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 1-40 are pending and currently under consideration for patentability under 37 CFR 1.104.
Priority
This application claims benefit of Provisional U.S. Application No. 63/375,936 filed on 09/16/2022. Applicant’s claim for the benefit of a prior-filed application under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, 365(c), or 386(c) is acknowledged.
Claims 37-40 contain subject matter which was not described in Provisional U.S. Application No. 63/375,936; consequently, their priority date will not correspond to the provisional application.
Claims 1-36 have an effective filing date of 09/16/2022 corresponding to Provisional U.S. Application No. 63/375,936. Claims 37-40 have an effective filing date of 09/15/2023 corresponding to the instant application.
Information Disclosure Statement
The information disclosure statement filed on 05/13/2024 has been considered. All references considered unless marked with strikethrough. Signed copies are enclosed.
The information disclosure statement filed 05/13/2024 fails to comply with 37 CFR 1.98(a)(2), which requires a legible copy of each cited foreign patent document; each non-patent literature publication or that portion which caused it to be listed; and all other information or that portion which caused it to be listed. It has been placed in the application file, but the information referred to therein has not been considered.
Notably, the disclosure statement filed lists a Search Report. The listing of the references cited in a Search Report itself is not considered to be an information disclosure statement (IDS) complying with 37 CFR 1.98. 37 CFR 1.98(a)(2) requires a legible copy of: (1) each foreign patent; (2) each publication or that portion which caused it to be listed; (3) for each cited pending U.S. application, the application specification including claims, and any drawing of the application, or that portion of the application which caused it to be listed including any claims directed to that portion, unless the cited pending U.S. application is stored in the Image File Wrapper (IFW) system; and (4) all other information, or that portion which caused it to be listed. In addition, each IDS must include a list of all patents, publications, applications, or other information submitted for consideration by the Office (see 37 CFR 1.98(a)(1) and (b)), and MPEP § 609.04(a), subsection I. states, "the list ... must be submitted on a separate paper." Therefore, the references cited in the Search Report have not been considered. Applicant is advised that the date of submission of any item of information or any missing element(s) will be the date of submission for purposes of determining compliance with the requirements based on the time of filing the IDS, including all "statement" requirements of 37 CFR 1.97(e). See MPEP § 609.05(a).
Note: If copies of the individual references cited on the Search Report are also cited separately on the IDS (and these references have not been lined-through) they have been considered.
Specification
Applicant is reminded of the proper language and format for an abstract of the disclosure.
The abstract should be in narrative form and generally limited to a single paragraph on a separate sheet within the range of 50 to 150 words in length. The abstract should describe the disclosure sufficiently to assist readers in deciding whether there is a need for consulting the full patent text for details.
The language should be clear and concise and should not repeat information given in the title. It should avoid using phrases which can be implied, such as, “The disclosure concerns,” “The disclosure defined by this invention,” “The disclosure describes,” etc. In addition, the form and legal phraseology often used in patent claims, such as “means” and “said,” should be avoided.
The abstract of the disclosure is objected to because “The present disclosure relates to” is used. A corrected abstract of the disclosure is required and must be presented on a separate sheet, apart from any other text. See MPEP § 608.01(b).
Claim Rejections - 35 USC § 112(b)
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 29 -30 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claim 29 recites “a process of producing an antibody comprising culturing the cell of claim 25 under conditions such that the antibody is expressed and recovering the expressed antibody from the culture medium” (lines 1-3).
The phrase “under conditions such that the antibody is expressed” is indefinite because it fails to specify what exact conditions are required for expression. The claim does not identify parameters such as how the antibody is marked for secretion nor how the vector encoding the antibody is introduced into the host cell.
In the specification, paragraph 0047 describes how ”an expression vector may include a sequence that encodes one or more signal peptides that facilitate secretion” and paragraph 0048 describes how a host cell can be “stably or transiently transfected, transformed, transduced or infected” for the expression of all or a portion of an anti-LAIR1 antibody.
