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 .
Response to Amendment/Status of Claims
Receipt of Arguments/Remarks filed on 10/17/2025 is acknowledged. Claims 12 and 13 were amended. Claims 14-19 were cancelled. Claims 20-23 are new. Claims 12,13 and 20-23 are pending and under examination.
Response to Arguments
Applicant’s arguments, see page 5, filed 10/17/2025, with respect to the objection to the specification for embedded hyperlinks have been fully considered and are persuasive due to correcting the embedded hyperlinks in paragraphs 0058 and 0075.
Applicant’s arguments and amendments, see pages 7-8, filed 10/17/2025, with respect to the 35 U.S.C. 103 rejection of claims 12,13 and 16-19 over Smith in view of Millena et al. have been fully considered and are persuasive, due to the amendments to claims 12,13 and new claims 20-23 which no longer recite that the inhibitor administered is an inhibitor of JunD and the recitation of the specific JunD target genes that are inhibited (PRDX3, PEA15, STX6, MCMBP, KIF2C, PRPS2, EMBL4, CTNNA3, ESPL1, CDK2, CDK4, EIF1, EPHAS, CCNA1, NAGA, ADRB2, F2RL2, CBX4, STX6 and NDUFAF4) that are not taught by Smith or Millena et al. Therefore, the rejection has been withdrawn.
The following rejections and/or objections are either reiterated or newly applied and are necessitated by amendment. They constitute the complete set presently being applied to the instant application.
Claim Objections
Claim 13 is objected to because of the following informalities: line 3 recites “comprising the set of” rather than “comprising the step of”. Appropriate correction is required.
Claim Rejections - 35 USC § 112
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 12,13 and 20-23 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
Claim 12 encompasses an in vivo method of treating prostate cancer in a subject in need of treatment by inhibiting the expression of c-MYC and c-MYC protein levels comprising the step of administering an effective amount of a large genera of inhibitors to the subject, wherein the inhibitor inhibits the expression of one or more JunD target genes selected from the group consisting of PRDX3, PEA15, STX6, MCMBP, KIF2C, PRPS2, EMBL4, CTNNA3, ESPL1, CDK2, CDK4, EIF1, EPHAS, CCNA1, NAGA, ADRB2, F2RL2, CBX4, STX6 and NDUFAF4. Claim 13 encompasses an in vivo method of inhibiting prostate cancer cell growth in a subject in need of treatment by inhibiting the expression of c-MYC and c-MYC protein levels comprising the step of administering an effective amount of a large genera of inhibitors to the subject, wherein the inhibitor inhibits the expression of one or more JunD target genes selected from the group consisting of PRDX3, PEA15, STX6, MCMBP, KIF2C, PRPS2, EML4, CTNNA3, ESPL1 and CDK2. New claims 20-21 depend from claim 12, and claims 22-23 depend from claim 13 and further limit the target genes that the inhibitor inhibits expression of. Based on the broadest reasonable interpretation, these claims read on administering an inhibitor that inhibits the expression of c-MYC and the expression of one or more of the recited JunD target genes, and no longer recite that the inhibitor that is administered is an inhibitor of JunD transcription factor, and encompass a large number of compounds including antisense oligonucleotides, anti-miRs, antagomirs, aptamers, ribozymes, CRISPR-Cas complex, RNAi, siRNA, shRNA, small molecules and antibodies, thereby treating prostate cancer or inhibiting prostate cancer cell growth in a subject.
The state of the art does not show that administering an inhibitor that inhibits expression of c-MYC would also inhibit the recited JunD target genes and result in treatment prostate cancer or inhibiting prostate cancer cell growth in a subject. The state of the art shows various inhibitors of JunD transcription factor, as well as the association of JunD with cancer, including prostate cancer, however the state of the art does not teach a representative number of inhibitors that inhibit expression of c-MYC and c-MYC protein levels as well as inhibit the expression of one or more of the JunD target genes recited in claims 12,13 and 20-23, thereby resulting in treating prostate cancer or inhibiting prostate cancer cell growth in a subject.
