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 .
DETAILED ACTION
Applicant’s Remarks filed on 01 December 2025 are fully considered here.
The previous rejection of Claims 9-12 under 35 U.S.C. §112(b), in the Non-Final Office Action mailed on 04 September 2025, is withdrawn in view of Applicants’ amendment filed on 01 December 2025.
The previous rejection of Claims 7 and 8 under 35 U.S.C. §102(a)(1) as being anticipated by Stankowska et al., in the Non-Final Office Action mailed on 04 September 2025, is withdrawn in view of Applicants' amendment of claim 7 on 01 December 2025.
The previous rejection of Claims 1 and 7-12 under 35 U.S.C. §103 as being unpatentable over Stankowska et al. in view of Xiang et al., in the Non-Final Office Action mailed on 04 September 2025, is withdrawn in view of Applicants' amendment on 01 December 2025.
The previous rejection of Claim 5 under 35 U.S.C. §103 as being unpatentable over Stankowska et al. in view of Xiang et al., and further in view of Chen et al., in the Non-Final Office Action mailed on 04 September 2025, is withdrawn in view of Applicants' amendment on 01 December 2025.
This action is a Final Office Action, based on new grounds under 35 U.S.C. §103 over Stankowska et al. in view of Xiang et al., and Chen et al., necessitated by Applicants’ amendment in claims 1 and 7 filed on 01 December 2025.
Claims 1-3, 7, 9-13 and 15-16 are pending. Claims 2-3, 13 and 15-16 are withdrawn. Claims 1, 7 and 9-12 are rejected.
Priority
Applicant’s claim for the benefit of a prior-filed application under 35 U.S.C. §119(e) or under 35 U.S.C. §120, §121, or §365(c) is acknowledged. As noted in the Non-Final Office Action mailed 04 September 2025, Applicant has claimed the benefit of the filing date of the prior application, and designates the instant application as a "CON" of PCT/CN2021/072108.
Applicant has complied with all of the conditions for receiving the benefit of an earlier filing date under 35 U.S.C. §120 or §365(c).
Claims 1, 7 and 9-12 have the effective filing date of 15 January 2021.
Claim Objections
Claims 2-3, 13 and 15-16 show incorrect status identifiers. Applicant is reminded that claims 2-3, 13 and 15-16 should be labeled: “(Withdrawn)”; remaining claims should be identified appropriately (MPEP 714 (II)(C)(A)) (See 37 CFR 1.121 (c)).
Applicant is required to provide a new claim set showing correct status identifiers in the response to this Office Action.
Claims 1 and 7 are objected to because of the following informalities:
Claim 1 recites: "..., comprising increasing the biological activity, in the amacrine cell, of genes of POU class 4 homeobox 2 (Bm3B) and SRY-box transcription factor 4 (Sox4),...", which should read: "..., comprising increasing the biological activity, in the amacrine cell, of the genes POU class 4 homeobox 2 (Bm3B) and SRY-box transcription factor 4 (Sox4),..."
Claim 7 recites: "..., comprising increasing the biological activity, in the RGC, of genes of Bm3B and Sox4,...", which should read: "..., comprising increasing the biological activity, in the RGC, of the genes Bm3B and Sox4,..."
Appropriate correction is required.
Claim Interpretations
(1) Claim 1 recites language which is considered to be an inherent feature or property.
Claim 1 recites: "A method for preparing an amacrine cell responsive to visual signals, comprising increasing the biological activity, in the amacrine cell, of genes of POU class 4 homeobox 2 (Brn3B) and SRY-box transcription factor 4 (Sox4),..."
The specification does not describe, define or explain what type of visual signals the amacrine cell is responsive to after it has been prepared within the context of the claimed subject matter. In fact, Cherry et al. (cited in the Non-Final Office Action mailed 04 September 2025) teaches that amacrine cells, a class of interneurons, are thought to mediate much of the processing of the visual signal that occurs within the retina (pg. 9495, column 1, Abstract). That is, it appears as though (native) amacrine cells are inherently responsive to visual signals.
