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 .
Claims 7, 12-17, 29-31, 39-49, submitted on 22 November 2023, represent all claims currently under consideration.
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.
Priority
This application is a continuation of PCT/US2022/016270, filed 14 February 2022, which claims priority to provisional US 63/149,944, filed on 16 February 2021. The effective filing date is 16 February 2021.
Information Disclosure Statement
One Information Disclosure Statement (IDS), filed 22 November 2023, is acknowledged and has been considered.
Claim Objections
Claim 7 is objected to because of the following informalities: “QD” should be defined prior to the first usage in the claim limitations. Appropriate correction is required.
Claim 14 is objected to because of the following informalities: “PIK3CA” should be defined prior to the first time it is used in the claim limitation. Appropriate correction is required.
Claim 14 is objected to because of the following informalities: There appears to be an errant semi-colon after “R88Q”. Appropriate correction is required.
Claim Rejections - 35 USC § 112(b)
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 42 and 43 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention. Claim 42 recites the limitation "GDC-0007" in Line 2. There is insufficient antecedent basis for this limitation in the claim. Claim 43 recites the limitation "GDC-007" in Line 1. There is insufficient antecedent basis for this limitation in the claim. The Examiner is assuming these are typographic errors, and should read “GDC-0077”.
Claim 42 is rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention. Claim 42 has the limitation of “does not substantially alter the exposure of either agent in the patient”. The specification does not define what encompasses “substantially”, leading to subjectivity in what exactly “substantially alter” means with respect to the exposure of each agent, causing the metes and bounds of the claim to be undefined, and therefore, indefinite.
Claim 16 is rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention. Claim 16 recites the limitations "E726K" and “M1043L” in Line 4. There is insufficient antecedent basis for this limitation in the claim as Claim 15 does not claim these specific mutations.
Claim Rejections - 35 USC § 112(d)
The following is a quotation of 35 U.S.C. 112(d):
(d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
The following is a quotation of pre-AIA 35 U.S.C. 112, fourth paragraph:
Subject to the following paragraph [i.e., the fifth paragraph of pre-AIA 35 U.S.C. 112], a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
Claims 16 and 17 are rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends. Claims 16 and 17 recite the limitations of mutations to PIK3CA which includes E726K and M1043L. Claims 16 and 17 depend on Claim 15, and Claim 15 does not contain these mutations within the limitations, and as such, Claims 16 and 17 are broader than, and do not further limit, Claim 15. Applicant may cancel the claim(s), amend the claim(s) to place the claim(s) in proper dependent form, rewrite the claim(s) in independent form, or present a sufficient showing that the dependent claim(s) complies with the statutory requirements.
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.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 7, 12-17, 29-31, 39-43, and 45-49 are rejected under 35 U.S.C. 103 as being unpatentable over Greene (WO 2020/023297; Publication Date: 30 January 2020) in view of Goodacre (WO 2017/216280; Publication Date: 21 December 2017), Harmon (WO 2021/178846; Publication Date: 10 September 2021; Priority to 6 March 2020), Dumont (Chinese Journal of Cancer, 2012 July, 31, 7, 327-334), and Loftsson (Essential Pharmacokinetics, Chapter 5-Pharmacologic Response and Drug Dosage Adjustments, Pages 119-130, Volume 1, 2015).