Kajanne et al. (International Journal of Oncology 35: 1175-1182, 10 July 2009) of record, teaches expression of AP-1 proteins has been associated with more aggressive clinical outcome in prostate cancer (page 1176, left column), and that PC-3 cells transfected with JunD siRNA further sensitized the cells to irradiation and reduced their growth rate significantly (page 1181, right column).
US 20130210772, (hereinafter “’772”), Published 15 August 2013, cited on an IDS, teaches a method of treating prostate cancer and inhibiting the growth of human prostate cancer in a subject comprising administering to a mammal one or more pharmaceutically acceptable salts of the present disclosure comprising an inhibitor of the JunD-AR interaction [0138], and recites the inhibitor is a compound of claim 1 (claims 71-72) of formula I.
US 20100172966 (hereinafter “Smith”), Published 8 July 2010, cited on an IDS, teaches two junD antisense ODNs of SEQ ID NOs: 5 and 6 [0205], that the H(1)junD antisense ODN has a great antileukemic effect and has anticancer effects on solid tumors [0206], and using ODNs to suppress expression of junD in cancer cells derived from prostate cancer can reverse multidrug resistance resulting from a variety of mechanisms [0208].
Millena et al. (J Biol Chem. Vol. 291(34): 17964-17976, Published 19 August 2016), cited on an IDS, teach using siRNAs to knock down Jun proteins in DU145 and PC3 cells which caused significant reduction in proliferation of both DU145 and PC3 cells (page 17966, left column). Millena et al. also teach that knockdown of endogenous JunD showed a significant decrease in the levels of c-Myc, Ki-67 and Id-1 proteins (page 17966, right column), and that JunD may provide a significant therapeutic target for treatment of prostate cancers (page 17972, right column).
When claims 12,13 and 20-23 are analyzed in light of the specification, the as-filed specification encompasses knocking out JunD in PC3 cells using CRISPR/Cas9 single guide RNAs of SEQ ID NO: 1 and 2 targeting 2 locations on JunD exon 1 [00061]. The specification discloses using CRISPR/Cas9 genome editing to generate JunD knock out prostate cancer, and results showed that in the absence of JunD protein, cell proliferation is significantly reduced compared to the control cells, with a significant decrease in proliferation in a time dependent manner and decrease in cell size [00078]. The instant specification also shows knock-down of JunD or PRDX3 protein in PC3 and DU145 cells using siRNA (paragraphs 00062,00068,00069) and that JunD knock-down decreases the expression of cell cycle-related genes including MYC (paragraph 00079). Paragraph 00079 shows microarray analysis and proteomic analysis of differentially expressed genes and proteins that were down-regulated or up-regulated in PC3 JunD KD cells, and that the top 10 down-regulated genes from microarray data include JunD, PRDX3, EPHAS, CCNA1, NAGA, ADRB2, F2RL2, CBX4, STX6 and BDUFAF4 (Fig 3C, paragraph 00080). The specification also shows that CDK2 and CDK4 were significantly down-regulated in PC3-JunD KD cells (paragraph 00083). However, the specification does not identify the structure of the siRNA that performs this function.
The specification also shows that JQ1, a c-MYC inhibitor, suppresses JunD-mediated cell proliferation of prostate cancer cells by treating a JunD-overexpressing cell line with JQ1 which significantly reduced cell proliferation and decreased JunD target genes protein levels (paragraph 00084, Fig. 6D). Fig. 6D shows c-MYC, PRDX3, CDK2 and KIF2C as the JunD target genes whose protein levels were decreased. Supplemental table 4 on pages 27-28 shows JunD-regulated genes in PC3 JunD KD cells but does not show what the required structure is of the inhibitor.
However, there is still lack of written description of what the required structure of an inhibitor is that inhibits the expression of c-MYC and the expression of one or more of the recited JunD target genes and results in treating prostate cancer.
Vas-Cath Inc. v. Mahurkar, 19 USPQ2d 1111, (Fed. Cir. 1991), makes clear that "applicant must convey with reasonable clarity to those skilled in the art that, as of the filing date sought, he or she was in possession of the invention. The invention is, for purposes of the 'written description' inquiry, whatever is now claimed." (See page 1117.) The specification does not "clearly allow persons of ordinary skill in the art to recognize that [he or she] invented what is claimed." (See Vas-Cath at page 1116.)
