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 .
Claims 24-45 are pending.
Claims 1-23 are cancelled.
Claims 32-45 are withdrawn.
Claims 24 and 25 are amended.
Claim Rejections - 35 USC § 112
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.
Claim 27 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.
In regard to claim 27, it is unclear why the terms “I, III, IV, V”, “Cx37, Cx40, Cx43”, “CD11b, CD16, and CD66b”, “CD4, CD14, CD114, CD1la, CD11b, CD91, CD16”, “CD4, CD8, CD19, CD20, CD24, CD25, CD38, CD22”, “CD16, CD56, CD30, CD38”, “CD61”, “C5b9, C3a, C5a”, “IL2, IL6, IL 1-36”, “1-28”, “D, G, 5, B, K”, and “vascular endothelial growth factor, basic fibroblast growth factor, transforming growth factor beta” is in parenthesis. Thus, it is unclear if this is a limitation in the claim or just a preferred embodiment.
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.
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 24, and 26-29 rejected under 35 U.S.C. 103 as being unpatentable over PETERS (Targeting atherosclerosis by using modular, multifunctional micelles. PNAS. 2009.) in view of LIANG (ULTRASOUND-MEDIATED DELIVERY OF ECHOGENIC IMMUNOLIPOSOMES TO PORCINE VASCULAR SMOOTH MUSCLE CELLS IN VIVO. J Liposome Res. 2010.).
Regarding claim 24, PETERS teaches a method of targeting atherosclerosis (abstract). The method comprises a micelle, that comprises a lipid (figure 1), an antibody for CD31+ endothelial cells (figure 3), and a fluorescent dye (page 9817, paragraph 3). The micelle was injected into mice (page 8917, paragraph 1). The micelle bound in tissue area (page 9818, paragraph 11).
PETERS does not teach using a liposome or teach how the fluorescent moiety is attached.
LIANG teaches a method that comprises liposomes, which are made of lipids, that are conjugated to an antibody for smooth muscle cell actin, and is further loaded with calcein, which is a fluorescent moiety (abstract). The liposome is injected, which reads on administering the liposome to a subject (abstract). The method is intended to target and treat atherosclerosis (abstract).
Note, the references do not specifically state the liposome is for targeting a tissue area of an aneurysm, however the prior art' s composition would have the same chemical/physical properties of targeting this specific area as claimed by Applicant, because the prior art has the same components, i.e targeting antibody, and steps, i.e administration as claimed by Applicant, unless proven otherwise.
Regarding claim 26 and 27, PETERS teaches an antibody for CD31+ endothelial cells (figure 3).
Regarding claim 28, LIANG teaches the calcein, which is a fluorescent moiety, is loaded into the liposome (page 3, paragraph 3).
Regarding claim 29, PETERS teaches the anti-CD31 targeted micelles were seen in areas of high inflammation (page 9816, paragraph 2), which reads on the marker is presented due to an inflammation.
It would have been obvious to the person of ordinary skill in the art at the time the invention was made to incorporate a liposome with the fluorescent moiety loaded into it. The person of ordinary skill in the art would have been motivated to make those modifications and reasonably would have expected success because a liposome and a micelle are functional equivalents of carriers comprising an antibody, a fluorescent moiety that can be used for atherosclerosis commonly used in the pharmaceutical industry. Furthermore the method of attachment of the moiety is a common choice in the art.
Regarding claim 29, the anti-CD31 targeted micelles were seen in areas of high inflammation (page 9816, paragraph 2), which reads on the marker is presented due to an inflammation.
Claims 24, and 26-29 rejected under 35 U.S.C. 103 as being unpatentable over PETERS (Targeting atherosclerosis by using modular, multifunctional micelles. PNAS. 2009.) and LIANG (ULTRASOUND-MEDIATED DELIVERY OF ECHOGENIC IMMUNOLIPOSOMES TO PORCINE VASCULAR SMOOTH MUSCLE CELLS IN VIVO. J Liposome Res. 2010.) in view of TOGHILL (Abdominal aortic aneurysm—an independent disease to atherosclerosis?. Cardiovascular Pathology. 2017.).
PETERS and LIANG teach Applicant’s invention above.
PETERS and LIANG do not explicitly state the intended tissue area is of an aneurysm.
TOGHILL teaches that atherosclerosis is a significant independent risk factor for abdominal aortic aneurysms development, due to the effects of chronic inflammation, associated alternative risk factors (e.g., hypertension) and most obviously the destruction/weakening of the aortic wall, predisposing to the effects of blood pressure and mechanical wall stress on the aorta, resulting in its dilation (page 74, paragraph 1).
It would have been obvious to the person of ordinary skill in the art at the time the invention was made to incorporate the site being associated with an aneurysm. The person of ordinary skill in the art would have been motivated to make those modifications, because atherosclerosis commonly leads to aneurysms do to causing inflammation, hypertension and the destruction/weaking of the aortic wall, and reasonably would have expected success because the references are in the same field of endeavor, such as atherosclerosis and PETERS is specifically targeting areas of high inflammation.
