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 .
Election/Restrictions
Applicant’s election of a method of suppressing allergen-specific IgE antibodies/IgE-class-specific immune responses in a subject that is a child, wherein the method further includes additional immunotherapy using an allergen, in the reply filed on 11/25/2025 is acknowledged. Because applicant did not distinctly and specifically point out the supposed errors in the restriction requirement, the election has been treated as an election without traverse (MPEP § 818.01(a)).
Claims 8-12 and 22-26 are examined on the merits in the present Office Action.
Claim Rejections - 35 USC § 112
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.
Claims 8-12, 22-23, 25-26 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.
Claims 8, 9, and 12 do not disclose the amino acid sequences of six non-degenerate CDRs
for the genus of anti-IgE antibodies having the functional property of either suppressing production of allergen-specific IgE antibodies in a subject in infancy or suppressing IgE-class-specific immune responses in a subject during the fetal stage to infancy. Claims 10-11, 22-23, and 25-26, depend directly or indirectly from claims 8, 9, and 12, but do not cure the deficiencies of these claims and are thus also rejected.
The guidelines for the Examination of Patent Applications Under the 35 U.S.C. 112, § 1 "Written Description" Requirement make clear that if a claimed genus does not show actual reduction to practice for a representative number of species, then the Requirement may be alternatively met by reduction to drawings, or by disclosure of relevant, identifying characteristics, i.e., 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 applicant was in possession of the genus (MPEP 2163).
In The Regents of the University of California v. Eli Lilly (43 USPQ2d 1398-1412) 19 F. 3d 1559, the court held that disclosure of a single member of a genus (rat insulin) did not provide adequate written support for the claimed genus (all mammalian insulins). In this same case, the court also noted:
“A definition by function, as we have previously indicated, does not suffice to define the genus because it is only an indication of what the gene does, rather than what it is. See Fiers, 984 F.2d at 1169-71, 25 USPQ2d at 1605-06 (discussing Amgen). It is only a definition of a useful result rather than a definition of what achieves that result. Many such genes may achieve that result. The description requirement of the patent statute requires a description of an invention, not an indication of a result that one might achieve if one made that invention. See In re Wilder, 736 F.2d 1516, 1521, 222 USPQ 369, 372-73 (Fed. Cir. 1984) (affirming rejection because the specification does “little more than outlin [e] goals appellants hope the claimed invention achieves and the problems the invention will hopefully ameliorate."). Accordingly, naming a type of material generally known to exist, in the absence of knowledge as to what that material consists of, is not a description of that material.”
The court has further stated that “Adequate written description requires a precise definition, such as by structure, formula, chemical name or physical properties, not a mere wish or plan for obtaining the claimed chemical invention.” Id. at 1566, 43 USPQ2d at 1404 (quoting at 1171, 25 USPQ2d at 1606). Also see (CAFC 2002). Enzo-Biochem v. Gen-Probe Fiers, 984 F.2d 01-1230.
It is well-known in the art that, in order to bind antigen, an antibody or antigen-binding fragment must have six complementarity defining regions (CDRs) (Janeway, see selection, in particular section 3-6) (Janeway, Charles A. et al. "Immunobiology: The Immune System in Health and Disease." 2001). Because CDRs from both VH and VL domains contribute to the antigen-binding site, it is the combination of the heavy and the light chain, and not either alone, that determines the final antigen specificity. As presently written, however, claims 8, 9, and 12 do not disclose the amino acid sequences of six non-degenerate CDRs for the genus of anti-IgE antibodies having the functional property of either suppressing production of allergen-specific IgE antibodies in a subject in infancy or suppressing IgE-class-specific immune responses in a subject during the fetal stage to infancy. Although Applicant has disclosed the anti-IgE antibody omalizumab, such disclosure does not adequately represent the structural diversity of the claimed genus of anti-IgE antibodies capable of achieving the recited functional properties. Claims 10-11, 22-23, and 25-26, depend directly or indirectly from claims 8, 9, and 12, but do not cure the deficiencies of these claims and are thus also rejected.
Therefore, the claimed genus of antibodies lacks adequate written description because there does not appear there is no structural information or disclosure provided for the genus of anti-IgE antibodies capable of suppressing allergen-specific IgE/IgE-specific immune responses in a subject. Thus, one of ordinary skill in the art would reasonably conclude that the applicant was not in possession of the full breadth of the claimed genus of anti-IgE antibodies at the time the instant application was filed.
Enablement
Claims 9, 12, and 22-26 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 suppressing IgE-class-specific immune responses in a subject during after birth to infancy, does not reasonably provide enablement for suppressing IgE-class-specific immune responses in a subject during the fetal stage to infancy. 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.
