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 .
Status of Claims
Claims 1-47 are pending.
Priority
Instant application 18/274,441, filed 07/26/2023 claims priority as follows:
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Information Disclosure Statement
All references from IDS(s) received 10/03/2023, 10/04/2023, and 05/07/2025 have been considered unless marked with a strikethrough.
Election/Restrictions
Applicant’s election of Group II, claims 1-28 and 33-43; and the species compound 478 and cancer NSCLC in the reply filed on 01/15/2026 is acknowledged. Because applicant did not distinctly and specifically point out the supposed errors in the restriction requirement, the election has been treated as an election without traverse (MPEP § 818.01(a)).
The combination of elected species (compound 478 and cancer NSCLC) reads on claims 1-4, 7, 9-14, 19-28, 33-40.
Examination will begin with the combination of elected species. In accordance with MPEP 803.02, if upon examination of the elected species, no prior art is found that would anticipate or render obvious the instant invention based on the elected species, the search of the Markush-type claim will be extended. If prior art is then found that anticipates or renders obvious the non-elected species, the Markush-type claim will be rejected. Please note that the prior art search will not be extended unnecessarily to cover all non-elected species. Should Applicant overcome the rejection by amending the claim, the amended claim will be examined again. The prior art search will be extended to the extent necessary to determine patentability of the Markush-type claim. In the event prior art is found during further examination that renders obvious or anticipates the amended Markush-type claim, the claim will be rejected and the action made final.
The elected species compound 478 and cancer NSCLC were searched and applicable art was identified. The entire scope of claims 1-4, 7, 9-14, 19-28 and 33-40 has not yet been examined in accordance with Markush search practice. See MPEP 803.02.
Claims 5-6, 8, 15-18, and 29-31 and 41-47 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention/species, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 01/15/2026.
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 1-4, 7, 9-14, 19-28 and 33-38 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for treating a KRas G12C-associated cancer, particularly KRas G12C-mutated NSCLC, does not reasonably provide enablement for treating the broad genus of “cancer” or the extensive list of cancers recited in claim 38. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to practice the invention commensurate in scope with these claims.
Pursuant to In re Wands, 858 F.2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988), one considers the following factors to determine whether undue experimentation is required: (1) The breadth of the claims, (2) The nature of the invention, (3) The state of the prior art, (4) The level of one of ordinary skill, (5) The level of predictability in the art, (6) The amount of direction provided by the inventor, (7) The existence of working examples and (8) The quantity of experimentation needed to make or use the invention based on the content of the disclosure.
Breadth of the claims:
The claims are broadly directed to the use of a combination of a MEK inhibitor and KRAS G12C inhibitor of formula (I) to treat cancer. The breadth of claim 1 is extreme. The term “cancer” encompasses hundreds of distinct malignancies that differ fundamentally in tissue of origin, molecular driver pathways, genetic landscape, tumor microenvironment, immune context, and drug responsiveness. Even the lengthy enumeration of specific cancer types in claim 38 does not meaningfully narrow the scope of the claim; the list includes cancers from virtually every organ system, including cancers where KRAS G12C mutations are either extremely rare or essentially unknown.
Nature of the invention:
The invention is drawn to the administration of a combination of a MEK inhibitor and a KRAS G12C compound of Formula (I):
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to treat cancer in a subject. The combination is mechanistically targeted at KRAS G12C-driven signaling. The KRAS G12C inhibitors of the invention covalently and irreversibly bind to KRAS G12C (Specification, para. [0053]). The rationale for combining them with a MEK inhibitor rests on synergistic blockade of the RAS-MAPK pathway (para. [0090-0091]. Cancers that do not harbor a KRAS G12C mutation would not be expected to respond to a KRAS G12C-targeted inhibitor, because the drug’s target is simply absent.