For the purpose of examination, prior art which shows directly or indirectly the step of increasing the biological activity of POU class 4 homeobox 2 (Brn3B) in an amacrine cell will be considered to be showing an amacrine cell responsive to visual signals.
On the other hand, prior art which shows this inherent property will be noted at the discretion of the Examiner.
(2) Claim 1 recites: "A method for preparing an amacrine cell responsive to visual signals, comprising increasing the biological activity, in the amacrine cell, of genes of POU class 4 homeobox 2 (Brn3B) and SRY-box transcription factor 4 (Sox4),..."
Claim 1 recites the broad limitation 'increasing the biological activity,..., of genes of..."
The specification recites: "The reprogramming, in one embodiment, entails activation (or increasing the biological activity) of one or more transcription factors in a non-RGC neural cell" (originally-filed specification, pg. 14, para. [0045]); and "Methods of increasing the biological activity of a gene are known in the art. Increased biological activity can be increased expression of the protein or increased function of the protein, or both (spec., pg. 19, para. [0052]).
It is noted that increasing the expression or function of the protein not only includes using recombinant DNA techniques to construct expression vectors carrying the genes cited in the claim and transfecting amacrine cells therewith. In addition, a gene's function may be increased by its interaction with some protein or factor that binds to its promoter region to upregulate/up-express it. A protein's function may be increased by interacting or binding with a specific protein that results in its upregulation/up-expression. These indirect activities may be carried out by genes or proteins not cited in the instantly-claimed subject matter.
Therefore, for the purpose of examination, prior art which shows any method by which the expression (and, therefore, production) of the instantly-claimed genes is increased will be considered to be applicable prior art.
Claim Rejections - 35 U.S.C. § 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 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 of this title, 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.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. §102(b)(2)(C) for any potential 35 U.S.C. §102(a)(2) prior art against the later invention.
Claims 1, 7 and 9-12 are rejected under 35 U.S.C. §103 as being unpatentable over Stankowska et al. (Invest. Ophthalmol. Vis. Sci. 2015, 56: 893-907) in view of Xiang et al. (Pub. No. CN110302398A, Pub. Date: 2019-10-08; see NPL as English machine translation (EngMT) for page/para. numbers), and Chen et al. (Aging Cell, 2015, 14: 635-643).
Regarding claim 1, pertaining to a method for preparing a cell responsive to visual signals, comprising increasing the biological activity, in the cell, of the gene POU class 4 homeobox 2 (Brn3B), and regarding claim 7, pertaining to a method for improving the function of a retinal ganglion cell (RGC), comprising increasing the biological activity, in the RGC, of the gene Brn3B, Stankowska et al. shows the neuroprotective effects of transcription factor Brn3b in an ocular hypertension fat model of glaucoma (pg. 893, Title). Primary RGCs (retinal ganglion cells) were obtained from postnatal day 5 rat pup eyes and used to test the ability of AAV to transduce the RGCs. RGCs were transduced with either with rAAVCMV-GFP (control vector) or rAAV-CMV-Brn3b (encoding transcription factor Brn3b) viral constructs. rAAV-CMV-Brn3b virus was found to be capable of overexpressing the Brn3b protein in RGCs, as seen by increased immunostaining for Brn3b (pg. 898, column 1, para. 1 [i.e., increasing biological activity in a cell or RGC]).
Glaucoma is an optic neuropathy commonly associated with elevated intraocular pressure (IOP), leading to optic nerve head (ONH) cupping, axon loss, and apoptosis of retinal ganglion cells (RGCs), which could ultimately result in blindness (pg. 893, Abstract, Purpose).
Adeno-associated virus-mediated expression of the Brn3b protein in IOP-elevated rat eyes promoted an upregulation of growth associated protein-43 (GAP-43), actin binding LIM protein (abLIM) and acetylated a-tubulin (ac-Tuba) both posterior to the ONH and in RGCs. The RGC survival as well as axon integrity score were significantly improved in IOP-elevated rAAV-hsyn-Brn3b–injected rats (pg. 893, Abstract, Results). That is, data demonstrate that AAV-derived Brn3b overexpression in IOP-elevated rat eyes is able to reverse the damage to the optic nerve and restore transport along the axons into the myelinated region of the optic nerve (pg. 904, column 2, last para. thru pg. 905, column 1, lines 1-2 [improving the function of a cell or a(n) RGC]).
