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 .
Notice of Change in Art Unit
Effective March 23, 2026, the Art Unit location of your application in the USPTO has changed. To aid in correlating any papers for this application, all further correspondence regarding this application should be directed to Hannah Philipose, Art Unit 1631, whose contact information is provided at the end of this action.
Noncompliance with 37 CFR 1.121(c)
The amendment to the claims filed on 08/26/2025 does not comply with one or more of the requirements of 37 CFR 1.121(c). In this case, the text of any deleted subject matter must be shown by being placed within double brackets if strike-through cannot be easily perceived. Claims 4-6 and 9 contain text of deleted subject matter shown by being placed within single brackets. While it would be proper to reject entry of the present amendment for noncompliance, it is instead respectfully offered as a reminder that applicant must comply with the requirements of 37 CFR 1.121(c) when making amendments to the claims in order to avoid the issuance of a Notice of Non-responsive Amendment which would delay prosecution and potentially have an adverse effect on any patent term adjustment should the claims proceed to issue.
Restriction/Elections
The following is a summary of the restriction requirement. Applicant elected Group 1 without traverse. Therefore, claims 20-26 were withdrawn from consideration.
Claim Amendments
The amendment filed August 26, 2025 has been entered. Claims 1-2, 4-6, and 8-26 are pending. Claims 3 and 7 are cancelled. Claims 20-26 are withdrawn from consideration. Claims 1-2, 4-6, and 8-19 are under examination. Applicant’s amendments to the Drawings and Specification have overcome each objection. All rejections below that are newly applied are necessitated by applicant’s amendment.
Priority
The instant application is a national stage entry under 35 U.S.C 371 of PCT/US2020/043342 filed 07/23/2020, which claims the benefit of provisional application 62/877,544, filed 07/23/2019. Applicant’s amendment to claim 1 to remove the term “fragmented macromolecules” is acknowledged.
Withdrawal of Prior Rejections/Objections
Rejections and/or objections not reiterated from the previous Office action mailed 02/26/2025 are hereby withdrawn. The following rejections and/or objections are either newly applied or are reiterated and are the only rejections and/or objections presently applied to the instant application.
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.
The following rejection under 35 U.S.C. 112(b) is newly applied. Claims 9-10 and 16 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as failing to set forth 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.
Claims 9 and 16 recite the limitation "the fragmented macromolecules" in the first sentence of the claims. There is insufficient antecedent basis for this limitation in the claim.
Dependent claim 10 is included in the basis of the rejection because it does not correct the deficiencies of the claim upon which it depends.
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
The following rejection under 35 U.S.C. 102(a)(1) is newly applied. Claims 1-2, 4-6, 15, and 17-18, are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Mazza et al. (WO 2015185912 A1; 06/03/2014), as evidenced by Brown et al. (Translational Research, 2014 April, 163(4): 268–285) and Booth et al. (Am J Respir Crit Care Med, 2012 Nov, 186(9): 866–876).
Regarding claim 1, Mazza teaches an acellular human liver ECM (i.e. the scaffold is decellularized) (page 4, lines 8-9). Mazza teaches the liver tissue may be pathological tissue which displays pathology associated with damage or disease. For example, liver tissue may be fatty, fibrotic, inflamed or display one or more other features associated with disease or damage (page 5, lines 17-20). Mazza teaches that sequential exposures to different decellularization reagents detach cells and cell debris from the ECM and remove them from the liver tissue (page 8, lines 33-35). Mazza discloses the absence of cells and/or the presence of ECM components, such as collagen, laminin, elastin, proteoglycans, hyaluronic acid, fibronectin, growth factors and extracellular proteases (page 18, lines 8-10). As evidenced by reference, Brown et al. (Translational Research, 2014 April; 163(4): 268–285) provides the ECM is a combination of both structural and functional components arranged in a 3-dimensional, tissue specific architecture. These components of ECM include collagens, glycoproteins, proteoglycans, mucins, elastic fibers, and growth factors (ECM composition, page 3-4). Brown further discloses the ECM can transmit mechanical cues, provides signaling cues through direct cellular binding to ECM components, and regulates access to soluble growth factors and cytokines (Dynamic reciprocity, page 4). Thus, cytokines as sequestered and regulated by the ECM and are functionally associated with and included as part of the ECM composition. Therefore, Mazza, as evidenced by Brown, discloses a substrate comprising fragmented macromolecules that include collagens, glycoproteins, proteoglycans, laminins, extracellular matrix associate proteins, soluble growth factors, inflammatory cytokines, and immune mediators as recited in claim 1. Mazza teaches that cells were found to be absent from the decellularized tissues while collagen and elastin were present (Figure 12). As evidenced by reference, Booth et al. (Am J Respir Crit Care Med, 2012 Nov, 186(9): 866–876) teaches acellular normal and fibrotic human lung matrices as a culture system for in vitro investigation. Booth discloses the relative expression of elastin in acellular idiopathic pulmonary fibrosis (IPF) lung is reduced compared to acellular normal lung, as indicated by an IPF:Normal fold change of 0.73 (Table 2). Therefore, Mazza, as evidenced by Booth, discloses a substrate wherein a concentration of elastin is reduced with respect to healthy, non-fibrotic tissue as recited in claim 1.
