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 .
Claim Status
Claims 1-9 are pending and under examination. See claim listing filed August 7, 2023.
Priority
Acknowledgment is made of applicant’s claim for foreign priority under 35 U.S.C. 119 (a)-(d). The certified copy has been filed in parent Application No. KR 20220061950, filed on 05/20/2022.
Claim Rejections - 35 USC § 112(a) Scope of Enablement
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 1-9 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for treating acute kidney injury, does not reasonably provide enablement for preventing acute kidney injury. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims.
Enablement is considered in view of the Wands factors (MPEP 2164.01(a)). The court in Wands states: "Enablement is not precluded by the necessity for some experimentation such as routine screening. However, experimentation needed to practice the invention must not be undue experimentation. The key word is ‘undue,’ not 'experimentation.'" (Wands, 8 USPQ2d 1404). Clearly, enablement of a claimed invention cannot be predicated on the basis of quantity of experimentation required to make or use the invention. "Whether undue experimentation is needed is not a single, simple factual determination, but rather is a conclusion reached by weighing many factual considerations." (Wands, 8 USPQ2d 1404). The factors to be considered in determining whether undue experimentation is required include: (1) the quantity of experimentation necessary, (2) the amount or direction or guidance presented, (3) the presence or absence of working examples, (4) the nature of the invention, (5) the state of the prior art, (6) the relative skill of those in the art, (7) the predictability or unpredictability of the art, and (8) the breadth of the claims. While all of these factors are considered, a sufficient amount for a prima facie case are discussed below.
The nature of the invention
The instantly claimed invention encompasses a method for preventing acute kidney injury in a subject comprising administering sestrin2 or pharmaceutical composition comprising said active ingredient, i.e. sestrin2.
The breadth of the claims
The claim is broad in that it encompasses the prevention of acute kidney injury.
The specification defines “prevention” as including “all actions that suppress or delay acute kidney injury by administration of the pharmaceutical composition according to the invention.”
Thus, in its broadest reasonable interpretation, the prevention of acute kidney injury indicates that that the onset of the acute kidney injury, or symptoms thereof, never occurs.
The amount or direction provided by the inventor / the existence of working examples
The examples of the instant disclosure describe the design and construction of sestrin2 (GenBank accession no.NP_113647.1), a protein encoded by the SESN2 gene located on human chromosome 1, and consists of a sequence of 480 amino acids. Sestrin2 is known as a protein involved
in regulating cellular responses to stress such as oxidative stress and metabolic stress (pages 4-5). The examples do not describe a study concerning the prevention of acute kidney injury.
Additionally, the disclosure does not identify a method through which an ordinarily skilled artisan would be able to predictably determine that a subject or individual would have developed acute kidney injury in order to determine that the claimed method resulted in prevention of the acute kidney injury.
The state of the prior art / the level of predictability in the art
Wang, M., et al., (M. Wang, Y. Xu, J. Liu, J. Ye, W. Yuan, H. Jiang, Z. Wang, H. Jiang, J. Wan, Recent Insights into the Biological Functions of Sestrins in Health and Disease – review paper Cellular Physiology and Biochemistry, 43:1731-1741, 2017) teaches that Sestrins (Sesns) have been identified as a family of highly conserved stress-inducible proteins that are strongly up-regulated by various stresses, including DNA damage, oxidative stress, and hypoxia. The Sesns play protective roles in most physiological and pathological conditions mainly through the regulation of oxidative stress, inflammation, autophagy, endoplasmic reticulum stress, and metabolic homeostasis (abstract). Wang, M., et al., discusses the expression, regulation and protective function of Sens in heart diseases, lung diseases, gastrointestinal tract diseases, liver and metabolism diseases, neurological diseases, kidney diseases and immunological diseases (pages 1732-1737). Wang, M., et al., also teaches that in renal tubular cells, the expression of Sesn2 was significantly increased after renal I/R injuries. Overexpression of Sesn2 in renal tubular cells could protect the cells against acute renal injuries through activating autophagy process (page 1736).
