DETAILED ACTION Notice of Pre-AIA or AIA Status 1. 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 2. Applicant’s correspondence filed August 17 , 202 5 is acknowledged; claims 1- 8 are pending. Claim Objections 3. Claims 1 and 3 are objected to because of the following informalities: the terms “TGF-1” and “Smad 2 and Smad 3” are abbreviations/acronyms that lack definition in the claims. Appropriate correction is required. Claim Rejections - 35 USC § 112 4 . 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. Written Description 5 . Claims 1 - 8 are rejected 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. The claims contain subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention. The MPEP states that the purpose of the written description requirement is to ensure that the inventor had possession, as of the filing date of the application, of the specific subject matter later claimed. The MPEP lists factors that can be used to determine if sufficient evidence of possession has been furnished in the disclosure of the application. These include “level of skill and knowledge in the art, partial structure, physical and/or chemical properties, functional characteristics alone or coupled with a known or disclosed correlation between structure and function, and the method of making the claimed invention.” The written description requirement for a claimed genus may be satisfied through sufficient description of a representative number of species by actual reduction to practice, disclosure of drawings, or by disclosure of relevant identifying characteristics, for example, structure or other physical and/or chemical properties, by functional characteristics coupled with a known or disclosed correlation between function and structure, or by a combination of such identifying characteristics, sufficient to show the Applicants were in possession of the claimed genus . Vas-Cath Inc. v. Mahurkar, 19 USPQ2d 1111, makes clear that: "applicant must convey with reasonable clarity to those skilled in the art that, as of the filing date sought, he or she was in possession of the invention. The invention is, for purposes of the 'written description' inquiry, whatever is now claimed." (See page 1117.) The specification does not "clearly allow persons of ordinary skill in the art to recognize that [he or she] invented what is claimed." (See Vas-Cath at page 1116.) T he claims are directed to peptides and pharmaceutical compositions comprising the peptides for preventing or treating fibrosis represented by “ an ” amino acid sequence of SEQ ID NO: 1 or SEQ ID NO: 2. Claims 1 and 4-8 therefore encompass any fragment of the peptides, including any two amino acids within SEQ ID NO: 1 or SEQ ID NO: 2. The claims recite a phrase “represented by. ” The term “represented by” is not a common transitional phrase such as “comprising” or “consisting of,” and therefore the claims must be given their broadest reasonable interpretation: the term “represented by” is open-ended and these claims therefore encompass any protein that contains the sequence of the respective SEQ ID N o s . The claimed peptides must possess specific functions, including preventing fibrosis, treating fibrosis, inhibiting dissociation of TGF-b from a large latent complex by binding to integrin, inhibiting epithelial-mesenchymal transition, binding to Smad2 and Smad3 through cell penetration to inhibit phosphorylation. There is no structure presented that would correlate with these functions. The specification only sets forth SEQ ID NO:1 and 2 specifically as potentially having the required functions, but these two species are not sufficiently representative of such a broad genus of peptides. A. No Written Description for Fragments The claimed invention recites “represented by an amino acid sequence, ” and the broadest reasonable interpretation for this recitation is: the claim language reads on a fragment of a peptide, or a longer peptide comprising the SEQ ID NOs. However, the specification only discloses peptides consisting of SEQ ID NOs 1 and 2, as set out below. The specification discloses biochemical mechanism s of action for the peptides of SEQ ID N O s: 1 and 2 at FIGs. 1-7 , including that SEQ ID NO: 1 binds to various integrins and that SEQ ID NO2: binds to Smads and prevents phosphorylation of the Smads ; results showing the treatment of a pulmonary fibrosis animal model with the peptides of SEQ ID Nos: 1 and 2 at FIG 8; and results showing the treatment of a hepatic fibrosis animal model with the peptides of SEQ ID Nos: 1 and 2 at FIG 9. No specific fragments of SEQ ID NO: 1 or SEQ ID NO: 2 or longer peptides comprising SEQ ID NO: 1 or SEQ ID NO: 2 are disclosed in the specification . However, t he specification teaches at paragraph [0073]: In the present invention, a specific amino acid sequence of SEQ ID NO: 1 or SEQ ID NO: 2 is described, but it will be apparent to those skilled in the art that, within the scope of the technical idea of the present invention, an amino acid sequence of an equivalent range in which the amino acid sequence of the present invention is partially modified is construed as being within the scope of the present invention. This teaching suggests that potentially hundreds of “partially modified” peptides are encompassed by the claims, but the specification does not define any structural features commonly possessed by members of the genus. The claims recite functional language of the peptides, such as “treats fibrosis” and “inhibits epithelial-mesenchymal transition,” however a definition by