Regarding claim 2, Mazza discloses the use of a human liver scaffold or artificial liver tissue for in vitro disease modelling (page 43, claim 55, lines 22-23).
Regarding claims 4-6, Mazza discloses that human liver scaffolds produced from fibrotic source liver tissue display the increased ECM components characteristic of the source tissue (page 20, lines 21-23). While Mazza does not explicitly specify which ECM components are elevated, a person of ordinary skill in the art would recognize that collagens, glycoproteins, and laminins are fundamental ECM components that are commonly elevated in fibrotic tissue. As evidenced by reference, Brown teaches the extracellular matrix (ECM) composition and organization change as a function of the metabolic adaptations of the cells in response to shifts in the mechanical properties, pH, oxygen concentration, and other variables in the microenvironment (Abstract, page 1). Therefore, these disclosures support the elevated concentration of collagens, glycoproteins, and laminins in fibrotic tissue aligning with the limitations of claims 4-6.
Regarding claim 15, Mazza discloses methods in modelling liver diseases or diseases affecting the liver, such as liver fibrosis (page 20, lines 36-37).
Regarding claim 17, Mazza discloses that human liver scaffolds produced from fibrotic source liver tissue display the increased ECM components characteristic of the source tissue (page 20, lines 21-23). Mazza also discloses that for the morphology of the pathological scaffold or the relative amounts of ECM components, such as collagen, tenascin, and laminin may be altered in scaffolds from pathological tissue compared to healthy liver tissue. Mazza teaches that this may be useful in obtaining specific disease-modified liver scaffolds for disease modeling (page 5, lines 34-37 and page 6, lines 1-2).
While Mazza does not explicitly specify which ECM components are elevated or reduced, a person of ordinary skill in the art would recognize that collagens are fundamental ECM components that are commonly elevated in fibrotic tissue. As evidenced by reference, Brown teaches the extracellular matrix (ECM) composition and organization change as a function of the metabolic adaptations of the cells in response to shifts in the mechanical properties, pH, oxygen concentration, and other variables in the microenvironment (Abstract, page 1). Booth further discloses elevated or reduced relative expression of collagens in acellular fibrotic lung compared to acellular normal lung, reported as the fold change of IPF:Normal (Table 2).
As provided in MPEP 2112, "[T]he discovery of a previously unappreciated property of a prior art composition, or of a scientific explanation for the prior art’s functioning, does not render the old composition patentably new to the discoverer." Atlas Powder Co. v. IRECO Inc., 190 F.3d 1342, 1347, 51 USPQ2d 1943, 1947 (Fed. Cir. 1999). Thus the claiming of an unknown property which is inherently present in the prior art does not necessarily make the claim patentable. In re Best, 562 F.2d 1252, 1254, 195 USPQ 430, 433 (CCPA 1977).
Therefore, these disclosures support the elevated concentration of collagen type XIV α l chain or collagen type XII αl chain and the reduced concentration of collagen type IV α1 chain and collagen type VI α6 chain, with respect to healthy, non-fibrotic liver tissue, aligning with the limitations of claim 17.