The claims are broadly drawn to a method that suppresses IgE-class-specific immune responses in a subject during the fetal stage to infancy, comprising administering an anti-IgE antibody to the subject at any point from after birth to infancy.
The specification teaches neonatal mice treated with anti-mouse IgE antibody one day after birth and then sensitized with OVA 0, 2 or 6 weeks after birth showed no increase in the OVA-specific IgE antibody titer compared to neonatal mice treated with isotype-matched control antibody. Thus, administration of anti- IgE antibody to newborn mice inhibited allergen-specific IgE antibody production for at least six weeks (Para. 0019 and 0149). Because the half-lives of mouse and human IgG antibodies are 6-8 days and 22-23 days, respectively, an age of 6 weeks in mice can be considered equivalent to an age of about 3-4 months in humans when converted on the basis of the half-life of IgG (Para. 0020). However, the phrase “fetal stage” is defined as the second and third trimesters after conception (see Para. 0015 of the Specification). If the anti-IgE antibody is administered to the subject at any point after birth to infancy, then artisans would not reasonably expect IgE-specific immune responses to be suppressed in the subject during the fetal stage prior to birth of the subject commensurate in scope of the claims.
Therefore, the specification is not enabling over the full scope of the claims.
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claims 8-12, 25, and 26 are rejected under 35 U.S.C. 102(a)(1) and (a)(2) as being anticipated by Penn (US20100166804A1).
Penn discloses methods for prophylactically treating, reducing, delaying or controlling severe allergic reaction to food allergen (e.g. peanut allergen) in patients at risk of systemic anaphylaxis comprising administering a mast cell stabilizer in combination with an additional therapeutic agent such as an anti-IgE antagonist antibody (Abstract, Para. 0006-0007, including Embodiments 1.12, 1.21, and 1.29), wherein the patient is an infant defined as anyone who is one month to two years of age (Para. 0007, particularly Embodiments 1.45, and Para. 0179). The patient can be undergoing oral allergen desensitization therapy wherein the allergen, is a peanut allergen (Para. 0007, particularly Embodiments 1.33, 1.34, 1.42, 1.43, and 1.44). Per the instant claims, the minimal steps required for suppressing production of allergen-specific IgE antibodies/an IgE-specific immune response in infancy—or during the fetal stage to infancy – is administering an anti-IgE antibody to a subject at any point after birth to infancy. Further, the “wherein” clause recited in instant claim 10 —“wherein the method prevents the onset of allergic disorders in infancy and later”—merely states the intended result of the claimed method and thus does not provide patentable distinctiveness to the claimed methods over the prior art. The courts have held that a “…whereby [or, in this case, wherein] clause in a method claim is not given weight when it simply expresses the intended result of a process step positively recited.”) (quoting Minton v. Nat’l Ass’n ofSecurities Dealers, Inc., 336 F.3d 1373, 1381, 67 USPQ2d 1614, 1620 (Fed. Cir. 2003)) (see MPEP 2111.04). Accordingly, the methods of Penn would necessarily be capable of suppressing production of allergen-specific IgE antibodies (or IgE-specific immune responses) in the subject and preventing the onset of allergic disorders in the subject in infancy and later.
Thus, Penn meets the limitations of instant claims 8-12, 25, and 26.
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.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 22 and 24 are rejected under 35 U.S.C. 103 as being unpatentable over Penn, as applied to claims 8-12, 25, and 26 above, in view of Yalcin et al, (Yalcin, Arzu Didem. “An overview of the effects of anti-IgE therapies.” Medical science monitor : international medical journal of experimental and clinical research vol. 20 1691-9. 22 Sep. 2014, doi:10.12659/MSM.890137), hereinafter Yalcin.
The teachings of Penn have been discussed above and differ from the instantly claimed invention in that it is not taught that the anti-IgE antibody binds to the Cε3 region of IgE or comprises omalizumab.
However, Yalcin teaches that omalizumab –a humanized monoclonal antibody that binds to the CH3 domain of human IgE (Cε3 domain) near the binding site for the high-affinity type-I IgE Fc receptors—can neutralize free IgE and inhibit the IgE allergic pathway without sensitizing mast cells and basophils. The interaction between Omalizumab and free IgE interrupts a key step in the allergic inflammatory cascade, preventing IgE from binding to mast cells, basophils, and dendritic cells, and down-regulating IgE receptor expression on these inflammatory cells, thereby inhibiting degranulation and the release of inflammatory mediators (Background and “Omalizumab and IgE Receptors” sections).