Claims 24-29 rejected under 35 U.S.C. 103 as being unpatentable over PETERS (Targeting atherosclerosis by using modular, multifunctional micelles. PNAS. 2009.), LIANG (ULTRASOUND-MEDIATED DELIVERY OF ECHOGENIC IMMUNOLIPOSOMES TO PORCINE VASCULAR SMOOTH MUSCLE CELLS IN VIVO. J Liposome Res. 2010.) and TOGHILL (Abdominal aortic aneurysm—an independent disease to atherosclerosis?. Cardiovascular Pathology. 2017.) in view of JAMINON (The Role of Vascular Smooth Muscle Cells in Arterial Remodeling: Focus on Calcification-Related Processes. International Journal of Molecular Sciences. 2019.).
PETERS, LIANG and TOGHILL teach Applicant’s invention as discussed above.
PETERS, LIANG and TOGHILL do not teach using an antibody for alpha smooth muscle cell actin, although LIANG does teach using an antibody for smooth muscle cell actin.
Regarding claim 25, JAMINON teaches that α-smooth muscle cell actin is highly expressed in VSMCs (Page 6, paragraph 5).
It would have been obvious to the person of ordinary skill in the art at the time the invention was made to incorporate having the antibody for α-smooth muscle cell actin. The person of ordinary skill in the art would have been motivated to make those modifications, and reasonably would have expected success because LIANG is towards targeting VSMCs using an antibody for smooth muscle cell actin and JAMINON teaches that α-smooth muscle cell actin is highly expressed in VSMCs. Additionally, LIANG does teach using an antibody for smooth muscle cell actin, just not specifically alpha smooth muscle cell actin
Claims 24-31 rejected under 35 U.S.C. 103 as being unpatentable over PETERS (Targeting atherosclerosis by using modular, multifunctional micelles. PNAS. 2009.), LIANG (ULTRASOUND-MEDIATED DELIVERY OF ECHOGENIC IMMUNOLIPOSOMES TO PORCINE VASCULAR SMOOTH MUSCLE CELLS IN VIVO. J Liposome Res. 2010.), TOGHILL (Abdominal aortic aneurysm—an independent disease to atherosclerosis?. Cardiovascular Pathology. 2017.) and JAMINON (The Role of Vascular Smooth Muscle Cells in Arterial Remodeling: Focus on Calcification-Related Processes. International Journal of Molecular Sciences. 2019.) in view of FUJII (Histopathological Characteristics of Post-inflamed Coronary Arteries : in Kawasaki Disease-like Vasculitis of Rabbits. Acta Histochem Cytochem. 2016.).
PETERS, LIANG, TOGHILL and JAMINON teach Applicant’s invention as discussed above.
PETERS, LIANG, TOGHILL and JAMINON do not specifically teach that alpha smooth muscle cell actin is associated with an infection, such as vasculitis.
Regarding claim 30-31, FUJII teaches that vasculitis, an infection, is associated with alpha smooth muscle cell actin and is expressed when vasculitis is present in a subject (abstract) in VSMCs (page 32, paragraph 3).
It would have been obvious to the person of ordinary skill in the art at the time the invention was made to incorporate having alpha smooth muscle cell actin being associated with vasculitis. The person of ordinary skill in the art would have been motivated to make those modifications, because vasculitis is associated with alpha smooth muscle cell actin and reasonably would have expected success because the references are in the same field of endeavor such as conditions relating to smooth muscle cell actin and inflammation.
Response to Arguments
Applicant argues, Applicant asserts that the presently claimed invention is directed to anchoring a liposome to an aneurysmal tissue presenting with at least one vascular inflammatory marker, and that the at least one vascular inflammatory marker includes a CD31+ endothelial cell, cyclooxygenase-2, or CD45+ leukocytes. Applicant further asserts that the presently claimed invention is directed to targeting liposome to an aneurysmal tissue, which differs from Liang's teaching of targeting VSMCs in the arterial wall. Further, neither Liang nor Jaminon disclose targeting liposomes to an aneurysmal tissue presenting with at least one vascular inflammatory marker, such as CD31+ endothelial cell, cyclooxygenase-2, or CD45+ leukocytes. Applicant asserts that it would not have been obvious to apply the a-smooth muscle cell actin as allegedly taught by Jaminon to the methods of Liang with the expectation of arriving at the presently claimed invention.
The examiner does not find the arguments persuasive because as discussed above, PETERS teaches a micelle, that comprises a lipid (figure 1), an antibody for CD31+ endothelial cells (figure 3), and a fluorescent dye (page 9817, paragraph 3). The micelle bound in tissue area (page 9818, paragraph 11).
Note, the references do not specifically state the liposome is for targeting a tissue area of an aneurysm, however the prior art' s composition would have the same chemical/physical properties of targeting this specific area as claimed by Applicant, because the prior art has the same components, i.e targeting antibody, and steps, i.e administration as claimed by Applicant, unless proven otherwise.