Further regarding claim 7, pertaining to the RGC is a damaged or normal retinal ganglion cell (RGC),
Stankowska et al. shows that primary RGCs (retinal ganglion cells) were obtained from postnatal day 5 rat pup eyes and used to test the ability of AAV to transduce the RGCs (pg. 898, column 1, para. 1). The described study shows the use of an IOP-elevated rat model of optic nerve damage to assess the ability of adeno-associated virus serotype 2 (AAV-2) overexpressing transcription factor Brn3b to promote neuroprotection of RGCs and maintenance of axonal integrity (pg. 893, column 2, lines 11-16). Data demonstrate that AAV-derived Brn3b overexpression in IOP-elevated rat eyes is able to reverse the damage to the optic nerve and restore transport along the axons into the myelinated region of the optic nerve (pg. 904, column 2, last para. thru pg. 905, column 1, lines 1-2).
Stankowska et al. does not show: 1) an amacrine cell [Claim 1]; 2) the amacrine cell is a Lgr5+ amacrine cell [Claim 1]; and 3) increasing the biological activity of SRY-box transcription factor 4 (Sox4) [Claims 1 and 7].
Xiang et al. provides information that would have motivated one of ordinary skill in the art to have increased the biological activity of an amacrine cell, in addition to that of a retinal ganglion cell, as shown by Stankowska et al.
Xiang et al. shows a composition containing Atoh7 and/or Pou4f. The composition contains a virus carrier for several transcription factors, including Atoh7+Pou4f2 and Pou4f2 alone (pg. 2, para. 1 [nexus to Stankowska et al.- recombinant virus carrying Brn3B] [Pou4f2 = POU class 4 homeobox 2 = Brn3B]). The transcription factor(s) is/are overexpressed in the Muller cells of a human or animal retina, thus directionally differentiating the cells into retinal ganglion cells (RGCs) (pg. 2, para. 1 [nexus to Stankowska et al.- increasing the biological activity of Brn3B in RGCs]). The RGCs regenerated through the composition can be migrated to a ganglion cell layer and integrated to a local neutral network, have the normal RGC form and function, and are connected to different brain areas. The RGCs express various specific markers of normal ganglion cells and have activity such as electrophysiology similar to normal RGCs in vivo. The composition can make the RGCs in vivo be regenerated and can be applied to the aspects such as cell replacement therapy of neurologic diseases such as glaucoma (pg. 2, para. 1 [nexus to Stankowska et al.- Brn3B overexpression improves the function of RGCs in rat glaucoma animal model]).
Regarding claim 1, Xiang et al. teaches that the mature retina is composed of 7 major types of cells, including ganglion cells, horizontal cells, amacrine cells, bipolar cells, Mueller cells, cone cells, and rod cells. All of these cells are obtained by proliferation and differentiation of a small population of precursor cells (pg. 9, last para. thru pg. 10 lines 1-2). Muller cells proliferated by methods shown in the described prior art can develop into amacrine cells (pg. 8, para. 3).
Xiang et al. shows that after infecting Muller cells with a virus carrying Atoh7 and/or Pou4f2, these genes are specifically expressed in Muller cells, and Muller cells are differentiated into RGCs (pg. 22, last para.).
Regarding claims 1 and 7, pertaining to Sox4, Xiang et al. teaches that during retinal development, the development of RGC is regulated by a series of transcription factors such as Atoh7 (Math5), Six6, Brn3a/b, Ebf, and Sox4/11 (pg. 5, para. 1 [nexus to Stankowska et al.- Brn3b gene expression]). The SoxC family is a small protein of high mobility group (HMG), in which Sox4 and Sox11 play an indispensable role in retinal development. Sox4 and Sox11 overlap in expression and function and they are highly expressed in RGC. It was found that Sox4, Sox11, and Sox12 primarily control the development of RGC (pg. 12, para. 1).
Chen et al. would have motivated one of ordinary skill in the art of producing amacrine cells responsive to visual signals, as shown by Stankowska et al. in view of Xiang et al., to have incorporated Brn3B into an Lgr5+ amacrine cell specifically.