function does not suffice to define the genus because it is only an indication of what the peptide does, rather than what it is; therefore, it is only a definition of a useful result rather than a definition of what achieves that result. In addition, because the genus of peptide is highly variable (i.e., each active fragment would necessarily have a unique structure; see MPEP 2434), the generic description of the substance is insufficient to describe the genus. Thus, the encompassed peptide fragments and proteins comprising the peptides have no correlation between their structure and function. Souza‐Silva et al. ("Peptide fragments of bradykinin show unexpected biological activity not mediated by B1 or B2 receptors." British Journal of Pharmacology 179.12 (2022): 3061-3077) teaches regarding fragments of the Bradykinin peptide: “ BK-(1–7) and BK-(1–5) are produced in vivo from BK-(1–9). Both peptides induced NO production in all cell types tested . However, unlike BK-(1–9), NO production elicited by BK-(1–7) or BK-(1–5) was not inhibited by B1 or B 2 receptor antagonists.” Souza‐Silva et al. at abstract. Therefore, it was surprising and not predictable that the fragments of peptide had substantially altered and different biological activity compared to the full-length peptide . In contrast, Zablocki et al. ("Potent in vitro and in vivo inhibitors of platelet aggregation based upon the Arg-Gly-Asp-Phe sequence of fibrinogen. A proposal on the nature of the binding interaction between the Arg-guanidine of RGDX mimetics and the platelet GP IIb-IIIa receptor." Journal of medicinal chemistry 36.13 (1993): 1811-1819) teaches regarding a fragment of the RGDF peptide that surprisingly: “[p]reviously, we had shown that the inherent inhibitory potency of Arg-Gly-Asp-Phe [RGDF] for disrupting the fibrinogen-GP Ilb-IIIa interaction can be enhanced 15-fold by removing the Arg-NH2 and the Arg-Gly amide bond to obtain 8-guanidinooctanoyl-Asp-Phe[GOA-Asp Phe] ” Zablocki et al. at introduction. In other words, the fragment of the tetrapeptide showed a large increase in inhibitory activity compared to the full-length tetrapeptide. The above juxtaposition of a fragmenting a peptide resulting in substantially altered and different biological activity as illustrated by Souza‐Silva et al. compared to fragmenting a peptide resulting in a large increase in (inhibitory) activity illustrated by Zablocki et al. shows it is very unpredictable what effects will be obtained with all the possible fragments of SEQ ID NOs: 1 and 2 as instantly claimed. These two studies also show the reverse, i.e., the unpredictable effects of comprising a peptide in a larger peptide/protein because, for example, the original Bradykinin peptide comprised the fragments and therefore showed substantially different biological activity compared to the fragments , and the full length RGDF peptide shows significantly less inhibitory activity . Therefore, neither the art nor the specification provides a sufficient representative number of peptide fragments or proteins comprising peptide species that retain normal biological activity when compared to the original peptide to meet the written description requirement for instant claims directed to peptides and pharmaceutical compositions . It is therefore unknown how the genus of peptide fragments would bind to integrins/smads and effect a treatment for pulmonary or hepatic fibrosis . Applicant has not shown possession of a representative number of species that have the claimed function(s). The specification therefore provides insufficient written description to support the genus fragments of and peptides comprising SEQ ID Nos: 1 and 2 encompassed by the claims . Given all of the above, Applicant does not have written description for “fragment” or “variants” of SEQ ID Nos. 1 and 2. B. No Written Description for the Breath of the Claims The claims recite peptides and pharmaceutical compositions comprising a peptide for preventing or treating fibrosis represented by an amino acid sequence of SEQ ID NO: 1 or SEQ ID NO: 2, but the specification only provides examples of treating pulmonary or hepatic fibrosis. Therefore, the breath of the claims encompasses all form of fibrosis. To address this issue, a brief assessment of the state of the art regarding the genus “fibrosis” is made herein. To address the scope of the claimed invention, the following is an assessment of the state of the art regarding challenges in fibrosis treatment. The instant peptides target the TGF-b/smad 2/3 pathway, which is considered a canonical signaling pathway in many types of fibrosis ( see Chen , Feilong, et al. ("The pivotal role of TGF-β/Smad pathway in fibrosis pathogenesis and treatment." Frontiers in Oncology 15 (2025): 1649179) in general). Chen et al. teach es that f ibrotic diseases involve complex pathogenic mechanisms that frequently progress to organ failure, yet effective therapeutic interventions remain limited. Therefore, this review aims to elucidate the molecular mechanisms through which the TGF-β1/Smad signaling pathway drives fibrotic pathogenesis. Specifically, we focus on its core biological functions: (1) driving pathological cellular phenotypic transitions, (2) promoting excessive extracellular matrix (ECM) deposition, and (3) suppressing ECM degradation—collectively culminating in structural disruption and functional decline of affected organs (see Discussion section). Chen et al. ’s teach ings suggest that therapeutic strategies targeting a single pathway may be insufficient, necessitating a