It would have been obvious to one of ordinary skill in the art to administer omalizumab as the anti-IgE antibody which binds to the Cε3 region of IgE to a subject after birth to infancy in order to suppress production of allergen-specific IgE in the subject. One of ordinary skill in the art would have been motivated to do so since omalizumab is blocks the binding of free IgE to its receptors on various effector cells, thereby inhibiting degranulation and the release of inflammatory mediators and preventing IgE-mediated allergic immune response as taught by Yalcin. Therefore, one of ordinary skill in the art would expect that the anti-IgE antibody omalizumab administered to a subject after birth to infancy can effectively suppress production of allergen-specific IgE in the subject.
Claim 23 is rejected under 35 U.S.C. 103 as being unpatentable over Penn, as applied to claims 8-12, 25, and 26 above, in view of Fleischer et al, (Fleischer, David M et al. “Primary prevention of allergic disease through nutritional interventions.” The journal of allergy and clinical immunology. In practice vol. 1,1 (2013): 29-36. doi:10.1016/j.jaip.2012.09.003), hereinafter Fleischer.
The teachings of Penn have been discussed above and differ from the instantly claimed invention in that it is not specifically taught that the infant patient at risk of systemic anaphylaxis in response to an allergen is not diagnosed with an allergic disorder.
However, Fleischer teaches that infants having at least one first-degree relative (parent or sibling) with a documented allergic condition are at high risk of developing an allergic disease, and represent a patient population often targeted in strategies for primary prevention, or inhibiting the development of clinical disease before it occurs (see Abstract and 1st paragraph of Introduction on Page 29). In other words, high-risk infants are those not having an allergic disorder but possess a greater likelihood of developing one due to family history.
It would have been obvious to one of ordinary skill in the art to administer an anti-IgE antibody a high-risk infant patient not having an allergic disorder. One of ordinary skill in the art would have been motivated to do so since high-risk infant patients have a greater likelihood of developing an allergic disorder and represent a patient population often targeted in strategies for primary prevention as taught by Fleischer. Therefore, one of ordinary skill in the art would reasonably expect that that the anti-IgE antibody omalizumab administered to a high-risk infant subject not having an allergic disease can effectively suppress production of allergen-specific IgE/IgE-specific immune responses in the subject.
Claims 8-12, 22, and 24-26 are rejected under 35 U.S.C. 103 as being unpatentable over Penn (US20100166804A1) in view of Yalcin et al, (Yalcin, Arzu Didem. “An overview of the effects of anti-IgE therapies.” Medical science monitor : international medical journal of experimental and clinical research vol. 20 1691-9. 22 Sep. 2014, doi:10.12659/MSM.890137), hereinafter Yalcin.
Penn discloses methods for prophylactically treating, reducing, delaying or controlling severe allergic reaction to food allergen (e.g. peanut allergen) in patients at risk of systemic anaphylaxis comprising administering a mast cell stabilizer defined as a compound or agent capable of inhibiting or reducing the release of inflammatory mediators or other autacoids (Abstract, Para. 0006-0007, including Embodiments 1.12, 1.21, and 1.29, and Para. 0183), The patient is an infant –anyone who is one month to two years of age (Para. 0179)— and can be undergoing oral allergen desensitization therapy wherein the allergen, is a peanut allergen. allergen (Para. 0007, particularly Embodiments 1.33, 1.34, 1.42, 1.43, and 1.44).
Penn does not specifically teach that an anti-IgE antibody such as omalizumab is a mast cell stabilizer.
However, Yalcin teaches that omalizumab –a humanized monoclonal antibody that binds to the CH3 domain of human IgE (Cε3 domain) near the binding site for the high-affinity type-I IgE Fc receptors—can neutralize free IgE and inhibit the IgE allergic pathway without sensitizing mast cells and basophils. The interaction between Omalizumab and free IgE interrupts a key step in the allergic inflammatory cascade, preventing IgE from binding to mast cells, basophils, and dendritic cells, and down-regulating IgE receptor expression on these inflammatory cells, thereby inhibiting degranulation and the release of inflammatory mediators (Background and “Omalizumab and IgE Receptors” sections). Thus, the anti-IgE antibody omalizumab can be considered a mast cell stabilizer as defined by Penn.