The teachings of Wang, M., et al. demonstrate that, while it was known that Sesns are regarded as stress-responsive under physiological conditions, and have been found to have a variety of functions in health and disease in different organs due to their responses to DNA damage, oxidative stress, hypoxia, metabolic stresses etc. However, a better understanding of the upstream regulators and downstream pathways of Sesns would further facilitate the development of therapeutics that modulate Sesns signaling to treat human diseases These teachings demonstrate that there was no specific known method to predictably determine that acute kidney disease was prevented using the claimed method.
Wang, J, et al., (J. Wang, S. Wang, M. Xiao, J. Zhang, J. Wang, Y. Guo, Y. Tang, J. Gu, Regulatory mechanisms of Sesn2 and its role in multi-organ diseases – review paper Pharmacological Research, 164 (2021) 105331, 2021) teaches Sestrin2 (Sesn2) is a powerful anti-oxidant that can prevent acute and chronic diseases (abstract). The review provides a systematic analysis of the role and regulatory mechanism of Sesn2 in heart, vascular, respiratory, and kidney diseases (page 1, right column, paragraph 1). Wang, J, et al., teaches the role of sesn2 as a downstream target of stress - imbalance between oxidation and oxidation resistance, disorder of endoplasmic reticulum homeostasis, DNA damage, oxygen deprivation, mitochondrial dysfunction; as well as sesn2 as an upstream target of stress – regulating ROS accumulation, protective role against endoplasmic reticulum stress, regulating DNA damage and mitochondrial dysfunction, regulating autophagy and related disorders, modulating apoptosis, and inhibiting the inflammatory response (pages 1-4). With regards to role of sesn2 in kidney disease, Wang, J, et al., summarizes that I/R-induced AKI showed that autophagy was the major mechanisms underlying renal I/R-induced AKI. A study of glomerular mesangial cells (MCs) treated with high glucose (HG) highlighted that Sesn2 plays a protective role in MCs by mediating AMPK activity and subsequently alleviating Nox4-mediated peroxynitrite generation and decreasing fibronectin, thus attenuating ROS generation and protecting MCs from injury. Protective function of Sesn2 mediated AMPK activation could improve the mitochondrial dysfunction in podocytes under high glucose condition, which illustrates a vital role of Sesn2 in suppressing diabetic kidney disease development. Further assessment is required to identify the specific mechanisms of Sesn2 in kidney disease and move them closer to clinical application (page 7).
The teachings of Wang, J, et al. demonstrate that there was no known method to predict the preventative role of exogenous sestrin2 in treating kidney disease suggesting that studies should be conducted to fully understand the relationship between Sesn2 levels and multi-organ disease progression and to explore the biochemical pathways regulated by Sesn2 to uncover new treatment strategies for a variety of diseases. As such, there was no known method that could be used to predictably identify subjects or individuals for whom acute kidney injury was prevented using the claimed methods.
The quantity of experimentation needed to make or use the invention based on the content of the disclosure
As discussed in detail above, there is no disclosed or art recognized method through which an ordinarily skilled artisan would be able to determine that a subject or an individual would have predictably developed acute kidney injury in order to apply the claimed method as a preventative measure. Furthermore, as there is no known or disclosed method that could be used to establish that acute kidney injury was prevented using the claimed method as there is no way to conclusively know that the subject would have developed acute kidney injury without the claimed method. Therefore, in order to implement the invention as claimed, one of ordinary skill in the art would have to participate in undue experimentation to find a method that could be used to determine that acute kidney injury was prevented.
In view of the Wands factors discussed above, a person of ordinary skill in the art would have to engage in undue experimentation to practice the full scope of the claimed invention. As such, the instant claims were determined to not meet the scope of enablement requirement of 35 USC 112(a).
Claim Rejections - 35 USC § 101
35 U.S.C. 101 reads as follows:
Whoever invents or discovers any new and useful process, machine, manufacture, or composition of matter, or any new and useful improvement thereof, may obtain a patent therefor, subject to the conditions and requirements of this title.
