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 .
Priority
This Application claims foreign priority to KR10-2021-0166728, filed Nov. 29, 2021 in the Republic of Korea.
Claim Status
Claims 1-9 and 12 are currently pending.
Applicant’s election without traverse of Group III, claims 8-12, in the reply filed on Aug. 4, 2025 is acknowledged.
Claims 8-9 and 12 are active and subject to examination.
Claims 1-7 are withdrawn.
Drawings
The corrected Drawings submitted on Dec. 17, 2025 are acceptable.
Claim Rejections – 35 USC § 103 – Withdrawn – Overcome by Amendment
The rejection of claim(s) 8-10 and 12 under 35 U.S.C. 103 as being unpatentable over Cutshall et al. (Bioorganic & Medicinal Chemistry Letters, 15 (2005), 3374–3379) in view of An et al. (Cancer Res; 73(4) February 15, 2013, 1374-1385) is withdrawn.
The above rejection was overcome by Applicant’s amendments to the claims.
Claim Rejections – 35 USC § 103 – Previously Presented
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
“A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.”
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
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.
The rejection of claim(s) 8-9 and 12 under 35 U.S.C. 103 as being unpatentable over Cutshall et al. (Bioorganic & Medicinal Chemistry Letters, 15 (2005), 3374–3379) in view of An et al. (Cancer Res; 73(4) February 15, 2013, 1374-1385), as applied to claims 8-10 and 12 above, and further in view of Saus et al. (US20140005134A1) citing to CFTR(inh)-172 (PubChem CID 504670, published July 10, 2005) is maintained.
Response to Arguments
The Applicant argues that the present application presents a different mechanism of action than the prior art and therefore a skilled artisan would have had no motivation to apply the teachings of the prior art to the macrophage mediated mechanism of the present Application (Remarks, p. 7-8). These arguments were fully considered but are not persuasive. The Applicant is claiming a method for treating RCC. One of ordinary skill in the art would have a reasonable expectation of success to apply the claimed compound for the treatment of RCC because the prior art teaches that similar compounds should have activity against RCC. The mechanism does not impart patentability. “"[T]he discovery of a previously unappreciated property of a prior art composition, or of a scientific explanation for the prior art’s functioning, does not render the old composition patentably new to the discoverer." Atlas Powder Co. v. IRECO Inc., 190 F.3d 1342, 1347, 51 USPQ2d 1943, 1947 (Fed. Cir. 1999).” (MPEP § 2112.I).
The Applicant argues that one of ordinary skill in the art could not have predicted the specific therapeutic effect of the claimed compounds because Cutshall only discloses compounds which have the same scaffold as the claimed compound (Remarks, p. 8-9). These arguments were fully considered but are not persuasive. “A prima facie case of obviousness may be made when chemical compounds have very close structural similarities and similar utilities.” (MPEP § 2144.09). One of ordinary skill in the art would have a reasonable expectation of success to apply the claimed compound to the treatment of RCC because the claimed compound is known in the art and is known to have a similar utility to the compound of Cutshall (cancer treatment).
The Applicant argues that the Examiner’s argument is based on hindsight reasoning (Remarks, p. 9). 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). The analysis only applies the teachings of the prior art and thus the reconstruction is proper.
Reiterated Rejection
Claim(s) 8-9 and 12 is/are rejected under 35 U.S.C. 103 as being unpatentable over Saus et al. (US20140005134A1) citing to CFTR(inh)-172 (PubChem CID 504670, published July 10, 2005) in view of Cutshall et al. (Bioorganic & Medicinal Chemistry Letters, 15 (2005), 3374–3379) and An et al. (Cancer Res; 73(4) February 15, 2013, 1374-1385).
Claim 8 is directed towards a method of treating renal cell carcinoma (RCC) comprising administering a pharmaceutical composition comprising a DUSP22 inhibitor as an active ingredient to a subject, wherein the DUSP22 inhibitor is the compound of formula 2:
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231
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.
Saus teaches that CFTR-inhibitor-172, which is the compound of formula 2,
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(CFTR(inh)-172, PubChem, p. 1-2),
is an anticancer agent that reduces the viability of lung cancer cells:
“FIG. 7. CFTR inhibition reduces cell viability of A549 cultures treated with T12. A549 cells were seeded on 96-well culture plates and after 4 h were treated with the indicated concentrations of doxorubicin in absence or presence of T12 (50 μM) and/or CFTR-inhibitor-172 (25 μM).”
Saus, Specification, paragraph 0040.
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Saus, Fig. 7.
While Saus does not teach that the cancer is RCC, one of ordinary skill in the art would have a reasonable expectation of success to apply the compound of formula 2 to the treatment of RCC because structural analogs of the compound of formula 2 are known in the art to be DUSP22 inhibitors which have putative activity against RCC.