“If the language of the claim is such that a person of ordinary skill in the art could not interpret the metes and bounds of the claim so as to understand how to avoid infringement, a rejection of the claim under 35 U.S.C. 112(b) or pre-AIA 35 U.S.C. 112, second paragraph, is appropriate” (MPEP 2173.02[II]).
Claim 29 fails to clearly and distinctly point out the conditions for anti-LAIR1 antibody expression that the applicant regards as the invention, as indicated in the specification of the instant application. As a result, a person having ordinary skill in the art would not be able to determine the metes and bounds of the claim. Claim 30 is included in this rejection as it is dependent on and/or incorporates claim 29.
Claim Rejections - 35 USC § 112(a)
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Written Description
Claims 37-38 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
The MPEP states that the purpose of the written description requirement is to ensure that the inventor had possession, as of the filing date of the application, of the specific subject matter later claimed. The MPEP lists factors that can be used to determine if sufficient evidence of possession has been furnished in the disclosure of the application, including “the level of skill and knowledge in the art, partial structure, physical and/or chemical properties, functional characteristics alone or coupled with a known or disclosed correlation between structure and function, and the method of making the claimed invention” (MPEP 2163[II][A][2]).
The written description requirement for a claimed genus may be satisfied through sufficient description of a representative number of species by actual reduction to practice, disclosure of drawings, or by disclosure of relevant identifying characteristics, for example, structure or other physical and/or chemical properties, by functional characteristics coupled with a known or disclosed correlation between function and structure, or by a combination of such identifying characteristics, sufficient to show the Applicants were in possession of the claimed genus.
Claim 37
Instant claim 37 is directed to an anti-LAIR1 antibody (referred to as mAb1 or mAb3 in the specification of the instant application) that does not form a complex with LAIR1 ligand complement component 1q (C1q).
However, Provisional U.S. Application No. 63/375,936 and instant application do not adequately describe anti-LAIR1 antibody and C1q binding for claim 37; it does not disclose through drawings nor through functional characteristics alone or coupled with a known or disclosed correlation between structure and function. There is no mention of C1q-binding in relation to the anti-LAIR1 antibody of claim 37. The specification of the instant application only describes C1q-binding of mAb4, a distinct anti-LAIR1 antibody.
According to Wang et al., C1q and hexamers of IgG antibodies can form complexes (Molecular Cell, 2016, Pg. 135, Summary). As the antibody isotype of the anti-LAIR1 antibody is not indicated for claim 37, the broadest reasonable interpretation of the claim includes an anti-LAIR1 antibody with an IgG isotype. Therefore, the anti-LAIR1 antibody from claim 37 of the instant application could form a complex with C1q, with the specification failing to provide evidence to the contrary.
University of California v. Eli Lilly and Co., 43 USPQ2d 1398, 1404. 1405 held that: To fulfill the written description requirement, a patent specification must describe an invention and does so in sufficient detail that one skilled in the art can clearly conclude that "the inventor invented the claimed invention.” Lockwood v. American Airlines Inc., 107 F.3d 1565, 1572, 41 USPQ2d 1961, 1966 (1997); In re Gosteli , 872 F.2d 1008, 1012, 10 USPQ2d 1614, 1618 (Fed. Cir. 1989) ("[T]he description must clearly allow persons of ordinary skill in the art to recognize that [the inventor] invented what is claimed."). Thus, an applicant complies with the written description requirement "by describing the invention, with all its claimed limitations, not that which makes it obvious," and by using "such descriptive means as words, structures, figures, diagrams, formulas, etc., that set forth the claimed invention" Lockwood, 107 F.3d at 1572, 41 USPQ2datl966.
The specification does not reasonably convey possession of the subject matter of claim 37. Claim 37 fails to comply with the written description requirement of 35 U.S.C. 112(a) as a person having ordinary skill in the art cannot reasonably conclude that the applicant had possession of the claimed invention at the time the instant application was filed.
Claim 38
Instant claim 38 is directed to an anti-LAIR1 antibody (referred to as mAb1 or mAb3 in the specification of the instant application) that does not require full receptor occupancy to elicit agonism.
