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 .
Status of Claims
Applicant' s amendment filed 11/10/2025 is acknowledged. Claims 1-2, 5-9, and 15-16 have been amended. Claims 3-4 have been cancelled. Claims 1-2 and 5-16 are pending in the instant application and the subject of this final office action.
All of the amendments and arguments have been reviewed and considered. Any rejections or objections not reiterated herein have been withdrawn in light of amendments to the claims or as discussed in this office action.
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Previous Rejection
Status of Prior Rejections/Objections:
Color drawings were identified in the file, and Applicant was asked to provide a statement that there was no intention to file color drawings or submit a petition for color drawings in the previous action. No statement or petition was identified. Therefore, the drawings have not been accepted. See the Drawings section for further information.
The objection to the specification regarding trademarks is withdrawn.
The claim objection to claim 2 and claim duplicate advisory for claims 3 and 4 are withdrawn in view of the amendment or cancellation, respectively.
The 112(b) rejections to claim(s) 15-16 are withdrawn in view of the amendments to the claims.
The 112(b) rejection of claim 2, now of amended claim 1, and claims 5 and 6 are maintained and clarified in view of the amendment. The 112(b) rejections of claims 8-9 are maintained and clarified. The 112(b) rejections of claim 7 is in part withdrawn in view of amendments and in part maintained and clarified. See also Specification objection and Response.
The prior art rejection(s) under 35 USC 103 directed to the following are maintained and modified/clarified as necessitated by the amendments:
Claims 1-2 and 5-6 over Dobi in view of Ebner
Claims 7-9 over Dobi in view of Ebner and UCSC
Claim 10 over Dobi in view of Ebner and of Shenoy
Claims 11-13 over Shenoy and Slade
Claim 14 over Shenoy in view of Slade and further in view of Dobi and Ebner
New Ground(s) of Rejections
The new ground(s) of rejections were necessitated by applicant’s amendment of the claims.
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Drawings
Color photographs and color drawings are not accepted in utility applications unless a petition filed under 37 CFR 1.84(a)(2) is granted. Any such petition must be accompanied by:
I. The appropriate fee set forth in 37 CFR 1.17(h);
II. One set of color drawings or color photographs, as appropriate, if submitted via EFS-Web or three sets of color drawings or color photographs, as appropriate, if not submitted via EFS-Web; and, unless already present,
III. An amendment to include the following language as the first paragraph of the brief description of the drawings section of the specification:
The patent or application file contains at least one drawing executed in color. Copies of this patent or patent application publication with color drawing(s) will be provided by the Office upon request and payment of the necessary fee.
Color photographs will be accepted if the conditions for accepting color drawings and black and white photographs have been satisfied. See 37 CFR 1.84(b)(2).
A statement from Applicant that there is no intention to have color drawings will result in acceptance of the drawings; otherwise, the conditions set forth above must be met in order for the color drawings to be accepted.
Please respond with either a statement regarding the color drawings or filing the necessary petition for color drawings.
Claim Interpretation
In evaluating the patentability of the claims presented in this application, claim terms have been given their broadest reasonable interpretation (BRI) consistent with the specification, as understood by one of ordinary skill in the art, as outlined in MPEP 2111.
Regarding claim 1, the claim recites “nucleic acid molecules the same chromosomal region of CHD1”. The specification states that the chromosomal band 5q15-q21 comprises the CHD1 gene (pg. 5, para 7). Said nucleic acid molecules were interpreted to encompass those that comprise sequence from this range of chromosomal bands.
Further, the term “from” was interpreted broadly to include those molecules derived directly from chromosomal DNA (e.g., unamplified digested gDNA) and those that comprise sequence from said region (e.g., cloned sequences, transcribed RNAs, and synthesized oligos).
The term “a nucleic acid probe” lacks a limiting definition in the specification regarding the structure. Thus, it was interpreted broadly to encompass a composition of multiple separate nucleic acid molecules, joined nucleic acid molecules, and combinations thereof.
The term “different proportions from each other” is interpreted to mean any discernable difference of proportion, e.g., 1X and 4X or 1X and 1.0001X, that can be determined by means known in the art.
Specification
The disclosure is objected to because it contains an embedded hyperlink and/or other form of browser-executable code. Applicant is required to delete the embedded hyperlink and/or other form of browser-executable code; references to websites should be limited to the top-level domain name without any prefix such as http:// or other browser-executable code. See MPEP § 608.01.
The incorporation of essential material in the specification by reference to an unpublished U.S. application, foreign application or patent, or to a publication is improper. Applicant is required to amend the disclosure to include the material incorporated by reference, if the material is relied upon to overcome any objection, rejection, or other requirement imposed by the Office. The amendment must be accompanied by a statement executed by the applicant, or a practitioner representing the applicant, stating that the material being inserted is the material previously incorporated by reference and that the amendment contains no new matter. 37 CFR 1.57(g).
Where Applicant incorporates sequences, they will need to comply with 37 CFR 1.821(a)(1).
Claim Rejections - 35 USC § 112(b)
Claim 1-2 and 5-10 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.
Regarding claims 1, 5, and 6, the claims recite “different proportions than they occur in nature in non-cancerous cells” (claim 1) or “than they occur in nature” (claims 5 and 6). The specification fails to provide a limiting definition for this phrase and the metes and bounds are not obvious to one of ordinary skill in the art.
First, the claim relies on a comparison to values that occur “in nature” but such values are not fixed and vary based on the context. In the absence of a defined reference condition or standard, the claim does not provide a consistent basis for determining whether the limitation is met, rendering the scope unclear.
For example, is also noted that pre-implantation embryos have a similarly notable level of chromosomal abnormality to cancerous cells. It is further noted that a lack of fetuses making it to term with structural variation in this region does not preclude such duplications/deletions that would result in 1X, 2X, 4X, etc. from existing “in nature” in these regions. It is also noted that while the amended claim 1 restricts the molecules relative to proportions other than those in which they occur in non-cancerous cells, the molecules having sequences of LSAMP or PTEN remain unrestricted in claims 5 and 6, respectively.