Regarding claim 18, Mazza discloses that following decellularization and sterilization, the liver scaffolds may be tested, for example for the absence of cells and/or the presence of ECM components, such as laminin, fibronectin, and growth factors (page 18, lines 6-10). Mazza also discloses that for the morphology of the pathological scaffold or the relative amounts of ECM components, such as collagen, tenascin, and laminin may be altered in scaffolds from pathological tissue compared to healthy liver tissue. Mazza teaches that this may be useful in obtaining specific disease-modified liver scaffolds for disease modeling (page 5, lines 34-37 and page 6, lines 1-2). Brown teaches the extracellular matrix (ECM) composition and organization change as a function of the metabolic adaptations of the cells in response to shifts in the mechanical properties, pH, oxygen concentration, and other variables in the microenvironment (Abstract, page 1). A person of ordinary skill in the art would recognize that laminin, fibronectin, and growth factors are fundamental ECM components that are commonly elevated in fibrotic tissue. After decellularizing fibrotic tissue, the structural components of elevated concentration growth factors as stated in claim 18 would naturally flow from the process of making the product.
Therefore, Mazza anticipates claims 1-2, 4-6, 15, and 17-18.
Response to Arguments
Applicant's arguments filed August 26, 2025, with respect to claim 1, in response to the claim rejections under 35 U.S.C. 102 have been fully considered but they are not persuasive. Claim 1 was not found novel over Mazza as evidenced by Brown and Booth, which disclose the natural components of the ECM and the concentration of elastin in acellular normal and fibrotic human lung matrices.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The following rejection under 35 U.S.C 103 is newly applied. Claims 8, 10-15, and 19 are rejected under 35 U.S.C. 103 as being unpatentable over Mazza et al. (WO 2015185912 A1; 06/03/2014) and Booth et al. (Am J Respir Crit Care Med, 2012 Nov, 186(9): 866–876) as evidenced by Brown et al. (Translational Research, 2014 April, 163(4): 268–285) and Wells et al. (Biochim Biophys Acta. 2013 July; 1832(7): 884–890).
The teachings of Mazza are relied on above.
Regarding claim 8, Mazza discloses an in vitro cell culture substrate of claim 1 as set forth in the anticipation rejection under 35 U.S.C. 102(a)(1).
However, Mazza does not disclose fibrotic tissue is tissue exhibiting pulmonary fibrosis.
As stated above, Booth teaches acellular normal and acellular idiopathic pulmonary fibrosis (IPF) human lung matrices as a culture system for in vitro investigation.
It would have been obvious to an artisan of ordinary skill in the art, before the effective filing date of the claimed invention to modify Mazza’s liver in vitro cell culture substrate by substituting the extracellular matrix (ECM) of fibrotic liver tissue with the fibrotic lung ECM disclosed by Booth. These disclosures align with the limitations of claim 8, which recites a substrate comprising a tissue-specific extracellular matrix derived from fibrotic tissue exhibiting pulmonary fibrosis. An artisan of ordinary skill in the art would have been motivated to combine Mazza’s liver in vitro cell culture substrate because Booth teaches that the in vitro cell culture substrate comprised of fibrotic human lung extracellular matrix highlights the feasibility of using an entirely human in vitro system to study lung ECM biology in a manner that takes into account tissue stiffness, architecture, and matrix composition and will enable biologically relevant, mechanistic study of ECM in a fully humanized system that can be adapted to any disease state (page 868). The artisan would reasonably expect success because Mazza demonstrates tissue engineering by combining cells and scaffolds regenerates organs and recapitulates disease in vitro (page 1, lines 10-12).
Regarding claim 10, Mazza discloses that human liver scaffolds produced from fibrotic source liver tissue display the increased ECM components characteristic of the source tissue (page 20, lines 21-23). Mazza also discloses that for the morphology of the pathological scaffold or the relative amounts of ECM components, such as collagen, tenascin, and laminin may be altered in scaffolds from pathological tissue compared to healthy liver tissue. Mazza teaches that this may be useful in obtaining specific disease-modified liver scaffolds for disease modeling (page 5, lines 34-37 and page 6, lines 1-2).