Claims 1-5 are rejected under 35 U.S.C. 101 because the claimed invention is directed to natural product without significantly more. Claim 1 recites a pharmaceutically composition. There is at least one embodiment within the broadest reasonable interpretation (BRI) of the composition that encompasses a natural product which is not markedly different from its naturally occurring counterpart. Sestrin2 is a naturally occurring product. Sestrin2 is a highly conserved protein expressed in animals including one invertebrate and mammals (see Velasco-Miguel et al., PA26, a novel target of the p53 tumor suppressor and member of the GADD family of DNA damage and growth arrest inducible genes, Oncogene. (1999) 18, no. 1, 127–137). The sestrin family proteins (including sestrin2) are upregulated in cells exposed to a variety of stresses, including DNA damage, oxidative stress, and hypoxia (see Lee et al., Sestrins orchestrate cellular metabolism to attenuate aging, Cell Metab., 18 (6) (2013), pp. 792-801).The claim recites sestrin2 as an active ingredient. This judicial exception is not integrated into a practical application because claim 1 encompass nothing more than a product of nature.
Claims 2 and 3 recites the intended use of the pharmaceutical composition in claim 1. The claims define acute kidney injury (AKI) is induced by a contrast medium. Sestrin2 is the only active ingredient in the pharmaceutical composition, and there is nothing else in the claim to be that is substantially different. Sestrin2 plays a vital role in AKI (see Ishihara et al., Sestrin-2 and BNIP3 regulate autophagy and mitophagy in renal tubular cells in acute kidney injury, Am J Physiol Renal Physiol 305: F495–F509, 2013) and protects renal function by mediating oxidative stress, fibrosis, inflammation, and autophagy, as well as attenuating endoplasmic reticulum stresses and mitochondrial dysfunction (see Wang et al., Regulatory mechanisms of Sesn2 and its role in multi-organ diseases, Pharmacological Research, Volume 164, February 2021, 105331). This judicial exception is not integrated into a practical application because claims 2 and 3 encompasses nothing more than a product of nature, and the function of the composition is an intrinsic property of the product of nature.
Claim 4 recites the function of the composition and intended use (function) of the pharmaceutical composition in claim 1. Lee et al., and Wang et. al, discloses that sestrin proteins (including sestrin1, sestrin2, and sestrin3) are stress-induced proteins that are upregulated in response to oxidative stress, DNA damage, and hypoxia. More significantly, sestrin2 has anti-oxidant properties and regulatory effects in response to multiple stressors. This judicial exception is not integrated into a practical application because claim 4 encompasses nothing more than a product of nature, and the function of the composition is intrinsic property by nature, but only an intended use of the product of nature. Both the claims are directed to a product of nature; naturally occurring proteins and recombinant proteins thereof. Utilizing the markedly different characteristic analysis, the nature-based product limitations are compared to its naturally occurring counterpart in its natural state. In the present case, the closest naturally occurring counterpart in its natural state is naturally occurring sestrin proteins and recombinant sestrin2 thereof. There are no additional elements integrated into the judicial exception (i.e., naturally occurring sestrin2 protein thereof) into a practical application because only the sestrin2 protein is claimed.
Claim 5 recites a pharmaceutical composition of claim 1, further comprising a pharmaceutically acceptable carrier, excipient or diluent. The specification defines a "pharmaceutical excipient" or a "pharmaceutically acceptable excipient" refers to a carrier, excipient and diluent that do not stimulate an organism and do not inhibit the biological activity or properties of an administered compound. The specification teaches that examples of a suitable carrier, diluent, and excipient that may be included in such a composition include saline, sterile water, Ringer's solution, buffered saline, an albumin injection solution, glycerol, ethanol, lactose, dextrose,25 sucrose, sorbitol, mannitol, xylitol, erythritol, maltitol, starch, acacia rubber, alginate,8 gelatin, calcium phosphate, calcium silicate, cellulose, methylcellulose, microcrystalline cellulose, hypromellose, polyvinylpyrrolidone, water, methylhydroxybenzoate, propylhydroxybenzoate, talc, magnesium stearate, mineral oil, and the like.