Likewise, the claims are not limited genomic DNA molecules or sequences/fragments thereof. RNAs transcribed in the region are nucleic acid molecules “from” the same chromosomal region of CHD1 and exist in different proportions to each other. As the proportions of RNA expression are known to vary based on context, as the claims lack sufficient basis for the artisan to determine whether the limitation is met, the claim is unclear.
Second, the claim recites “portion different than … in non-cancerous cells”. It is not clear whether the claim intends the proportion to be met in any grouping of non-cancerous cells, all single cells that are non-cancerous, or some combination thereof. For example, a decaying body (i.e., a collection of non-cancerous cells) may have a 1:1 staring ratio of two regions in each individual cell but due to different chromatin wrapping that differentially protects the regions, may have different rates of degradation of the regions as one stays relatively stable and other degrades at, say, 10X faster. All points in the decay could be considered “natural” proportions in such non-cancerous cells. Thus, it is unclear based on the scope of “in … cells” being considered.
Claims 2 and 5-10 are indefinite for depending on claim 1 and not rectifying the deficiency.
Regarding claims 8-9, claims 8 and 9 are indefinite of the recitation of Table 1. As stated in MPEP 2173.05(s), claims should be complete to themselves and the reference to figures or tables renders the claims incomplete. Claims that recite tables are only permitted in exceptional circumstances where there is no practical way to define the invention in words and where it is more concise to incorporate by reference than duplicating a drawing or table into a claim.
It is noted that Table 1 encompasses many overlapping sets and thus could be represented in a similar manner to the amendment of claim 7, or more preferably, by SEQ ID NO once the sequence are properly incorporated by reference. See below.
Regarding claims 7-9, the claims require “molecules having sequences” (claim 7) or “molecules selected from the clone sets” (claims 8 or 9) from artificial chromosome IDs. As the IDs require an externally hosted database to understand the content of (e.g., ftp.ncbi.nih.gov/repository/clone/reports or the UCSC Genome Browser) and such databases are not a part of the filing and further may not be maintained through the life of any patent granted. Therefore, as the claims and application are not complete in and of themselves with regard to these BAC IDs, the metes and bounds cannot be determined by one of ordinary skill in the art.
Claim Rejections - 35 USC § 101
Claims 1-2 and 5-7 are rejected under 35 U.S.C. 101 because the claimed invention is directed to judicial exceptions without significantly more. The claim(s) recite(s) products of nature and/or abstract ideas. This judicial exception is not integrated into a practical application. The claim(s) does/do not include additional elements that are sufficient to amount to significantly more than the judicial exception
The following three inquiries are used to determine whether a claim is drawn to patent-eligible subject matter:
Step 1. Is the claim to a process, machine, manufacture, or composition of matter?
Yes, the claims 1-2 and 5-7 are directed to a composition.
Step 2A, prong 1. Does the claim recite a law of nature, a natural phenomenon, or an abstract idea (recognized judicial exceptions)?
Regarding claim 1, the claim recites “a nucleic acid probe for hybridization to chromosomal DNA, comprising at least two different nucleic acid molecules from the same chromosomal region of CHD1, where said nucleic acid molecules are present in different proportions from each other and in proportions different than those in which they occur in nature”. Therefore, the structures required are two nucleic acid sequences each comprising a sequence complementary to at least a portion of the chromosomal CHD1 gene region and further comprising some difference between the two. The claim further recites that the two molecules are in different proportions to each other.
Because this is a nature-based product, it is necessary to evaluate this product on markedly different characteristics. The claims encompass probes solely consisting of chromosomal DNA in the CHD1 region. MPEP 2106.04(c)(II)(A) instructs that:
Although the selected counterpart should be in its natural state, examiners should take care not to confuse the counterpart with other material that may occur naturally with, or adjacent to, the counterpart. For example, assume that applicant claims a nucleic acid having a nucleotide sequence derived from naturally occurring gene B. Although gene B occurs in nature as part of a chromosome, the closest natural counterpart for the claimed nucleic acid is gene B, and not the whole chromosome. See, e.g., Ass’n for Molecular Pathology v. Myriad Genetics, Inc., 569 U.S. 576, 591-94, 106 USPQ2d 1972, 1979-81 (2013) (comparing isolated BRCA1 genes and BRCA1 cDNA molecules to naturally occurring BRCA1 gene); Roche Molecular System, Inc. v. CEPHEID, 905 F.3d 1363, 1371, 128 USPQ2d 1221, 1227 (Fed. Cir. 2018) (comparing claimed primers to "their corresponding nucleotide sequences on the naturally occurring DNA"). Similarly, assume that applicant claims a single-stranded piece of DNA (a primer) having a nucleotide sequence derived from the sense strand of naturally occurring nucleic acid C. Although nucleic acid C occurs in nature as a double-stranded molecule having a sense and an antisense strand, the closest natural counterpart for the claimed nucleic acid is the sense strand of C only. See, e.g., University of Utah Research Foundation v. Ambry Genetics, 774 F.3d 755, 760, 113 USPQ2d 1241, 1241 (Fed. Cir. 2014) (comparing single-stranded nucleic acid to the same strand found in nature, even though "single-stranded DNA cannot be found in the human body").
Therefore, one or more fragments or region of CHD1 wherein the sequences are identical to natural products are not markedly different, following the logic of the findings of Myriad.
Next, it is considered, whether molecules being present in different proportions to one another is a “marked” difference. Following the logic of the finding in Ambry, wherein the proportion strands of the product considered is different than that found in the human body, this too is not found to be a markedly different characteristic. The structure of the sequences remains the same and no evidence has been presented that behavior is markedly different than the sequences of the genome regions or processed RNA from the region by the combination in different proportions.