comprehensive approach that considers the interplay of multiple signaling networks ( See the Discussion section). Poo et al . (“ Challenges in treating liver fibrosis, ” Annals of Hepatology, Vol. 13, Issue 6, November -December 2014, pages 845-846) teach “There are many challenges to consider. Histopathological changes seen in cirrhosis include complex modifications in hepatocyte patterns, bile duct proliferation, stellate-cell transformation, and complex microcirculation and lymphatic abnormalities, all contributing to decreased liver function, increased intrahepatic resistance and portal hypertension. Vascular changes are also present in the splanchnic organs, heart, lungs, kidney, brain, and skin. Complete resolution of all abnormalities may require long duration treatments. ” Poo et al. at paragraph 3. As a further example of the unpredictability in treating other forms of fibrosis based on success in one or two types of fibrosis: even fibrosis drugs in phase 3 clinical trials fail to successfully treat the fibrosis. See UW Medicine press release; //newsroom.uw.edu/news-releases/idiopathic-pulmonary-fibrosis-drug-fails-in-phase-3-trial/ , published May 29, 2024 . To be in phase 3, significant evidence suggested the drug may successfully treat a specific type of fibrosis; however, the cited reference demonstrates that a possible or even likely treatment may fail to work for a specific form of fibrosis. Therefore, without actually performing the required experiments, it is unpredictable if the instantly claimed peptides can treat every type of fibrosis. Given all of the above, Applicant does not have written description for entire genus of treating “fibrosis”. C) No Written Description for “Preventing”. The claims recite peptides and pharmaceutical compositions comprising a peptide for preventing or treating fibrosis represented by an amino acid sequence of SEQ ID NO: 1 or SEQ ID NO: 2, but the specification only provides examples of treating pulmonary or hepatic fibrosis. To address this issue, a brief assessment of the state of the art regarding “preventing” fibrosis is made herein. Zhao et al. ("Targeting fibrosis: mechanisms and clinical trials." Signal transduction and targeted therapy 7.1 (2022): 206) summarizes the state of the art for fibrosis therapeutics near the time of the present invention. Zhao et al. shows that there had been approximately 130 clinical trials for fibrosis therapeutics of various classes, including drugs targeting TGF-b, RTKs, CTGF, PI3K, JAKs, b-catenin, ASK-1, PPARs, FXR, and other signaling pathways. Zhao et al. at Table 1. These clinical trials targeted fibrotic conditions such as NASH, liver fibrosis, cystic fibrosis, IPF, and myelofibrosis. Id. However, these clinical trials all recruited subjects already having fibrosis, and then treated the fibrosis. The clinical trials did not attempt to pick healthy people who would later develop fibrosis to demonstrate a prophylactic effect of any of the therapeutics. For example, Senhaji et al. ("Idiopathic Pulmonary Fibrosis: A Comprehensive Review of Risk Factors, Genetics, Diagnosis, and Therapeutic Approaches." Biomedicines 14.1 (2026): 90), details the clinical trials for Idiopathic Pulmonary Fibrosis (IPF) that resulted in FDA drug approvals for Nintedanib and Pirfenidone. The results of the clinical trials showed reductions in disease progression and mortality compared to placebo. See Senhaji et al. Table 3. This is treating fibrosis, and the treatments did not cure fibrosis, let alone prevent fibrosis. An additional challenge with demonstrating the prevention of fibrosis is that it would also be necessary to first predict subjects who would later get fibrosis, and then prophylactically treat them to prevent the fibrosis’s occurrence. However, the instant specification and the art fail to provide any examples of this . It is also unpredictable how a treatment that may beneficially treat fibrosis may function in the prevention of the disease because the TGF-b, RTKs, CTGF, PI3K, JAKs, b-catenin, ASK-1, PPARs, FXR, and other signaling pathways implicated in fibrosis interact in complex ways, meaning a therapeutic that showed beneficial effect for the treatment of fibrosis may not function similarly for the prevention of fibrosis. It is also clear that none of the 130 clinical trials disclosed by Zhao et al. ( see Table 1 ) cured fibrosis, but rather the drugs merely reduced the symptomology of fibroses; a therapeutic with curative power may provide some credibility to the notion that said drug targeted a master regulator of fibrosis etiology and may work to also prevent fibrosis, however no such therapeutic is demonstrated in the specification or known in the art. It is also unpredictable what subjects will later develop fibrosis, and such predictions would be necessary in order to enable prophylactic treatments that may prevent the fibrosis. For example, as detailed by Zheng et al. ("Biomarkers in idiopathic pulmonary fibrosis: current insight and future direction." Chinese medical journal pulmonary and critical care medicine 2.02 (2024): 72-79), biomarkers are known to be associated with fibrosis, however none of biomarkers are known to have the actual predictive power that would be required to enable identification of a subject who does not yet have fibrosis and prophylactically treatment the subject, to thereby prevent fibrosis. See Zheng et al. at Tables. The cited references therefore demonstrate that the prevention that Applicants are not possession of a method of preventing fibrosis in a