State of the prior art and predictability in the art:
At the time of filing, KRAS G12C mutations are predominantly found in non-small cell lung cancer (NSCLC), accounting for approximately 13% of NSCLC carcinomas. See KIM et al. (Cell, vol. 183, no. 4, Nov. 2020, pp. 850–59). They also occur in a smaller fraction of colorectal cancers and pancreatic cancers (KIM, pages 850-851, “KRAS Activation in Cancer”):
“KRAS mutations are found predominantly in lung (approximately 25% of cases and estimated to affect 57,000 patients per year in the US), pancreatic (∼95% of cases and ∼54,000 patients), and colorectal (∼35% of cases and ∼36,000 patients) cancer… In addition to being found in ∼13% of patients with lung adenocarcinoma, the KRAS(G12C) allele is found at a lower frequency in those with colorectal cancer (∼3%), uterine cancer (∼2%), mesothelioma (∼1%), pancreatic cancer (<1%), cervical cancer (<1%), bladder cancer (<1%) and gastric cancer (<1%).”
The prior art does not support the extreme breadth of cancers recited in the instant claims. While MEK inhibitors have some broader activity across RAS-MAPK pathway-activated tumors, the claimed combination specifically requires a KRAS G12C inhibitor, and the synergistic rationale depends on the presence of the KRAS G12C target, which is largely only present in NSCLC and sporadically found in colorectal, uterine, pancreatic, cervical, bladder, gastric cancers or mesothelioma.
Pharmacological activity in general is a very unpredictable area. Note that in cases involving physiological activity such as the instant case, “the scope of enablement obviously varies inversely with the degree of unpredictability of the factors involved.” See In re Fisher, 427 F.2d 833, 839, 166 USPQ 18, 24 (CCPA 1970). Moreover, cancer treatment is a field of high unpredictability. The instant specification itself acknowledges this at paras. [0006]-[0007], noting that the relative potency of any given KRAS G12C inhibitor varies between KRAS mutant cell lines, that the reasons for this variation are not fully understood, and that certain cell lines appear to possess differing intrinsic resistance.
Level of ordinary skill in the art:
The person of ordinary skill would hold an advanced degree in oncology, pharmacology, or a related discipline, and possess several years of professional experience, with some familiarity for KRAS-targeted therapeutics and the MAPK signaling pathway. Such a person would understand that the KRAS G12C inhibitors described in the instant application are mutation-specific covalent inhibitors and would not reasonably expect them to treat cancers lacking the KRAS G12C mutation.
The amount of direction provided and working examples:
The specification provides direction concentrated on KRAS G12C-mutant cancer cell lines. The background discussion (para. [0002]-[0007]) frames the invention in the context of KRAS G12C-driven oncology. The specification provides no mechanistic rationale, data, or guidance for treating cancers that lack KRAS G12C mutations with the claimed combination. There is no discussion of how a KRAS G12C inhibitor would provide therapeutic benefit to patients whose tumors lack the drug’s molecular target.
The working examples include Example A (in vitro studies with KRAS G12C mutant cell lines) and Example B (the only disclosed in vivo study, in mice inoculated with H2122, an NSCLC mutant cell line). Every working example involves a KRAS G12C-mutant lung, colorectal, cervical, or bladder cancer cell line. There are no working examples in pancreatic cancer, any hematological malignancy, any sarcoma, any CNS tumor, or any of the other dozens of other cancer types enumerated in claim 38.
Quantity of experimentation needed to use the invention based on the content of the disclosure:
The quantity of experimentation needed is undue experimentation. One of skill in the art would need to determine which of the claimed cancer types even harbor KRAS G12C mutations at a meaningful frequency and conduct in vitro testing to determine whether the combination shows synergistic activity in those mutants. For non-KRAS G12C cancers the experimentation would be essentially futile, as the molecular target of the KRAS G12C inhibitor is absent. Nevertheless, to practice the full scope of claim 1, one would need to confirm this experimentally for each cancer type embraced by the claims.