Example 10 of the USPTO guidance on subject matter eligibility (https://www.uspto.gov/sites/default/files/documents/101_examples_1to36.pdf) provides guidance regarding claims of a combination of natural elements that further illustrates the markedly different characteristics analysis of MPEP 2106.04(c)(I). Claim 2 of Example 10 is eligible because the bacterial species, when combined, have different characteristics from either species on its own such that the combination with the milk has markedly different characteristics than any component individually or either bacteria with the milk. These differences rise to the level of a “marked difference”.
This contrasts with the instant claims where the claims require only sequences from the chromosomal region(s). There is no evidence to suggest that the combination in the composition results in a material transformation of the claimed molecules beyond what exists naturally to give the molecules different characteristics.
For argument, even should the proportion introduce some novel behavior, the amended claim now encompass the proportions that occur for cancerous cells, which encompass part of nature. Accordingly, such as probe composition is found to be a natural product.
Regarding claim 2, the claim further recites that the nucleic acid probe “comprises at least 10 molecules”. The nucleic acid molecules are not further structurally defined and thus also encompass natural products.
Regarding claims 5 and 6, the claims recite “further comprising additional molecules having sequences from the LSAMP gene deleted in patients with prostate cancer” (claim 5) or “further comprising additional molecules having sequences from the PTEN gene deleted in patients with prostate cancer” (claim 6).
As with claims 1 and 2, sequence directed to these genes in differing proportions to the genome and to each other is not held to be a markedly different characteristic from the chromosomal/RNA sequence and thus these are also held to be natural products natural products.
Regarding claims 7, this claim recites molecules having sequences from BACs. As the claim requires only “molecules having sequences from” the clones, it is held the entire BAC is not required. Therefore, the claim encompasses chromosomal sequence comprised within the BACs and thus encompasses natural products.
Step 2A, prong 2. Are the judicial are integrated into a practical application?
Regarding claims 1-2 and 5-7, no other transformative matter is recited to integrate the natural products into a practical application, as previously discussed.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
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 1-6 are rejected under 35 U.S.C. 103 as being unpatentable over Dobi (WO 2020/123880 A2; effectively filed 12/12/2019) and Ebner (WO 2017/007739 A2; published 01/12/2017).
It is noted that the courts have held that when a claim recites using an old composition or structure and the “use” is directed to a result or property of that composition or structure, then the claim is anticipated In re May, 574 F.2d 1082, 1090, 197 USPQ 601, 607 (CCPA 1978)). The phrase “for hybridization” clearly defines a use of the composition, and thus does not further distinguish the composition over the prior art. See MPEP 2112.02.
Regarding claims 1-6, Dobi teaches a kit for use in diagnosing or prognosing prostate cancer comprising at least two oligonucleotide probes, wherein in the probes comprise a first oligonucleotide probe for detecting a first genomic rearrangement that results in deletion of a human LSAMP gene (instant claim 5) and a second oligonucleotide probe for detecting a second genomic rearrangement that results in a deletion of a human CHD1 gene (claim 17; instant claims 1). Dobi further teaches that the kit further comprises an oligonucleotide for detecting a human gene selected from PTEN (claim 18; instant claim 6).
Dobi teaches identifying or characterizing prostate cancer comprising detecting in a biological sample the presence or absence of a genomic rearrangement that results in a deletion a genomic rearrangement that results in a deletion of a CHD1 gene, wherein CHD1 genomic rearrangements serve as a biomarker for prostate cancer and can be used to stratify prostate cancer based the severity or aggressiveness of prostate cancer (Abstract).
While Dobi teaches an oligonucleotide, i.e., nucleic acid probe, for detecting a region of CHD1, Dobi fails to explicitly teach how many molecules are present and the proportions in which they are present.
Ebner teaches probes that may be useful for detecting deletions in the PTEN and LSAMP genes as diagnostic for prostate cancer (para [0009]). Ebner teaches that the nucleic acid probe for detecting a deletion in the LSAMP gene by in situ hybridization to chromosomal DNA, comprising at least two different nucleic acid molecules comprising DNA from the LSAMP gene, where the amounts of each nucleic acid molecule present in the probe are in different proportions from each other and in different proportions in which they are present in the gene as it occurs in nature (claim 1; instant claims 1 and 5-6). Ebner further teaches a probe comprising at least two different nucleic acid molecules comprising DNA from the PTEN gene for use in detecting prostate cancer, where the amounts of each nucleic acid molecule present in the probe are in different proportions from each other and in different proportions in which they are present in the gene as it occurs in nature (claim 18; instant claim 6).
Ebner further teaches that in addition to not being a continuous region, the probe preferably does not contain equal representations or proportions of each sub-region within the target region; for example, the probe will contain fragments of [a gene] in unequal quantities, i.e., if the region has ten different fragments [i.e., 10 molecules] within it, fragment 1 may be present in 1x quantity, fragment 2 in 2x quantity, fragment 3 in 3x quantity, fragment 4 in 4x quantity, and so on, (instant claim 1) wherein such unequal representations from the molecules as they occur in nature [i.e., proportions different than “natural non-cancerous” cells] result from the selection of non-overlapping molecules from which to prepare the probe, and subsequent amplification reactions which unequally amplify parts of the target nucleic acid (para [0022]).
Ebner teaches using sets of tiled candidate nucleic acids in desired chromosomal regions in greater quantity than other regions and in higher amounts than in the native chromosome (para [0037]). Ebner teaches its probes for characterizing prostate cancer as being aggressive (para [0052]). Ebner teaches that determination of specific probes is routine within the art and may be selected [i.e., optimized[ based on numerous properties (para [0036]; see also para [0037-0042]).
Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to utilize the single probes targets, i.e., each of the genes CHD1, LSAMP, and PTEN, of Dobi with the multiple fragment [molecule] probes in differing “non-natural” concentrations in the same region of said targets of Ebner. The artisan would have been motivated to do so because additional probe molecules allow for redundancy/tiling, as taught by Ebner, which is advantageous in the case of detecting deletions in a region and that is a stated goal of Dobi, and particularly for the stratifying prostate cancer based on the aggressiveness of said cancer as taught by Dobi and Ebner. The results of the combination would have been predictable as both Ebner and Dobi teach the probes for the same purpose, Ebner teaches means for selecting such probes for various targets and that they’re routine.