However, Provisional U.S. Application No. 63/375,936 and instant application do not adequately describe the receptor occupancy of anti-LAIR1 antibody of claim 38 needed for agonism; it does not disclose through drawings nor through functional characteristics alone or coupled with a known or disclosed correlation between structure and function. There is no mention of receptor occupancy in relation to the anti-LAIR1 antibody of claim 38. The specification of the instant application only describes receptor occupancy of mAb4, a distinct anti-LAIR1 antibody.
According to Schrage et al., agonistic ligands can induce signaling less than, similar to, or greater than the endogenous ligand (British Journal of Pharmacology, 2016, Pg. 3020, column 1, first paragraph). Agonists with high efficiency in signaling would potentially require a smaller percentage of receptor occupancy to elicit a response similar to the endogenous ligand at the same concentration. As the receptor occupancy of anti-LAIR1 antibody is not indicated for claim 38, the broadest reasonable interpretation includes an anti-LAIR1 antibody with agonism less than or similar to the endogenous ligand. Therefore, an anti-LAIR1 antibody from claim 38 of the instant application could require full receptor occupancy for agonism, with the specification failing to provide evidence to the contrary.
University of California v. Eli Lilly and Co., 43 USPQ2d 1398, 1404. 1405 held that: To fulfill the written description requirement, a patent specification must describe an invention and does so in sufficient detail that one skilled in the art can clearly conclude that "the inventor invented the claimed invention.” Lockwood v. American Airlines Inc., 107 F.3d 1565, 1572, 41 USPQ2d 1961, 1966 (1997); In re Gosteli, 872 F.2d 1008, 1012, 10 USPQ2d 1614, 1618 (Fed. Cir. 1989) ("[T]he description must clearly allow persons of ordinary skill in the art to recognize that [the inventor] invented what is claimed."). Thus, an applicant complies with the written description requirement "by describing the invention, with all its claimed limitations, not that which makes it obvious," and by using "such descriptive means as words, structures, figures, diagrams, formulas, etc., that set forth the claimed invention" Lockwood, 107 F.3d at 1572, 41 USPQ2datl966.
The specification does not reasonably convey possession of the subject matter of claim 38. Claim 38 fails to comply with the written description requirement of 35 U.S.C. 112(a) as a person having ordinary skill in the art cannot reasonably conclude that the applicant had possession of the claimed invention at the time the instant application was filed.
Scope of Enablement
Claims 33-36 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for a method of treating graft vs. host disease and lupus nephritis in a subject comprising administration of anti-LAIR1 antibody, does not reasonably provide enablement for a method of treating all autoimmune and fibrotic diseases in a subject comprising administration of anti-LAIR1 antibody. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims.
As a general rule, enablement must be commensurate with the scope of claim language. MPEP 2164.08 states, “The Federal Circuit has repeatedly held that “the specification must teach those skilled in the art how to make and use the full scope of the claimed invention without undue experimentation’.” In re Wright, 999 F.2d 1557, 1561, 27 USPQ2d 1510, 1513 (Fed. Cir. 1993)” (emphasis added). The “make and use the full scope of the invention without undue experimentation” language was repeated in 2005 in Warner-Lambert Co. v. Teva Pharmaceuticals USA Inc., 75 USPQ2d 1865, and Scripps Research Institute v. Nemerson, 78 USPQ2d 1019 asserts: “A lack of enablement for the full scope of a claim, however, is a legitimate rejection.” The principle was explicitly affirmed most recently in Auto. Tech. Int’l, Inc. v. BMW of N. Am., Inc., 501 F.3d 1274, 84 USPQ2d 1108 (Fed. Cir. 2007), Monsanto Co. v. Syngenta Seeds, Inc., 503 F.3d 1352, 84 U.S.P.Q.2d 1705 (Fed. Cir. 2007), and Sitrick v. Dreamworks, LLC, 516 F.3d 993, 85 USPQ2d 1826 (Fed. Cir. 2008). See also In re Cortright, 49 USPQ2d 1464, 1466 and Bristol-Myers Squibb Co. v. Rhone-Poulenc Rorer Inc., 49 USPQ2d 1370.