Univ. of Rochester v. G.D. Searle, 69 USPQ2d 1886, 1892 (CAFC 2004), further supports this by stating that: The appearance of mere indistinct words in a specification or a claim, even an original claim, does not necessarily satisfy that requirement. A description of an anti-inflammatory steroid, i.e., a steroid (a generic structural term) described even in terms of its functioning of lessening inflammation of tissues fails to distinguish any steroid from others having the same activity or function. A description of what a material does, rather than of what it is, usually does not suffice…. The disclosure must allow one skilled in the art to visualize or recognize the identity of the subject matter purportedly described. (Emphasis added).
In analyzing whether the written description requirement is met for genus claims, it is first determined whether a representative number of species have been described by their complete structure. In the instant case the specification discloses the complete structure of JQ1, a c-MYC inhibitor and which is shown to decrease protein levels of c-MYC, PRDX3, CDK2 and KIF2C (paragraph 00084, Fig. 6D). The specification does not describe that the sgRNAs of SEQ ID NOs: 1 and 2 have the recited function of inhibiting the expression of the JunD target genes recited in the instant claims as amended, and as stated earlier, the specification does not identify the structure of the siRNA in paragraphs 00062,00068,00069.
Therefore, as JQ1 is the only inhibitor disclosed as inhibiting c-MYC, PRDX3, CDK2 and KIF2C, the number of complete structures do not represent the broad genus of inhibitors with the function of inhibiting expression of c-MYC and inhibiting expression of one or more JunD target genes selected from the group consisting of PRDX3, PEA15, STX6, MCMBP, KIF2C, PRPS2, EMBL4, CTNNA3, ESPL1, CDK2, CDK4, EIF1, EPHAS, CCNA1, NAGA, ADRB2, F2RL2, CBX4, STX6 and NDUFAF4 or selected from the group consisting of PRDX3, PEA15, STX6, MCMBP, KIF2C, PRPS2, EML4, CTNNA3, ESPL1 and CDK2 and resulting in treating prostate cancer or inhibiting prostate cancer cell growth in a subject.
The genus of inhibitors encompasses a large number of variants and molecules (antisense oligonucleotides, anti-miRs, antagomirs, aptamers, ribozymes, CRISPR-Cas complex, RNAi, siRNA, shRNA, small molecules and antibodies) that have different structures, and the specification does not describe an essential structure of a representative number of species of the large genus of inhibitors or functional equivalents thereof. The specification does not provide description for which species of inhibitors within the broad genus would or would not result in inhibiting the expression of c-MYC and c-MYC protein and inhibiting the expression of one or more JunD target genes selected from the group consisting of PRDX3, PEA15, STX6, MCMBP, KIF2C, PRPS2, EMBL4, CTNNA3, ESPL1, CDK2, CDK4, EIF1, EPHAS, CCNA1, NAGA, ADRB2, F2RL2, CBX4, STX6 and NDUFAF4 or selected from the group consisting of PRDX3, PEA15, STX6, MCMBP, KIF2C, PRPS2, EML4, CTNNA3, ESPL1 and CDK2, thereby treating prostate cancer or reducing prostate cancer cell growth in a subject. See Amgen Inc. v. Sanofi 872 F.3d 1367, 1378, 124 USPQ2d 1354, 1361 (Fed. Cir. 2017) cited in MPEP 2163.II.3(a). Therefore, the number of species disclosed by complete structure is not sufficient to provide written description support for the entire broad genus of inhibitors with the recited function (inhibiting the expression of c-MYC and c-MYC protein and inhibiting the expression of one or more JunD target genes selected from the group consisting of PRDX3, PEA15, STX6, MCMBP, KIF2C, PRPS2, EMBL4, CTNNA3, ESPL1, CDK2, CDK4, EIF1, EPHAS, CCNA1, NAGA, ADRB2, F2RL2, CBX4, STX6 and NDUFAF4 or selected from the group consisting of PRDX3, PEA15, STX6, MCMBP, KIF2C, PRPS2, EML4, CTNNA3, ESPL1 and CDK2, thereby treating prostate cancer or reducing prostate cancer cell growth in a subject).