Further, the courts have found that it is prima facie obvious to combine two compositions each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose... (In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980)). See MPEP 2144.06. It is therefore obvious to provide a mixture of two probes’ molecules because both are known to be useful for detection of prostate cancer. That is to say, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to provide combined compositions a molecule targeting CHD1 and LSAMP and/or CHD1 and PTEN because both were taught to be useful for detecting prostate cancer and/or stratifying aggressiveness.
It is also noted that the proportions compared to non-cancerous cells would also be a matter of routine optimization based on the tiling selections and amplification reaction efficiencies, as taught by Ebner. As discussed in MPEP 2144 rebutting routine optimization requires a teaching away and/or a showing that the amount is critical; in the instant case, no data was identified in the specification regarding that the particular amount recited within the claims is critical because no data was identified that compares sets of probes based on proportions.
Claims 7-9 are rejected under 35 U.S.C. 103 as being unpatentable over Dobi (WO 2020/123880 A2; effectively filed 12/12/2019) and Ebner (WO 2017/007739 A2; published 01/12/2017), as applied to claim 1 above and further in view of UCSC (Mapping of clone libraries end placements [Internet]. UCSC; 2015 [retrieved 2025 May 2]. Available from: https://genome.ucsc.edu/cgi-bin/hgTrackUi?g=cloneEndSuper).
Regarding claims 7-9, in the nucleic acid probe of Dobi in view of Ebner, Dobi teaches obtaining commercially available probes including BAC clones and utilizing them in a FISH experiment (para [00110]).
Ebner also teaches publicly available BAC clones that include sequences from LSAMP or directly adjacent to it, and that two or more clones and be selected to make a probe, e.g., where the clones are amplified separately or in combination by nick-translation, random primer, etc. (para [0059]). As cited above, Ebner teaches 4 fragments “and so on” of differing proportions. Ebner teaches BAC clones from the RP11 BAC library (Fig. 3 and Fig. 4).
Ebner further teaches that when a certain chromosomal region is targeted, a set of tiled or overlapping candidate nucleic acids may be selected, such as tiled BAC clones to unique sequences in the desired chromosomal regions (para [0037]).
Ebner additionally teaches that a useful probe can be made by selecting DNA, such as from a BAC clone, where two or more of the DNAs overlap with each other in such a way that the completed probe contains a higher representation of the overlapped region than regions which show no overlap, wherein such a probe can be designed utilizing overlapping middle regions of the gene and non-overlapping 3' and 5' regions (para [0058]).
Dobi in view of Ebner fail to teach the specific probes of the list of instant claim 7 and Table 1.
UCSC teaches BACs comprising RP11-416O8, RP11-90M19, RP11-384D8, RP11-98E9, RP11-644F13, RP11-533M23, RP11-813D1, RP11-1093B19, RP11-430B3, RP11-719G24, and RP11-720G19 in the region of CHD1 (see attachment of the action dated 05/09/2025). UCSC teaches the BACs may be useful biological reagents and the Genome Browser track comprising said BACs may be used for determining which BAC contains a gene, useful for certain wet lab experiments (Description).
Therefore, it is held that one of ordinary skill in the art before the effective filing date of the claimed invention would have simply substituted the RP11 probes of UCSC into the multiple nucleic acid probes in different proportions for each other of Dobi in view of Ebner. The artisan would have been so motivated as UCSC teaches that said probes are useful in wet lab experiments, which one of ordinary skill would understand to include the FISH experiments of Dobi, wherein the choice of such probes in a region would be obvious given the teaching of Ebner target a certain region by choosing tiled BAC clones to unique sequences in the desired chromosomal region. Such would have been predictable as Ebner teaches clones in the RP11 library, the sequences were known as taught by UCSC, and the means of using such BACs was taught by Ebner.
It is further held to be a matter of routine optimization to choose a particular number (i.e., comprising five) of molecules having sequences from Table 1 under MPEP 2144.05(II). Ebner discloses tiling candidate nucleic acids in a desired regions, and further teaches the use of 4 and 10 fragments (i.e., molecules). Ebner teaches that a useful probe may be designed using BAC DNA with two or more overlapping molecules over the gene and non-overlapping regions in the 3’ and 5’ regions. Therefore, it is held that one of ordinary skill in the art, in choosing from the BACs of UCSC to target the region of CHD1 would choose a number to test, and guided by Ebner’s direction of two or more over the gene and the implied at least one non-overlapping in the 3’ or 5’ and to generate sequences from them using nick-translation or random priming would have arrived at a set of probes comprising five sequences from claimed BAC(s).
Claims 10 is rejected under 35 U.S.C. 103 as being unpatentable over Dobi (WO 2020/123880 A2; effectively filed 12/12/2019), Ebner (WO 2017/007739 A2; published 01/12/2017) as applied to claim 1 above and in further view of Shenoy (Shenoy TR, et al. CHD1 loss sensitizes prostate cancer to DNA damaging therapy by promoting error-prone double-strand break repair. Ann Oncol. 2017 Jul 1;28(7):1495-1507).
Regarding claim 10, Shenoy teaches deficiency [i.e., deletion] of CHD1 In prostate cancers (page 1495, Background), and a method of confirming homozygous deletion in CHD1 in samples generated from mCRPC [metastatic castration resistant prostate cancers; see pg. 1496, col 1, para 1] biopsies using FISH, wherein the generated organoids were more sensitive to olaparib compared to those with normal CHD1 copy number (pg. 1503, mCRPC with homozygous CHD1 loss is sensitive to olaparib and carboplatin ex vivo and in vivo; Figure S7).
Shenoy further teaches that similar to BRCA1, CHD1 loss sensitizes cells to olaparib treatment in vitro and in vivo (pg. 1503, Loss of CHD1 leads to hypersensitivity to PARP inhibition and DNA damaging agents, para 1), wherein while WT and Chd1-/- mESC-derived tumors grew at similar rates in the absence of any treatment, Chd1-/- mESC-derived tumors were more sensitive to olaparib (pg. 1503, Loss of CHD1 leads to hypersensitivity to PARP inhibition and DNA damaging agents, para 1; Fig. 6B).