While Mazza does not explicitly specify which ECM components are elevated or reduced, a person of ordinary skill in the art would recognize that collagens are fundamental ECM components that are commonly elevated in fibrotic tissue. As evidenced by reference, Brown teaches the extracellular matrix (ECM) composition and organization change as a function of the metabolic adaptations of the cells in response to shifts in the mechanical properties, pH, oxygen concentration, and other variables in the microenvironment (Abstract, page 1). Booth further discloses elevated or reduced relative expression of collagens in acellular IPF lung compared to acellular normal lung, reported as the fold change of IPF:Normal (Table 2).
As provided in MPEP 2112, "[T]he discovery of a previously unappreciated property of a prior art composition, or of a scientific explanation for the prior art’s functioning, does not render the old composition patentably new to the discoverer." Atlas Powder Co. v. IRECO Inc., 190 F.3d 1342, 1347, 51 USPQ2d 1943, 1947 (Fed. Cir. 1999). Thus the claiming of an unknown property which is inherently present in the prior art does not necessarily make the claim patentable. In re Best, 562 F.2d 1252, 1254, 195 USPQ 430, 433 (CCPA 1977).
Therefore, these disclosures support the elevated concentration of collagen type II α1 chain or collagen type XVI α1 chain in fibrotic tissue and the reduced concentration of collagen type IV α1 chain, collagen type IV α2 chain, collagen type IV α3 chain, collagen type IV α4 chain, collagen type IV α5 chain, or collagen type XXI α1 chain, aligning with the limitations of claim 10.
Regarding claim 11, Booth discloses the relative expression of fibulin-2, periostin, and vitronectin in acellular idiopathic pulmonary fibrosis (IPF) lung is elevated compared to acellular normal lung, as indicated by an IPF:Normal fold change of 3.25, 3.49, and 1.18, respectively (Table 2). Booth also discloses the relative expression of laminin γ-1, laminin β-2, nidogen 1, and laminin α-3 in acellular idiopathic pulmonary fibrosis (IPF) lung is reduced compared to acellular normal lung, as indicated by an IPF:Normal fold change of 0.61, 0.46, 0.89, and 0.14, respectively (Table 2).
Regarding claims 12-13, Mazza discloses that following decellularization and sterilization, the liver scaffolds may be tested, for example for the absence of cells and/or the presence of ECM components, such as growth factors (page 18, lines 6-10). Booth teaches that the ECM acts as a reservoir for growth factors and cytokines that, during tissue injury and repair, help to localize and direct the wound healing response. A person of ordinary skill in the art would recognize that growth factors are fundamental ECM components that are commonly elevated in fibrotic tissue. After decellularizing fibrotic tissue, the structural components of elevated concentration growth factors as stated in claims 12-13 would naturally flow from the process of making the product.
Regarding claim 14, as evidenced by Wells, teaches fibrotic lungs become stiffer in fibrosis, with elastic modulus values ranging from approximately 2 kPa for normal tissue to approximately 17 kPa for fibrotic tissue (page 3). Claim 14 recites, “…wherein the substrate comprises an elastic modulus of at least about 20kPa”. Because ‘at least about 20kPa’ allows for a reasonable variance and 17 kPa is sufficiently close to 20 kPa the lower limit of 20 kPa no longer has to be considered because of “about”.
Regarding claims 15 and 19, as evidenced by Wells also teaches fibrotic livers range from 3 kPa to 22 kPa (page 3). Additionally, Wells describes typical elastic modulus of less than 5 kPa for normal livers and greater than 12 kPa for cirrhotic livers (page 3). Claim 19 recites, “…wherein the substrate comprises an elastic modulus of at least about 15 kPa”. Because Wells teaches fibrotic livers have an elastic modulus that ranges up to 22 kPa it is reasonable to expect an elastic modulus of ‘at least about 15 kPa’ be encompassed in the disclosed range. Claim 15 is included in this rejection since claim 19 depends on claim 15.
Therefore, the combined prior art references render the claims obvious.