Regarding claim 1, Chen et al. shows that the adult stem cell marker, leucine-rich repeat-containing G-protein-coupled receptor 5 (Lgr5), is expressed in the retina of adult mice. Lgr5+ cells are generated at late stages of retinal development and exhibit properties of differentiated amacrine interneurons (amacrine cells). Nevertheless, Lgr5+ amacrine cells contribute to regeneration of new retinal cells in the adult stage. The generation of new retinal cells, including retinal neurons and Muller glia from Lgr5+ amacrine cells, begins in early adulthood and continues as the animal ages. Lgr5+ amacrine cells function as an endogenous regenerative source. The identification of such cells in the mammalian retina may provide new insights into neuronal regeneration and point to therapeutic opportunities for age-related retinal degenerative diseases (pg. 635, column 1, Summary).
Absence of (retinal neuron) regeneration is thought to contribute to a host of retinal degenerative diseases, including age-related macular degeneration, glaucoma and retinitis pigmentosa, which have been viewed as consequences of the irreversible loss of retinal neurons (pg. 635, column 2, lines 14-20).
Accordingly, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention, to have modified the method of preparing a retinal ganglion cell (RGC) responsive to visual signals, as shown by Stankowska et al., by also preparing an amacrine cell responsive to visual signals [Claim 1], with a reasonable expectation of success.
Xiang et al. shows that Muller cells can be propagated in such a way so as to become amacrine cells, and can also become RGCs by the overexpression of Brn3B/Pou4f2 (MPEP 2143 (I)(G)). Therefore, it would have been obvious to one of ordinary skill in the art to have overexpressed Brn3B in amacrine cells directly (e.g., rather than in Muller cells, as shown by Xiang et al., or RGCs, as shown by Stankowska et al.), with the reasonably predictable expectation that Brn3B would have been overexpressed in the amacrine cells, because Xiang et al. and Stankowska et al. show that Brn3B can be transfected into (and successfully expressed in) these different types of retinal cells (MPEP 2143 (I)(G)).
It would have been further obvious to have incorporated the POU class 4 homeobox 2/Brn3B/Pou4f2 gene, into an Lgr5+ amacrine cell specifically [Claim 1], with a reasonable expectation of success, because Chen et al. shows that Lgr5+ amacrine cells have the ability to regenerate (lost or damaged) retinal neurons (MPEP 2143 (I)(G)).
Therefore, it would have been obvious and one of ordinary skill in the art of using amacrine cells as a therapeutic, would have been motivated to have increased the biological activity of Brn3B in an Lgr5+ amacrine cell, because Chen et al. teaches that the Lgr5+ amacrine cell already has some endogenous neural regeneration capacity. Because Brn3B, when introduced into a retinal cell, also has the ability to restore retinal ganglion morphology and function, the therapeutic cells would become optimized or improved by the overexpression Brn3B in an Lgr5+ amacrine cell via the increase in the cells' ability to produce retinal ganglion cells (MPEP 2143 (I)(F,G)).
It would have been further obvious to have incorporated the SRY-box transcription factor 4 (Sox4) gene, into an amacrine cell or a(n) RGC [Claims 1 and 7], with a reasonable expectation of success, because Xiang et al. teaches that Sox4 is highly expressed in RGC, and primarily controls the development of RGC (MPEP 2143 (I)(G)). That is, Xiang et al. teaches that the biological activity of both Brn3b and Sox4 is increased in RGCs and, therefore, amacrine cells (pg. 5, para. 1) (MPEP 2143 (I)(G)).
One of ordinary skill in the art would have been motivated to have made those modifications, because Stankowska et al. teaches that Brn3b has been shown to be a key regulator of axon outgrowth and pathfinding in RGCs and contributes to their proper polarization. The predominant phenotype in Brn3b-deficient mice was loss of most ganglion cells, with approximately 70% of RGCs undergoing apoptosis. Lack of Brn3b expression also caused a decline in the number of optic nerve fibers and thinning of the mouse optic nerve. A lack of Brn3b resulted in a developmental loss of RGCs due to the inability to develop axons (Stankowska et al., pg. 893, column 1, para. 2 thru column 2, lines 1-10).