Shenoy teaches that CHD1 status may be a predictive biomarker for PARPi for mCRPC (pg. 1503, mCRPC with homozygous CHD1 loss is sensitive to olaparib and carboplatin ex vivo and in vivo, para 2, spanning pg. 1504).
Thus, Shenoy teaches an assessment of a patient with a prostate cancer associated with a CHD1 loss, as evaluated by FISH to CHD1 performed on a nucleic acid sample obtained from the subject, that treating with a PARP inhibitor is effective in subjects with CHD1 deficiency, and CHD1 as a predictive marker for PARP inhibitors in prostate cancer.
Shenoy does not explicitly teach the nucleic acid probe of claim 1 or performing FISH on the samples obtained from the subjects that are treated with olaparib.
As cited in claim 1 above, Dobi in view of Ebner teach a nucleic acid probe for hybridization to chromosomal DNA comprising at least two different nucleic acid molecules from the same chromosomal region of CHD1 present in different proportions from one another and in proportions different than “natur[al] non-cancerous cells”.
Dobi further teaches that CHD1 genomic rearrangements serve as biomarkers for prostate cancer and can be used to stratify prostate cancer based on the severity or aggressiveness of prostate cancer and/or identify a patient for prostate cancer treatment (Abstract).
Therefore, it is held that it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to simply substitute the FISH probes of Dobi in view of Ebner for the probes of Shenoy. The artisan would have been motivated to do so because the probes of Dobi allow for stratifying patients based on the severity of the prostate cancer as taught by Dobi. The results of the substitution would have been predictable as both Shenoy and Dobi in view of Ebner teach the probes for the same purpose (detecting CHD1).
Claims 11-13 are rejected under 35 U.S.C. 103 as being unpatentable over Shenoy (Shenoy TR, et al. CHD1 loss sensitizes prostate cancer to DNA damaging therapy by promoting error-prone double-strand break repair. Ann Oncol. 2017 Jul 1;28(7):1495-1507) in view of Slade (Slade D. PARP and PARG inhibitors in cancer treatment. Genes Dev. 2020 Mar 1;34(5-6):360-394).
Regarding claims 11-13, Shenoy teaches deficiency [i.e., deletion] of CHD1 In prostate cancers (page 1495, Background), and a method of confirming homozygous deletion in CHD1 in samples generated from mCRPC [metastatic castration resistant prostate cancers; see pg. 1496, col 1, para 1] (pg. 1503, mCRPC with homozygous CHD1 loss is sensitive to olaparib and carboplatin ex vivo and in vivo; Figure S7).
Shenoy teaches that similar to BRCA1, CHD1 loss sensitizes cells to olaparib and carboplatin treatment in vitro and in vivo (pg. 1503, Loss of CHD1 leads to hypersensitivity to PARP inhibition and DNA damaging agents, para 1), wherein while WT and Chd1-/- mESC-derived tumors grew at similar rates in the absence of any treatment, Chd1-/- mESC-derived tumors were more sensitive to both olaparib and carboplatin (pg. 1503, Loss of CHD1 leads to hypersensitivity to PARP inhibition and DNA damaging agents, para 1; Fig. 6B).
Shenoy further teaches treatment of a patient from whom CHD1 loss organoids were derived and was too unwell to be treated on a PARPi clinical treated with carboplatin, wherein after two doses his symptoms had fully resolved and his CT scan indicated a major response (pg. 1503, mCRPC with homozygous CHD1 loss is sensitive to olaparib and carboplatin ex vivo and in vivo, para 2, spanning pg. 1504). Shenoy teaches that these clinical data support the preclinical evidence and suggest that CHD1 status may be a predictive biomarker for DNA damaging agents such as carboplatin or PARPi for mCRPC (pg. 1503, mCRPC with homozygous CHD1 loss is sensitive to olaparib and carboplatin ex vivo and in vivo, para 2, spanning pg. 1504). Shenoy teaches that said patient (V5272) is the patient evaluated by FISH (Fig. S7; pg. 1503, mCRPC with homozygous CHD1 loss is sensitive to olaparib and carboplatin ex vivo and in vivo, para 2).
Shenoy teaches that CHD1 status may be a predictive biomarker for DNA damaging agents or PARPi for mCRPC (pg. 1503, mCRPC with homozygous CHD1 loss is sensitive to olaparib and carboplatin ex vivo and in vivo, para 2, spanning pg. 1504).
Thus, Shenoy teaches assessment of a patient with a prostate cancer associated with a CHD1 loss on a nucleic acid sample obtained from the subject, that treating with a DNA damaging agent (instant claim 11) or PARP inhibitor (instant claims 12 and 13) is effective in subjects with CHD1 deficiency, and CHD1 as a predictive marker for DNA damaging agents and PARP inhibitors in prostate cancer. See also Abstract and pg. 1506, para 4.
Shenoy further teaches CHD1 loss decreases HR-mediated DSB repair and increases error-prone NHEJ activity (pg. 1506, col 1, para 4).
Shenoy does not explicitly teach that the DNA damaging agent is bleomycin or treating with both bleomycin and a PARP inhibitor (instant claim 12), wherein the PARP inhibitor is olaparib.
Slade rectifies this by teaching that chemotherapeutic drugs that damage DNA by inducing DSBs comprise bleomycin (pg. 365, col 1, para 2).
Slade teaches that precision medicine has revolutionized cancer therapy by putting forth the concept of selective targeting of cancer cells, wherein PARP inhibitors represent a successful example of precision medicine applied in the clinic, wherein carriers of heterozygous BRCA1/2 mutations are sensitive to PARP inhibitor treatment as they lose the wild-type allele during tumorigenesis and thereby become BRCA1/2-null (pg. 365, col 1, para 2). Slade further teaches that it has become clear that oxidative stress and genomic instability, manifested not just through mutations in DNA repair proteins but also replication stress, sensitize cells to PARP and PARG inhibitors, and that additional genes have since shown synthetic lethality in combination with PARP inhibitors (pg. 365, col 1, para 2, spanning col 2).
