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 .
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 04/01/2026 has been entered.
Response to Amendment/Status of Claims
Receipt of Arguments/Remarks filed on 04/01/2026 is acknowledged. Claims 12 and 13 were amended. Claims 12,13 and 20-23 are pending and under examination.
Withdrawn Rejections
Applicant’s arguments and amendments, see page 4, filed 04/01/2026, with respect to claim 13 have been fully considered and are persuasive due to the amendment correcting the typo. The objection to claim 13 has been withdrawn.
Applicant’s arguments and amendments, see page 6, filed 04/01/2026, with respect to the 35 U.S.C. 102(a)(1) rejection of claims 12,13 and 20-23 as anticipated by Wang et al. (US 20150246923) have been fully considered and are persuasive due to the amendments to claims 12 and 13 requiring that the inhibitor administered is an inhibitor of JunD transcription factor, rather than the prior recitation of administering an inhibitor (any inhibitor), and Wang et al. does not teach administering an effective amount of an inhibitor of JunD. The 35 U.S.C. 102(a)(1) rejection of claims 12,13 and 20-23 has been withdrawn.
The following rejections and/or objections are either reiterated or newly applied. They constitute the complete set presently being applied to the instant application.
Drawings
The drawings are objected to because figure(s) 1-11 recite “Figure X” and each view is identified as A., B., C., D., etc. However, 37 CFR 1.84(u) shown below requires partial views to be identified by the same number followed by a capital letter and preceded by “FIG”. For example, the correct label is FIG. 1A, FIG. 1B, FIG. 1C, etc.
(u) Numbering of views.
(1) The different views must be numbered in consecutive Arabic numerals, starting with 1, independent of the numbering of the sheets and, if possible, in the order in which they appear on the drawing sheet(s). Partial views intended to form one complete view, on one or several sheets, must be identified by the same number followed by a capital letter. View numbers must be preceded by the abbreviation "FIG."
Corrected drawing sheets in compliance with 37 CFR 1.121(d) are required in reply to the Office action to avoid abandonment of the application. Any amended replacement drawing sheet should include all of the figures appearing on the immediate prior version of the sheet, even if only one figure is being amended. The figure or figure number of an amended drawing should not be labeled as “amended.” If a drawing figure is to be canceled, the appropriate figure must be removed from the replacement sheet, and where necessary, the remaining figures must be renumbered and appropriate changes made to the brief description of the several views of the drawings for consistency. Additional replacement sheets may be necessary to show the renumbering of the remaining figures. Each drawing sheet submitted after the filing date of an application must be labeled in the top margin as either “Replacement Sheet” or “New Sheet” pursuant to 37 CFR 1.121(d). If the changes are not accepted by the examiner, the applicant will be notified and informed of any required corrective action in the next Office action. The objection to the drawings will not be held in abeyance.
Claim Objections
Claims 12,13 and 20-23 are objected to because of the following informalities: Claims 12,13 and 20-23 recite many acronyms of genes/proteins, including c-MYC, JunD, as well as PRDX3, PEA15, STX6, MCMBP, KIF2C, PRPS2, EMBL4, CTNNA3, ESPL1, CDK2, CDK4, EIF1, EPHAS, CCNA1, NAGA, ADRB2, F2RL2, CBX4, STX6 and NDUFAF4. For clarity, at least the first recitation of a gene/protein name should be fully written, for example Peroxiredoxin-3 (PRDX3). 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.
Claims 12,13 and 20-23 encompass an in vivo method of treating prostate cancer or 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 administering an effective amount of a large genera of inhibitors of JunD transcription factor to the subject, and 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 12); 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 (claim 13); wherein the inhibitor inhibits the expression of PRDX3, CDK2, CDK4, EIF1, KIF2C or PEA15 (claim 20); wherein the inhibitors inhibits the expression of PRDX3 (claim 21); wherein the inhibitor inhibits the expression of PRDX3, CDK2, CDK4, EIF1, KIF2C or PEA15 (claim 22); wherein the inhibitor inhibits the expression or PRDX3 (claim 23).