Therefore, it would have been obvious, and one of ordinary skill in the art of using amacrine cells or RGCs as a therapeutic would have been motivated, to have increased the biological activity of Brn3B or Sox4 in an Lgr5+ amacrine cell, because Chen et al. teaches that the Lgr5+ amacrine cell already has some endogenous neural regeneration capacity. Because Brn3B, when introduced into a retinal cell, also has the ability to restore retinal ganglion morphology and function, the therapeutic cells would become optimized or improved by the overexpression Brn3B in an Lgr5+ amacrine cell via the increase in the cells' ability to produce retinal ganglion cells (MPEP 2143 (I)(F,G)). In addition, Sox4 also controls the development of RGCs.
Therefore, the invention as a whole would have been prima facie obvious to a person of ordinary skill before the effective filing date of the claimed invention.
Regarding claims 9, 10 and 11, Stankowska et al. shows that recombinant AAV vectors were prepared using plasmids. pAAV-Brn3b vector encoding transcription factor Brn3b was constructed by insertion of a mouse Brn3b cDNA clone. After DNA sequence validation, the pAAV-Brn3b plasmid was used for AAV-2 virus production (pg. 894, column 1, para. 1). Primary RGCs (retinal ganglion cells) were obtained from postnatal day 5 rat pup eyes and used to test the ability of AAV to transduce the RGCs. RGCs were transduced with either rAAVCMV-GFP (control vector) or rAAV-CMV-Brn3b (encoding transcription factor Brn3b) viral constructs (pg. 898, column 1, para. 1).
Regarding claim 12, glaucoma is an optic neuropathy commonly associated with elevated intraocular pressure (IOP), leading to optic nerve head (ONH) cupping, axon loss, and apoptosis of retinal ganglion cells (RGCs), which could ultimately result in blindness (pg. 893, Abstract, Purpose). Intravitreal injections were carried out using an ultrafine 30.5-G disposable needle connected to a 50-lL Hamilton syringe in anesthetized rats (pg. 894, column 2, para. 3). Brn3b overexpression using the rAAV-hsyn-Brn3b vector was efficacious since it was able to significantly restore the visual acuity that was compromised in IOP-elevated rat eyes (pg. 905, column 1, para. 3).
Response to Arguments
Applicant’s arguments, pp. 5-6, filed on 01 December 2025, with respect to the prior art references cited in the 35 U.S.C. §103 rejections, and the 35 U.S.C. §102(a)(1) rejection, have been fully considered, and they persuasive, in part. On the other hand, some of the arguments are either not persuasive or are moot because the arguments do not apply to the references as they are applied in the context of the current rejection, or as new grounds necessitated by Applicant’s amendment, in which claims 1 and 7 were amended.
1. Applicant remarks (pg. 5, para. 9), with regard to the 102 rejection, that Stankowska et al. did not mention simultaneously increasing the expression of both Brn3B and Sox4 in RGCs.
In response to Applicant, the rejection of claims 7 and 8 as being anticipated by Stankowska et al. under 35 USC §102(a)(1) is withdrawn in view of Applicant's amendment.
2. Applicant remarks (pg. 5, para. 10 thru pg.6), with regard to the 103 rejection, that claim 1 is amended to include limitations of "increasing the biological activity, in the amacrine cell, of genes of POU class 4 homeobox 2 (Brn3B) and SRY-box transcription factor 4 (Sox4)" and "the amacrine cell is a Lgr5+ amacrine cell or a Prokr2+ displaced amacrine cell". Neither Stankowska et al. nor Xiang et al. mentioned simultaneously increasing the biological activity of both Brn3B and Sox4 in amacrine cells. The present invention has demonstrated that the combination of Brn3B and Sox4 can significantly synergistically enhance reprogramming activity, thereby increasing the regeneration of retinal ganglion cells. As shown in Figure 2c of the drawings as filed in the present application, while Brn3B and Sox4 alone can reprogram retinal neurons into retinal ganglion cells, their efficiency is significantly low, while the combination of Brn3B and Sox4 greatly improves the reprogramming efficiency of retinal neurons.