One embodiment within the BRI is a mixture of sestrin2 and water. Because the sestrin2 and saline water do not occur together in nature, there is no naturally occurring counterpart mixture for comparison; thus, the claimed mixture is compared to its naturally occurring counterparts, i.e., sestrin2 and saline water. Both sestrin2 and saline water occur naturally and there is no indication that mixing sestrin2 and saline water changes the structure, function or other properties of sestrin2 and saline water. Therefore, judicial exception is not integrated into a practical application because claim 5 encompasses nothing more than a product of nature. Claim 5 does not include additional elements that are sufficient to amount to significantly more than the judicial exception.
With regard to the formulation of the composition, the specification discloses that the composition may additionally include a typical dispersing agent, filler, extender, binder, disintegrating agent, surfactant, anti-aggregating agent, lubricant, wetting agent, fragrant, emulsifier, preservative, lyophilized formulation and the like. The claim does not include additional elements that are sufficient to amount to significantly more than the judicial exception because only the active ingredient sestrin2 are claimed. The claim directed to the intended purpose of the dispersing agent, filler, extender, binder, disintegrating agent, surfactant, anti-aggregating agent, lubricant, wetting agent, fragrant, emulsifier, preservative, lyophilized formulation, do not amount to significantly more because it does not change the structure or function of the composition such that the claimed active ingredient differ from the judicial exception, naturally occurring pharmaceutically active composition comprising sestrin2.
Therefore, the reasons set for the above, claims 1-5 are rejected under 35 U.S.C. 101.
Claim Rejections - 35 USC § 102
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 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 1-5 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by He et al. (T. He, W. Li, Y. Song, Z. Li, Y. Tang, Z. Zhang, G-Y Yang, Sestrin2 regulates microglia polarization through mTOR-mediated autophagic flux to attenuate inflammation during experimental brain ischemia, Journal of Neuroinflammation, 17:329, 2020).
Regarding claim 1, He et al. discloses a composition comprising 1 and 3 microg of sestrin2 as the active ingredient (see p.3, §Method- Transient middle cerebral artery occlusion surgery). With regard to the limitation “for preventing or treating acute kidney injury”, a recitation of the intended use of the claimed invention must result in a structural difference between the claimed invention and the prior art in order to patentably distinguish the claimed invention from the prior art. If the prior art structure is capable of performing the intended use, then it meets the claim.
Regarding claims 2 and 3 and its limitation ‘wherein the acute kidney injury is induced by a contrast medium,’ and ‘wherein the contrast medium is iohexol,….., or iodixanol.’, a statement of intended use does not impart patentable weight unless it corresponds to a structural difference over the prior art. Where the prior art discloses a structure or composition capable of performing the recited use, that limitation is not met by the applicant’s claim. In the present case, the composition of He et al. contains the same active ingredient that is claimed to treat and prevent acute kidney injury induced by a contrast medium. Accordingly, the ‘contrast-medium-induced acute kidney injury’ limitation fails to distinguish the claimed composition from He et al.’s disclosure. Regarding claim 4, He et al. discloses the same active ingredient claimed to reduce intracellular oxidative stress. Accordingly, the “reducing intracellular oxidative stress” limitation does not distinguish the claimed subject matter from He et al.’s disclosure.
Regarding claim 5, He et al. disclose the composition comprises saline. See p.3, §Method- Transient middle cerebral artery occlusion surgery.
Therefore, the disclosures of He et al. anticipate the instantly claimed invention.
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 6 is rejected under 35 U.S.C. 103 as being unpatentable over He et al. (T. He, W. Li, Y. Song, Z. Li, Y. Tang, Z. Zhang, G-Y Yang, Sestrin2 regulates microglia polarization through mTOR-mediated autophagic flux to attenuate inflammation during experimental brain ischemia, Journal of Neuroinflammation, 17:329, 2020).