The following rejection under 35 U.S.C. 103 is newly applied. Claims 9 and 16 are rejected under 35 U.S.C. 103 as being unpatentable over Mazza et al. (WO 2015185912 A1; 06/03/2014) and Booth et al. (Am J Respir Crit Care Med, 2012 Nov, 186(9): 866–876) as evidenced by Wells et al. (Biochim Biophys Acta. 2013 July; 1832(7): 884–890) as applied to claims 1, 8, 11-15, and 17-19 above, and further in view of Frenguelli et al. (WO 2019122351 A1; ISR of record 01/21/2022).
Regarding claims 9 and 16, the teachings of Mazza, Booth, and Wells are relied on above.
However, Mazza and Booth do not specifically disclose the concentration of collagen or subunits.
Frenguelli teaches ECM material is specific for and obtained from decellularized human tissues chosen from healthy and pathological liver, intestine, pancreas, lung,…(page 47, claim 10, lines 11-13). Frenguelli teaches sampled tissue may be pathological tissue which displays pathology associated with damage or disease, for example fibrotic liver tissue or fibrotic lung tissue (page 24, lines 7-8 and 13-16). Frenguelli teaches the composition of pathological (fibrotic) human or animal tissue-specific extracellular matrix (ECM) material comprises collagen and the concentration of the ECM material is in the interval from 0.001 to 50 mg/ml (pages 46-47, lines 21-22). The concentration range of up to 50 mg/mL= 50,000 µg/mL, encompasses the disclosed concentration range of 100 µg/mL to 400 µg/mL in claim 9. The concentration range of up to 50 mg/mL= 50,000 µg/mL, fully encompasses the disclosed range of 500 µg/mL to 700 µg/mL as required in claim 16.
It would have been obvious to an artisan of ordinary skill in the art, before the effective filing date of the claimed invention to combine Frenguelli’s teaching of the concentration of fragmented macromolecules, particularly collagen, with Mazza’s liver in vitro cell culture substrate and Booth’s teaching of fibrotic lung extracellular matrix (ECM) compositions. An artisan of ordinary skill in the art would have been motivated to combine the prior art references because Frenguelli demonstrates that tissue-specific ECM materials would naturally comprise collagen and other macromolecules in interval concentrations. Additionally, Booth demonstrates ECM components in idiopathic pulmonary fibrosis (IPS) tissues have increased collagen concentrations (Table 2). The artisan would reasonably expect success because extracellular matrix materials from liver and lung fibrosis models share common ECM compositions to predictably yield the concentration of collagen in claims 9 and 16.
Therefore, the combined prior art references render the claims obvious.
Response to Arguments
Applicant’s arguments filed August 26, 2025 in response to the claim rejections under 35 U.S.C. 103 have been fully considered and are persuasive. Germanguz is not considered prior art for claims with a priority date of 07/23/2019. Therefore, the rejections in view of Germanguz have been withdrawn. However, new grounds of rejection are made in view of Booth.
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.
The following rejection under 35 U.S.C. 101 is reiterated from the previous non-final rejection. Claims 1-2, 4-6, and 8-19 are rejected under 35 U.S.C. 101 because the claimed invention is drawn to a product of nature without significantly more.
The claims recite “tissue-specific extracellular matrix”. According to the 2019 Revised Patent Subject Matter Eligibility Guidelines (2019PEG), the claim is first analyzed to determine if it is directed to one of the acceptable statutory categories of invention (i.e., process, machine, manufacture, and composition of matter). Claims 1-2, 4-6, and 8-19 are drawn to a composition of matter comprising an extracellular matrix. Thus, claims 1-2, 4-6, and 8-19 meet the requirements for step 1 of the analysis.
Second the claim is assessed to determine if it is directed to a judicial exception under step 2A. Under 2019PEG, “directed to” is determined via a two-prong inquiry: (1) Does the claim recite a law of nature, a product of nature, or natural phenomenon, or an abstract idea; and (2) Does the claim recite additional element(s) that integrate the judicial exception into a practical application. The phrase, “integration of a practical application”, requires the presence of an additional claim element(s) or a combination thereof to apply, rely on or use the judicial exception in a manner that imposes a meaningful limitation on the judicial exception, such that the claim does not monopolize the judicial exception. (See MPEP § 2103.05 for examples of integration of practical application).