Slade further teaches administration of PARP inhibitors following chemotherapy [i.e., bleomycin] is a better strategy [than combining treatments] and that mutations that cause resistance to PARP inhibitors, such as loss of NHEJ factors, PARP1, or PARG, were shown to sensitize cells to different DNA-damaging agents [i.e., bleomycin] (pg. 379, PARP inhibitor combination therapies, para 1).
Therefore, it is held that one of ordinary skill in the art before the effective filing date of the claimed invention would have simply substituted the DNA damage-inducing carboplatin of Shenoy for another DNA damage-inducing treatment such a bleomycin as taught by Slade, wherein the results would have been predictable as the purpose of both is the same. The artisan would have been so motivated because Slade teaches that such genotoxic agents including bleomycin induce high levels of DNA damage that render cancer cells particularly vulnerable due to their high proliferation rates.
It further would have been prima facie obvious to one of ordinary skill in the art to improve the therapy by combing with the PARP inhibitor olaparib of Shenoy by treating in sequence in view of Slade in order to effectively utilize precision medicine techniques as taught by Slade by targeting the mutations in the cancer cells that decrease HR-mediated DSB repair as taught by Shenoy. There would have been a strong expectation for success as the purpose of each and the efficacy of the combination was known.
Claims 14-16 are rejected under 35 U.S.C. 103 as being unpatentable over Shenoy (Shenoy TR, et al. CHD1 loss sensitizes prostate cancer to DNA damaging therapy by promoting error-prone double-strand break repair. Ann Oncol. 2017 Jul 1;28(7):1495-1507) in view of Slade (Slade D. PARP and PARG inhibitors in cancer treatment. Genes Dev. 2020 Mar 1;34(5-6):360-394) as applied to claim 11 above and further in view of Dobi (WO 2020/123880 A2; effectively filed 12/12/2019) and Ebner (WO 2017/007739 A2; published 01/12/2017).
Regarding claim 14, in the method of Shenoy and Slade, Shenoy teaches confirming homozygous deletion in CHD1 in samples generated from mCRPC [metastatic castration resistant prostate cancers; see pg. 1496, col 1, para 1] biopsies using FISH (pg. 1503, mCRPC with homozygous CHD1 loss is sensitive to olaparib and carboplatin ex vivo and in vivo; Figure S7).
Shenoy and Slade fail to explicitly teach the probe of claim 1 wherein the CHD1 probe comprises at least two different molecules in different proportions from each other.
As cited in claim 1 above, Dobi in view of Ebner rectify this by teaching a nucleic acid probe for hybridization to chromosomal DNA comprising at least two different nucleic acid molecules from the same chromosomal region of CHD1 present in different proportions from one another and in proportions different than “natur[al] non-cancerous cells”.
Dobi teaches identifying or characterizing prostate cancer comprising detecting in a biological sample the presence or absence of a genomic rearrangement that results in a deletion a genomic rearrangement that results in a deletion of a CHD1 gene, wherein CHD1 genomic rearrangements serve as a biomarker for prostate cancer and can be used to stratify prostate cancer based the severity or aggressiveness of prostate cancer (Abstract).
Therefore, it is held that it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to simply substitute the FISH probes of Dobi in view of Ebner for the probes of Shenoy. The artisan would have been motivated to do in order to stratify the prostate cancers of patients based on the severity of their cancers as taught by Dobi. The results of the substitution would have been predictable as both Shenoy and Dobi in view of Ebner teach the probes for the same purpose (detecting CHD1).
Regarding claim 15, in the method of Dobi, Ebner, and Shenoy, Shenoy teaches performing FISH on a lymph node biopsy (Supplementary Fig. 7B). Shenoy teaches previously obtaining mCRPC biopsies and generating organoids [i.e., a nucleic acid sample obtained from a subject] (pg. 1503, mCRPC with homozygous CHD1 loss is sensitive to olaparib and carboplatin ex vivo and in vivo, para 1).
Dobi teaches performing FISH on whole-mounted prostate sections (para [00112]) and that CHD1 genomic rearrangements serve as a biomarker for prostate cancer and can be used to stratify prostate cancer based on the severity or aggressiveness (Abstract).
Ebner teaches performing an in situ hybridization on prostate tissue in a method of detecting prostate cancer using a nucleic acid probe comprising at least two different nucleic acid molecules in different proportions to each other (claim 15).
Therefore, it is held that one of ordinary skill in the art before the effective filing date of the claimed invention could have simply substituted the prostate cancer biopsy for the lymph node biopsy as it was known in the art how to perform FISH on prostate cancer tissue and the artisan would be motivated to do so if the patient had not had any metastases or the prostate was already undergoing surgical removal and because Dobi teaches that CH1 can be used to stratify patients based on genomic rearrangements. The substitution was predictable Dobi teaches performing FISH on prostate samples.
Regarding claim 16, in the method of Dobi, Ebner and Shenoy, Shenoy teaches performing a circulating tumor cell count (pg. 1503, mCRPC with homozygous CHD1 loss is sensitive to olaparib and carboplatin ex vivo and in vivo, para 2).
Dobi teaches performing FISH for the detection of CHD1 in prostate cancer patients (para [00110]). Dobi further teaches that the sample may contain circulating tumor cells and that said cells have detached from a primary tumor (para [0084]). Dobi teaches CHD1 genomic rearrangements serve as biomarkers for prostate cancer and can be used to stratify prostate cancer based the severity or aggressiveness of prostate cancer (Abstract).
Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to simply substitute the sample of Shenoy for the circulating tumor cell sample of Dobi in the method of Dobi, Ebner, and Shenoy. The artisan would have been so motivated to monitor the patient for metastatic cells [i.e., cells that have detached from a primary tumor] to stratify patients. There would have been a strong expectation of success as both Dobi and Shenoy teach performing FISH and obtaining samples comprising CTCs.