subject. MPEP § 2163.02 states, “[a]n objective standard for determining compliance with the written description requirement is, 'does the description clearly allow person of ordinary skill in the art to recognize that he or she invented what is claimed’”. The courts have decided: the purpose of the "written description" requirement is broader than to merely explain how to "make and use"; the Applicant must convey with reasonable clarity to those skilled in the art, that as of the filing date sought, he or she was in possession of the invention. The invention is for purposes of the “written description” inquiry, whatever is now claimed. See Vas-Cath, Inc v. Mahurkar, 935 F.2d 1555, 1563-64, 19 USPQ2d 1111, 1117 (Federal Circuit, 1991). Furthermore, the written description provision of 35 USC §112 is severable from its enablement provision; and adequate written description requires more than a mere statement that it is part of the invention and reference to a potential method for isolating it. Fiers v. Revel, 25 USPQ2d 1601, 1606 (CAFC 1993). And Amgen Inc. v. Chugai Pharmaceutical Co. Ltd., 18 USPQ2d 1016. Moreover, an adequate written description of the claimed invention must include sufficient description of at least a representative number of species by actual reduction to practice, reduction to drawings, or by disclosure of relevant, identifying characteristics sufficient to show that Applicant was in possession of the claimed genus. However, factual evidence of an actual reduction to practice has not been disclosed by Applicant in the specification; nor has Applicant shown the invention was “ready for patenting” by disclosure of drawings or structural chemical formulas that show that the invention was complete; nor has the Applicant described distinguishing identifying characteristics sufficient to show that Applicant were in possession of the claimed invention at the time the application was filed. Therefore, for all these reasons the specification lacks adequate written description, and one of skill in the art cannot reasonably conclude that Applicant had possession of the claimed invention at the time the instant application was filed. Enablement 6 . Claims 1- 8 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 pulmonary and hepatic fibrosis, with SEQ ID NO: 1 or 2, does not reasonably provide enablement for treating or preventing the genera “ fibrosis ” in general with SEQ ID NO: 1 or 2 , let alone with fragments of SEQ ID NO: 1 or 2 . The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the invention commensurate in scope with these claims. It is noted that MPEP 2164.03 teaches that “the amount of guidance or direction needed to enable the invention is inversely related to the amount of knowledge in the state of the art as well as the predictability of the art. In re Fisher, 427 F.2d 833, 839, 166 USPQ 18, 24 (CCPA 1970). The amount of guidance or direction refers to that information in the application, as originally filed, that teaches exactly how to make or use the invention. The more that is known in the prior art about the nature of the invention, how to make, and how to use the invention, and the more predictable the art is, the less information needs to be explicitly stated in the specification. In contrast, if little is known in the prior art about the nature of the invention and the art is unpredictable, the specification would need more detail as how to make and use the invention in order to be enabling.” As a general rule, enablement must be commensurate with the scope of claim language. MPEP 2164.08 states, “The Federal Circuit has repeatedly held that “the specification must teach those skilled in the art how to make and use the full scope of the claimed invention without undue experimentation’.” In re Wright, 999 F.2d 1557, 1561, 27 USPQ2d 1510, 1513 (Fed. Cir. 1993)” (emphasis added). The “make and use the full scope of the invention without undue experimentation” language was repeated in 2005 in Warner-Lambert Co. v. Teva Pharmaceuticals USA Inc., 75 USPQ2d 1865, and Scripps Research Institute v. Nemerson, 78 USPQ2d 1019 asserts: “A lack of enablement for the full scope of a claim, however, is a legitimate rejection.” The principle was explicitly affirmed most recently in Auto. Tech. Int’l, Inc. v. BMW of N. Am., Inc., 501 F.3d 1274, 84 USPQ2d 1108 (Fed. Cir. 2007), Monsanto Co. v. Syngenta Seeds, Inc., 503 F.3d 1352, 84 U.S.P.Q.2d 1705 (Fed. Cir. 2007), and Sitrick v. Dreamworks, LLC, 516 F.3d 993, 85 USPQ2d 1826 (Fed. Cir. 2008). See also In re Cortright, 49 USPQ2d 1464, 1466 and Bristol-Myers Squibb Co. v. Rhone-Poulenc Rorer Inc., 49 USPQ2d 1370. Enablement is considered in view of the Wands factors (MPEP 2164.01 (A)). The factors considered when determining if the disclosure satisfies the enablement requirement and whether any necessary experimentation is undue include, but are not limited to (In re Wands, 858 F.2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988)): 1) nature of the invention; 2) the breadth of the claims; 3) the state of the prior art; 4) the level of one of ordinary skill; 5) the level of predictability in the art; 6) the amount of direction or guidance provided by the inventor; 7) the existence of working examples; and 8) the quantity of experimentation needed to make or use the invention based on the content of the disclosure. When the above factors are weighed, it is the examiner’s position that one skilled in the art could not practice the invention without undue experimentation. Some experimentation is not fatal; the