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 .
DETAILED ACTION
Applicant’s election without traverse of the anti-PD-1 antibody comprising heavy and light chain variable regions (VHs and VLs) of (F) in claim 21 and the anti-CTLA-4 antibody comprising heavy and light chain variable regions of (C) in claim 22 in the reply filed on 06/26/2026 is acknowledged.
Claims 21-38 are pending.
Claim 23 is withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected species, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 06/26/2026.
Claims 21, 22, and 24-38 are under examination on the merits.
Claim Rejections
35 U.S.C. 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 29-37 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.
Claims 29 and 30 rejected under 35 U.S.C. 112(b), because claims are “use” claims. According to MPEP 2173.05(q), “[a]ttempts to claim a process without setting forth any steps involved in the process generally raises an issue of indefiniteness under 35 U.S.C. 112(b) or pre-AIA 35 U.S.C. 112, second paragraph. For example, a claim which read: ‘[a] process for using monoclonal antibodies of claim 4 to isolate and purify human fibroblast interferon’ was held to be indefinite because it merely recites a use without any active, positive steps delimiting how this use is actually practiced. Ex parte Erlich, 3 USPQ2d 1011 (Bd. Pat. App. & Inter. 1986).” Claim 29 recites the use of a bispecific antibody that binds to PD-1 for promoting stimulation of an immune-mediated response of a subject in need thereof; however the claim does not recite any active, positive steps defining how this use is actually practiced and is therefore rejected under 35 U.S.C. 112(b). Claim 30 recites the use of a bispecific antibody that binds to PD-1 for treating a disease or condition associated with a suppressed immune system; however the claim does not recite any active, positive steps defining how this use is actually practiced and is therefore rejected under 35 U.S.C. 112(b). Claim 37 recites the use of a bispecific antibody that binds to PD-1 for manufacturing a medicament for promoting stimulation of an immune-mediated response or for treating a disease or condition associated with a suppressed immune system; however the claim does not recite any active, positive steps defining how this use is actually practiced and is therefore rejected under 35 U.S.C. 112(b). Claims 31-36 are included in this rejection, because these claims depend, either directly or indirectly, from claim 30 but do not remedy the deficiencies of claim 30 with respect to 35 U.S.C. 112(b).
Nonstatutory 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 21, 22, 24, 25, 27, 28, and 38 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 3 and 6 of U.S. Patent No. 10,954,301.
Although the claims at issue are not identical, they are not patentably distinct from each other, because the instant claims and the conflicting claim comprise a bispecific antibody comprising an anti-PD-1 VH that shares 100% homology with instant SEQ ID NO: 57, an anti-PD-1 VL that shares 100% homology with the instant SEQ ID NO: 58, an anti-CTLA-4 VH that shares 100% homology with the instant SEQ ID NO: 90, an anti-CTLA-4 VL that shares 100% homology with the instant SEQ ID NO: 91. The conflicting claims also recite a construct comprising an IgG4 Fc region with M252Y/S254T/T256E substitutions, and claim 3 recites pharmaceutical compositions that comprise a bispecific molecule and a pharmaceutically acceptable carrier.
Claims 21, 22, 24, 25, 27, and 28 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 11 of U.S. Patent No. 11,840,571.
Although the claims at issue are not identical, they are not patentably distinct from each other, because the instant claims and the conflicting claim comprise a bispecific antibody comprising an anti-PD-1 VH that shares 100% homology with instant SEQ ID NO: 57, an anti-PD-1 VL that shares 100% homology with the instant SEQ ID NO: 58, an anti-CTLA-4 VH that shares 100% homology with the instant SEQ ID NO: 90, an anti-CTLA-4 VL that shares 100% homology with the instant SEQ ID NO: 91. The conflicting claims also recite a construct comprising an IgG4 Fc region with M252Y/S254T/T256E substitutions.
Claim 38 is rejected on the ground of nonstatutory double patenting as being unpatentable over over claim 11 of U.S. Patent No. 11,840,571 in view of Roschke et al. (WO 2014/144600, publication date: 09/18/2014).
With respect to claim 38, at [0636], Roschke et al. teach that therapeutic formulations of bispecific or multi-specific molecules may contain pharmaceutically acceptable carriers, excipients or stabilizers.
Based upon the teachings of the conflicting claims and Roschke et al., one of ordinary skill in the art would have been motivated to prepare a pharmaceutical composition that comprises the bispecific antibody of the conflicting claim and a pharmaceutically acceptable carrier. One of ordinary skill in the art would have been motivated to do so, because there would have been a reasonable expectation that the resultant pharmaceutical composition could be used in the treatment of cancer.
Claims 21, 24-28, and 38 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 4 of U.S. Patent No. 10,577,422 in view of Roschke et al. (WO 2014/144600, publication date: 09/18/2014) and Saha et al. (WO 2014/209804, publication date 12/31/2014).
The conflicting claims recite an anti-PD-1 antibody that comprises a VH that shares 100% homology with the instant SEQ ID NO: 57 and a VL that shares 100% homology with the instant SEQ ID NO: 58.
The conflicting claims do not teach a bispecific antibody that comprises an anti-PD-1-binding moiety and a specificity for another antigen, such as CTLA-4; however this deficiency is remedied by Roschke et al. and Saha et al.
At [0003], Roschke et al. teach that “[t]he development of bispecific or multi-specific molecules that target two or more targets simultaneously offers a novel and promising solution for discovering new systems-oriented multitargeted agents demonstrating improved efficacy and pharmacological properties over conventional monotherapies.” At [0006], Roschke et al. teach that said bispecific molecules may be used to treat cancer.
At the Abstract, Saha et al. teach bispecific antibodies that bind CTLA-4 and PD-1 for use in the treatment of cancer.