For example, Cutshall teaches very similar DUSP22 inhibitors such as compound 15a:
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(Cutshall, Table 3, p. 2278) and An teaches Jnk pathway inhibitors for the treatment of clear cell RCC:
Clear cell renal cell carcinomas (RCC), the major histologic subtype of RCC accounting for more than 80% of cases, are typified by biallelic inactivation of the von Hippel–Lindau (VHL) tumor suppressor gene. Although accumulation of hypoxia-inducible factor alpha (HIF-a) is the most well-studied effect of VHL inactivation, direct inhibition of HIFa or restoration of wild-type pVHL protein expression has not proved readily feasible, given the limitations associated with pharmacologic targeting of transcription factors (i.e., HIF-a) and gene replacement therapy of tumor suppressor genes (i.e., VHL). Here, we have established that phosphorylated c-Jun, a substrate of the c-Jun-NH2-kinase (JNK), is selectively activated in clear cell RCC patient specimens. Using multiple isogenic cell lines, we show that HIF-a–independent JNK hyperactivation is unique to the pVHL-deficient state. Importantly, pVHL-deficient RCCs are dependent upon JNK activity for in vitro and in vivo growth. A multistep signaling pathway that links pVHL loss to JNK activation involves the formation of a CARD9/BCL10/TRAF6 complex as a proximal signal to sequentially stimulate TAK1 (MAPKKK), MKK4 (MAPKK), and JNK (MAPK). JNK stimulates c-Jun phosphorylation, activation, and dimerization with c-Fos to form a transcriptionally competent AP1 complex that drives transcription of the Twist gene and induces epithelial–mesenchymal transition. Thus, JNK represents a novel molecular target that is selectively activated in and drives the growth of pVHL-deficient clear cell RCCs. These findings can serve as the preclinical foundation for directed efforts to characterize potent pharmacologic inhibitors of the JNK pathway for clinical translation.
An, Abstract (emphasis added).
Therefore, claim 8 was prima facie obvious at the time of filing.
Claim 9 is directed towards the method of claim 8, wherein the DUSP22 inhibitor inhibits the invasion and metastasis of RCC.
As shown above, Saus teaches that the compound of formula 2 inhibits the viability of cancer cells.
While Saus does not teach that the DUSP22 inhibitor inhibits the invasion and metastasis of RCC, one of ordinary skill in the art would have a reasonable expectation of success to inhibit the invasion and metastasis of RCC with the compound of formula 2 because it is known that inhibition of the JNK pathway can inhibit the invasion and metastasis of RCC.
For example, An teaches that VHL deficient RCC cells have a heightened invasiveness that can be reversed by the pharmacologic inhibition of JNK:
Moreover, compared with VHLþ cells, pVHL-deficient cells showed markedly heightened invasiveness in a Matrigel chamber, a finding that further supports the notion of EMT induced by pVHL deficiency (Fig. 6C and Supplementary Fig. S4B) that has been described (26–28). Although these prior studies have implicated HIF-a as a pivotal factor in the EMT observed in pVHL-deficient RCCs, we investigated the potential for JNK/AP1 to function in a parallel pathway to mediate EMT in this context.
RNAi with c-Jun–specific siRNA reversed the mesenchymal cadherin expression pattern in VHLlow cells (Fig. 6D). Similar effects on cadherin expression were observed when JNK-specific shRNA was introduced (Fig. 6E). In pVHL deficient cells, the JNKi induced a dose- and time-dependent reversion of the "cadherin switch" back to that of VHLþ cells (Fig. 6F and Supplementary Fig. S5). Similarly, the heightened invasiveness of pVHL-deficient cells was reversed by the JNKi as well as c-Jun–specific siRNA (Fig. 6G and H and Supplementary Fig. S6).
An, col. 1, p. 1383.
Therefore, claim 9 was prima facie obvious at the time of filing.
Claim 12 us directed towards the method of claim 8, wherein the RCC is clear cell RCC.
While Saus does not teach that the RCC is clear cell RCC, one of ordinary skill in the art would have a reasonable expectation of success to treat clear cell RCC because An specifically teaches that clear cell RCC is responsive to JNK inhibitors.
Therefore, claim 12 was prima facie obvious at the time of filing.
Given the above teachings, the invention as a whole was prima facie obvious at the time of filing.
Conclusion
No claim is found to be allowable.
THIS ACTION IS MADE FINAL. Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any extension fee pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to HEATHER DAHLIN whose telephone number is (571)270-0436. The examiner can normally be reached 9-5.
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Jeffrey Lundgren can be reached on (571) 272-5541. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/HEATHER DAHLIN/Examiner, Art Unit 1629
/JEFFREY S LUNDGREN/Supervisory Patent Examiner, Art Unit 1629
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