Furthermore, TOGHILL teaches that atherosclerosis is a significant independent risk factor for abdominal aortic aneurysms development, due to the effects of chronic inflammation, associated alternative risk factors (e.g., hypertension) and most obviously the destruction/weakening of the aortic wall, predisposing to the effects of blood pressure and mechanical wall stress on the aorta, resulting in its dilation (page 74, paragraph 1).
It would have been obvious to the person of ordinary skill in the art at the time the invention was made to incorporate the site being associated with an aneurysm. The person of ordinary skill in the art would have been motivated to make those modifications, because atherosclerosis commonly leads to aneurysms do to causing inflammation, hypertension and the destruction/weaking of the aortic wall, and reasonably would have expected success because the references are in the same field of endeavor, such as atherosclerosis and PETERS is specifically targeting areas of high inflammation.
Applicant argues, The Office alleges that Liang teaches a composition comprising an antibody for smooth muscle cell actin that is specifically used to target vascular smooth muscle cells (VSMCs), and that liposomes are conjugated to an antibody for smooth muscle cell actin and are further loaded with calcein. The Office alleges that Jaminon discloses a-smooth muscle cell actin is an inflammatory marker that is highly expressed in VSMCs. The Office acknowledges that neither Liang nor Jaminon teach that a-smooth muscle cell actin is associated with an infection, such as vasculitis. To overcome the deficiencies of Liang and Jaminon, the Office relies on Fujii, which allegedly discloses that vasculitis is associated with a-smooth muscle cell actin and is expressed when vasculitis is presented in a subject in VSMCs. Thus, the Office alleges that it would have been obvious to one of skill in the art to incorporate having a-smooth muscle cell actin, as taught by Liang and Jaminon, being associated with vasculitis, as taught by Fujii. Applicant traverses the rejection.
The examiner does not find the argument persuasive because FUJII teaches that vasculitis, an infection, is associated with alpha smooth muscle cell actin and is expressed when vasculitis is present in a subject (abstract) in VSMCs (page 32, paragraph 3).
It would have been obvious to the person of ordinary skill in the art at the time the invention was made to incorporate having alpha smooth muscle cell actin being associated with vasculitis. The person of ordinary skill in the art would have been motivated to make those modifications, because vasculitis is associated with alpha smooth muscle cell actin and reasonably would have expected success because the references are in the same field of endeavor such as conditions relating to smooth muscle cell actin and inflammation.
Applicant argues, Claim 24 has been amended to recite anchoring a liposome to an aneurysmal tissue presenting with at least one vascular inflammatory marker, and that the at least one vascular inflammatory marker includes a CD3 l + endothelial cell, cyclooxygenase-2, or CD45+ leukocytes. Applicant further asserts that the presently claimed invention differs from Liang by teaching a method of targeting a liposome to an aneurysmal tissue. Contrarily, Liang teaches targeting VSMCs in the arterial wall. Applicant asserts that neither Jaminon nor Fujii remedies the defects of Liang. Therefore, Applicant asserts that it would not have been obvious to apply the teachings of Fujii to the teachings of Liang and Jaminon with an expectation of arriving of the presently claimed invention. Applicant also asserts that the presently claimed invention is patentable over Liang in view of Jaminon and Fujii and also respectfully requests withdrawal of the rejection.
The examiner does not find the arguments persuasive because as discussed above, PETERS teaches a micelle, that comprises a lipid (figure 1), an antibody for CD31+ endothelial cells (figure 3), and a fluorescent dye (page 9817, paragraph 3). The micelle bound in tissue area (page 9818, paragraph 11).
Note, the references do not specifically state the liposome is for targeting a tissue area of an aneurysm, however the prior art' s composition would have the same chemical/physical properties of targeting this specific area as claimed by Applicant, because the prior art has the same components, i.e targeting antibody, and steps, i.e administration as claimed by Applicant, unless proven otherwise.
Furthermore, TOGHILL teaches that atherosclerosis is a significant independent risk factor for abdominal aortic aneurysms development, due to the effects of chronic inflammation, associated alternative risk factors (e.g., hypertension) and most obviously the destruction/weakening of the aortic wall, predisposing to the effects of blood pressure and mechanical wall stress on the aorta, resulting in its dilation (page 74, paragraph 1).
It would have been obvious to the person of ordinary skill in the art at the time the invention was made to incorporate the site being associated with an aneurysm. The person of ordinary skill in the art would have been motivated to make those modifications, because atherosclerosis commonly leads to aneurysms do to causing inflammation, hypertension and the destruction/weaking of the aortic wall, and reasonably would have expected success because the references are in the same field of endeavor, such as atherosclerosis and PETERS is specifically targeting areas of high inflammation.
Conclusion
No claims are allowable.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to SAMANTHA L. MEJIAS whose telephone number is (703)756-5666. The examiner can normally be reached M-F.
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/S.L.M./Examiner, Art Unit 1618
/Michael G. Hartley/Supervisory Patent Examiner, Art Unit 1618
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