A person having ordinary skill in the art at the time the invention was made would be faced with an undue amount of experimentation to use the combination of the invention according to the full scope of the claimed method.
Therefore claims 1-4, 7, 9-14, 19-28 and 33-38 are rejected.
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.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claims 1-4, 7, 9-14, 19-24, 28, 33, and 38-40 are rejected under 35 U.S.C. 102(a)(2) as being anticipated by PACHTER (WO 2021154929 A1; cited in IDS; filed 28 January 2021).
PACHTER discloses combination therapies for treating cancer, particularly the combination of a KRAS G12C inhibitor and a FAK and/or MEK or dual RAF/MEK inhibitor (title, abstract). PACHTER discloses the particular KRAS G12C inhibitor MRTX849, aka adagrasib, which is applicant’s elected species compound 478 (see e.g. page 9 and claims 4 and 6). PACHTER also discloses MEK inhibitors including binimetinib, cobimetinib, trametinib, selumetinib or RO5126766 (also known as “CH5126766 or VS-6766”) (see e.g. page 2, lines 20-28 and claim 8). In the examples, PACHTER demonstrates synergy between VS-6766, which is a MEK inhibitor, and the KRAS G12C inhibitor MRTX849 in NSCLC cell lines (see e.g. page 5, lines 1-21; and Example 1, pages 32-35; FIGs 1-7).
PACHTER therefore anticipates instant claims 1-4, 7, 9-14, 19-23, and 38-40.
For claim 24, PACHTER discloses the administration of VS-6766 and adagrasib on the same day (see e.g. page 32, line 31 to page 33, line 7).
For claim 28, PACHTER discloses that administration of VS-6766 and adagrasib was synergistic in reducing viability of KRAS G12C mutant NSCLC cell lines (e.g. page 34, lines 6-14; FIG. 1A). The results recited in claim 28 (i.e. increase in survival or tumor growth regression or inhibition relative to treatment with only KRAS G12C inhibitor) would necessarily occur in view of the synergy demonstrated by PACHTER. See also page 22, lines 7-16, which states “In some embodiments, the method increases the average length of survival, increases the average length of progression-free survival, and/or reduces the rate of recurrence of subjects treated with the combinations described herein in a statistically significant manner”.
For claim 33, PACHTER anticipates administering to a subject the combination of a KRAS G12C inhibitor reading on applicant’s elected species (adagrasib) and a MEK inhibitor (see claim 7 or 35 of PACTHER); and discloses that the combination increased sensitivity of NSCLC cells to KRAS G12C inhibitor adagrasib (e.g. page 34, lines 6-14; FIG. 1A).
Claim Rejections - 35 USC § 103
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.
Claims 1-4, 7, 9, 14, 23-28, and 33-40 are rejected under 35 U.S.C. 103 as being unpatentable over ENGSTROM (WO 2020055760 A1; published 19 March 2020; cited in IDS).
ENGSTROM discloses combination therapies for treating KRas G12C cancers (title, abstract) comprising a combination of a Raf family kinase inhibitor and a KRAS G12C inhibitor. ENGSTROM discloses a combination of a KRAS G12C inhibitor of Formula (I) (including the elected species compound adagrasib) and RO5126766 for use in the treatment of cancer (see abstract; para. [0007], [0008], [0038], [0040], [0041], [0087], [0184]; and claims 1, 57-62, 67-85). R05126766 is a dual Raf/Mek inhibitor, and is being interpreted as reading on “MEK inhibitor” recited by the instant claims, particularly because dependent claims 9, 14, and 23 recite RO5126766.
ENGSTROM requires the selection of R05126766 from a list of 11 compounds to arrive at a method reading on instant claim 1.
Finding of prima facie obviousness
The Supreme Court in KSR Int'l Co. v. Teleflex Inc., 550 U.S. 398, 415-421, 82 USPQ2d 1385, 1395-97 (2007) identified a number of rationales to support a conclusion of obviousness which are consistent with the proper "functional approach" to the determination of obviousness as laid down in Graham. See MPEP 2143.