It would have been obvious to one of ordinary skill in the art to use the anti-IgE antibody omalizumab—which binds to the Cε3 region of IgE—as the mast cell stabilizer in the methods disclosed by Penn. One of ordinary skill in the art would have been motivated to do so since omalizumab blocks binding of free IgE to its receptors on various effector cells, thereby inhibiting degranulation and the release of inflammatory mediators and preventing IgE-mediated allergic immune response. Per the instant claims, the minimal steps required for suppressing production of allergen-specific IgE antibodies/ IgE-specific immune response in infancy—or during the fetal stage to infancy – is administering an anti-IgE antibody to a subject at any point after birth to infancy. Further, the “wherein” clause recited in instant claim 10 —“wherein the method prevents the onset of allergic disorders in infancy and later”—merely states the intended result of the claimed method and thus does not provide patentable distinctiveness to the claimed methods over the prior art. The courts have held that a “…whereby [or, in this case, wherein] clause in a method claim is not given weight when it simply expresses the intended result of a process step positively recited.”) (quoting Minton v. Nat’l Ass’n ofSecurities Dealers, Inc., 336 F.3d 1373, 1381, 67 USPQ2d 1614, 1620 (Fed. Cir. 2003)) (see MPEP 2111.04). Therefore, one of ordinary skill in the art would expect that the anti-IgE antibody omalizumab administered as a mast cell stabilizer to infant subjects according to the methods of Penn can effectively suppress production of allergen-specific IgE (or IgE-specific immune responses) in the subject and prevent the onset of allergic disorders in infancy and later.
Claim 23 is rejected under 35 U.S.C. 103 as being unpatentable over Penn and Yalcin, as applied to claims 8-12, 22, and 24-26 above, and further in view of Fleischer et al, (Fleischer, David M et al. “Primary prevention of allergic disease through nutritional interventions.” The journal of allergy and clinical immunology. In practice vol. 1,1 (2013): 29-36. doi:10.1016/j.jaip.2012.09.003), hereinafter Fleischer.
The teachings of Penn and Yalcin have been discussed above and differ from the instantly claimed invention in that it is not specifically taught that the infant patient at risk of systemic anaphylaxis in response to an allergen is not diagnosed with an allergic disorder.
However, Fleischer teaches that infants having at least one first-degree relative (parent or sibling) with a documented allergic condition are at high risk of developing an allergic disease, and represent a patient population often targeted in strategies for primary prevention, or inhibiting the development of clinical disease before it occurs (see Abstract and 1st paragraph of Introduction on Page 29). In other words, high-risk infants are those not having an allergic disorder but possess a greater likelihood of developing one due to family history.
It would have been obvious to one of ordinary skill in the art to administer an anti-IgE antibody a high-risk infant patient not having an allergic disorder. One of ordinary skill in the art would have been motivated to do so since high-risk infant patients have a greater likelihood of developing an allergic disorder and represent a patient population often targeted in strategies for primary prevention as taught by Fleischer. Therefore, one of ordinary skill in the art would reasonably expect that that the anti-IgE antibody omalizumab administered to a high-risk infant subject not having an allergic disease can effectively suppress production of allergen-specific IgE in the subject.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 8-12 and 23-26 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-12 and 14-18 of copending Application No. 18516127 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because the co-pending claims either anticipate or are obvious variants over the instant claims. (Of note, a Notice of Allowance was issued for the co-pending application on 10/28/2025; however, the claims have not yet issued).
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
The co-pending claims recite a method decreasing a risk of an allergic predisposition in a subject comprising administering an effective amount of an anti-IgE antibody to the subject and administering an effective amount of an allergen to the subject, wherein 1) the subject is not sensitized to an allergen that causes the allergic predisposition and is in infancy or younger; 2) the subject is not diagnosed with an allergic disorder or asthma; 3) the allergen comprises a peanut; and 4) and the anti-IgE antibody is omalizumab and administered during a newborn stage, early infancy, or infancy (co-pending claims 1, 7, 8, 14, 15, and 16). As evidenced by Yalcin, omalizumab is an anti-IgE antibody that binds to the CH3 domain of IgE (Cε3 domain). The method is also capable of decreasing the probability for an onset of an allergic disorder in a subject during infancy or later (co-pending claim 12). Further recited is a method of suppressing production of allergen-specific IgE antibodies in a subject comprising administering an effective amount of an anti-IgE antibody to the subject wherein the subject is not sensitized to an allergen that causes allergic predisposition and is in infancy or younger (co-pending claim 2). It is noted that per the instant claims, the minimal steps required for suppressing production of allergen-specific IgE antibodies in infancy—or during the fetal stage to infancy – is administering an anti-IgE antibody to a subject at any point after birth to infancy. Further, the “wherein” clause recited in instant claim 10 —“wherein the method prevents the onset of allergic disorders in infancy and later”—merely states the intended result of the claimed method and thus does not provide patentable distinctiveness to the claimed methods over the prior art. The courts have held that a “…whereby [or, in this case, wherein] clause in a method claim is not given weight when it simply expresses the intended result of a process step positively recited.”) (quoting Minton v. Nat’l Ass’n ofSecurities Dealers, Inc., 336 F.3d 1373, 1381, 67 USPQ2d 1614, 1620 (Fed. Cir. 2003)) (see MPEP 2111.04). Accordingly, the methods of the co-pending claims can effectively suppress production of allergen-specific IgE (or IgE-specific immune responses) in the subject and prevent the onset of allergic disorders in infancy and later.