Next, then, it is determined whether a representative number of species have been sufficiently described by other relevant identifying characteristics (i.e., other than nucleotide sequence), specific features and functional attributes that would distinguish different members of the claimed genus. In the instant case, the functional characteristics in claims 12,13 and 20-23 are not coupled with a known structure. The specification fails to identify a core structure of an inhibitor that inhibits the expression of c-MYC and c-MYC protein levels and inhibits the expression of the recited JunD target genes and results in treatment of prostate cancer or inhibiting prostate cancer cell growth in a subject, as well as a partial structure, physical or chemical property, or functional characteristic coupled with a structure/function relationship responsible for inhibiting c-MYC and the recited JunD target genes to treat prostate cancer or inhibit prostate cancer cell growth in a subject to demonstrate possession of the full invention as claimed at the time of filing.
Applicant’s attention is directed to the Guidelines for the Examination of Patent Applications Under the 35 U.S.C. 112(a) or Pre-AIA 35 U.S.C. 112, first paragraph, "Written Description" Requirement (MPEP2163).
In conclusion, the disclosure regarding JQ1 as the inhibitor for the claimed broad genus of inhibitors with the recited functions of inhibiting c-MYC and the recited JunD target genes and result in treating prostate cancer or inhibiting prostate cancer cell growth, is not deemed sufficient to reasonably convey to one skilled in the art that the instant disclosure was in possession of the claimed broad genus of inhibitors at the time the effective filing date. Thus, it is concluded that the written description requirement is not satisfied for the claimed genus.
Response to Arguments
Applicant’s arguments, see pages 6-7, filed 10/17/2025, with respect to the 35 U.S.C. 112(a) Written description rejection of claims 12,13 and 16-19 has been fully considered but is not persuasive. The above 35 U.S.C. 112(a) Written Description rejection has been modified based on the claim amendments to claims 12 and 13, cancelation of claims 16-19 and new claims 20-23.
Applicant argues on page 6, that they traverse the Written Description rejection but have amended the claims to further specify the target genes of the claimed inhibitors, i.e., JunD target genes recited in claim 12. Applicant argues that the claims are not directed to the discovery or generation of new compounds (e.g. inhibitor of JunD factor as recited in the claims) but rather to the novel use of known compounds (inhibitors of the c-MYC pathway) in a particular therapeutic application (i.e. a method of treating prostate cancer by inhibiting the recited target genes). Applicant argues that the description necessary to establish written description for a genus of compounds logically differs from that needed to establish written description for a method of using a genus of compounds to achieve a particular purpose and that the courts have recognized a distinction between these two types of claims and have warned against viewing such method claims like composition claims when assessing written description, citing Erfindergemeinschaft UroPep GbR v. Eli Lilly and Co., 276 F.Supp.3d 629 (E.D. Tex. Oct. 21, 2017), affirmed by United States Court of Appeals, Federal Circuit on October 10, 2018; see also Ex parte AMBATI, Appeal 2017-011580 at 6 (PTAB Jan 29, 2019). Recently, the court in UroPep discussed the important differences between claims drawn to the identification of particular inhibitors versus claims to the use of compounds having the inhibiting feature for a particular therapeutic purpose, as in the present claims (citing University of Rochester v. G.D. Searle & Co., Inc., 358 F.3d 916 (Fed. Cir. 2006). The PTAB in Ex parte AMBATI took a similar position, noting that the level and type of description needed for claims drawn to compounds (antibodies in that case) differs from that needed for claims drawn to a new use of such compounds.