Examples of rationales that may support a conclusion of obviousness include:
(A) Combining prior art elements according to known methods to yield predictable results;
(B) Simple substitution of one known element for another to obtain predictable results;
(C) Use of known technique to improve similar devices (methods, or products) in the same way;
(D) Applying a known technique to a known device (method, or product) ready for improvement to yield predictable results;
(E) "Obvious to try" – choosing from a finite number of identified, predictable solutions, with a reasonable expectation of success;
(F) Known work in one field of endeavor may prompt variations of it for use in either the same field or a different one based on design incentives or other market forces if the variations are predictable to one of ordinary skill in the art;
(G) Some teaching, suggestion, or motivation in the prior art that would have led one of ordinary skill to modify the prior art reference or to combine prior art reference teachings to arrive at the claimed invention.
Applying at least KSR example rationale (G), it would have been prima facie obvious to select the combination of a compound of Formula (I), particularly adagrasib (taught in e.g. para. [0125] or claim 60 of ENGSTROM, and the dual Raf/Mek inhibitor R05126766 (taught in e.g. para. [0145] or claim 62 of ENGSTROM). ENGSTROM teaches that the combination therapy of a KRas G12C inhibitor and a Raf kinase inhibitor (which includes the dual Raf/Mek inhibitor R05126766 specifically contemplated by ENGSTROM) synergistically increases the potency of KRas G12C inhibitors resulting in improved efficacy (see e.g. page 2, para. [0007]).
Moreover, the concept of the present invention is implied by teachings in ENGSTROM. ENSTROM specifically teaches that the combination of KRas G12C inhibitors and a Raf family kinase inhibitor effectively blocks upstream signaling from KRas G12C, wild type KRas and/or N-Ras to shut down further Mek and Erk signaling through Raf thereby blocking this potential resistance mechanism and enhancing the overall tumor response. Therefore, dual inhibition of Raf and the direct downstream target of Raf, which is Mek, in combination with a KRas G12C inhibitor would have been prima facie obvious in view of ENGSTROM’s teachings.
Therefore claims 1-4, 7, 9, 14, and 23 are obvious over ENGSTROM.
For claims 24-25, ENGSTROM teaches same day (claim 67) or different day (claim 68) administration of the KRAS G12C and Raf kinase inhibitor. Therefore claims 24-25 are obvious over ENGSTROM.
For claims 26-27, ENGSTROM teaches that (para. [0141]) oncology drugs are typically administered at the maximum tolerated dose (“MTD”), which is the highest dose of drug that does not cause unacceptable side effects. In one embodiment, the KRas G12C inhibitor and the Raf family kinase inhibitor are each dosed at their respective MTDs. Therefore claims 26-27 are obvious over ENGSTROM.
For claim 28, ENGSTROM teaches that (claim 71 or e.g. para. [0079]) the therapeutically effective amount of the combination of the Raf family kinase inhibitor and the KRAS G12C inhibitor results in an increased duration of overall survival, an increased duration of progression free survival, an increase in tumor growth regression, an increase in tumor growth inhibition or an increased duration of stable disease in the subjects relative to treatment with only the KRas G12C inhibitor. Therefore claim 28 is obvious over ENGSTROM.
For claim 33, ENSTROM teaches the steps of administering the KRAS G12C inhibitor adagrasib in combination with R05126766 to a subject undergoing treatment for cancer, and teaches that the invention provides for synergistically increasing the sensitivity of a KRas G12C-associated cancer to the KRas G12C inhibitor (see e.g. para. [0039] and para. [0040]). Therefore claim 33 is obvious over ENGSTROM.