Response to Arguments
Applicant's arguments filed 11/10/2025 have been fully considered but they are not persuasive.
Applicant argues on pg. 8 of the Remarks that the claim amendments render the claims not indefinite under 112(b).
The 112(b) rejections regarding the phrases “in nature” were not limited to cancerous cells; this was provided as an example. Other illustrative examples have been provided. Further, the subsequent references to the phrase in the dependent claim were unaddressed.
The 112(b) rejections regarding the Tables and the identifiers of the BACs/YACs remain unaddressed. The threshold of including a reference to a Table is one of necessity. As the unique clones of Table 1 are a smaller number than those now recited in words in Claim 7, this does not appear to be such a case and no argument was provided to justify such an inclusion. Further, the claims recite either directly or through the table the reference identifiers of BACs/YACs. The specification attempts to incorporate the clones of Fig. 3 by reference on pg. 11; however, as essential material (i.e., claimed material), this is not sufficient.
37 C.F.R. 1.57 states that essential material, i.e., claimed sequence, may be incorporated by reference but only by way of reference to a US patent of US patent application publication. Attempts to incorporate essential material, including sequences or molecules, from external databases are not effective. Thus, as the material has not been incorporated, the metes and bounds remain unclear to one of skill in the art. See also the specification objection.
Applicant argues on pgs. 8-9 of the Remarks that the claims are directed to subject eligible matter because the claimed probe is a synthetic diagnostic tool that must be constructed. Applicant argues that Myriad doesn’t apply because the claimed probe is not a mere isolated fragment, but an engineered mixture of multiple CDH1-derived molecules that are non-contiguous, deliberately combined, and present in stoichiometric ratios that do not occur in non-cancerous human cells. The Applicant alleges that the composition therefore possesses “markedly different characteristics” from natural DNA.
In response to applicant's argument that the references fail to show certain features of the invention, it is noted that the features upon which applicant relies (i.e., “non-contiguous”) are not recited in the rejected claim(s). Although the claims are interpreted in light of the specification, limitations from the specification are not read into the claims. See In re Van Geuns, 988 F.2d 1181, 26 USPQ2d 1057 (Fed. Cir. 1993). For clarity, it is noted that while the claim recites “different nucleic acid molecules”, broadly interpreted, the claims do not require the molecules be non-contiguous in a probe (e.g., 5’-A-B-A-3’). However, such joined probes where the component molecules are present in different proportions, would be outside of a natural products analysis.
Regarding the arguments that the composition has markedly different characteristics from natural DNA, the claims encompass compositions of sequences and fragments of natural DNA. MPEP 2106.04(c)(II)(B) provides examples of characteristics considered including biological functions, physical properties, phenotype (functional/structural characteristics), and genetics/physical structure and form. Applicant has failed to identify any ways in which the “non-natural” ratios of the claimed invention cause the nucleic acid molecules of the claim—which encompass natural structures—to differ functionally or structurally from the natural sequences themselves. And, indeed, the amended claims now exclude proportions for those from the CHD1 region that may be found in cancer cells, i.e., clearly encompass natural proportions of those found in cancer cells.
Further, as discussed in the 101, University of Utah v. Ambry also presents a situation where the closest counterpart differs, in essence, by a ratio of nucleic acids (single-stranded in the invention vs. double-stranded in the natural product); this difference in stoichiometry and the “deliberate intervention” were insufficient to make the subject matter eligible.
As clarified in the 101 rejection, Example 10 presents a situation of combining products that does result in a marked difference based on a transformation of properties based on the human intervention. However, the sequences here have no evidence that the combination or a combination in particular ratios results in such a material transformation.
For these reasons, the arguments regarding the alleged marked difference are not found persuasive.
Applicant argues on pgs. 9-10 of the Remarks that Dobi and Ebner fail to individually teach the claimed invention and that the combination is based on hindsight because Dobi and Ebner do not teach or suggest the structural configuration of a probe composition.
In response to applicant's arguments against the references individually, one cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986).
In response to applicant's argument that the examiner's conclusion of obviousness is based upon improper hindsight reasoning, it must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon hindsight reasoning. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made, and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin, 443 F.2d 1392, 170 USPQ 209 (CCPA 1971).
In response to applicant’s argument that there is no teaching, suggestion, or motivation to combine the references, the examiner recognizes that obviousness may be established by combining or modifying the teachings of the prior art to produce the claimed invention where there is some teaching, suggestion, or motivation to do so found either in the references themselves or in the knowledge generally available to one of ordinary skill in the art. See In re Fine, 837 F.2d 1071, 5 USPQ2d 1596 (Fed. Cir. 1988), In re Jones, 958 F.2d 347, 21 USPQ2d 1941 (Fed. Cir. 1992), and KSR International Co. v. Teleflex, Inc., 550 U.S. 398, 82 USPQ2d 1385 (2007). In this case, Dobi teaches the targets and single probe composition for each of the CHD1, PTEN, and LSAMP regions/genes and Ebner teaches a composition of multiple probes for such targets and different proportions from a “natural” molecules and among probes, as cited in the 103. Dobi and Ebner teach each the composition for detecting/stratifying aggressiveness of prostate cancer, and MPEP 2144.06 provides a basis that it is prima facie obvious to combine two compositions taught by the prior art to be useful for the same purpose in order to form a composition to be used for the same purpose. This has been clarified in the rejection to specify the particular combinations.
It is also noted, based on the amended claim language, that the proportion different than those in which they occur in nature in non-cancerous cells is a matter of routine optimization based on selected tiling molecules and amplification reaction efficiencies, as taught by Ebner.
Applicant argues on pgs. 10-11 of the Remarks that neither Shenoy nor Slade teach the method of claim 11 and that the art’s reliance on preclinical insights does not provide a motivation for specific treatment steps recited in these claims, nor provide a reasonable expectation of success that a CHD-1 deficient prostate cancer patient should be treated with bleomycin or bleomycin in combination with PARP inhibitors. Applicant argues that Slade does not teach a clinical treatment protocol.