issue is whether the amount of experimentation is “undue”; see In re Vaeck, 20 USPQ2d 1438, 1444. (1) The nature of the invention and (5) The breadth of the claims: The claims are drawn to peptides and pharmaceutical compositions comprising peptides “represented by” an amino acid sequence of SEQ ID NO: 1 or 2 . The claims further recite various intended uses of the peptides, including preventing or treating the genera “ fibrosis ” in general . The claims are therefore broad and encompass preventing or treating all types of fibrosis with peptides, including fragments, of SEQ ID NO: 1 or 2. However, t he claims are extremely broad for not only by encompassing all forms of fibrosis, but also for encompassing the prevention of fibrosis. The term “p revention ” means prophylaxis for the disease, or in other words, to prevent the disease from happening in the first place. In order to prevent fibrosis, therefore, a subject would need to first be identified who would later get fibrosis to allow prophylactic treatment and prevention of the fibrosis . Therefore, the claims also inherently encompass identifying subjects who would have been diagnosed with fibrosis in the future, in order to prophylactically “prevent” it with the peptides of the instant invention. (2) The state of the prior art and (4) The predictability or unpredictability of the art: A) While the state of the art is relatively high with regard to the treatment of specific fibrosis types , the state of the art with regard to preventing fibrosis is underdeveloped. In particular, there is no known prophylactic suitable for preventing fibrosis. The lack of significant guidance from the present specification or prior art with regard to the actual prevention of fibrosis makes practicing the claimed invention highly unpredictable. To address the scope of the claimed invention, the following is an assessment of the state of the art regarding challenges in fibrosis treatment. Chen et al. teach es that f ibrotic diseases involve complex pathogenic mechanisms that frequently progress to organ failure, yet effective therapeutic interventions remain limited. Therefore, this review aims to elucidate the molecular mechanisms through which the TGF-β1/Smad signaling pathway drives fibrotic pathogenesis. Specifically, we focus on its core biological functions: (1) driving pathological cellular phenotypic transitions, (2) promoting excessive extracellular matrix (ECM) deposition, and (3) suppressing ECM degradation—collectively culminating in structural disruption and functional decline of affected organs (see Discussion section). Chen et al. teachings suggest that therapeutic strategies targeting a single pathway may be insufficient, necessitating a comprehensive approach that considers the interplay of multiple signaling networks (See the Discussion section). Poo et al . (“ Challenges in treating liver fibrosis, ” Annals of Hepatology, Vol. 13, Issue 6, November -December 2014, pages 845-846) teach “There are many challenges to consider. Histopathological changes seen in cirrhosis include complex modifications in hepatocyte patterns, bile duct proliferation, stellate-cell transformation, and complex microcirculation and lymphatic abnormalities, all contributing to decreased liver function, increased intrahepatic resistance and portal hypertension. Vascular changes are also present in the splanchnic organs, heart, lungs, kidney, brain, and skin. Complete resolution of all abnormalities may require long duration treatments .” Poo et al. at paragraph 3. Zhao et al. ("Targeting fibrosis: mechanisms and clinical trials." Signal transduction and targeted therapy 7.1 (2022): 206) summarizes the state of the art for fibrosis therapeutics near the time of the present invention. Zhao et al. shows that there had been approximately 130 clinical trials for fibrosis therapeutics of various classes, including drugs targeting TGF-b, RTKs, CTGF, PI3K, JAKs, b-catenin, ASK-1, PPARs, FXR, and other signaling pathways. Zhao et al. at Table 1. These clinical trials target ed fibrotic conditions such as NASH, liver fibrosis, cystic fibrosis, IPF, and myelofibrosis. Id. However, these clinical trials all recruited subjects already having fibrosis, and then treated the fibrosis . The clinical trials did not attempt to pick healthy people who would later develop fibrosis to demonstrate a prophylactic effect of any of the therapeutics . For example, Senhaji et al. ( "Idiopathic Pulmonary Fibrosis: A Comprehensive Review of Risk Factors, Genetics, Diagnosis, and Therapeutic Approaches." Biomedicines 14.1 (2026): 90), details the clinical trials for Idiopathic Pulmonary Fibrosis (IPF) that resulted in FDA drug approvals for Nintedanib and Pirfenidone. The results of the clinical trials showed reductions in disease progression and mortality compared to placebo. See Senhaji et al. Table 3 . This is treating fibrosis, and the treatments did not cure fibrosis, let alone prevent fibrosis. A n additional challenge with demonstrating the prevention of fibrosis is that it would also be necessary to first predict subjects who would later get fibrosis, and then prophylactically treat them to prevent the fibrosis’s occurrence . However, t he instant specification and the art fail to provide any examples of this. It is also unpredictable how a treatment that may beneficially treat fibrosis may function in the prevention of the disease because the TGF-b, RTKs, CTGF, PI3K, JAKs, b-catenin, ASK-1, PPARs, FXR, and other signaling pathways implicated in fibrosis interact in complex