Based upon the teachings of the conflicting claims, Roschke et al. and Saha et al., one of ordinary skill in the art would have been motivated to prepare a bispecific antibody that comprises an anti-PD-1-binding moiety, such as that recited by the conflicting claims, and a specificity for another antigen, such as CTLA-4, because there would have been a reasonable expectation that the resultant bispecific antibody would be useful in the treatment of cancer. The invention of the conflicting claims, Roschke et al., and Saha et al. meets the limitations of claims 21 and 28.
With respect to claims 24-27, at [0249], Roschke et al. teach that Fc region mutations IgG1-L234A and IgG1-L235A may used to decrease antibody-dependent cellular cytotoxicity. At [0425], Roschket et al. teach that “IgG4 antibodies are known to have decreased ADCC activity and half-life compared to other immunoglobulins subclasses such as, IgGl and IgG3. Accordingly, IgG4 subclass-based formats provide an attractive format for developing therapeutics that bind to and block cell receptors, but do not deplete the target cell. Alternatively, in those embodiments for which increased effector activity is desired, an IgG4 heavy chain of a composition of the invention can be modified as described herein or otherwise known in the art, so as to increase effector function (e.g., modification of the residues at positions 327, 330 and 331; numbering according to EU index of Kabat). Similarly, where increased half-life is desired, an IgG4 heavy chain of a composition of the invention can be engineered as described herein, or otherwise known in the art to more selectively bind the FcRn at pH 6.0, but not pH 7.4, by for example, incorporating mutations located at the interface between the CH2 and CH3 domains, such as substitutions at T250Q/M428L as well as M252Y/S254T/T256E and H433K/N434F (numbering according to the EU index of Kabat).”
With respect to claim 38, at [0636], Roschke et al. teach that therapeutic formulations of bispecific or multi-specific molecules may contain pharmaceutically acceptable carriers, excipients or stabilizers.
Claim 22 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 4 of U.S. Patent No. 10,577,422 in view of Roschke et al. (WO 2014/144600, publication date: 09/18/2014) and Saha et al. (WO 2014/209804, publication date 12/31/2014), as applied to claims 21, 24-28, and 38, and further in view of Korman et al. (US PG PUB 2002/0086014, publication date: 07/04/2002).
The invention of the conflicting claims, Roschke et al., and Saha et al. is detailed above. These references do not teach or suggest an anti-CTLA-4 antibody that comprises a) the VH of the instant SEQ ID NO: 90 and b) the VL of the instant SEQ ID NO: 91; however this deficiency is remedied by Korman et al.
At [0027], Korman et al. teach an anti-CTLA-4 antibody that comprises a) the VH of SEQ ID NO: 19, which shares 100% homology with the instant SEQ ID NO: 90 and b) the VL of SEQ ID NO: 9, which shares 100% homology with the instant SEQ ID NO: 91. At [0212], Korman et al. teach that “[p]harmaceutical compositions of the invention also can be administered in combination therapy, i.e., combined with other agents. For example, in treatment of cancer, the combination therapy can include a composition of the present invention with at least one anti-tumor agent…”
Based upon the teachings of the conflicting claims, Roschke et al., Saha et al., and Korman et al., one of ordinary skill in the art would have been motivated to prepare a bispecific antibody that comprises an anti-PD-1-binding moiety, such as that recited by the conflicting claims, and a specificity for another antigen, such as CTLA-4, wherein said anti-CTLA-4-binding moiety comprises a) the VH of the instant SEQ ID NO: 90 and b) the VL of the instant SEQ ID NO: 91, because there would have been a reasonable expectation that the resultant bispecific antibody is useful in the treatment of cancer. The invention of the conflicting claims, Roschke et al., Saha et al., and Korman et al. meets the limitations of claim 22.
Claims 21, 24-28, and 38 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 4 of U.S. Patent No. 11,623,959 in view of Roschke et al. (WO 2014/144600, publication date: 09/18/2014) and Saha et al. (WO 2014/209804, publication date 12/31/2014).
The conflicting claims recite an anti-PD-1 antibody that comprises a VH that shares 100% homology with the instant SEQ ID NO: 57 and a VL that shares 100% homology with the instant SEQ ID NO: 58.
The conflicting claims do not teach a bispecific antibody that comprises an anti-PD-1-binding moiety and a specificity for another antigen, such as CTLA-4; however this deficiency is remedied by Roschke et al. and Saha et al.
At [0003], Roschke et al. teach that “[t]he development of bispecific or multi-specific molecules that target two or more targets simultaneously offers a novel and promising solution for discovering new systems-oriented multitargeted agents demonstrating improved efficacy and pharmacological properties over conventional monotherapies.” At [0006], Roschke et al. teach that said bispecific molecules may be used to treat cancer.
At the Abstract, Saha et al. teach bispecific antibodies that bind CTLA-4 and PD-1 for use in the treatment of cancer.
Based upon the teachings of the conflicting claims, Roschke et al. and Saha et al., one of ordinary skill in the art would have been motivated to prepare a bispecific antibody that comprises an anti-PD-1-binding moiety, such as that recited by the conflicting claims, and a specificity for another antigen, such as CTLA-4, because there would have been a reasonable expectation that the resultant bispecific antibody is useful in the treatment of cancer. The invention of the conflicting claims, Roschke et al., and Saha et al. meets the limitations of claims 21 and 28.