The factors to be considered in determining whether a disclosure meets the enablement requirement of 35 U.S.C. 112, first paragraph, have been described in In re Wands, 8 USPQ2d 1400 (Fed. Cir. 1988). Among these factors are: (1) the nature or the invention; (2) the state of the prior art; (3) the relative skill of those in the art; (4) the predictability or unpredictability of the art; (5) the breadth of the claims; (6) the amount of direction or guidance presented; (7) the presence or absence of working examples; and (8) the quantity of experimentation necessary. When the above factors are weighed, it is the examiner’s position that one skilled in the art could not practice the invention without undue experimentation. Some experimentation is not fatal; the issue is whether the amount of experimentation is “undue”; see In re Vaeck, 20 USPQ2d 1438, 1444.
With regard to claims 33 and 35, the claims are drawn to “a method of treating an autoimmune or fibrotic disease” comprising administration of anti-LAIR1 antibody (claim 33, lines 1-3; claim 35, lines 1-3). Claims 33 and 35 do not specify which autoimmune or fibrotic diseases.
Claims 34 and 36 further specify that “the autoimmune disease or fibrotic disease is selected from rheumatoid arthritis, psoriasis, systemic lupus erythematosus, lupus nephritis, pemphigus vulgaris, systemic sclerosis, idiopathic pulmonary fibrosis, scleroderma, ulcerative colitis, Crohn's disease, hidradenitis suppurativa, atopic dermatitis, multiple sclerosis, scleroderma-associated interstitial lung disease, IgG4 related disease or chronic fibrosing interstitial lung diseases” (claim 34, lines 1-6; claims 36, lines 1-6).
These diseases have distinct and often unrelated pathogenic mechanisms, some of which are not associated with LAIR1 signaling. As such, the claims 33-36 generally read on the treatment of a subject with anti-LAIR1 antibody of 1) all autoimmune and fibrotic disease for claims 33 and 35 and 2) any of the listed autoimmune and fibrotic diseases for claims 34 and 36, the full scope of which is not enabled by the method as instantly claimed.
(1) The nature or the invention and (5) the breadth of the claims
The autoimmune and fibrotic diseases are varied in pathogenesis and mechanism of action. The pathogeneses can be 1) related to LAIR1 dysfunction but having different mechanisms of action, 2) unrelated to LAIR1 dysfunction, or 3) poorly understood and not well characterized.
LAIR1 dysfunction is indicated in some autoimmune and fibrotic diseases. However, the mechanism of action varies. According to Zhang et al., in patients with rheumatoid arthritis, LAIR1 is overexpressed in the synovia which leads to inflammation (Clinical and Experimental Immunology, 2018, Pg. 193, Summary). Conversely, according to Son, LAIR1 expression is lower in plasmacytoid dendritic cells and B cells in patients with systemic lupus erythematosus, subsequently reducing LAIR1 inhibition (Experimental & Molecular Medicine, 12 May 2022, Pg. 569, second column, second paragraph).
In addition, not all of autoimmune and fibrotic diseases require LAIR1 dysfunction for pathogenesis. According to Zhou et al., psoriasis can be triggered by keratinocytes (CDDpress, 24 Jan 2022, Pg. 1, Introduction, second paragraph, last 3 lines) with rapid and uncontrolled growth. Liu et al. state regarding IgG4-related disease that “the exact pathophysiology standing behind this fibroinflammatory condition still remains enigmatic” (Journal of Translational Autoimmunity, 2020, Pg. 4, Conclusions).
In the example of psoriasis and IgG4-related disease, their treatment plans differ. Psoriasis is skin-focused while IgG4-related disease affects “essentially every organ in the body” (Liu et al., Pg. 1, first paragraph, line 5). This difference suggests that psoriasis might respond to topical treatments while IgG4-relate disease would not.