ways, meaning a therapeutic that showed beneficial effect for the treatment of fibrosis may not function similarly for the prevention of fibrosis. It is also clear that none of the 130 clinical trials cured fibrosis ( see Zhao et al. at Table 1) , but rather the drugs merely reduced the symptomology of fibroses; a therapeutic with curative power may provide some credibility to the notion that said drug targeted a master regulator of fibrosis etiology and may work to also prevent fibrosis , however no such therapeutic is demonstrated in the specification or known in the art . It is also unpredictable what subjects will later develop fibrosis , and such predictions would be necessary in order to enable prophylactic treatments that may prevent the fibrosis. For example, as detailed by Zheng et al. ("Biomarkers in idiopathic pulmonary fibrosis: current insight and future direction." Chinese medical journal pulmonary and critical care medicine 2.02 (2024): 72-79) , biomarkers are known to be associated with fibrosis, however none of biomarkers are known to have the actual predictive power that would be required to enable identification of a subject who does not yet have fibrosis and prophylactically treatment the subject, to thereby prevent fibrosis . S ee Zheng et al. at Tables. The cited references therefore demonstrate that the prevention of fibrosis is highly unpredictable, if even possible. B) The prior art also indicates it is unpredictable what peptide fragments of SEQ ID NOs: 1 or 2 would maintain the biological activity necessary to treat fibrosis. For example, Souza‐Silva et al. ("Peptide fragments of bradykinin show unexpected biological activity not mediated by B1 or B2 receptors." British Journal of Pharmacology 179.12 (2022): 3061-3077) teaches regarding fragments of the Bradykinin peptide: “ BK-(1–7) and BK-(1–5) are produced in vivo from BK-(1–9). Both peptides induced NO production in all cell types tested . However, unlike BK-(1–9), NO production elicited by BK-(1–7) or BK-(1–5) was not inhibited by B1 or B 2 receptor antagonists.” Souza‐Silva et al . at abstract. Therefore, it was surprising and not predictable that the fragments of peptide had substantially altered and different biological activity compared to the full-length peptide . In contrast, Zablocki et al. ("Potent in vitro and in vivo inhibitors of platelet aggregation based upon the Arg-Gly-Asp-Phe sequence of fibrinogen. A proposal on the nature of the binding interaction between the Arg-guanidine of RGDX mimetics and the platelet GP IIb-IIIa receptor." Journal of medicinal chemistry 36.13 (1993): 1811-1819) teaches regarding a fragment of the RGDF peptide that surprisingly: “[p]reviously, we had shown that the inherent inhibitory potency of Arg-Gly-Asp-Phe [RGDF] for disrupting the fibrinogen-GP Ilb-IIIa interaction can be enhanced 15-fold by removing the Arg-NH2 and the Arg-Gly amide bond to obtain 8-guanidinooctanoyl-Asp-Phe[GOA-Asp Phe] ” Zablocki et al. at introduction. In other words, the fragment of the tetrapeptide showed a large increase in inhibitory activity compared to the full-length tetrapeptide. The above juxtaposition of a fragmenting a peptide resulting in substantially altered and different biological activity as illustrated by Souza‐Silva et al. compared to fragmenting a peptide resulting in a large increase in (inhibitory) activity illustrated by Zablocki et al. shows it is very unpredictable what effects will be obtained with all the possible fragments of SEQ ID NOs: 1 and 2 as instantly claimed . These two studies also show the reverse, i.e., the unpredictable effects of comprising a peptide in a larger peptide/protein because, for example, the original Bradykinin peptide comprised the fragments and therefore showed substantially different biological activity compared to the fragments , and the full length RGDF peptide shows significantly less inhibitory activity . Therefore, neither the art nor the specification provides a sufficient representative number of peptide fragments or proteins comprising peptide species that retain normal biological activity when compared to the original peptide to meet the written description requirement for instant claims directed to peptides and pharmaceutical compositions comprising a peptide for preventing or treating fibrosis represented by an amino acid sequence of SEQ ID NO: 1 or SEQ ID NO: 2 . C) The prior art also indicates it is unpredictable what types of fibrosis may be treated with the instant peptides, other than the pulmonary and hepatic fibrosis. The instant peptides target the TGF-b/smad 2/3 pathway, which is considered a canonical signaling pathway in many types of fibrosis (see generally Chen, Feilong, et al. ("The pivotal role of TGF-β/Smad pathway in fibrosis pathogenesis and treatment." Frontiers in Oncology 15 (2025): 1649179) in general). However, other signaling pathways are also important in the etiology of fibrosis, e.g., signaling pathways through smad 1/5, ERK, JNK/p38, PI3K-Akt, Abl, ROCK, and STAT3 are known to be important to the etiology of systemic sclerosis fibrosis (see generally Finnson, Kenneth W., Yasser Almadani, and Anie Philip. "Non-canonical (non-SMAD2/3) TGF-β signaling in fibrosis: Mechanisms and targets." Seminars in cell & developmental biology . Vol. 101. Academic Press, 2020) . It is therefore unknown if, e.g., SEQ ID NO: 2, which according to claim 3 “binds to smad 2 and smad 3” may treat forms of fibrosis where other non-smad 2/3 signaling pathways may predominate. As a further example of the unpredictability in treating other forms of fibrosis based on success in one or two types of fibrosis: even fibrosis drugs in phase 3 clinical trials fail to successfully treat the fibrosis. See UW Medicine press release; //newsroom.uw.edu/news-releases/idiopathic-pulmonary-fibrosis-drug-fails-in-phase-3-trial/ published May 29, 2024 . To be in phase 3, significant evidence suggested the drug may successfully treat a specific type of fibrosis; however, the cited reference demonstrates that a possible or even likely treatment may fail to work for a specific form of fibrosis . Therefore, without actually performing the required experiments, it is unpredictable if the instantly claimed peptides can treat every type of fibrosis. 