Greene (See IDS, 22 November 2023) discloses methods of treating PI3KCA-mutant cancer patients by administering metformin and GDC-0077 (Abstract). Non-clinical studies demonstrate that GDC-0077 specifically degrades mutant p110α, inhibits proliferation and induces apoptosis in PIK3CA-mutant breast cancer lines, inhibits tumor growth in human breast xenograft models harboring PIK3CA mutations, and reduces downstream PI3K-pathway markers, including pAKT, pPRAS40, and pS6 (Page 9, Lines 9-13). A multi-center, international, open-label, Phase I trial is designed to evaluate the safety, tolerability, and pharmacokinetics of GDC-0077 administered orally as a single agent in patients with locally advanced or metastatic PIK3CA-mutant solid tumors, including breast cancers for the treatment of locally advanced or metastatic PIK3CA-mutant HR positive/EGFR2 negative breast cancer (Page 13, Lines 6-11). Target population inclusion and exclusion criteria are determination of PIK3CA-mutant tumor status based on results from archival or fresh tumor tissue or ctDNA. PIK3CA mutants are defined as follows: H1047R/Y/L, E542K, E545K/D/GΑ, Q546/K/R/E/L, N345K, C420R, G1049R, R88Q, M1043I (Page 13, Lines 12-17). Women of childbearing potential (i.e., pre-menopausal) can be treated using this method following an agreement to remain abstinent or use a non-hormonal contraceptive method with a failure rate of <1% per year, and agreement to refrain from donating eggs during treatment period and for at least 60 days after the last dose of study treatment (Page 14, Lines 29-33). In an exemplary embodiment, the therapeutically effective amount of GDC-0077 is about 1 mg to about 15 mg, administered once per day. In an exemplary embodiment, the therapeutically effective amount of GDC-0077 is about 9 mg. In an exemplary embodiment, the patient has locally advanced or metastatic PIK3CA-mutant solid tumors. In an exemplary embodiment, the patient has locally advanced or metastatic PIK3CA-mutant hormone-receptor positive breast cancer. In an exemplary embodiment, the breast cancer is HER2-negative (Page 24, Lines 12-27). In an exemplary embodiment, the patient is administered an additional therapeutic agent. In an exemplary embodiment, the additional therapeutic agent is a selective estrogen receptor modulator (SERM) or a selective estrogen-receptor degrader (SERD) (Page 25, Line 20, 31-32).
Greene fails to disclose GDC-9545 as the selective estrogen-receptor degrader.
Goodacre (See IDS, 22 November 2023) discloses compounds with estrogen receptor modulation activity or function, compositions and medicaments comprising these compounds, as well as methods of using such ER modulators, alone and in combination with other therapeutic agents, for treating diseases or conditions that are mediated or dependent upon estrogen receptors (Abstract). Recently, the next generation whole genome and targeted sequencing has identified ESR1 (estrogen receptor alpha gene) mutations in up to 20% of tumors from patients with advanced breast cancer who have progressed on endocrine therapies. These mutations can confer high basal activity of the apo-receptor rendering them ligand independent and thus active in the setting of low estradiol. There is a need for therapies that target ER signaling with robust activity in the setting of progressive disease including the subset of patients harboring ESR1 mutant tumors. In some embodiments, compounds of the invention are used in methods for treating a hormone resistant ER positive breast cancer in a patient characterized as having a mutation in the ESR1 gene (Page 20, Line 23- Page 24, Line 12). Given the central role of ER-α in breast cancer development and progression, compounds disclosed herein are useful in the treatment of breast cancer, either alone or in combination with other agents that can modulate critical pathways in breast cancer, including those that target the PI3K/AKT/mTOR axis (Page 21, Lines 13-17). Formula I compounds disclosed herein are useful in the treatment of breast cancer, either alone or in combination with other agents used to treat cancer, including PI3K inhibitors (Page 21, Lines 18-24). In some embodiments, compounds disclosed herein are used to treat HR positive metastatic breast cancer following disease progression following anti-estrogen therapy (Page 22, Lines 22-24). In some embodiments, the compounds disclosed herein are used to treat cancer in a mammal wherein the mammal is chemotherapy-naïve (Page 23, Lines 3-4). Compound A (Table 2) is GDC-9545 (Page 47), and has an EC50 against ERα of 0.000027 µM. A dose to treat human patients may range from about 10 mg to about 1000 mg of compounds of the invention. A dose may be administered once a day (QID), twice a day (BID), or more frequently, depending on the pharmacokinetic and pharmacodynamic properties. In addition, toxicity factors may influence the dosage and administration regimen. When administered orally, the pill, capsule, or tablet may be ingested daily or less frequently for a specified period of time. The regimen may be repeated for a number of cycles of therapy (Page 48, Lines 3-10). Suitable dosages for co-administered agents are those presently used and may be lowered due to the combined action of the newly identified agent and other therapeutic agents or treatments. A synergistic effect may be attained when the active ingredients are co-formulated and administered or delivered simultaneously in a combined, unit dosage form; delivered by alternation or in parallel as separate formulations; or by some other regimens (Page 56, Lines 25-33). In some embodiments, a compound of the invention is used in combination with a PI3K inhibitor (Page 58, Lines 18-20). Claim 35 claims the compound for use or the composition for use in the treatment of ER-related disease, including breast cancer, in combination with a PI3K/mTOR pathway inhibitor.