This is not found persuasive. Applicant has amended claims 12 and 13, canceled claims 14-19 and provided new claims 20-23. Amended claims 12 and 13 are now broader than they previously were regarding the inhibitor being administered, and encompass administering an inhibitor that inhibits the expression of c-MYC and inhibits the expression of the recited JunD target genes and results in treating prostate cancer or inhibiting prostate cancer cell growth, rather than administering an inhibitor of JunD transcription factor as previously recited. The inhibitor being administered could be a JunD inhibitor, but as instantly claimed does not have to be a JunD inhibitor, just that the inhibitor has the function of inhibiting expression of c-MYC and c-MYC protein levels and one or more of the instantly recited JunD target genes (one or more JunD target genes selected from the group consisting of PRDX3, PEA15, STX6, MCMBP, KIF2C, PRPS2, EMBL4, CTNNA3, ESPL1, CDK2, CDK4, EIF1, EPHAS, CCNA1, NAGA, ADRB2, F2RL2, CBX4, STX6 and NDUFAF4 or selected from the group consisting of PRDX3, PEA15, STX6, MCMBP, KIF2C, PRPS2, EML4, CTNNA3, ESPL1 and CDK2). In addition, applicant has canceled claims 14 and 15 reciting species of inhibitors of JunD transcription factor being CRISPR/Cas9 single guide RNAs comprising the nucleotide sequence set forth in SEQ ID NO: 1 and 2. New claims 20-23 narrow the target genes whose expression is being inhibited that are recited in amended claims 12 and 13. Therefore applicant has broadened the claims with regard to the genus of inhibitors being administered with the recited functions. The specification does not provide a structure-function correlation for the genus of inhibitors being administered with the recited function of inhibiting the expression of c-Myc and the instant recited JunD target genes that results in treating prostate cancer or inhibiting prostate cancer cell growth in a subject.
Applicant argues on page 6 that the present claims are not drawn to a genus of compounds, but rather to a new use for known compounds in a particular therapeutic indication (i.e., treatment of prostate cancer). In this regard, the specification provides working evidence and a clear rationale as to why inhibition of c-MYC and c-MYC protein levels by an inhibitor of JunD transcription factor is effective in the treatment of prostate cancer and that compounds falling within this class of inhibitors were well known at the relevant filing date. Applicant argues it is well established that the written description requirement must be applied in the context of the particular invention and the state of the knowledge in the art. As each field evolves, the balance also evolves between what is known and what is added by each inventive contribution (emphasis added) (Capon v. Eshhar, 418 F.3d 1349, 1357, 76 USPQ2d 1078, 1085 (Fed. Cir. 2005)). Applicant argues given the description in the present specification and the knowledge in the art at the relevant filing date, the skilled artisan would clearly recognize that Applicant was in possession of a method of treating prostate cancer by inhibiting c- MYC, regardless of the specific inhibitor of JunD transcription factor used for this purpose and that the specification demonstrates the proof-of-principle that inhibition of c-MYC and c-MYC protein by administering an inhibitor of JunD transcription factor can reduce prostate cancer cell growth (see, e.g., paragraphs [00055] and [00056] of the published application), which is sufficient to establish possession of a method of using these inhibitors to treat prostate cancer.
This is not found persuasive. The Written Description rejection in the non-final office action does not focus on a genus of compounds as applicant suggests, but rather the use of a genus of compounds with a particular function. The non-final office action of 07/21/2025 says that the functional characteristics in claims 12,13 and 16-19 are not coupled with a known structure, and the specification fails to identify a core structure necessary for inhibiting JunD that inhibits the expression of c-MYC and c-MYC protein levels and that results in treatment of prostate cancer or inhibiting prostate cancer cell growth in a subject, as well as a partial structures, physical or chemical property or functional characteristic coupled with a structure/function relationship responsible for inhibiting JunD to treat prostate cancer or inhibit prostate cancer cell growth in a subject to demonstrate possession of the full invention (Office Action, page 9). It is not clear from the state of the art that there are well known inhibitors that inhibit c-MYC as well as one or more of the recited JunD target genes, and it is also not clear based on the instant specification if the same structural requirements for the inhibitor are required for each of the JunD target genes or if a different structure is required in order to inhibit expression of certain JunD target genes. The specification does not show the structure of the siRNA used in paragraphs 00062,00068,00069. Aside from JQ1, there is no structure provided that achieves the recited effects, and there is no evidence provided that administering a different inhibitor has this effect. Therefore, with no structure given for the siRNA tested and no guidelines provided by the specification regarding a required structure to achieve the recited function, and no evidence that the recited JunD target genes are known to be associated with JunD and c-MYC, the written description requirement has not been satisfied. JQ1 is not representative of the genus of inhibitors with the recited functions.