However, in response to Applicant, the combination of Stankowska et al. and Xiang et al. shows that the expression of transcription factors Brn3b and Sox4 during RGC development drives said RGC development. In addition, it is not clear that the synergism between Sox4 and Brn3B with regard to the regeneration of RGCs would have been unexpected or non-obvious. For example, Jiang et al (cited on the IDS submitted on 13 July 2022 and on the record) teaches that the formation of RGCs is a stepwise process involving extensive and precise molecular factors. MATH5 (ATOH7-Mouse Genome Informatics) and BRN3B (POU4F2-Mouse Genome Informatics) are two of the most important transcription factors (TFs) involved in regulatory pathway of RGCs. Brn3b functions in terminal differentiation and survival of RGCs by regulating axon outgrowth and apoptosis (pg. 18429, column 2, lines 10-15). The Sry-related high mobility group (HMG) box (SOX) family of transcription factors have been reported as critical regulators to control cell fate and differentiation in multiple processes during development (pg. 18429, column 2, para. 1). The expression of Sox4 and Sox11 was highly overlapping in the developing retina during embryonic stages, as demonstrated in the described study (pg. 18430, column 1, lines 10-12). Overexpression of Sox4 or Sox11 stimulated BRN3B expression in vitro (pg. 18430, column 1, lines 21-24).
That is, it appears as though the Brn3b and Sox4 genes participate in the development of RGCs in a non-overlapping manner (i.e., Brn3b functions in terminal differentiation and axon outgrowth, whereas Sox4 expression is notable during the embryonic stage of RGC development). In addition, Sox4 overexpression stimulated Brn3b expression. Therefore, one of ordinary skill in the art of gene expression and RGC development would have understood from the information shown by Jiang et al. that either gene alone would show little, if any, RGC regeneration, whereas the combination of Brn3b and Sox4 would show, minimally, an additive, if not most certainly a synergistic effect with regard to RGC regeneration, given their complementary roles and the interdependence of their gene expressions.
3. Applicant remarks (pg. 6, para. 11) that there is no teaching, suggestion or motivation in Stankowska to directly transfect amacrine cells with Brn3B; Stankowska is concerned with the effects of Brn3B on RBC differentiation into multiple cell types. The Examiner proposes that an artisan would want to directly transfect amacrine cells with Brn3B (instead of RBCs) because amacrine cells have the ability to 'regenerate retinal neurons'. This is inconsistent with the fundamental precepts of developmental biology. There is no plausible scenario where an artisan of ordinary skill would expect to obtain the seven different differentiated cell types of RBCs taught by Stankowska and Xiang by transfecting one of the differentiated cell types instead of the progenitor cell itself.
However, in response to Applicant, the argument of Applicant appears to be 'opinion evidence'. It is well known that to be of probative value, any objective evidence should be supported by actual proof. The arguments of counsel cannot take the place of evidence in the record. In re Schulze, 346 F.2d 600, 602, 145 USPQ 716, 718 (CCPA 1965) (MPEP 716.01 (c)(I)(II)). In addition, the Examiner is not suggesting that seven different differentiated cell types of RBCs would result from transfecting the progenitor cell itself. Stankowska et al. shows that RGCs can be transfected with Brn3b (via an adenovirus vehicle), Xiang et al. teaches that transfected Muller cells can develop into amacrine cells, and Chen et al. teaches that Lgr5+ cells are generated at late stages of retinal development and exhibit properties of differentiated amacrine interneurons (amacrine cells). Therefore, it would have been obvious to have transfected any type of cell associated with retinal ganglion cell development (e.g., Muller cells or amacrine cells) with the transcription factors Brn3b or Sox4. Mammalian cell transfection is a well- known, well-established laboratory protocol.
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 extension fee 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 date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to SHARON M PAPCIAK whose telephone number is (571)272-6235. The examiner can normally be reached M-F 8:30am-5:00pm.
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/LOUISE W HUMPHREY/Supervisory Patent Examiner, Art Unit 1657
/SMP/Examiner, Art Unit 1657