Harmon discloses methods of treating estrogen receptor-associated diseases, disorders, and conditions (Abstract). In some embodiments, the present disclosure teaches that one or more of the following compounds may be particularly useful as described herein, including GDC-9545 (Paragraph 0021). The present disclosure provides various effective dosing regimens for certain complete estrogen antagonists as described herein. The present disclosure provides methods for treating an ER-associated disease disorder or condition by administering such complete estrogen receptor antagonists according to such regimen (Paragraph 0024). Other selective ER degraders or antagonists such as fulvestrant suffer from numerous deficiencies, including poor bioavailability (Paragraph 0118). In some embodiments, a complete estrogen receptor antagonist is GDC-9545 (Paragraph 0127). Additionally, in some embodiments, particularly useful ER antagonist agents are further characterized by one or more of the following: oral bioavailability and a long half-life, and blood brain barrier penetration (Paragraph 0163). In some embodiments, an ER-associated disorder is a cancer. In some embodiments, an ER-associated disorder is a breast cancer (Paragraph 0165). The present disclosure provides dosing regimens where compounds reported herein are dosed at levels and/or according to regimens corresponding to those exemplified herein for Compound 1. That is a dosage refers to a particular ratio of compound weight per kilogram of subject. In some embodiments, the human subject is provided a dosage that corresponds to 3 through 30 mg/kg in a mouse (Paragraph 0176). In some embodiments, a composition comprising a complete estrogen receptor antagonist is administered as a unit dosage form. In some embodiments, a composition comprising a complete estrogen receptor antagonist is administered in the form of a capsule or a tablet (Paragraph 0177). In some embodiments, a composition comprising a complete estrogen receptor antagonist is administered as a daily dose (QD). In some embodiments, a composition comprising a complete estrogen receptor antagonist is administered as a twice daily dose (BID) (Paragraph 0178). The present disclosure encompasses the recognition that a combination of certain agents can beneficially be used to completely antagonize the estrogen receptor. Accordingly, in some embodiments the present disclosure provides a method for treating a subject suffering from an ER-associated disorder (e.g., a cancer or breast cancer) comprising administering a complete estrogen receptor antagonist and an anti-cancer agent. In some embodiments, the anti-cancer agent is a PI3KCA inhibitor (Paragraph 0180). It is understood that administering a complete estrogen receptor antagonist and an anti-cancer agent described herein can be administered simultaneously or separately (Paragraph 0184).
Dumont provides an overview of mutations in PIK3CA. Mutations in the gene PIK3CA that encodes the p110α catalytic subunit of the PI3K enzymes result in cell proliferation and resistance to apoptosis in vitro and induce breast tumors in transgenic mice. These data underscore the role of this pathway during oncogenesis. Thus, an ongoing large-scale effort is underway to develop clinically active drugs that target elements of the PI3K pathway. However, conflicting data suggest that gain of function PI3KCA mutations may be associated with either a favorable or a poor clinical outcome, compared with the wild-type PIK3CA gene. The authors performed a systematic review of breast cancer clinical studies. Upon evaluation, the data showed that patients with tumors harboring a PI3KCA mutation have a better clinical outcome than those with a wild-type PIK3CA gene. This improved prognosis may pertain only to patients with mutations in the kinase domain of p110α and to postmenopausal women with ER+ breast cancer. These mutations may interfere with metastasis, induce senescence, increase early tumor diagnosis by modification of the actin cytoskeleton in tumor cells, and may be a favorable predictive factor for response to hormonal therapy, giving a therapeutic advantage to these patients. An improved understanding of the clinical impact of PIK3CA mutations is critical for the development of optimally personalized therapeutics against breast cancer (Abstract).
The prior references fail to specifically disclose the claimed dosage regimen.
Loftsson teaches dosing of pharmaceuticals and that drugs are administered on the basis of their average pharmacokinetic parameters in normal patients populations (Page 119). Many drugs have a wide therapeutic window and can easily remain within their therapeutic window (Page 119). Pharmacodynamics describes the relationship between drug concentration at the receptor and the drug effect, with the receptor being a well-defined place within the body, or on or within the surface of a microorganism within the body (Section 5.3, Pharmacodynamics). The relationship between drug concentration and drug effect is shown in Figure 5.2A; at high drug concentrations, the drug effect approaches a maximum value where 100% drug response is obtained. At this concentration, virtually all receptors have formed a drug-receptor complex. This relationship is sigmoidal (Section 5.3, Pharmacodynamics).