With respect to claims 24-27, at [0249], Roschke et al. teach that Fc region mutations IgG1-L234A and IgG1-L235A may used to decrease antibody-dependent cellular cytotoxicity. At [0425], Roschket et al. teach that “IgG4 antibodies are known to have decreased ADCC activity and half-life compared to other immunoglobulins subclasses such as, IgGl and IgG3. Accordingly, IgG4 subclass-based formats provide an attractive format for developing therapeutics that bind to and block cell receptors, but do not deplete the target cell. Alternatively, in those embodiments for which increased effector activity is desired, an IgG4 heavy chain of a composition of the invention can be modified as described herein or otherwise known in the art, so as to increase effector function (e.g., modification of the residues at positions 327, 330 and 331; numbering according to EU index of Kabat). Similarly, where increased half-life is desired, an IgG4 heavy chain of a composition of the invention can be engineered as described herein, or otherwise known in the art to more selectively bind the FcRn at pH 6.0, but not pH 7.4, by for example, incorporating mutations located at the interface between the CH2 and CH3 domains, such as substitutions at T250Q/M428L as well as M252Y/S254T/T256E and H433K/N434F (numbering according to the EU index of Kabat).”
With respect to claim 38, at [0636], Roschke et al. teach that therapeutic formulations of bispecific or multi-specific molecules may contain pharmaceutically acceptable carriers, excipients or stabilizers.
Claim 22 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 4 of U.S. Patent No. 11,623,959 in view of Roschke et al. (WO 2014/144600, publication date: 09/18/2014) and Saha et al. (WO 2014/209804, publication date 12/31/2014), as applied to claims 21, 24-28, and 38, and further in view of Korman et al. (US PG PUB 2002/0086014, publication date: 07/04/2002).
The invention of the conflicting claims, Roschke et al., and Saha et al. is detailed above. These references do not teach or suggest an anti-CTLA-4 antibody that comprises a) the VH of the instant SEQ ID NO: 90 and b) the VL of the instant SEQ ID NO: 91; however this deficiency is remedied by Korman et al.
At [0027], Korman et al. teach an anti-CTLA-4 antibody that comprises a) the VH of SEQ ID NO: 19, which shares 100% homology with the instant SEQ ID NO: 90 and b) the VL of SEQ ID NO: 9, which shares 100% homology with the instant SEQ ID NO: 91. At [0212], Korman et al. teach that “[p]harmaceutical compositions of the invention also can be administered in combination therapy, i.e., combined with other agents. For example, in treatment of cancer, the combination therapy can include a composition of the present invention with at least one anti-tumor agent…”
Based upon the teachings of the conflicting claims, Roschke et al., Saha et al., and Korman et al., one of ordinary skill in the art would have been motivated to prepare a bispecific antibody that comprises an anti-PD-1-binding moiety, such as that recited by the conflicting claims, and a specificity for another antigen, such as CTLA-4, wherein said anti-CTLA-4-binding moiety comprises a) the VH of the instant SEQ ID NO: 90 and b) the VL of the instant SEQ ID NO: 91, because there would have been a reasonable expectation that the resultant bispecific antibody is useful in the treatment of cancer. The invention of the conflicting claims, Roschke et al., Saha et al., and Korman et al. meets the limitations of claim 22.
Claims 21, 24-28, and 38 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 4 of U.S. Patent No. 12,534,531 in view of Roschke et al. (WO 2014/144600, publication date: 09/18/2014) and Saha et al. (WO 2014/209804, publication date 12/31/2014).
The conflicting claims recite an anti-PD-1 antibody that comprises a VH that shares 100% homology with the instant SEQ ID NO: 57 and a VL that shares 100% homology with the instant SEQ ID NO: 58.
The conflicting claims do not teach a bispecific antibody that comprises an anti-PD-1-binding moiety and a specificity for another antigen, such as CTLA-4; however this deficiency is remedied by Roschke et al. and Saha et al.
At [0003], Roschke et al. teach that “[t]he development of bispecific or multi-specific molecules that target two or more targets simultaneously offers a novel and promising solution for discovering new systems-oriented multitargeted agents demonstrating improved efficacy and pharmacological properties over conventional monotherapies.” At [0006], Roschke et al. teach that said bispecific molecules may be used to treat cancer.
At the Abstract, Saha et al. teach bispecific antibodies that bind CTLA-4 and PD-1 for use in the treatment of cancer.
Based upon the teachings of the conflicting claims, Roschke et al. and Saha et al., one of ordinary skill in the art would have been motivated to prepare a bispecific antibody that comprises an anti-PD-1-binding moiety, such as that recited by the conflicting claims, and a specificity for another antigen, such as CTLA-4, because there would have been a reasonable expectation that the resultant bispecific antibody is useful in the treatment of cancer. The invention of the conflicting claims, Roschke et al., and Saha et al. meets the limitations of claims 21 and 28.
With respect to claims 24-27, at [0249], Roschke et al. teach that Fc region mutations IgG1-L234A and IgG1-L235A may used to decrease antibody-dependent cellular cytotoxicity. At [0425], Roschket et al. teach that “IgG4 antibodies are known to have decreased ADCC activity and half-life compared to other immunoglobulins subclasses such as, IgGl and IgG3. Accordingly, IgG4 subclass-based formats provide an attractive format for developing therapeutics that bind to and block cell receptors, but do not deplete the target cell. Alternatively, in those embodiments for which increased effector activity is desired, an IgG4 heavy chain of a composition of the invention can be modified as described herein or otherwise known in the art, so as to increase effector function (e.g., modification of the residues at positions 327, 330 and 331; numbering according to EU index of Kabat). Similarly, where increased half-life is desired, an IgG4 heavy chain of a composition of the invention can be engineered as described herein, or otherwise known in the art to more selectively bind the FcRn at pH 6.0, but not pH 7.4, by for example, incorporating mutations located at the interface between the CH2 and CH3 domains, such as substitutions at T250Q/M428L as well as M252Y/S254T/T256E and H433K/N434F (numbering according to the EU index of Kabat).”