Even seemingly comparable diseases can have drastically different underlying mechanisms. Scleroderma and lupus nephritis are both characterized as connective tissue disorders. However, their pathogeneses, while resulting in a similar presentation, are distinct. “The pathogenesis of scleroderma involves dysregulation of the immune system, leading to fibroblast activation and excessive collagen deposits. On the other hand, immunological complexes develop and deposit in the glomeruli of patients with membranous lupus nephritis, causing glomerular injury and initiating an inflammatory cascade” (Reddy et al., Overlap of Scleroderma and Class V Lupus Nephritis: A Rare Autoimmune Confluence, Cureus, 2024, Pg. 5, fourth paragraph).
In another example, rheumatoid arthritis and multiple sclerosis share a similar pathogenesis linked to inflammatory cytokines, TNF-α and IL-6, but the roles of these cytokines are different. Konen et al. state “TNF-α and IL-6 were found to be elevated in both diseases”; yet, in multiple sclerosis, “these cytokines also appear to be involved in neuroprotection and tissue repair” (Management of disease-modifying therapies in multiple sclerosis and comorbid rheumatoid arthritis, Neurol Res Pract, 2025, Pg. 4, second column, first paragraph). In addition, multiple sclerosis targets the central nervous system while rheumatoid arthritis targets joints.
In the specification, an in vivo study in a mouse model with anti-LAIR1 antibody demonstrated that “a surrogate agonistic antibody can modulate disease in a pre-clinical model of lupus nephritis” (¶ 0160) and “anti-human LAIR1 antibodies have immunomodulatory effects on human immune cells in a humanized mouse model of [graft vs. host] disease” (¶ 0147). The specification does not provide additional examples or guidance on how to use anti-LAIR1 antibody to treat any other autoimmune or fibrotic diseases in a subject.
The treatment of the autoimmune and fibrotic diseases with one anti-LAIR1 antibody generically may not be effective as described above, relating to Wands factors (1) the nature or the invention and (5) the breadth of the claims. The claims recite multiple diseases that require the specification of the instant application to provide support for the entire scope of the claims. The specification fails to show that a person having ordinary skill in the art could treat all recited diseases without undue experimentation.
Moreover, as described above, the diseases do not share a common mechanism of action nor functional link. Evidence of efficacy of anti-LAIR1 antibody in treatment of graft vs. host disease and lupus nephritis is provided in the specification.
Therefore, the method of treating using an anti-LAIR1 antibody is not adequately supported for autoimmune and fibrotic diseases besides graft vs. host disease and lupus nephritis.
(2) The state of the prior art
The prior art teaches that the treatment of autoimmune and fibrotic diseases is difficult. There is no known molecule that is broadly effective across a range of autoimmune and fibrotic diseases.
Fugger et al. state “present therapies [to treat autoimmune diseases] are broadly acting and non-disease specific; consequently, they are associated with numerous side effects” (Challenges, Progress, and Prospects of Developing Therapies to Treat Autoimmune Diseases, Cell, 2020, Pg. 63, first paragraph in green text, lines 2-3). Walraven and Hinz indicate “there is still no effective cure for fibrosis - organ replacement (e.g., lung or skin transplants) is often the only available option for severely affected patients” (Therapeutic approaches to control tissue repair and fibrosis: Extracellular matrix as a game changer, Laboratory of Tissue Repair and Regeneration, 2018, Pg. 206, first column, third paragraph).
The closest prior art to the instant application refers to cancer treatments with anti-LAIR1 antibodies in mouse models (WO 2021262597 A2, 2021, Pg. 171, ¶ 00386; US 11377491 B2, 2018, Fig. 55). Prior to the effective filing date of the application, there was not adequate support for anti-LAIR1 antibody treatment in autoimmune and fibrotic diseases using in vivo models.
While LAIR1 dysfunction is indicated in some autoimmune and fibrotic diseases (see above), it is not clear in the prior art that an anti-LAIR1 antibody could broadly treat autoimmune and fibrotic diseases in a subject, applicable to Wands factor (2) the state of the prior art.