University of California v. Eli Lilly and Co., 43 USPQ2d 1398, 1404, 1405 (Fed. Cir. 1997) held that:
...To fulfill the written description requirement, a patent specification must describe an invention and do so in sufficient detail that one skilled in the art can clearly conclude that "the inventor invented the claimed invention." Lockwood v. American Airlines, Inc., 107 F.3d 1565, 1572, 41 USPQ2d 1961, 1966 (Fed. Cir. 1997); In re Gosteli, 872 F.2d 1008, 1012, 10 USPQ2d 1614, 1618 (Fed. Cir. 1989) (" [T]he description must clearly allow persons of ordinary skill in the art to recognize that [the inventor] invented what is claimed."). Thus, an applicant complies with the written description requirement "by describing the invention, with all its claimed limitations, not that which makes it obvious," and by using "such descriptive means as words, structures, figures, diagrams, formulas, etc., that set forth the claimed invention." Lockwood, 107 F.3d at 1572, 41 USPQ2d at 1966.
As shown above in the 35 U.S.C. 112(a) Written Description rejection for 12,13 and 20-23 and the arguments above, neither the state of the art nor the specification teach a representative number of compounds for the genus of inhibitors with the function of inhibiting the expression of c-MYC and c-MYC protein levels, and inhibiting expression of one or more JunD target genes selected from the group consisting of PRDX3, PEA15, STX6, MCMBP, KIF2C, PRPS2, EMBL4, CTNNA3, ESPL1, CDK2, CDK4, EIF1, EPHAS, CCNA1, NAGA, ADRB2, F2RL2, CBX4, STX6 and NDUFAF4 or selected from the group consisting of PRDX3, PEA15, STX6, MCMBP, KIF2C, PRPS2, EML4, CTNNA3, ESPL1 and CDK2, thereby resulting in treating prostate cancer or inhibiting prostate cancer cell growth. Therefore, the 35 U.S.C. 112(a) Written Description rejection is maintained for claims 12,13 and 20-23.
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.
Claims 12,13 and 20-23 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Wang et al. (US 20150246923, Published 3 Sept 2015).
Claim Interpretation: The active method step of claims 12 and 13 only requires administering an effective amount of an inhibitor, wherein the inhibitor inhibits the expression of c-MYC and c-MYC protein levels and inhibits the expression of one or more JunD target genes as recited in claims 12,13 and 20-23. The instant specification demonstrates that treatment of JunD over-expressing cell lines with 5 um of JQ1, a c-MYC inhibitor, significantly reduced proliferation and reduced JunD target genes protein levels (Paragraph 00084 and Fig 6D), which shows the target genes reduced as c-MYC, PRDX3, CDK2 and KIF2C. Therefore, administering an effective amount of JQ1 to a prostate cancer patient reads on the active method step, and would result in inhibition of c-MYC expression and PRDX3, CDK2 and KIF2C expression.
Regarding claims 12,13 and 20-23, Wang et al. teach treatment of VCaP prostate cancer tumor-bearing mice with JQ1 led to significant reduction in tumor volume/weight (Figs. 23-25; paragraph 1123, page 261). Wang et al. teach that FIG. 23 is a line graph comparison of JQ1 and MDV3100VCaP, Xenografted mice were randomized and then received vehicle or 50 mg/kg JQ1 or 10 mg/kg MDV3100 as indicated 5 days/week (paragraph 0050).
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Wang et al. also teach that a 50% reduction in castration-resistant tumors by JQ-1 treatment was observed (Fig. 26; paragraph 1123).
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Wang et al. teach that a loss of the MYC associated gene signature was observed in AR-positive cells lines upon JQ1 treatment (Table 7), and MYC levels were attenuated by JA1 in cells which are AR-positive and sensitive to JQ1 inhibition (paragraphs 1118, 1159).
Regarding the expression of the JunD target genes recited in claims 12,13 and 20-23, as explained in the above claim interpretation, as Wang et al. teach administering an effective amount of JQ1 to the same patient population as the instant claims (prostate cancer subject), and in addition teaches JQ1 treatment reduces MYC levels, and would therefore result in inhibiting the expression of PRDX3, CDK2 and KIF2C target genes.
Conclusion
Claims 12,13 and 20-23 are rejected.
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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/STEPHANIE L SULLIVAN/Examiner, Art Unit 1635
/ABIGAIL VANHORN/ Primary Examiner, Art Unit 1636