With respect to claim 38, at [0636], Roschke et al. teach that therapeutic formulations of bispecific or multi-specific molecules may contain pharmaceutically acceptable carriers, excipients or stabilizers.
Claim 22 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 4 of U.S. Patent No. 12,534,531 in view of Roschke et al. (WO 2014/144600, publication date: 09/18/2014) and Saha et al. (WO 2014/209804, publication date 12/31/2014), as applied to claims 21, 24-28, and 38, and further in view of Korman et al. (US PG PUB 2002/0086014, publication date: 07/04/2002).
The invention of the conflicting claims, Roschke et al., and Saha et al. is detailed above. These references do not teach or suggest an anti-CTLA-4 antibody that comprises a) the VH of the instant SEQ ID NO: 90 and b) the VL of the instant SEQ ID NO: 91; however this deficiency is remedied by Korman et al.
At [0027], Korman et al. teach an anti-CTLA-4 antibody that comprises a) the VH of SEQ ID NO: 19, which shares 100% homology with the instant SEQ ID NO: 90 and b) the VL of SEQ ID NO: 9, which shares 100% homology with the instant SEQ ID NO: 91. At [0212], Korman et al. teach that “[p]harmaceutical compositions of the invention also can be administered in combination therapy, i.e., combined with other agents. For example, in treatment of cancer, the combination therapy can include a composition of the present invention with at least one anti-tumor agent…”
Based upon the teachings of the conflicting claims, Roschke et al., Saha et al., and Korman et al., one of ordinary skill in the art would have been motivated to prepare a bispecific antibody that comprises an anti-PD-1-binding moiety, such as that recited by the conflicting claims, and a specificity for another antigen, such as CTLA-4, wherein said anti-CTLA-4-binding moiety comprises a) the VH of the instant SEQ ID NO: 90 and b) the VL of the instant SEQ ID NO: 91, because there would have been a reasonable expectation that the resultant bispecific antibody is useful in the treatment of cancer. The invention of the conflicting claims, Roschke et al., Saha et al., and Korman et al. meets the limitations of claim 22.
Claims 21, 24-28, and 38 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 4 of U.S. Patent No. 11,623,959 in view of Roschke et al. (WO 2014/144600, publication date: 09/18/2014) and Saha et al. (WO 2014/209804, publication date 12/31/2014).
The conflicting claims recite an anti-PD-1 antibody that comprises a VH that shares 100% homology with the instant SEQ ID NO: 57 and a VL that shares 100% homology with the instant SEQ ID NO: 58.
The conflicting claims do not teach a bispecific antibody that comprises an anti-PD-1-binding moiety and a specificity for another antigen, such as CTLA-4; however this deficiency is remedied by Roschke et al. and Saha et al.
At [0003], Roschke et al. teach that “[t]he development of bispecific or multi-specific molecules that target two or more targets simultaneously offers a novel and promising solution for discovering new systems-oriented multitargeted agents demonstrating improved efficacy and pharmacological properties over conventional monotherapies.” At [0006], Roschke et al. teach that said bispecific molecules may be used to treat cancer.
At the Abstract, Saha et al. teach bispecific antibodies that bind CTLA-4 and PD-1 for use in the treatment of cancer.
Based upon the teachings of the conflicting claims, Roschke et al. and Saha et al., one of ordinary skill in the art would have been motivated to prepare a bispecific antibody that comprises an anti-PD-1-binding moiety, such as that recited by the conflicting claims, and a specificity for another antigen, such as CTLA-4, because there would have been a reasonable expectation that the resultant bispecific antibody is useful in the treatment of cancer. The invention of the conflicting claims, Roschke et al., and Saha et al. meets the limitations of claims 21 and 28.
With respect to claims 24-27, at [0249], Roschke et al. teach that Fc region mutations IgG1-L234A and IgG1-L235A may used to decrease antibody-dependent cellular cytotoxicity. At [0425], Roschket et al. teach that “IgG4 antibodies are known to have decreased ADCC activity and half-life compared to other immunoglobulins subclasses such as, IgGl and IgG3. Accordingly, IgG4 subclass-based formats provide an attractive format for developing therapeutics that bind to and block cell receptors, but do not deplete the target cell. Alternatively, in those embodiments for which increased effector activity is desired, an IgG4 heavy chain of a composition of the invention can be modified as described herein or otherwise known in the art, so as to increase effector function (e.g., modification of the residues at positions 327, 330 and 331; numbering according to EU index of Kabat). Similarly, where increased half-life is desired, an IgG4 heavy chain of a composition of the invention can be engineered as described herein, or otherwise known in the art to more selectively bind the FcRn at pH 6.0, but not pH 7.4, by for example, incorporating mutations located at the interface between the CH2 and CH3 domains, such as substitutions at T250Q/M428L as well as M252Y/S254T/T256E and H433K/N434F (numbering according to the EU index of Kabat).”
With respect to claim 38, at [0636], Roschke et al. teach that therapeutic formulations of bispecific or multi-specific molecules may contain pharmaceutically acceptable carriers, excipients or stabilizers.
Claim 22 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 4 of U.S. Patent No. 11,623,959 in view of Roschke et al. (WO 2014/144600, publication date: 09/18/2014) and Saha et al. (WO 2014/209804, publication date 12/31/2014), as applied to claims 21, 24-28, and 38, and further in view of Korman et al. (US PG PUB 2002/0086014, publication date: 07/04/2002).
The invention of the conflicting claims, Roschke et al., and Saha et al. is detailed above. These references do not teach or suggest an anti-CTLA-4 antibody that comprises a) the VH of the instant SEQ ID NO: 90 and b) the VL of the instant SEQ ID NO: 91; however this deficiency is remedied by Korman et al.