Based on the broadest reasonable interpretation, these claims read on administering a large number of compounds including antisense oligonucleotides, anti-miRs, antagomirs, aptamers, ribozymes, CRISPR-Cas complex, RNAi, siRNA, shRNA, small molecules and antibodies which are JunD transcription factor inhibitors, and also have the function of inhibiting expression of c-MYC and c-MYC protein levels, as well as inhibiting the expression of the one or more recited JunD target genes, thereby treating prostate cancer or inhibiting prostate cancer cell growth in a subject.
While the state of the art shows various inhibitors of JunD transcription factor, as well as the association of JunD with cancer, including prostate cancer, the state of the art does not teach a representative number of inhibitors of JunD transcription factor that also inhibit expression of c-MYC and c-MYC protein levels and the expression of one or more of the recited JunD target genes of the instant claims, 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 discloses 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 specification also discloses that PRDX3, CDK2, CDK4, EIF1, KIF2C and PEA15 were significantly down-regulated in PC3-JunD KD cells (paragraph 00083).
The instant specification discloses 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, EPHA5, CCNA1, NAGA, ADRB2, F2RL2, CBX4, STX6 and NDUFAF4 (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 discloses 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. However, JQ1 is a c-MYC inhibitor rather a JunD inhibitor as required by the instant claims. 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.
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 does not disclose the structure of any inhibitors of JunD transcription factor with the recited functions. The specification does not identify the structure of the siRNA in paragraphs 00062,00068,00069.
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 the same activity as a JunD inhibitor, however the genus encompasses a large number of variants and molecules that have different structures, and the specification does not describe an essential structure of a representative number of species of the large genus of JunD inhibitors or functional equivalents thereof. The specification does not provide description for which species of JunD inhibitors within the broad genus would or would not result in inhibiting the expression of c-MYC and c-MYC protein and 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 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 JunD inhibitors with the recited function (inhibiting the expression of c-MYC and c-MYC protein 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 necessary for inhibiting JunD that also inhibits the expression of c-MYC and c-MYC protein levels as also inhibits the expression of one or more JunD target genes recited in claims 12,13 and 20-23, 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 JunD, 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 for the claimed broad genus of JunD inhibitors with the recited functions 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 JunD 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 4-5, filed 04/01/2026, with respect to the 35 U.S.C. 112(a) Written description rejection of claims 12,13 and 20-23 has been fully considered but is not persuasive. The above Written Description rejection has been modified regarding the amendments to claims 12 and 13 regarding administering an effective amount of an inhibitor of JunD transcription factor, rather than any inhibitor as previously recited.
Applicant argues on pages 4-5 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.
Applicant argues that the claims are not drawn to a genus of compounds but rather a new use for known compounds in a particular therapeutic indication (the treatment of prostate cancer), and the specification provides working evidence and a clear rationale as to why inhibition of JunD transcription factors upstream of c-MYC and c-MYC protein expression is effective in treatment of prostate cancer. Applicant argues that compounds falling within this class of inhibitors were well known at the relevant filing date. 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)). 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. Indeed, 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 final office action dated 12/09/2025 pertains to the use of a genus of compounds with a particular function rather than just a genus of compounds. The functional characteristics in claims 12,13 and 20-23 are not coupled with a known structure and the specification and state of the art do not identify a core structure that is required for the recited functions. Not only do the claims require that what is administered is an inhibitor of JunD but also requires that c-MYC expression is inhibited as well as one or more of the recited JunD target genes and result in treating prostate cancer or inhibiting prostate cancer cell growth in a subject. It is not clear from the state of the art that there are well known JunD 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 JunD 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, which is a c-MYC inhibitor rather than a JunD inhibitor, 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.
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 claims 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 JunD inhibitors with the function of inhibiting 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
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 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 US 20130210772, hereinafter “’772”, (Published 15 August 2013) and cited on an IDS.
Claim Interpretation: Regarding claims 12,13 and 20-23, these claims recite an in vivo method of treating prostate cancer or 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 an inhibitor of JunD transcription factor to the subject, wherein the inhibitor inhibits the expression of one or more JunD target genes…. Based on the broadest reasonable interpretation these claims encompass administering any JunD inhibitor, as there is no definition of an inhibitor of JunD transcription factor in the specification, and no specific JunD inhibitor is claimed. Absent a demonstration of the criticality of the structure of the JunD inhibitor, the wherein clause is interpretated as a result that flows from the administration of the effective amount of the JunD inhibitor. "A 'whereby' clause that merely states the result of the limitations in the claim adds nothing to the patentability or substance of the claim." Texas Instruments, Inc. v. International Trade Comm., 988 F.2d 1165, 1172 (Fed. Cir. 1993). See also Minton v. National Assoc. of Securities Dealers, Inc., 336 F.3d 1373, 1381 (Fed. Cir. 2003) ("A whereby clause in a method claim is not given weight when it simply expresses the intended result of a process step positively recited."). Note MPEP 2111.04.