6) the amount of direction or guidance provided by the inventor; 7) the existence of working examples: The specification discloses biochemical mechanism of action for the peptides of SEQ ID NOs: 1 and 2 at FIGs. 1-7, including that SEQ ID NO: 1 binds to various integrins and that SEQ ID NO2: binds to Smads and prevents phosphorylation of the Smads; results showing the treatment of a pulmonary fibrosis animal model with the peptides of SEQ ID Nos: 1 and 2 at FIG 8; and results showing the treatment of a hepatic fibrosis animal model with the peptides of SEQ ID Nos: 1 and 2 at FIG 9. The specification therefore only discloses administering the peptides of the present invention (e.g., peptides consisting of SEQ ID NOs: 1 or 2) after the onset of pulmonary or hepatic fibrosis model s — this is treating pulmonary or hepatic fibrosis, not preventing fibrosis . Given the evidence above and (i) lack of known means for predicting the future occurrence of fibrosis in a subject, and (ii) lack of examples in the art of fibrosis being “prevented , ” one of skill in the art could not reasonably extrapolate the instant findings regarding beneficial treatment of fibrosis with the instant peptides to the prevention of fibrosis , without undue experimentation. It would also be undue experimentation to confirm which of the 1000s of peptide fragments encompassed by the claims could treat pulmonary or hepatic fibrosis, let alone other form of fibrosis encompassed by the claim-recited genera “fibrosis” in general. In conclusion, the claimed invention does not provide enablement for the prevention of fibrosis . Thus , for the reasons outlined above, the specification is not considered to be enabling for one skilled in the art to make and use the claimed invention as the amount of experimentation required is undue, due to the broad scope of the claims, the lack of guidance and working examples provided in the specification. Therefore, the specification is not representative of the instant claims and the specification is not fully enabled for the instant claims. In view of the above, one of skill in the art would be forced into undue experimentation to practice the claimed invention. 7 . 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 1-8 , 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. A) Claims 1-8 are drawn to peptides and pharmaceutical compositions for preventing or treating fibrosis represented by an amino acid sequence of SEQ ID NO: 1 or 2 . Transitional phrases other than comprising ; consisting of ; and consisting essentially of are permissible, however the term “represented by” requires interpretation in light of the specification. Although the specification indicates “represented by” includes peptides of “equivalent range” and “partially modified” peptides, no further guidance is provided in the specification as to what “equivalent” AA lengths are encompassed; or what modifications are encompassed by “partial modifications.” For example, SEQ ID NO: 2 is 15 AA long. If a peptide 14 or 16 AA long may be considered “ equivalent ” in length, how long or short would a peptide AA sequence need to be to cease being equivalent? Also, if 14 out of the 15 AAs are modified /substituted , rendering a “ partial ” modification under the broadest reasonable interpretation this term , would such a modified AA sequence be encompassed by the claims? In view of this, the scope of the claim-recited term “an amino acid” is also indefinite because it is not clear what actual structure the phrase imparts on the peptide (e.g. whether a fragment is encompassed, or only full length of SEQ ID NO of the peptide s or the . full length of SEQ ID NO of the peptides comprised in a larger sequence) . Clarification and/or correction is required. B) Claim s 2 and 3 are drawn to the peptide according to claim 1, wherein the peptide represented by the amino acid sequence of SEQ ID NO: 1 inhibits dissociation of TGF- 1 from a large latent complex (LLC) by binding to integrin (claim 2); and wherein the peptide represented by the amino acid sequence of SEQ ID NO: 2 inhibits epithelial-mesenchymal transition, or binds to Smad2 and Smad3 through cell penetration to thus inhibit phosphorylation thereof (claim 3). These claims lack antecedent basis because claim 1 is drawn to a peptide represented by an amino acid sequence of SEQ ID NO: 1 or 2 (a fragment, less than the fully sequence) , not the amino acid sequence of SEQ ID NO: 1 or 2 (fully length sequence of 1 or 2). A ppropriate clarification and/or correction is required. C) Claims 2 and 3 are drawn to the peptide according to claim 1, wherein the peptide represented by the amino acid sequence of SEQ ID NO: 1 i nhibits dissociation of TGF- 1 from a large latent complex (LLC) by binding to integrin (claim 2); or wherein the peptide represented by the amino acid sequence