In response to applicant's arguments against the references individually, one cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986).
Shenoy does teach evaluating a nucleic acid sample obtained from a subject using FISH (pg. 1503, mCRPC with homozygous CHD1 loss is sensitive to olaparib and carboplatin ex vivo and in vivo, para 2, spanning pg. 1504; Fig. S7 wherein the patient is V5272; pg. 1503, mCRPC with homozygous CHD1 loss is sensitive to olaparib and carboplatin ex vivo and in vivo, para 2), that CHD1 deficiency may be a predictive biomarker for DNA damaging agents or PARPi in metastatic prostate cancer (pg. 1503, mCRPC with homozygous CHD1 loss is sensitive to olaparib and carboplatin ex vivo and in vivo, para 2, spanning pg. 1504), and treating patients with tumors with CHD1 deletion with DNA damaging agents pg. (1506, col 1, para 4).
Contrary to the Applicant’s argument regarding Shenoy’s translational suggestion being specific to carboplatin and PARP inhibitors, Shenoy broadly states: “Our data provide a rationale for treating patients bearing tumors with CHD1 deletion in prospective clinical trials of PARP inhibitors or DNA damaging agents such as carboplatin to evaluate their potential clinical benefit in this subclass of PCa” (emphasis added; pg. 1506, col 1, para 4). Shenoy likewise broadly discusses the “the role of CHD1 in DSB repair and in response to DNA damaging therapy” (emphasis added; Abstract) and recites that “Loss of CHD1 sensitizes prostatic epithelial cells to DNA damaging treatments, including irradiation and drugs such as carboplatin and PARP inhibitors” (emphasis added; pg. 1496, col 1, para 2). It is clear that Shenoy does not believe the effects are constrained to the limited drugs presented.
Shade teaches that bleomycin is one such agent that causes DNA damage (e.g., pg. 365, para 1) and that administering PARP inhibitor and chemotherapy in sequence is an effective treatment strategy as PARP inhibitors sensitize cells to DNA damaging agents (pg. 379, PARP inhibitor combination therapies, para 1).
Therefore, it would have been obvious to utilize a DNA damaging agent such as bleomycin either in substitute of carboplatin or in addition to the PARP inhibitors, wherein such would have been predictable as one of the class of DNA damaging agents for the reasons further discussed in the 103 above.
Applicant’s argument that the prior art is deficient for relying on pre-clinical data is not persuasive because the present application also relies on in vitro experimental data for the claims relating to bleomycin and PARP inhibitors. Applicant has not adequately explained why such data would be sufficient to support and enable the claimed invention in the present application, but insufficient in the prior art.
In response to applicant's argument that the references fail to show certain features of the invention, it is noted that the features upon which applicant relies (i.e., “clinical treatment protocol”) are not recited in the rejected claim(s). Although the claims are interpreted in light of the specification, limitations from the specification are not read into the claims. See In re Van Geuns, 988 F.2d 1181, 26 USPQ2d 1057 (Fed. Cir. 1993). In the instant case, it is noted that claims neither require that the subject be a human nor the treatment be outside of a pre-clinical study. The claim requires “an effective amount of bleomycin” administered “to the subject” wherein the artisan would be able to determine the effective amount appropriate to the chosen subject. A particular treatment protocol, let alone a protocol targeted at the clinical setting, is not claimed.
For these reasons, the arguments regarding the art rejections are not found persuasive.
Conclusion
No claims are allowed.
The prior art made of record and not relied upon is considered pertinent to applicant's disclosure.
Mansoor (US 20040009493 A1; published 01/15/2004) teaches an array for the detection of chromosomal abnormality comprising a plurality of nucleic of nucleic acid segments immobilized to discrete spots (claim 1). Mansoor teaches a compilation of nucleic acids comprising a plurality of nucleic acid segments associated with a chromosomal abnormality (claim 126), wherein the segment may be an artificial chromosome (claims 183-185). Mansoor teaches detecting said chromosomal abnormality comprising providing an array of claim 1 or the compilation of claim 126, contacting gDNA from an individual with the array, and measuring the amount of specific hybridization, thereby making a diagnosis (claim 77; claim 194), wherein the disease may be a cancer (claim 83; claim 200). Mansoor teaches that at least one genomic nucleic acid segment is spotted in duplicate or triplicate on the array (claim 53) and the duplicate or triplicate spot has different amounts of nucleic acid segments immobilized [i.e., from the other probes] (claim 54).
Mansoor does not explicitly teach the targets of the instant application, though Mansoor teaches clones that represent all 24 human chromosomes at about 1 Mb resolution including clone RP11-90M19 (para [0213]; Table 2) and means of making such compilations/sets/libraries of nucleic acids (para [0212-0213]).
It is noted that the “probe” composition of claim 1 would encompass arrays.
Pinkel (US 5665549 A; granted 09/09/1997) teaches methods of in situ hybridization to detect abnormal nucleic acid sequence copy numbers, i.e., comparative genomic hybridization, including tumor cells (Abstract). Pinkel teaches that sensitivity of CDH is primarily limited by the granularity of the hybridization of signals and that further improvements in sensitivity will be achieved by optimization of the probe concentration (col 42, para 1). Pinkel teaches a mixture comprising unlabeled sequences designed to block sequences in the genomic DNA, wherein said DNA may be within a factor of 10 of the concentration of the labeled subject nucleic acids (col 14, para 2). Pinkel does not explicitly teach probes targeting the region of CHD1.
It is noted that claim 1 is product and the “probe” is not required to participate in hybridization, merely have structures from the same chromosomal region, and method teaching structures of products render the products obvious.
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.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Emma R Hoppe whose telephone number is (703)756-5550. The examiner can normally be reached Mon - Fri 11:00 am - 7:00 pm.
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/EMMA R HOPPE/Examiner, Art Unit 1683
/NANCY J LEITH/Primary Examiner, Art Unit 1636