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 .
Status of claims
The amendment filed 03/09/2026 is acknowledged. Claim 2 is cancelled. Claims 1 and 11-13 are amended. Claims 1 and 3-13 are pending and under review.
Election/Restrictions
During a telephone conversation with Hui Wauters on 11/04/2025 a
provisional election was made without traverse to prosecute the species of “a CCL7 neutralizing
antibody”, claim 2, and “diabetes”, claims 4-6 and 11-13. This election was made without traverse as acknowledged in applicant’s response filed 03/09/2026.
Withdrawn Rejections
The rejection of claims 1-13 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112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement is withdrawn in view of claim 1 being amended to require a CCL7 antibody.
The rejection of claims 1-13 under 35 U.S.C. 103 as being unpatentable over Sayyed et al. is withdrawn upon further consideration.
New Rejections
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
Claims 1 and 3-13 are rejected under 35 U.S.C. 103 as being unpatentable over Maddaluno et al. in view of Qi et al., and in further view of Soyoye et al.
Independent claim 1 is drawn to a method of treating peripheral artery disease in a subject. Claims 3-13 recite specific administration criteria, including specific disease causes, patient selection criteria, effective amounts, and outcomes.
Instant claim 6 states "wherein the subject suffers from T2DM with vascular endothelial cell damages" and this is interpreted as an inherent property of type 2 diabetes mellitus. Furthermore, instant claims 11-13 state "wherein the administering enhances angiogenesis", "protects endothelial cell functions", and "improves diabetic vascular disease", and are interpreted as inherent properties of the CCL7 antibody of claim 1.
Maddaluno et al. discloses that MCP-3, also known as CCL7, is involved in vascular pathological processes, such as smooth muscle cell proliferation associated with atherosclerosis (instant claim 4), restenosis (instant claim 3) [see abstract, lines 3-4], and intimal hyperplasia [see p. 117, col. 2, discussion, par. 1, lines 1-3]. Specifically, Maddaluno et al. discloses that MCP-3 directly promotes coronary artery smooth muscle cell (CASMC) proliferation through ERK1/2, MAPK, and PI3K signaling pathways [see p. 117, col. 2, discussion, par. 1, lines 6-9]. Maddaluno et al. further discloses that such smooth cell proliferation plays an important role in intimal thickening resulting from arterial injury and atherosclerosis [see p. 113, col. 2, par. 2, lines 1-3], which would necessarily contribute to arterial narrowing (stenosis) and vessel lumen obstruction (occlusion) (instant claim 3). Maddaluno et al. discloses that inhibition of MCP-3 using MCP-3 antibodies reduces smooth muscle cell proliferation induced by inflammatory mediators such as TNFa and IL-1B [see p. 117, col. 2, discussion, par. 1, lines 9-11], thereby establishing CCL7 as a known mediator of vascular remodeling and inflammation.
Maddaluno et al. does not expressly disclose administration of the CCL7 neutralizing antibody to a human or animal subject, treatment or prevention of peripheral artery disease (PAD) specifically, treatment of PAD associated with diabetes, or the claimed dosage ranges.
Qi et al. discloses administering a CCL7 neutralizing antibody to mice (instant claim 7) at a dose of 2ug intravenously [see p. 12, col. 2, par. 1, lines 20-22] (instant claim 10). This antibody mediated inhibition of CCL7 reduced macrophage infiltration, vascular remodeling, hypertension, inflammation, and medial aortic thickness [see abstract, lines 10-11; see p. 9, col. 1, par. 2, lines 10-13]. Qi et al. further teaches that vascular remodeling is a pathological basis for cardiovascular diseases including hypertension, atherosclerosis, and aortic aneurysm [see p. 9, par. 2, lines 1-3]. Thus, Qi et al. teach that CCL7 mediated inflammatory responses can be therapeutically suppressed in vivo through administration of CCL7 neutralizing antibodies and expressly states that CCL7 may serve as a therapeutic target for treating vascular remodeling related diseases [see p. 12, col. 1, par. 3, last sentence].
Neither Maddaluno et al. nor Qi et al. expressly disclose treatment of peripheral PAD specifically, treatment of PAD associated with diabetes, or the claimed dosage ranges.