of SEQ ID NO: 2 inhibits epithelial-mesenchymal transition, or binds to Smad2 and Smad3 through cell penetration to thus inhibit phosphorylation thereof (claim 3) . This is a products claims , however the inhibiting/penetrating terms may also be interpreted as method steps . A single claim which claims both an apparatus and the method steps of using the apparatus is indefinite under 35 U.S.C. 112(b) or pre-AIA 35 U.S.C. 112 , second paragraph. See In re Katz Interactive Call Processing Patent Litigation, 639 F.3d 1303, 1318, 97 USPQ2d 1737, 1748-49 (Fed. Cir. 2011). Appropriate clarification as to whether the claims are intended to be directed to a method or a product is required . D ) Claim 4 is drawn to a pharmaceutical composition for preventing or treating fibrosis comprising a peptide represented by an amino acid sequence of SEQ ID NO: 1 and/ or a peptide re presented by an amino acid sequence of SEQ ID NO: 2 as an active ingredient . It is unclear how the peptide can be represented by two different SEQ ID NOs simultaneously. Appropriate clarification and/or correction is required. E ) Claim 2 is drawn to wherein the peptide represented by the amino acid sequence of SEQ ID NO: 1 inhibits dissociation of TGF- 1 from a large latent complex (LLC) by binding to integrin. It is unclear if “integrin” refers to a specific integrin or the entire family of integrin proteins. Appropriate clarification and/or correction is required. F ) Claim 3 is drawn to wherein the peptide represented by the amino acid sequence of SEQ ID NO: 2 inhibits epithelial-mesenchymal transition, or binds to Smad2 and Smad3 through cell penetration to thus inhibit phosphorylation thereof. It is unclear (i) how the peptide may bind to Smad 2/3 “through ” cell penetration, and (ii) whether phosphorylation of Smad2/3 or the peptide is being inhibited. Appropriate clarification and/or correction is required. G ) Claim 7 is drawn to wherein the pharmaceutical composition further comprises an acceptable adjuvant . The term “ acceptable ” in the claim is a relative term which renders the claim indefinite. The term “ acceptable ” is not defined by the claim, the specification does not provide a standard for ascertaining the requisite degree, and one of ordinary skill in the art would not be reasonably apprised of the scope of the invention. Double Patenting 8 . Claim 1-8 of this application is patentably indistinct from claims 1-13 of Application No. 18/836,118. Pursuant to 37 CFR 1.78(f), when two or more applications filed by the same applicant or assignee contain patentably indistinct claims, elimination of such claims from all but one application may be required in the absence of good and sufficient reason for their retention during pendency in more than one application. Applicant is required to either cancel the patentably indistinct claims from all but one application or maintain a clear line of demarcation between the applications. See MPEP § 822. 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 1-8 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-13 of copending Application No. 18/836,118 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other. The instant claims are directed to peptides represented by amino acid sequences SEQ ID NO: 1 or SEQ ID NO: 2; pharmaceutical compositions comprising a peptide represented by amino acid sequences SEQ ID NO: 1 or SEQ ID NO:2; and intended uses of the peptides and pharmaceutical compositions (e.g., treatment of fibrosis). The reference application claims are directed to peptides represented by amino acid sequences SEQ ID NO: 1; pharmaceutical compositions comprising a peptide represented by amino acid sequences SEQ ID NO: 1; and intended uses of the peptides and pharmaceutical compositions (e.g., anti-inflammatory activity). As shown below, instant SEQ ID NO: 2 is identical the reference application’s SEQ ID NO: 1: Sequence 1, US/18836118 GENERAL INFORMATION APPLICANT: NIBEC Co., Ltd. (en) TITLE OF INVENTION: PEPTIDE HAVING ANTIBACTERIAL, ANTIINFLAMMATION OR TISSUE REGENERATION AND USES THEREOF (en) FILE REFERENCE: DPP20220087KR CURRENT APPLICATION NUMBER: US/18/836,118 CURRENT FILING DATE: 2024-08-06 NUMBER OF SEQ ID NOS: 1 SEQ ID NO 1 LENGTH: 15 TYPE: PRT FEATURE: NAME/KEY: REGION LOCATION: 1.. 15 QUALIFIERS: note = PEPTIDE HAVING ANTIBACTERIAL, ANTIINFLAMMATION OR TISSUE REGENERATION FEATURE: NAME/KEY: source LOCATION: 1.. 15 QUALIFIERS: mol_type = protein organism = synthetic construct Query Match 100.0%; Score 78; Length 15; Best Local Similarity 100.0%; Matches 15; Conservative 0; Mismatches 0; Indels 0; Gaps 0; Qy 1 GKCSTRGRKSSRRKK 15 ||||||||||||||| Db 1 GKCSTRGRKSSRRKK 15 The reference application claims anticipate the instant claims because recitation of the intended use of the claimed invention must result in a structural difference between the claimed inventions in order to patentably distinguish the claimed inventions. If the reference application peptide is capable of performing the intended use, then it meets the claim. See e.g., MPEP sections 2111.02, 2112. That is the case here since the reference application peptide and pharmaceutical compositions comprising the peptide was inherently capable of preventing or treating fibrosis, as demonstrated by the instant specification. Treating fibrosis with the peptide also results in no structural difference to the peptide. As the MPEP instructs at section 2112 (I): SOMETHING WHICH IS OLD DOES NOT BECOME PATENTABLE UPON THE DISCOVERY OF A NEW PROPERTY “[T]he discovery of a previously unappreciated pr