He et al. teaches mice underwent stereotactic injection of normal saline, 1 mg rh-sestrin2, or 3 μg rh-sestrin2 per 25-20 g of mice bodyweight each (See the methods,§ Transient middle cerebral artery occlusion surgery, paragraph 2, page 3). Dose equivalent to the range = 4x10-5 - 10x10-8 units.
At the time before the effective filing date of the claimed invention, it would have been obvious to use “sestrin2 is 20 pg/kg to 100 pg/kg based on a total weight of the composition” because the claimed range overlaps with and within the range disclosed by He et al. Claimed dose is equivalent to range = 2x10-14 - 10x10-14 units.
Prior art range fully overlaps and is broader than claimed range. Therefore, before the effective filing date of the claimed invention, the claimed invention was prima facie obvious to the artisan of ordinary skill.
Claim(s) 7-9 are rejected under 35 U.S.C. 103 as being unpatentable over Jeong et al (B. Y. Jeong, H. Y. Lee, C. G. Park, J. Kang, S-L. Yu, D-R. Choi, S-Y. Han, M. H. Park, S. Cho, S. Y. Lee, W-M. Hwang, S-R. Yun, H-M. Ryu, E-J. Oh, S-H. Park, Y-L. Kim, S-H. Yoon, Oxidative stress caused by activation of NADPH oxidase 4 promotes contrast-induced acute kidney injury, PLoS ONE 13 (1): e0191034., January 12, 2018) in view of Eid et al. (A. A. Eid, B. M. Ford, K. Block, B. S. Kasinath, Y. Gorin, G. Ghosh-Choudhury, J. L. Barnes, and H. E. Abboud, AMP-activated Protein Kinase (AMPK) Negatively Regulates Nox4-dependent Activation of p53 and Epithelial Cell Apoptosis in Diabetes, THE JOURNAL OF BIOLOGICAL CHEMISTRY VOL. 285, NO. 48, pp. 37503–37512, November 26, 2010) and Lin et al. (Q. Lin, Y. Ma, Z. Chen, J. Hu, C. Chen, Y. Fan, W. Liang and G. Ding, Sestrin 2 regulates podocyte mitochondrial dysfunction and apoptosis under high glucose conditions via AMPK, INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE 45: 1361-1372, January 28, 2020).
Regarding claim 7, Jeong et al. teaches the following -
• Intrarenal oxidative stress plays a critical role in contrast-induced acute kidney injury (CIAKI) (abstract).
• The role of NADPH oxidase-derived reactive oxygen species (Nox4) and benefit of Nox4 inhibition in CIAKI using in vivo and in vitro models (abstract).
• Nox4 is the predominant form in the kidney and has been implicated in the production of reactive oxygen species (ROS) in the kidneys in both basal and pathologic conditions such as diabetic nephropathy and chronic kidney disease; upregulation of Nox4 may be important in renal oxidative stress and kidney injury (page 2, paragraph 2).
• Nox4 was involved in iohexol-induced apoptosis in human proximal tubular cells. (page 7, paragraph 2); and also demonstrate the role of Nox4 as a key mediator of cellular apoptosis after contrast medium exposure (page 16, paragraph 1).
• Contrast medium upregulates Nox4 and causes increased ROS production, and direct targeting of Nox4 may be helpful in the prevention of ROS-mediated CIAKI and could provide novel potential strategies for reducing AKI-related mortality (page 18, paragraph 2).
Note: Nicotinamide adenine dinucleotide 3-phosphate (NADPH) oxidases (Noxs) are important sources of reactive oxygen species (ROS).
Jeong et al. does not teach regarding the method comprising administering the composition containing sestrin2 as an active ingredient for treating acute kidney injury, however, their results suggest the underlying mechanism caused by oxidative stress and apoptosis in the pathogenesis of CIAKI and provide a novel potential strategy for treatment of CIAKI.