Greene, Goodacre, Harmon, Dumont, and Loftsson are considered analogous to the claimed invention as all are involved in the study and treatment of disease using pharmaceuticals. Therefore, it would have been prima facie obvious to one of ordinary skill in the art the time of the effective filing date of the instant application to combine GDC-0077 and GDC-9545 in one treatment regimen for the treatment of locally advanced breast cancer (laBC) or metastatic breast cancer (mBC) in view of the cited teachings. Greene demonstrates that GDC-0077 is useful in the treatment of ER+/HER2- breast cancer with PI3K mutations, including those claimed in the examined application, and states that this method can further comprise a selective estrogen receptor modulator/degrader. Both Goodacre and Harmon teach the use of the SERM/SERD GDC-9545 for the treatment of ER+/HER2- breast cancer, and this can be done in combination with a PI3K inhibitor. Dumont demonstrates that screening for these mutations allows for determination of patients which may favorably respond to treatment, providing a motivation to screen for patients with these mutations prior to treatment. The combination of GDC-0077 and GDC-9545 for the treatment of these cancers is prima facie obvious combination of prior art elements according to known methods to yield predictable results (See MPEP § 2143 I (A)); both GDC-0077 and GDC-9545 are known in the art to be useful for the treatment of the claimed forms of breast cancer, and the prior art teaches that each class of these compounds can be used in combination with one another to treat these cancers. The artisan would recognize this, and could arrive at combining these two known drugs for the treatment of these cancers.
Regarding the specific dosages which are claimed, the optimization of dosages of each of these compounds is prima facie obvious in view of Greene, Goodacre, and Harmon, and further in view of Loftsson. Greene, Goodacre, and Harmon each establish basic dosing regimens for each compound individually, while Loftsson shows that in the field of medicine and pharmacology, dosage adjustments are a routine part of the development of treatments for patients suffering from various conditions, and would be obvious to the artisan, who is likely a medical doctor who has extensive training in the administration of chemotherapeutics.
Regarding Claim 12, the method described by Greene is taught for use in premenopausal women, assuming that they take appropriate precautions to prevent pregnancy. Thus, it would be obvious to apply the claimed method in the treatment of premenopausal women, as Greene demonstrates this method is safe for these women as long as precautions are followed.
Regarding Claim 13, Goodacre states that the efficacy of anti-ER drugs can be dependent upon the mutation status of the estrogen receptor, and thus, it would be obvious to screen for mutations in the target of interest prior to initiation of treatment. Moreover, it is routine in cancer treatment to screen the targets of interest for potential mutations that may confer sensitivity or chemoresistance towards treatments.
Regarding Claims 29-31 and 39-41, it would be obvious to apply these treatments to these specific patient populations. Patients previously treated with other chemotherapeutics, such as CDK4/6 inhibitors, fulvestrant, anastrozole, exemestae, or letrozole, would be a population which did not respond to these treatments, and thus, the artisan would recognize that another treatment method is necessary. GDC-9545, as taught by Harmon, has favorable pharmacokinetics compared to other estrogen modulators such as fulvestrant, providing a motivation to utilize this method.
Regarding Claim 42, determining the appropriate dosages for each compound and the timing of each dosage would ensure that the administration of each compound does not alter the exposure of either agent within the patient, and would be considered part of routine dosage optimization, which as described previously, would be obvious for the artisan due to their training in dosage administration.
Regarding Claims 45 and 46, it would be obvious to co-formulate these two compounds together in a single pharmaceutical composition. It flows from the prior art as it would be obvious to administer these compounds together, and thus, co-formulating these compounds would ensure consistent dosage and administration to the patient, and improve patient compliance.
Claims 7, 12-17, 29-31, and 39-49 are rejected under 35 U.S.C. 103 as being unpatentable over Greene (WO 2020/023297; Publication Date: 30 January 2020) in view of Goodacre (WO 2017/216280; Publication Date: 21 December 2017), Harmon (WO 2021/178846; Publication Date: 10 September 2021; Priority to 6 March 2020), Dumont (Chinese Journal of Cancer, 2012 July, 31, 7, 327-334), Loftsson (Essential Pharmacokinetics, Chapter 5-Pharmacologic Response and Drug Dosage Adjustments, Pages 119-130, Volume 1, 2015), Penault-Liorca (Pathology, 49, 2, February 2017, 166-171), and Ma (Molecular Cancer Research, 8(10), October 2010).