At [0027], Korman et al. teach an anti-CTLA-4 antibody that comprises a) the VH of SEQ ID NO: 19, which shares 100% homology with the instant SEQ ID NO: 90 and b) the VL of SEQ ID NO: 9, which shares 100% homology with the instant SEQ ID NO: 91. At [0212], Korman et al. teach that “[p]harmaceutical compositions of the invention also can be administered in combination therapy, i.e., combined with other agents. For example, in treatment of cancer, the combination therapy can include a composition of the present invention with at least one anti-tumor agent…”
Based upon the teachings of the conflicting claims, Roschke et al., Saha et al., and Korman et al., one of ordinary skill in the art would have been motivated to prepare a bispecific antibody that comprises an anti-PD-1-binding moiety, such as that recited by the conflicting claims, and a specificity for another antigen, such as CTLA-4, wherein said anti-CTLA-4-binding moiety comprises a) the VH of the instant SEQ ID NO: 90 and b) the VL of the instant SEQ ID NO: 91, because there would have been a reasonable expectation that the resultant bispecific antibody is useful in the treatment of cancer. The invention of the conflicting claims, Roschke et al., Saha et al., and Korman et al. meets the limitations of claim 22.
Claims 21, 24-28, and 38 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 1 of U.S. Patent No. 12,448,448 in view of Roschke et al. (WO 2014/144600, publication date: 09/18/2014) and Saha et al. (WO 2014/209804, publication date 12/31/2014).
The conflicting claim recites an anti-PD-1 antibody that comprises a VH that shares 100% homology with the instant SEQ ID NO: 57 and a VL that shares 100% homology with the instant SEQ ID NO: 58.
The conflicting claim does not teach a bispecific antibody that comprises an anti-PD-1-binding moiety and a specificity for another antigen, such as CTLA-4; however this deficiency is remedied by Roschke et al. and Saha et al.
At [0003], Roschke et al. teach that “[t]he development of bispecific or multi-specific molecules that target two or more targets simultaneously offers a novel and promising solution for discovering new systems-oriented multitargeted agents demonstrating improved efficacy and pharmacological properties over conventional monotherapies.” At [0006], Roschke et al. teach that said bispecific molecules may be used to treat cancer.
At the Abstract, Saha et al. teach bispecific antibodies that bind CTLA-4 and PD-1 for use in the treatment of cancer.
Based upon the teachings of the conflicting claim, Roschke et al. and Saha et al., one of ordinary skill in the art would have been motivated to prepare a bispecific antibody that comprises an anti-PD-1-binding moiety, such as that recited by the conflicting claim, and a specificity for another antigen, such as CTLA-4, because there would have been a reasonable expectation that the resultant bispecific antibody is useful in the treatment of cancer. The invention of the conflicting claim, Roschke et al., and Saha et al. meets the limitations of claims 21 and 28.
With respect to claims 24-27, at [0249], Roschke et al. teach that Fc region mutations IgG1-L234A and IgG1-L235A may used to decrease antibody-dependent cellular cytotoxicity. At [0425], Roschket et al. teach that “IgG4 antibodies are known to have decreased ADCC activity and half-life compared to other immunoglobulins subclasses such as, IgGl and IgG3. Accordingly, IgG4 subclass-based formats provide an attractive format for developing therapeutics that bind to and block cell receptors, but do not deplete the target cell. Alternatively, in those embodiments for which increased effector activity is desired, an IgG4 heavy chain of a composition of the invention can be modified as described herein or otherwise known in the art, so as to increase effector function (e.g., modification of the residues at positions 327, 330 and 331; numbering according to EU index of Kabat). Similarly, where increased half-life is desired, an IgG4 heavy chain of a composition of the invention can be engineered as described herein, or otherwise known in the art to more selectively bind the FcRn at pH 6.0, but not pH 7.4, by for example, incorporating mutations located at the interface between the CH2 and CH3 domains, such as substitutions at T250Q/M428L as well as M252Y/S254T/T256E and H433K/N434F (numbering according to the EU index of Kabat).”
With respect to claim 38, at [0636], Roschke et al. teach that therapeutic formulations of bispecific or multi-specific molecules may contain pharmaceutically acceptable carriers, excipients or stabilizers.
Claim 22 is rejected on the ground of nonstatutory double patenting as being unpatentable over claim 1 of U.S. Patent No. 12,448,448 in view of Roschke et al. (WO 2014/144600, publication date: 09/18/2014) and Saha et al. (WO 2014/209804, publication date 12/31/2014), as applied to claims 21, 24-28, and 38, and further in view of Korman et al. (US PG PUB 2002/0086014, publication date: 07/04/2002).
The invention of the conflicting claim, Roschke et al., and Saha et al. is detailed above. These references do not teach or suggest an anti-CTLA-4 antibody that comprises a) the VH of the instant SEQ ID NO: 90 and b) the VL of the instant SEQ ID NO: 91; however this deficiency is remedied by Korman et al.
At [0027], Korman et al. teach an anti-CTLA-4 antibody that comprises a) the VH of SEQ ID NO: 19, which shares 100% homology with the instant SEQ ID NO: 90 and b) the VL of SEQ ID NO: 9, which shares 100% homology with the instant SEQ ID NO: 91. At [0212], Korman et al. teach that “[p]harmaceutical compositions of the invention also can be administered in combination therapy, i.e., combined with other agents. For example, in treatment of cancer, the combination therapy can include a composition of the present invention with at least one anti-tumor agent…”
Based upon the teachings of the conflicting claim, Roschke et al., Saha et al., and Korman et al., one of ordinary skill in the art would have been motivated to prepare a bispecific antibody that comprises an anti-PD-1-binding moiety, such as that recited by the conflicting claims, and a specificity for another antigen, such as CTLA-4, wherein said anti-CTLA-4-binding moiety comprises a) the VH of the instant SEQ ID NO: 90 and b) the VL of the instant SEQ ID NO: 91, because there would have been a reasonable expectation that the resultant bispecific antibody is useful in the treatment of cancer. The invention of the conflicting claim, Roschke et al., Saha et al., and Korman et al. meets the limitations of claim 22.