Regarding claim 8, Eid et al. teaches -
• The underlying mechanism at physiological conditions: Diabetes and high glucose (HG) increase the generation of NADPH oxidase-derived reactive oxygen species (Noxs) and induce apoptosis of glomerular epithelial cells (podocytes) (abstract).
• HG inactivates AMP-activated protein kinase (AMPK), up-regulates Nox4, enhances NADPH oxidase activity, and induces podocyte apoptosis (abstract).
• Results demonstrate Nox4 mediates apoptosis Induced by HG (page 37505, Results, paragraph 1).
• AMPK activators or Nox4 inhibitors may represent an adjunct therapy in addition to metabolic control to reduce kidney damage in type 1 diabetes (page 37511, right column, paragraph 2).
Eid et al. does not disclose about the mechanism underlying oxidative stress caused during contrast medium in acute kidney injury; however, this study confirms the potential therapeutic utility of AMPK activators to block Nox4 and reactive oxygen species generation alleviating intracellular oxidative stress chronic kidney disease; which is in direct correlation with stress induced contrast induced acute kidney injury.
Regarding claim 9, Lin et al. teaches -
• The role of sesn2 (sestrin2) in podocyte mitochondrial dysfunction, the effects of sesn2 on the regulation of AMP activated protein kinase (AMPK) were examined in vitro and in vivo (abstract);
• The expression of the stress-inducible protein, sesn2, was decreased in high glucose (HG) stimulated podocytes, as well as those in diabetic rats and patients with diabetic kidney disease. Sesn2 ameliorated the apoptosis and function of mitochondria in podocytes through AMPK signaling (page 1369, left column, paragraph 2).
• With regard to diabetic kidney disease, sesn2 alleviates podocyte apoptosis under high glucose (HG) conditions, which may be attributed to the protection of the mitochondria via AMPK activation, including reduced reactive oxygen species( ROS) production (page 1371, right column, paragraph 3).
Although Lin et al. does not directly teach the method for treating acute kidney injury, and neither does it mention about the oxidative stress involved in acute kidney injury induced by a contrast medium, however, they revealed that the expression of the stress-inducible protein, sesn2, was decreased in HG stimulated (mimic diabetic conditions) podocytes, as well as those in diabetic rats and patients with diabetic kidney disease. Further, they disclosed that the antioxidant effects of sesn2 were active against diabetic kidney disease and decreased expression of sesn2 may be a therapeutic target for chronic kidney disease.
Therefore, regarding claims 7-9, it would have been prima facie obvious to incorporate the teachings of art before the effective filing date of the claimed invention to incorporate the teachings of Lin et al. and Eid et al. into the novel findings taught by Jeong, thereby arriving at the instant invention. One would have been motivated to incorporate the teachings of Lin et al. and Eid et al. with a reasonable expectation to success in order to improve the treatment for acute kidney injury, by corelating the key underlying mechanisms of podocyte apoptosis due to oxidative stress in chronic (diabetic) kidney disease along with the pathogenesis of contrast-induced acute kidney injury. Thus, one of ordinary skill in the art would have recognized that applying the known teachings of Lin et al. and Eid et al. would have yielded predictable results and resulted in a promising therapeutic approach for the treatment of acute kidney injury as deduced by Jeong et al., thereby utilizing the protective role of sestrin2 as a new antioxidant for contrast-induced acute kidney injury through the regulation of mitochondrial function, oxidative stress, and apoptosis.
Summary
Claims 1-9 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ). Claims 1-5 are rejected under 35 U.S.C. 101. Claims 1-5 are rejected under 35 U.S.C. 102(a)(1). Claims 6-9 are rejected under 35 U.S.C. 103.
Conclusion
No claim is allowed.
Correspondence
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/KOYELI BANERJEE/Examiner, Art Unit 1658
/LIANKO G GARYU/Supervisory Patent Examiner, Art Unit 1654