The teachings of Greene, Goodacre, Harmon, Dumont, and Loftsson are previously described and are fully incorporated into this rejection.
The previous teachings fail to specifically disclose testing a patient for mutations in Ki67 or prostaglandin receptors.
Penault-Liorca provides a review of Ki67 in breast cancer. Ki67 is principally used for estimation of prognosis and guiding the decision on adjuvant treatment choice, as well as for prediction of response to neoadjuvant treatment in ER+/HER2- breast cancer. In ER-/HER2+ and ER-/HER2- tumors, high post-neoadjuvant Ki67 index is associated with unfavorable prognosis (Abstract). Ki67 is mainly used to discriminate from luminal A from luminal B tumors in the ER+/HER2- breast cancers and guide the choice of chemotherapy, versus hormonotherapy alone. Denkert and colleagues have highlighted three different groups of tumors: low proliferating tumors are not responding to chemotherapy but have a good prognosis (low Ki67 linked to good outcome); in those high proliferating tumors that are therapy sensitive, high Ki67 is linked to an increased chance of pCR and improved survival (high Ki67 linked to good outcome); in contrast, in high proliferating tumors that are chemotherapy or hormone therapy resistant, increased Ki67 is linked to reduced survival (high Ki67 linked to poor outcome) (Synthesis on clinical utility of Ki67 in breast cancer). The authors conclude by stating that proliferation is a major biomarker in breast cancer, used for prognosis, prediction of treatment response, or both. Proliferation assessment is of paramount importance in ER+/HER2- breast cancers for guiding the choice of treatment. Ki67 is a popular and cheap biomarker, widely used for monitoring tumor proliferation in breast specimens (Conclusions).
Ma provides a meta-analysis of prostaglandin receptors in breast cancer. Cyclooxygenase-2 (COX-2) is frequently overexpressed and associated with poor prognosis in breast cancer. The COX-2 product prostaglandin-E2 (PGE2) elicits cellular responses through four GPCRs, EP1 to EP4. EP4, expressed on malignant breast cells, promotes metastasis. Using a murine model of metastatic breast cancer, the authors show that pharmacologic antagonism of EP1 promoted lung colonization of mammary tumors. Reducing EP1 gene expression by shRNA also increased metastatic capacity relative to cells transfected with non-silencing vector. Examination of invasive ductal carcinomas by IHC shows that EP1 was detected in both the cytoplasm and nucleus of benign ducts as well as malignant cells in some samples, but was absent or limited in either the nucleus or cytoplasm in other malignant samples. Overall survival for women with tumors that were negative for nuclear EP1 was significantly worse than for women with EP1 expression. There was no difference in survival for women with differences in cytoplasmic EP1 expression. Comparing EP1 mRNA in breast tumors from African American and European American women revealed that many more African American breast tumors lacked detectable EP1 mRNA. These studies support the hypothesis that EP1 functions as a metastasis suppressor and that loss of nuclear EP1 is associated with poorer overall survival and may contribute to disparities in outcome in different populations (Abstract).
Greene, Goodacre, Harmon, Dumont, Loftsson, Penault-Liorca, and Ma are considered analogous to the claimed invention as all are involved in the study and treatment of disease using pharmaceuticals. Therefore, it would have been prima facie obvious to one of ordinary skill in the art the time of the effective filing date of the instant application to test patients for mutations in Ki67 or prostaglandin receptors while using the combined method of Greene, Goodacre, and Harmon as Penault-Liorca and Ma show that both Ki67 and PGE receptors are heavily implicated in not only the prognosis of breast cancer, but also in determining the appropriate course of therapy. Testing for mutations in these markers is prima facie obvious use of a known technique to improve similar methods ready for improvement to yield predictable results (See MPEP § 2143 I (C)); these markers are known to be heavily implicated in breast cancer, and the artisan would recognize this, and would be motivated to screen for mutations in these markers in order to ensure that the therapy will be effective, and to monitor the progression and efficacy of the treatment which is being used.
Conclusion
Claims 7, 12-17, 29-31, and 39-49 are rejected.
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/P.M.R./Examiner, Art Unit 1625 /Andrew D Kosar/Supervisory Patent Examiner, Art Unit 1625