Claims 21, 24-28, and 38 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 9, and 13 of U.S. Patent No. 12,214,036 in view of Roschke et al. (WO 2014/144600, publication date: 09/18/2014) and Saha et al. (WO 2014/209804, publication date 12/31/2014).
The conflicting claims recite an anti-PD-1 antibody that comprises a VH that shares 100% homology with the instant SEQ ID NO: 57 and a VL that shares 100% homology with the instant SEQ ID NO: 58.
The conflicting claims do not teach a bispecific antibody that comprises an anti-PD-1-binding moiety and a specificity for another antigen, such as CTLA-4; however this deficiency is remedied by Roschke et al. and Saha et al.
At [0003], Roschke et al. teach that “[t]he development of bispecific or multi-specific molecules that target two or more targets simultaneously offers a novel and promising solution for discovering new systems-oriented multitargeted agents demonstrating improved efficacy and pharmacological properties over conventional monotherapies.” At [0006], Roschke et al. teach that said bispecific molecules may be used to treat cancer.
At the Abstract, Saha et al. teach bispecific antibodies that bind CTLA-4 and PD-1 for use in the treatment of cancer.
Based upon the teachings of the conflicting claims, Roschke et al. and Saha et al., one of ordinary skill in the art would have been motivated to prepare a bispecific antibody that comprises an anti-PD-1-binding moiety, such as that recited by the conflicting claims, and a specificity for another antigen, such as CTLA-4, because there would have been a reasonable expectation that the resultant bispecific antibody is useful in the treatment of cancer. The invention of the conflicting claims, Roschke et al., and Saha et al. meets the limitations of claims 21 and 28.
With respect to claims 24-27, at [0249], Roschke et al. teach that Fc region mutations IgG1-L234A and IgG1-L235A may used to decrease antibody-dependent cellular cytotoxicity. At [0425], Roschket et al. teach that “IgG4 antibodies are known to have decreased ADCC activity and half-life compared to other immunoglobulins subclasses such as, IgGl and IgG3. Accordingly, IgG4 subclass-based formats provide an attractive format for developing therapeutics that bind to and block cell receptors, but do not deplete the target cell. Alternatively, in those embodiments for which increased effector activity is desired, an IgG4 heavy chain of a composition of the invention can be modified as described herein or otherwise known in the art, so as to increase effector function (e.g., modification of the residues at positions 327, 330 and 331; numbering according to EU index of Kabat). Similarly, where increased half-life is desired, an IgG4 heavy chain of a composition of the invention can be engineered as described herein, or otherwise known in the art to more selectively bind the FcRn at pH 6.0, but not pH 7.4, by for example, incorporating mutations located at the interface between the CH2 and CH3 domains, such as substitutions at T250Q/M428L as well as M252Y/S254T/T256E and H433K/N434F (numbering according to the EU index of Kabat).”
With respect to claim 38, at [0636], Roschke et al. teach that therapeutic formulations of bispecific or multi-specific molecules may contain pharmaceutically acceptable carriers, excipients or stabilizers.
Claim 22 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 9, and 13 of U.S. Patent No. 12,214,036 in view of Roschke et al. (WO 2014/144600, publication date: 09/18/2014) and Saha et al. (WO 2014/209804, publication date 12/31/2014), as applied to claims 21, 24-28, and 38, and further in view of Korman et al. (US PG PUB 2002/0086014, publication date: 07/04/2002).
The invention of the conflicting claims, Roschke et al., and Saha et al. is detailed above. These references do not teach or suggest an anti-CTLA-4 antibody that comprises a) the VH of the instant SEQ ID NO: 90 and b) the VL of the instant SEQ ID NO: 91; however this deficiency is remedied by Korman et al.
At [0027], Korman et al. teach an anti-CTLA-4 antibody that comprises a) the VH of SEQ ID NO: 19, which shares 100% homology with the instant SEQ ID NO: 90 and b) the VL of SEQ ID NO: 9, which shares 100% homology with the instant SEQ ID NO: 91. At [0212], Korman et al. teach that “[p]harmaceutical compositions of the invention also can be administered in combination therapy, i.e., combined with other agents. For example, in treatment of cancer, the combination therapy can include a composition of the present invention with at least one anti-tumor agent…”
Based upon the teachings of the conflicting claims, Roschke et al., Saha et al., and Korman et al., one of ordinary skill in the art would have been motivated to prepare a bispecific antibody that comprises an anti-PD-1-binding moiety, such as that recited by the conflicting claims, and a specificity for another antigen, such as CTLA-4, wherein said anti-CTLA-4-binding moiety comprises a) the VH of the instant SEQ ID NO: 90 and b) the VL of the instant SEQ ID NO: 91, because there would have been a reasonable expectation that the resultant bispecific antibody is useful in the treatment of cancer. The invention of the conflicting claims, Roschke et al., Saha et al., and Korman et al. meets the limitations of claim 22.
Claims 21, 24-28, and 38 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 1 of copending Application No. 18/987,695 in view of Roschke et al. (WO 2014/144600, publication date: 09/18/2014) and Saha et al. (WO 2014/209804, publication date 12/31/2014).