For claims 34-37, ENGSTROM teaches an amount of the KRas G12C inhibitor ranging between about 0.01 to 100 mg/kg per day or about 0.1 to 50 mg/kg per day (claims 76-77) and teaches an amount of the Raf kinase inhibitor ranging between about 0.01 to 100 mg/kg per day or about 0.1 to 50 mg/kg per day (claims 78-79). Therefore claims 34-37 are obvious over ENGSTROM.
For claims 38-40, ENGSTROM teaches cancer and KRas G12C-associated cancer (e.g. para. [0036]). Note also that ENSTROM teaches NSCLC (claim 82) and provides an in vivo example demonstrating that the invention is effective in mice inoculated with NCI-H2122 cells, which are a human non-small cell lung cancer (NSCLC) model (Example B; Table 1). Therefore claims 38-40 are obvious over ENGSTROM.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 1-4, 7, 9-14, 19-28, 33-40 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-9 of U.S. Patent No. 12,208,099 (“the ‘099 patent”) in view of PACHTER (WO 2021154929 A1; cited in IDS; filed 28 January 2021).
The ‘099 patent is in the same family as ENGSTROM cited above. The teachings of PACHTER are disclosed above and those teachings are incorporated herein by reference.
The ‘099 patent recites:
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The claimed KRAS G12C inhibitor is applicant’s elected species. The difference between the ‘099 patent and the instant claims is that the ‘099 patent recites administering the Raf kinase inhibitor Lifirafenib instead of a MEK inhibitor.
However, as set forth above, PACHTER demonstrates synergy between VS-6766, which is a Raf inhibitor, and the KRAS G12C inhibitor MRTX849 in NSCLC cell lines (see e.g. page 5, lines 1-21; and Example 1, pages 32-35; FIGs 1-7).
Applying KSR example rationale (B), it would have therefore been prima facie obvious to substitute the Raf inhibitor lifirafenib with VS-6766 taught by PACHTER in the method of treating non-small cell lung cancer recited by the ‘099 patent.
Accordingly, claims 1-4, 7, 9-14, 19-28, 33-40 are unpatentable over the ‘099 patent in view of PACHTER.
Claims 1-4, 7, 9-14, 19-28, 33-40 rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-39 of copending Application No. 18/906,104 (“the ‘104 application”) in view of PACHTER (WO 2021154929 A1; cited in IDS; filed 28 January 2021).
The ‘104 application is in the same family as ENGSTROM and claims priority to the ‘099 patent cited above. The teachings of PACHTER are disclosed above and those teachings are incorporated herein by reference.
The ‘104 application recites:
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The ‘104 application recites the Raf kinase inhibitor RO5126766 aka VS-6766 (see e.g. claim 29 of the ‘104 application). Additionally, as set forth above, PACHTER demonstrates synergy between VS-6766, which is a dual Raf/Mek inhibitor, and the KRAS G12C inhibitor MRTX849 in NSCLC cell lines (see e.g. page 5, lines 1-21; and Example 1, pages 32-35; FIGs 1-7).
Applying KSR example rationale (G), it would have therefore been prima facie obvious to administer a combination of a KRAS G12C inhibitor of Formula (I) and the Raf/Mek inhibitor VS-6766 recited by the ‘104 application and taught by PACHTER in the method of treating non-small cell lung cancer recited by the ‘104 application.
Accordingly, claims 1-4, 7, 9-14, 19-28, 33-40 are unpatentable over the ‘104 patent in view of PACHTER.
This is a provisional nonstatutory double patenting rejection.
Conclusion
Claims 1-4, 7, 9-14, 19-28, 33-40 are rejected. Claims 5-6, 8, 15-18, and 29-31 and 41-47 are withdrawn.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Kyle Nottingham whose telephone number is (571)270-0640. The examiner can normally be reached M-F from 10:00 am - 6:00 pm.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Clinton Brooks can be reached at (571) 270-7682. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/K.N./Examiner, Art Unit 1621
/CLINTON A BROOKS/Supervisory Patent Examiner, Art Unit 1621