In this case, claims 12,13 and 20-23 use the term "wherein", rather than "whereby", but it is concluded that the terms should be treated the same…the wherein clause does not inform the artisan of how the “administering an effective amount of an inhibitor of JunD transcription factor to the subject" steps are performed; rather, the wherein clause merely characterizes the results of those steps. Therefore, the examiner is considering that as the only active method step is “administering an effective amount of an inhibitor of JunD transcription factor to the subject”, that the functional limitations of inhibiting the expression of c-MYC and c-MYC protein levels, as well as inhibiting the expression of the recited JunD target genes recited in claims 12,13 and 20-23 would be carried out by the active method step of administering an effective amount of an inhibitor of JunD transcription factor to the subject in need thereof.
Regarding claims 12,20 and 21, ‘772 teaches a method of treating or inhibiting the recurrence, progression or metastasis of prostate cancer consisting of administering to a mammal diagnosed as having prostate cancer, in an amount effective to treat or inhibit the occurrence, recurrence, progression or metastasis of the prostate cancer, one or more pharmaceutically acceptable salts of the present disclosure comprising an inhibitor of the JunD-AR interaction (paragraph 0138). Therefore, ‘772 recites administering an inhibitor of JunD to a subject having prostate cancer and is therefore in need of treatment. ‘772 teaches “effective amount” refers to the quantity of active therapeutic sufficient to yield a desired therapeutic or preventative response, and will vary with such factors as the particular condition being treated, the physical condition of the patient, the nature of concurrent therapy and the specific formulations employed and the specific structures of the compounds or its derivatives, and the optimum effective amounts can be readily determined by one of ordinary skill in the art using routine experimentation (paragraph 0141). Claims 12,20 and 21 recite wherein clauses that do not provide any additional steps to the active method step to provide additional claim limitations. See claim interpretation above.
Regarding claims 13,22 and 23, ‘772 recites a method of inhibiting the growth of human prostate cancer in a subject comprising administering to the subject an inhibitor of the JunD-AR interaction, wherein the inhibitor is a compound of claim 1 (claims 71-72) which is a compound having the structure of formula I in claim 1. Claims 13,22 and 23 recite wherein clauses that do not provide any additional steps to the active method step to provide additional claim limitations. See claim interpretation above.
Although the reference is silent about inhibiting the expression of c-MYC and c-MYC protein levels and inhibiting the expression of one or more of the recited JunD target genes, it does not appear that the claim language or limitations result in a manipulative difference in the method steps when compared to the prior art disclosure. See Bristol-Myers Squibb Company v. Ben Venue Laboratories, 58 USPQ2d 1508 (CAFC 2001). “It is a general rule that merely discovering and claiming a new benefit of an old process cannot render the process again patentable.” In re Woodruff, 16 USPQ2d 1934, 1936 (Fed. Cir. 1990). Granting a patent on the discovery of an unknown but inherent function would remove from the public that which is in the public domain by virtue of its inclusion in, or obviousness from, the prior art. In re Baxter Travenol Labs, 21 USPQ2d 1281 (Fed. Cir. 1991). See M.P.E.P. 2145. On this record, it is reasonable to conclude that the same patient is being administered the same active agent by the same mode of administration in the same amount in both the instant claims and the prior art reference. The fact that Applicant may have discovered yet another beneficial effect from the method set forth in the prior art does not mean that they are entitled to receive a patent on that method.
Thus, ‘772 teaches, either expressly or inherently implied, each and every limitation of the instant claims.
Conclusion
Claims 12,13 and 20-23 are rejected.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to STEPHANIE L SULLIVAN whose telephone number is (703)756-4671. The examiner can normally be reached Monday-Friday, 7:30-3:30 EST.
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/STEPHANIE L SULLIVAN/Examiner, Art Unit 1635
/ABIGAIL VANHORN/ Primary Examiner, Art Unit 1636
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