Thus, the co-pending claims meet the limitations of instant claims 8-12 and 23-26 .
Claims 8-12 and 23-36 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-8 of U.S. Patent No. 11185561B2 in view of Penn (US20100166804A1) in view of Yalcin et al, (Yalcin, Arzu Didem. “An overview of the effects of anti-IgE therapies.” Medical science monitor : international medical journal of experimental and clinical research vol. 20 1691-9. 22 Sep. 2014, doi:10.12659/MSM.890137), hereinafter Yalcin.
The issued claims recite an egg allergy prevention method for preventing a human infant who has not developed an egg allergy from developing an egg allergy, comprising administering an egg allergen to the infant according to the recited dosage regimens and schedules (i.e. a desensitization/allergen immunotherapy) (issued claims 1-8).
The issued claims do not recite further administration of an anti-IgE antibody such as omalizumab to the human infant.
However, Penn teaches methods for prophylactically treating, reducing, delaying or controlling severe allergic reaction to food allergen (e.g. egg allergen) in patients at risk of systemic anaphylaxis comprising administering a mast cell stabilizer defined as a compound or agent capable of inhibiting or reducing the release of inflammatory mediators or other autacoids (Abstract, Para. 0006-0007, including Embodiments 1.12, 1.21, and 1.29, and Para. 0183), The patient is an infant –anyone who is one month to two years of age (Para. 0179)— and can be undergoing oral allergen desensitization therapy, wherein the allergen, is an egg allergen (Para. 0007, particularly Embodiments 1.21, 1.33, 1.34, 1.42, and 1.44).
Yalcin further teaches that omalizumab –a humanized monoclonal antibody that binds to the CH3 domain of human IgE (Cε3 domain) near the binding site for the high-affinity type-I IgE Fc receptors—can neutralize free IgE and inhibit the IgE allergic pathway without sensitizing mast cells and basophils. The interaction between Omalizumab and free IgE interrupts a key step in the allergic inflammatory cascade, preventing IgE from binding to mast cells, basophils, and dendritic cells, and down-regulating IgE receptor expression on these inflammatory cells, thereby inhibiting degranulation and the release of inflammatory mediators (Background and “Omalizumab and IgE Receptors” sections). Thus, the anti-IgE antibody omalizumab can be considered a mast cell stabilizer as defined by Penn.
It would have been obvious to one of ordinary skill in the art to modify the method of the issued claims such that the anti-IgE antibody omalizumab is further administered to the human infant as a mast cell stabilizer. One of ordinary skill in the art would have been motivated to do so since administration of a mast cell stabilizer to infants undergoing oral allergen desensitization therapy can prevent severe allergic reactions to food allergens (e.g. egg allergen) as taught by Penn; and the anti-IgE antibody omalizumab prevents IgE binding to inflammatory cells, thereby inhibiting degranulation and inflammatory mediator release as taught by Yalcin. As such, omalizumab functions as a mast cell stabilizer. Further, per the instant claims, the minimal steps required for suppressing production of allergen-specific IgE antibodies/an IgE-specific immune response in infancy—or during the fetal stage to infancy – is administering an anti-IgE antibody to a subject at any point after birth to infancy. Further, the “wherein” clause recited in instant claim 10 —“wherein the method prevents the onset of allergic disorders in infancy and later”—merely states the intended result of the claimed method and thus does not provide patentable distinctiveness to the claimed methods over the prior art. The courts have held that a “…whereby [or, in this case, wherein] clause in a method claim is not given weight when it simply expresses the intended result of a process step positively recited.”) (quoting Minton v. Nat’l Ass’n ofSecurities Dealers, Inc., 336 F.3d 1373, 1381, 67 USPQ2d 1614, 1620 (Fed. Cir. 2003)) (see MPEP 2111.04). Therefore, one of ordinary skill in the art would reasonably expect that modifying the method of the issued claims such that the infant is further administered the anti-IgE antibody omalizumab can effectively suppress production of allergen-specific IgE (or IgE-specific immune responses) in the subject and prevent the onset of allergic disorders in infancy and later.
Conclusion
No claims are allowable.
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/LIA E TAYLOR/Examiner, Art Unit 1641
/MISOOK YU/Supervisory Patent Examiner, Art Unit 1641