAIT activity in immune response (Figure 9). Shaler teaches the manipulation of MAIT cells changes inflammatory response in cell and animal models (abstract).
Shaler thus teaches manipulation of MAIT cells can result in changes to the weight of a subject.
Regarding claim 1, Lantz teaches an antibody that inhibits MAIT cells (Example 2 and claims 1-37, 43, and 45-46) and further teaches the antibody as part of a composition that further comprises non-antibody therapeutics including ones that inhibit MAIT cells (claims 44 and 52). Lantz teaches a method of treating a patient by the manipulation of MAIT cells by inhibiting MAIT cells (claims 47-51). Lantz teaches the method of treatment includes numerous diseases with inflammation including irritable bowel syndrome, ulcerative colitis, and celiac disease (claim 49).
Rouxel teaches the administration of Ac-6-FP to NOD mice with type 1 diabetes (Figure 5). Type 1 diabetes would include high blood sugar which would be a metabolic syndrome as evidenced by Eckel (Entire text but in particular Table on page 182, page 181 in col 2 in par 1).
It would have been obvious at the time the application was filed to take the teachings of Khumar of MAIT cells being active in inflammation and obese adipose tissues and produce a method of treating obese patients with MAIT cell inhibition using the inhibitors taught by Lantz and Rouxel. Shaler teaches weight loss with MAIT cell manipulation that causes a loss in MAIT cell function in a mouse model. Lantz and Rouxel both teach effective methods of treatment by administration of their MAIT cell inhibitors. One of skill in the art would have been motivated by Khumar’s teaching of MAIT cell presence and activity in obese adipose tissue and Shaler’s resulting weight loss to explore administration to patients using safer therapeutic MAIT cell inhibitors taught by Lantz and Rouxel. One of skill in the art would not use SEB of Shaler given its potentially dangerous applications which is why one of skill in the art would explore inhibitors already taught to be used in patients with inflammatory issues like type 1 diabetes patients of Rouxel. There would have been a reasonable expectation of success as the art, Khumar, Shaler, Lantz, and Rouxel, teaches MAIT cells as having a role in inflammation, being used in patients with inflammatory related conditions and the success of those methods. Thus, a method of treating an obese patient with the MAIT cell inhibitor Ac-6-FP to treat the inflammation and having weight loss would be obvious in view of the art as MAIT cells are taught as a potential therapeutic target in obese adipose tissue (Khumar), weight loss is taught with MAIT cell manipulation (Shaler), and use of Ac-6-FP as a therapeutic to target MAIT cells in an inflammatory environment (Rouzel) are all known in the art.
Applicant Arguments
Applicant argues that Rouxel and Eckel are unrelated to the invention as the Metabolic Syndrome of the claims is limited to a subject characterized by three or more of the following symptoms: abdominal obesity, hyperglyceridemia, low HDL cholesterol, high blood pressure, and high fasting plasma glucose.
Applicant argues that Kumar and Shaler fail to compensate for the deficiencies of Rouxel being unrelated to the invention.
Applicant argues Kumar does not teach targeting MAIT cells as an effective treatment for obesity or type 2 diabetes.
Applicant argues Shaler teaches the activation rather than the inhibition of MAIT cells and would not provide one of skill in the art knowledge of inhibiting MAIT cells for use in a method of treating obesity.
Applicant argues that Lantz does not compensate for the deficiencies of Kumar and Shaler as Lantz is only teaching antibodies that inhibit MAIT cells in the adipose tissue of an obese subject.
Response to Arguments
Applicant's arguments filed 08/26/2025 have been fully considered but they are not persuasive.
Rouxel and Eckel remain relevant to the claims and the 103 rejection as they teach the pharmaceutical Ac-6-FP administered to patients that would inherently have the symptoms of hyperglycemia, high fasting blood sugar, and inflammation in a patient with an autoimmune disease. Rouxel provides teachings that location and activity of MAIT cells corresponds with disease progression and symptoms playing a key role in inflammatory and autoreactive T cells in the development to T1D (page 5 in par 1-2 and page 6 in par 1 in last 3 lines of paragraph). While the teachings of Rouxel do not anticipate the claims, Rouxel in combination with Eckel show that one of skill in the art would group Rouxel and its teachings on T1D with the teachings of Khumar.
Khumar and Shaler are not being relied upon to teach inhibition of MAIT cells. Khumar and Shaler are both teaching the location of MAIT cells in the patient population of interest and Shaler teaches that manipulating MAIT cell activity impacts the symptoms of the patient population of Khumar and the claims.
Khumar and Shaler are being relied upon in the rejection to teach the presence of MAIT cells in the adipose of obese and type 2 diabetic patients and the role of MAIT cells in inflammatory signals of patients with autoimmune disorders, inflammatory disorders, cancer, and infectious disease. Khumar specifically teaches MAIT cells deposited in the adipose tissue contributing to development of diabetes (page 101 in col 2 in lines 28-35.
Rouxel is then relied upon to teach not only the development of T1D from MAIT cell activity but that inhibition of MAIT cells led to delay in development of T1D while teaching Ac-6-FP as a known inhibitor of MAIT cells that worked in another condition characterized by inflammation and autoreactive immune response.
Lantz provides support for Rouxel showing that while Shaler only provides manipulation of MAIT cells, Lantz shows the art teaching treatment of inflammation using a MAIT inhibitor (claims 47-52).
Khumar and Shaler teach the presence of MAIT cells in the patient population of the claims and teaches MAIT cell activity is related to the disease state. Further, they teach MAIT cells as a potential target for treatment of obesity, T2D, inflammatory disease, and many chronic and infectious diseases. Rouxel and Lantz teach that the inhibition of MAIT cells is a method of treating inflammation and autoimmune disease when MAIT cells are present in the tissue related to disease.
Conclusion
THIS ACTION IS MADE FINAL. Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
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/F.E./Examiner, Art Unit 1643
/Meera Natarajan/Primary Examiner, Art Unit 1643