The conflicting claim recites an anti-PD-1 antibody that comprises a VH that shares 100% homology with the instant SEQ ID NO: 57 and a VL that shares 100% homology with the instant SEQ ID NO: 58.
The conflicting claim does not teach a bispecific antibody that comprises an anti-PD-1-binding moiety and a specificity for another antigen, such as CTLA-4; however this deficiency is remedied by Roschke et al. and Saha et al.
At [0003], Roschke et al. teach that “[t]he development of bispecific or multi-specific molecules that target two or more targets simultaneously offers a novel and promising solution for discovering new systems-oriented multitargeted agents demonstrating improved efficacy and pharmacological properties over conventional monotherapies.” At [0006], Roschke et al. teach that said bispecific molecules may be used to treat cancer.
At the Abstract, Saha et al. teach bispecific antibodies that bind CTLA-4 and PD-1 for use in the treatment of cancer.
Based upon the teachings of the conflicting claim, Roschke et al. and Saha et al., one of ordinary skill in the art would have been motivated to prepare a bispecific antibody that comprises an anti-PD-1-binding moiety, such as that recited by the conflicting claims, and a specificity for another antigen, such as CTLA-4, because there would have been a reasonable expectation that the resultant bispecific antibody is useful in the treatment of cancer. The invention of the conflicting claims, Roschke et al., and Saha et al. meets the limitations of claims 21 and 28.
With respect to claims 24-27, at [0249], Roschke et al. teach that Fc region mutations IgG1-L234A and IgG1-L235A may used to decrease antibody-dependent cellular cytotoxicity. At [0425], Roschket et al. teach that “IgG4 antibodies are known to have decreased ADCC activity and half-life compared to other immunoglobulins subclasses such as, IgGl and IgG3. Accordingly, IgG4 subclass-based formats provide an attractive format for developing therapeutics that bind to and block cell receptors, but do not deplete the target cell. Alternatively, in those embodiments for which increased effector activity is desired, an IgG4 heavy chain of a composition of the invention can be modified as described herein or otherwise known in the art, so as to increase effector function (e.g., modification of the residues at positions 327, 330 and 331; numbering according to EU index of Kabat). Similarly, where increased half-life is desired, an IgG4 heavy chain of a composition of the invention can be engineered as described herein, or otherwise known in the art to more selectively bind the FcRn at pH 6.0, but not pH 7.4, by for example, incorporating mutations located at the interface between the CH2 and CH3 domains, such as substitutions at T250Q/M428L as well as M252Y/S254T/T256E and H433K/N434F (numbering according to the EU index of Kabat).”
With respect to claim 38, at [0636], Roschke et al. teach that therapeutic formulations of bispecific or multi-specific molecules may contain pharmaceutically acceptable carriers, excipients or stabilizers.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claim has not in fact been patented.
Claim 22 is rejected on the ground of nonstatutory double patenting as being unpatentable over claim 1 of copending Application No. 18/987,695 in view of Roschke et al. (WO 2014/144600, publication date: 09/18/2014) and Saha et al. (WO 2014/209804, publication date 12/31/2014), as applied to claims 21, 24-28, and 38, and further in view of Korman et al. (US PG PUB 2002/0086014, publication date: 07/04/2002).
The invention of the conflicting claim, Roschke et al., and Saha et al. is detailed above. These references do not teach or suggest an anti-CTLA-4 antibody that comprises a) the VH of the instant SEQ ID NO: 90 and b) the VL of the instant SEQ ID NO: 91; however this deficiency is remedied by Korman et al.
At [0027], Korman et al. teach an anti-CTLA-4 antibody that comprises a) the VH of SEQ ID NO: 19, which shares 100% homology with the instant SEQ ID NO: 90 and b) the VL of SEQ ID NO: 9, which shares 100% homology with the instant SEQ ID NO: 91. At [0212], Korman et al. teach that “[p]harmaceutical compositions of the invention also can be administered in combination therapy, i.e., combined with other agents. For example, in treatment of cancer, the combination therapy can include a composition of the present invention with at least one anti-tumor agent…”
Based upon the teachings of the conflicting claim, Roschke et al., Saha et al., and Korman et al., one of ordinary skill in the art would have been motivated to prepare a bispecific antibody that comprises an anti-PD-1-binding moiety, such as that recited by the conflicting claims, and a specificity for another antigen, such as CTLA-4, wherein said anti-CTLA-4-binding moiety comprises a) the VH of the instant SEQ ID NO: 90 and b) the VL of the instant SEQ ID NO: 91, because there would have been a reasonable expectation that the resultant bispecific antibody is useful in the treatment of cancer. The invention of the conflicting claim, Roschke et al., Saha et al., and Korman et al. meets the limitations of claim 22.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claim has not in fact been patented.
Claims 21, 24-28, and 38 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 13 of copending Application No. 17/787,793 in view of Roschke et al. (WO 2014/144600, publication date: 09/18/2014) and Saha et al. (WO 2014/209804, publication date 12/31/2014).
The conflicting claims recite an anti-PD-1 antibody that comprises a VH that shares 100% homology with the instant SEQ ID NO: 57 and a VL that shares 100% homology with the instant SEQ ID NO: 58.
The conflicting claims do not teach a bispecific antibody that comprises an anti-PD-1-binding moiety and a specificity for another antigen, such as CTLA-4; however this deficiency is remedied by Roschke et al. and Saha et al.
At [0003], Roschke et al. teach that “[t]he development of bispecific or multi-specific molecules that target two or more targets simultaneously offers a novel and promising solution for discovering new systems-oriented multitargeted agents demonstrating improved efficacy and pharmacological properties over conventional monotherapies.” At [0006], Roschke et al. teach that said bispecific molecules may be used to treat cancer.