Regarding 2A, Prong 1, claims 1-2, 4-6, and 8-19 are directed to a decellularized tissue-specific extracellular matrix derived from a fibrotic tissue. As discussed above, Frenguelli teaches tissue-specific ECM material refers to extracellular matrix biomolecules…and are obtained from decellularized tissue, and allow the cells of the tissue to receive physiological and/or pathophysiological signals (page 16, lines 20-23). Additionally, Herrera et al. (J Clin Invest. 2018 Jan 2;128(1):45–53) describes the extracellular matrix (ECM) as dynamically tuned to optimized physiological function. When pathological changes in the ECM lead to impairment of organ function, we use the term “fibrosis.”…and the altered ECM is not only a consequence but also a driver of fibrosis (Abstract, page 45). Herrera provides that fibrosis progression involves both cell-intrinsic/autonomous and ECM-driven mechanisms… the idea that progressive fibrosis in the absence of ongoing injury occurs in a fibrogenic niche comprising fibrogenic progenitors and their fibrogenic progeny residing in an ECM that is itself fibrogenic (page 46). The test at prong 1 is whether the product of nature is markedly different. The tissue-specific extracellular matrix (ECM) as claimed does not exhibit structural, functional, or other characteristics that distinguish it from ECM naturally occurring in fibrotic tissue. As such, the claimed invention is drawn to a product of nature and the first prong of the inquiry demonstrates that claims 1-2, 4-6, and 8-19 are directed to a judicial exception.
Regarding 2A, Prong 2, claim 1 recites “a decellularized tissue-specific extracellular matrix”. For claim 1, there are no additional elements or steps that apply or use the ECM in a meaningful way that limits the judicial exception. In the instant case, the extracellular matrix (ECM) is a naturally occurring product and its recitation in the claim merely describes its inherent features and properties, which are consistent with extracellular matrix’s natural function and do not impose meaningful limitations.
Claims 1-2, 4-6, and 8-19, recite wherein the tissue-specific ECM comprises collagens, glycoproteins, proteoglycans, laminins,…elevated and reduced concentration ranges,…an elastic modulus. However, these elements do not integrate the ECM into practical application because they are merely inherent properties of naturally derived ECM from fibrotic tissue. The concentration ranges and matrix composition are known characteristics of the ECM. As such, the recited “a decellularized tissue-specific extracellular matrix” does not integrate the judicial exception into a practical application as required by prong 2 of the analysis.
Step 2B-Third, if a judicial exception is present in the claim, it is further assessed to determine if the claims recite any additional elements or steps that are sufficient to ensure that the claim as a whole amounts to significantly more than the judicial exception. As discussed above, the additional elements recited in the claims such as the specified concentration ranges for collagens and the additional element describing the composition of the ECM reflects the inherent characteristics of the natural extracellular matrix derived from fibrotic tissue. The claims do not include any structural or functional modifications that would distinguish the claimed invention from its natural product. Therefore, claims 1-2, 4-6, and 8-19 do not recite significantly more than the judicial exception and fail the requirements of step 2B of the analysis.
In conclusion, claims 1-2, 4-6, and 8-19 are deemed patent ineligible.
Response to Arguments
Applicant's arguments filed August 26, 2025 in response to the claim rejections under 35 U.S.C. 101 have been fully considered but they are not persuasive. The amendment from “an acellular tissue-specific extracellular matrix” to “a decellularized tissue-specific extracellular matrix” in claim 1 is being interpreted as a product-by-process limitation to produce an acellular product. Decellularization is being interpreted as merely a process of isolation of the product found in nature. Applicant has not provided sufficient explanation or evidence to show why the amendment to the claims results in subject matter that has not been shown as a product found in nature in the prior rejection under 35 U.S.C. 101.
Conclusion
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
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/H.P./Examiner, Art Unit 1631
/JAMES JOSEPH GRABER/Examiner, Art Unit 1631
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