(3) The relative skill of those in the art, (4) the predictability or unpredictability of the art, and (8) the quantity of the experimentation
In the specification, an in vivo study in a mouse model with anti-LAIR1 antibody demonstrated that “a surrogate agonistic antibody can modulate disease in a pre-clinical model of lupus nephritis” (¶ 0160) and “anti-human LAIR1 antibodies have immunomodulatory effects on human immune cells in a humanized mouse model of [graft vs. host] disease” (¶ 0147). The specification does not provide additional examples or guidance on how to use anti-LAIR1 antibody to treat any other autoimmune or fibrotic diseases in a subject.
Since autoimmune and fibrotic diseases arise from different biological pathways as described above, a person having ordinary skill in the art (i.e. someone with a PhD or MD) would need to determine independently whether treatment with anti-LAIR1 antibody is therapeutically relevant for each disease. An ordinary artisan would not know nor anticipate how an anti-LAIR1 antibody would affect autoimmune and fibrotic disease broadly, relating to Wands factor (3) the relative skill of those in the art.
The amount of experimentation needed would not be reasonable due to the unpredictability of how an anti-LAIR1 antibody would treat a wide variety of diseases, relating to Wands factors (4) the predictability or unpredictability of the art and (8) the quantity of experimentation, as it would require extensive screening and mechanistic investigation to determine dosage and efficacy.
It is not routine to determine or predictable to a person having ordinary skill in the art how anti-LAIR1 antibody will treat a broad array of diseases. Therefore, the method of treating using an anti-LAIR1 antibody is not adequately supported for autoimmune and fibrotic diseases besides graft vs. host disease and lupus nephritis.
6) The amount of direction or guidance provided by the inventor and 7) the existence of working examples
In the specification, an in vivo study in a mouse model with anti-LAIR1 antibody demonstrated that “a surrogate agonistic antibody can modulate disease in a pre-clinical model of lupus nephritis” (¶ 0160) and “anti-human LAIR1 antibodies have immunomodulatory effects on human immune cells in a humanized mouse model of [graft vs. host] disease” (¶ 0147).
The specification does not provide additional working examples, further direction, or guidance on how to use anti-LAIR1 antibody to treat any other autoimmune or fibrotic diseases in a subject, relating to Wands factors 6) The amount of direction or guidance provided by the inventor and 7) the existence of working examples.
Thus, the specification provides sufficient teachings only for the enablement of the treatment of lupus nephritis and graft vs. host disease is a subject with an anti-LAIR1 antibody. Diseases with similar LAIR1-related mechanisms of action to lupus nephritis and graft vs. host disease are enabled for treatment with anti-LAIR1 antibody. Prior art discloses anti-LAIR antibodies are useful in treatment of cancer, outside of the scope of the instant application.
Therefore, the method of treating using an anti-LAIR1 antibody does not have sufficient working examples or guidance for autoimmune and fibrotic diseases besides graft vs. host disease and lupus nephritis.
Claims 33 and 35 are not enabled because a person having ordinary skill in the art as of the effective filing date of the application would not be able to treat all autoimmune and fibrotic diseases with anti-LAIR1 antibody. Claims 34 and 36 are included in this rejection as they depend on and/or incorporate claims 33 and 35.
Art-Free Subject Matter
It is noted that proteins sequences of SEQ ID NOs: 1-10, 13-16, 18-22, 25, 27 and nucleic acids sequences encoding SEQ ID NOs: 9-10, 21-22, 25, and 27 have been thoroughly searched corresponding to the limitations of the claims and are free of prior art.
Conclusion
Claims 1-40 are pending. Claims 29-30 and 33-38 are rejected. Claims 1-28, 31-32, and 39-40 are potentially allowable.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Jessica M Priest whose telephone number is (571)272-8469. The examiner can normally be reached Mon-Fri 8am-5pm.
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/J.M.P./Examiner, Art Unit 1642
/SAMIRA J JEAN-LOUIS/Supervisory Patent Examiner, Art Unit 1642