At the Abstract, Saha et al. teach bispecific antibodies that bind CTLA-4 and PD-1 for use in the treatment of cancer.
Based upon the teachings of the conflicting claims, Roschke et al. and Saha et al., one of ordinary skill in the art would have been motivated to prepare a bispecific antibody that comprises an anti-PD-1-binding moiety, such as that recited by the conflicting claims, and a specificity for another antigen, such as CTLA-4, because there would have been a reasonable expectation that the resultant bispecific antibody is useful in the treatment of cancer. The invention of the conflicting claims, Roschke et al., and Saha et al. meets the limitations of claims 21 and 28.
With respect to claims 24-27, at [0249], Roschke et al. teach that Fc region mutations IgG1-L234A and IgG1-L235A may used to decrease antibody-dependent cellular cytotoxicity. At [0425], Roschket et al. teach that “IgG4 antibodies are known to have decreased ADCC activity and half-life compared to other immunoglobulins subclasses such as, IgGl and IgG3. Accordingly, IgG4 subclass-based formats provide an attractive format for developing therapeutics that bind to and block cell receptors, but do not deplete the target cell. Alternatively, in those embodiments for which increased effector activity is desired, an IgG4 heavy chain of a composition of the invention can be modified as described herein or otherwise known in the art, so as to increase effector function (e.g., modification of the residues at positions 327, 330 and 331; numbering according to EU index of Kabat). Similarly, where increased half-life is desired, an IgG4 heavy chain of a composition of the invention can be engineered as described herein, or otherwise known in the art to more selectively bind the FcRn at pH 6.0, but not pH 7.4, by for example, incorporating mutations located at the interface between the CH2 and CH3 domains, such as substitutions at T250Q/M428L as well as M252Y/S254T/T256E and H433K/N434F (numbering according to the EU index of Kabat).”
With respect to claim 38, at [0636], Roschke et al. teach that therapeutic formulations of bispecific or multi-specific molecules may contain pharmaceutically acceptable carriers, excipients or stabilizers.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claim 22 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 13 of copending Application No. 17/787,793 in view of Roschke et al. (WO 2014/144600, publication date: 09/18/2014) and Saha et al. (WO 2014/209804, publication date 12/31/2014), as applied to claims 21, 24-28, and 38, and further in view of Korman et al. (US PG PUB 2002/0086014, publication date: 07/04/2002).
The invention of the conflicting claims, Roschke et al., and Saha et al. is detailed above. These references do not teach or suggest an anti-CTLA-4 antibody that comprises a) the VH of the instant SEQ ID NO: 90 and b) the VL of the instant SEQ ID NO: 91; however this deficiency is remedied by Korman et al.
At [0027], Korman et al. teach an anti-CTLA-4 antibody that comprises a) the VH of SEQ ID NO: 19, which shares 100% homology with the instant SEQ ID NO: 90 and b) the VL of SEQ ID NO: 9, which shares 100% homology with the instant SEQ ID NO: 91. At [0212], Korman et al. teach that “[p]harmaceutical compositions of the invention also can be administered in combination therapy, i.e., combined with other agents. For example, in treatment of cancer, the combination therapy can include a composition of the present invention with at least one anti-tumor agent…”
Based upon the teachings of the conflicting claims, Roschke et al., Saha et al., and Korman et al., one of ordinary skill in the art would have been motivated to prepare a bispecific antibody that comprises an anti-PD-1-binding moiety, such as that recited by the conflicting claims, and a specificity for another antigen, such as CTLA-4, wherein said anti-CTLA-4-binding moiety comprises a) the VH of the instant SEQ ID NO: 90 and b) the VL of the instant SEQ ID NO: 91, because there would have been a reasonable expectation that the resultant bispecific antibody is useful in the treatment of cancer. The invention of the conflicting claims, Roschke et al., Saha et al., and Korman et al. meets the limitations of claim 22.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claim has not in fact been patented.
Claims 21, 22, and 24-28 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 31, 32, and 36 of copending Application No. 18/006,294 (reference application).
Although the claims at issue are not identical, they are not patentably distinct from each other, because the instant claims and the conflicting claim comprise a bispecific antibody comprising an anti-PD-1 VH that shares 100% homology with instant SEQ ID NO: 57, an anti-PD-1 VL that shares 100% homology with the instant SEQ ID NO: 58, an anti-CTLA-4 VH that shares 100% homology with the instant SEQ ID NO: 90, an anti-CTLA-4 VL that shares 100% homology with the instant SEQ ID NO: 91. The conflicting claims also recite a construct comprising an Fc region with L234A and/or L235A and M252Y/S254T/T256E substitutions.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claim 38 is provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 31 and 32 of copending Application No. 18/006,294 in view of Roschke et al. (WO 2014/144600, publication date: 09/18/2014).
With respect to claim 38, at [0636], Roschke et al. teach that therapeutic formulations of bispecific or multi-specific molecules may contain pharmaceutically acceptable carriers, excipients or stabilizers.
Based upon the teachings of the conflicting claims and Roschke et al., one of ordinary skill in the art would have been motivated to prepare a pharmaceutical composition that comprises the bispecific antibody of the conflicting claim and a pharmaceutically acceptable carrier. One of ordinary skill in the art would have been motivated to do so, because there would have been a reasonable expectation that the resultant pharmaceutical composition could be used in the treatment of cancer.
This is a provisional nonstatutory double patenting rejection.
Conclusion
No claims are allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to NELSON B MOSELEY II whose telephone number is (571)272-6221. The examiner can normally be reached on M-F, 9:00-6:00 EST.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Samira Jean-Louis, can be reached at 571-270-3503. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/NELSON B MOSELEY II/Primary Examiner, Art Unit 1642
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