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 .
Election/Restrictions
Applicant's election with traverse of Group I (claims 1-9) in the reply filed on 12/22/2025 is acknowledged. The traversal is on the ground(s) that the cited reference in the Election/Restriction requirement (Ericksson et al.) does not teach the specific methods claimed. This is not found persuasive because, while the reference does not teach the specific effects of the method, it teaches a method comprising administering an effective amount of a PDGFcc antagonist to a subject. Thus, the shared technical feature is present, irrespective of the effects that are due to the treatment and not to the desires of an artisan.
The requirement is still deemed proper and is therefore made FINAL.
Claims 1-11, 17 and 24-31 are pending. Claims 10-11, 17 and 24-31 are withdrawn from prosecution for being drawn to non-elected subject matter. Claims 1-9 are examined.
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.
Claims 1, 3, 4 and 8 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Eriksson et al. (WO2007136679- cited by Applicant).
The reference disclosed methods for modulating FATP (fatty acid transport protein) expression and/or activity in vivo. Lipid accumulation in tissues, particularly of skeletal muscle induces diabetic and FATP4 had been shown linked to dyslipidemia, hypertension, and the procoagulant state (abstract; p 2). The reference taught a method of reducing lipid accumulation in any mammalian subject that has any disease or condition for which lipid reduction is a desirable therapeutic goal (as well as for subjects at risk for developing such disease or condition), comprising administering a VEGF-B inhibitor administered in conjunction with a PDGF-CC inhibitor (p.46).
Thus, in broadest reasonable interpretation, the reference anticipates claims 1, 3, 4 and 8.
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.
Claims 2 and 5 are rejected under 35 U.S.C. 103 as being unpatentable over
Eriksson et al. (WO2007136679- cited by Applicant) in view of Zeitelhofer et al. (Preclinical toxicological assessment of a novel monoclonal antibody targeting human platelet-derived growth factor CC (PDGF-CC) in PDGF-CC hum mice. PLoS 13, article e0200649; pages 1-16; 2018- cited by Applicant).
The claims add the limitation that the PDGFcc antagonist is an anti-PDGFcc antibody.
The teachings of Eriksson et al. were presented supra and they do not disclose that the PDGFcc antagonist is an anti-PDGFcc antibody.
Zeitelhofer et al. reports about a newly generated monoclonal anti-human PDGF-CC antibody 6B3 (mAb 6B3) and its effects in PDGF-CC humanized mice. The antibody is free of adverse effects and it may be used in clinical settings (abstract). The reference investigates the effect of the antibody in different aspects, including lipid metabolism (p.7).
It would have been obvious for a person of ordinary skill in the art at the time that the invention was filed to have used the antibody of Zeitelhofer et al. in the method of Eriksson et al. and treat lipid accumulation or obesity with a reasonable expectation of success. This is because Eriksson et al. indicated that the antibody may be used in a clinical setting and thus in one of the settings from Eriksson et al. A skilled artisan would have used a known product with proven effects of blocking the PDGFcc effects.
Claims 6 and 7 are rejected under 35 U.S.C. 103 as being unpatentable over Eriksson et al (cited supra) in view of Zeitelhofer et al. (cited by Applicant) and in further view of Zhang et al. (WO2010/121036 – cited by Applicant).
The claims add the limitations that the method of treating obesity comprises administering a combination therapy of: i) a PDGFcc antagonist/an anti- PDGFcc antibody, an active fragment, or a homolog thereof; and ii) at least one of a CCR2 antagonist or an anti-CCR2 antibody.
Eriksson et al. does not disclose administering at least one of a CCR2 antagonist in combination with a PDGFcc antagonist/antibody.
As indicated above, Zeitelhofer et al. investigated the effect of the anti-PDGFcc antibody in different aspects, including lipid metabolism and proved its usefulness in various clinical settings.
Janssen disclosed a method of treating of obesity by inhibiting CCR2 activity in a mammal, obese animals are orally treated with vehicle or CCR2 antagonists (example 46, claims 17, 18 and 20).
It would have been obvious to a person of ordinary skill in the art, at the time that the invention was filed , to have modified the method of Eriksson with the teachings of Zeitelhofer et al. and further with the teachings of Zhang et al. and improve the effectiveness of reducing lipid accumulation in obesity with a reasonable expectation of success. This is because the methods and the reagents were known and routinely used in the art and thus the skilled artisan would have applied known methods and reagents to solve a therapeutic problem.
Claim 9 is rejected under 35 U.S.C. 103 as being unpatentable over Eriksson et al. in view of Ferro et al. (POPs' effect on cardiometabolic and inflammatory profile in a sample of women with obesity and hypertension. Arch. Environ. Occup. Health., 74, 310-321, 2019).
The claim adds the limitation that the obesity is characterized by adipocyte hypertrophy.
The teachings of Eriksson were presented above and they were silent about obesity characterized by adipocyte hypertrophy.
Ferro discloses that the obesity is characterized by adipocyte hypertrophy and hyperplasia (abstract, p. 317).
It would have been obvious to a person of ordinary skill in the art, at the time that the invention was filed, to have considered the method of Eriksson of treating obesity and consider the teachings of Ferro et al. that provide additional information on the pathophysiology of obesity and treat obesity with a reasonable expectation of success. This is because Eriksson and Ferro both disclose methods of treatment of obesity or risk factors that provide an input for manifestation of obesity.
The prior art made of record and not relied upon is considered pertinent to applicant's disclosure:
Huh et al. (Dual CCR2/5 antagonist attenuates obesity-induced insulin resistance by regulating macrophage recruitment and M1/M2 status. Obesity, 26, 378-386, 2018).
Eriksson et al. (WO2018005904), which relates to isolated antibodies that specifically interact with and show measurable binding affinity to an epitope of platelet derived growth factor C (PDGF-C). Such antibodies may be used for the modulation of PDGF-C activity in or secreted from a cell to study its effects on cell function and, in certain embodiments, for the treatment and/or prevention of a disease or condition associated with PDGF-C signing pathway (abstract).
Tateya et al. (An increase in the circulating concentration of monocyte chemoattractant protein-1 elicits systemic insulin resistance irrespective of adipose tissue inflammation in mice. Endocrin. 151, 971-979, 2010) teaches that inhibition of signaling by MCP-1 and its receptor CCR2 by administration of a novel CCR2 antagonist ameliorated insulin resistance in mice fed a high-fat diet without affecting macrophage infiltration into adipose tissue.
Sullivan et al. (Experimental evidence for the use of CCR2 antagonists in the treatment of type 2 diabetes. Metabolism Clin. & Exp. 62, 1623-1632, 2013) shows that pharmacological inhibition of CCR2 in models of T2D can reduce inflammation in adipose tissue, alter hepatic metabolism and ameliorate multiple diabetic parameters. These mechanisms may contribute to the promising antidiabetic effects seen in humans with at least one CCR2 antagonist.
Conclusion
No claims are allowed.
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ELLY-GERALD STOICA
Primary Examiner
Art Unit 1647
/Elly-Gerald Stoica/ Primary Examiner, Art Unit 1647