Soyoye et al. teaches that the central pathophysiological basis of PAD in type 2 diabetes mellitus (T2DM) is atherosclerosis, which involves progressive arterial obstruction and reduction of blood flow [see p. 829, pathophysiology, lines 1-3] (instant claims 3-6). Soyoye et al. further teaches that vascular inflammation, endothelial dysfunction, vascular smooth muscle cell dysfunction, and vascular remodeling, are key mechanisms underlying diabetic PAD and atherosclerosis [see p. 829, pathophysiology, lines 6-7].
It would have been obvious to combine these teachings and administer an effective amount of a CCL7 antibody to a subject in need in order to treat or prevent PAD because the prior art collectively teaches that CCL7 functions as an upstream mediator of vascular remodeling processes underlying occlusive vascular disease, including PAD and atherosclerosis. More specifically, the prior art teaches that atherosclerosis, which underlies and contributes to PAD, is driven by vascular inflammation, endothelial cell dysfunction, smooth muscle cell activation, and macrophage infiltration. Maddaluno et al. teaches that CCL7 promotes smooth muscle cell proliferation associated with atherosclerosis and restenosis, while Qi et al. teaches that antibody mediated inhibition of CCL7 suppresses macrophage infiltration, vascular inflammation, vascular remodeling, and medial thickening in vivo. Soyoye et al. further teaches that these same vascular remodeling and inflammatory processes underlie diabetic PAD and atherosclerotic occlusive disease. Accordingly, one would have been motivated to inhibit CCL7 signaling using a neutralizing antibody in order to attenuate vascular remodeling and inflammatory processes associated with PAD and atherosclerosis, with a reasonable expectation of success because the prior art demonstrates that CCL7 functions as an upstream inflammatory chemokine driving leukocyte recruitment, smooth muscle cell proliferation, and vascular remodeling, all of which are suppressible through antibody mediated neutralization in vivo (instant claim 1). Furthermore, because PAD in T2DM is driven by atherosclerotic vascular remodeling and endothelial dysfunction, a person having ordinary skill in the art would have reasonably expected that therapeutic suppression of CCL7 mediated vascular inflammation and remodeling would similarly provide benefit in treating or preventing diabetic PAD and endothelial dysfunction associated with diabetic PAD (instant claims 5, 6, 12, and 13).
Although the prior art does not expressly disclose the claimed antibody dosage ranges, Qi et al. establishes that CCL7 neutralizing antibodies are effective in vivo at low microgram dosing levels. Therefore, determination of a specific therapeutically effective dosage within the claimed range would have constituted routine optimization of a result-effective variable within the skill of an ordinary artisan (instant claim 1), absent evidence of unexpected results (instant claims 8 and 9).
Therefore, claims 1 and 3-13 are
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 1 and 3-13 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6 and 8-12 of copending Application No. 18649626 (reference application), in view of Garimella et al.
Although the claims at issue are not identical, they are not patentably distinct from each other because they recite the method of administering a CCL7 antagonist to a subject in need thereof to inhibit CCL7 activity and thereby treat an inflammatory mediated pathology. Garimella et al. establishes that chronic kidney disease (CKD) and PAD are closely linked vascular complications sharing common atherosclerotic and inflammatory mechanisms [see abstract, lines 3-6]. Specifically, Garimella et al. teaches that patients with CKD are at significantly increased risk of developing PAD due to shared pathogenic processes including chronic inflammation, endothelial cell dysfunction, and atherosclerotic disease progression [see p. 3, par. 3]. Accordingly, it would have been obvious to a person having ordinary skill in the art that treatment of diabetic PAD using a CCL7 neutralizing antibody is an obvious variation of methods for treatment of diabetic kidney disease using the same CCL7 targeted approach given the shared diabetic vascular inflammatory disease process.
Therefore, claims 1 and 3-13 are provisionally rejected on the ground of nonstatutory double patenting. This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Response to arguments
Applicant’s remarks regarding the prior art rejection of claims 1-13 based on Sayyed et al. have been fully considered and found persuasive. The rejection is withdrawn.
Conclusion
No claims are allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Tirone D Johnson whose telephone number is (571)272-1256. The examiner can normally be reached M-F, 9-5 ET.
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Jeffrey Stucker can be reached at (571)272-0911. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
/TIRONE D. JOHNSON/ Examiner, Art Unit 1675
/JEFFREY STUCKER/ Supervisory Patent Examiner, Art Unit 1675
Prosecution Insights