DETAILED ACTION
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 the Claims
Claims 1-41 are pending.
Status of Priority
The present application is a 35 U.S.C. § 371 national stage patent application of International patent application PCT/US2023/063641, filed on March 3, 2023. This application also claims the benefits of priority to U.S. Provisional Application no. 63/316,437, filed on March 4, 2022.
Specification - Abstract
The abstract of the disclosure is objected to because it is not in compliance with 37 C.F.R. 1.72 (b). Specifically, the sheet presenting the abstract includes other parts of the application or other material. A corrected abstract of the disclosure is required and must be presented on a separate sheet, apart from any other text. See MPEP § 608.01(b).
In the amended abstract, please keep the structure of instant Formula (I).
Appropriate correction is required.
Specification - Disclosure
The specification has not been checked to the extent necessary to determine the presence of all possible minor errors. Applicant’s cooperation is requested in correcting any errors of which applicant may become aware in the specification.
Claim Objections
Claims 8 and 36 are objected to because of the following informalities:
For grammatical consistency, claim 8 should read:
“…5-membered monocyclic heteroaryl having 1-4 heteroatoms wherein the heteroatom is a nitrogen atom.”
There is a spelling error in claim 36:
“mutant PI3Kα over wide-type PI3Kα” should read“mutant PI3Kα over wild-type PI3Kα”
Appropriate correction is required.
Examiner’s note on novelty and nonobviousness
The closest prior art is:
Boezio et al. (Boezio) (WO2021222556A1; published November 4, 2021).
Novelty:
Boezio discloses PI3Kα inhibitors and methods of use thereof (see abstract) wherein the PI3Kα inhibitors are represented by formula I-1 (see claim 1):
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.
The variables of formula I-1 are defined in claim 1 of Boezio. The PI3Kα inhibitors represented by formula I-1 as disclosed in Boezio differ from those presently claimed in that all the compounds of Boezio comprise a fused bicyclic ring whereas the instant claims encompass compounds comprising a fused tricyclic ring.
Thus, the instant invention is considered novel.
Nonobviousness:
Both Boezio and the present invention disclose PI3Kα inhibitors. One of the PI3Kα inhibitors disclosed by Boezio has the following structure (see the left compound in the table below):
Compound I-194 (see Boezio, pg. 206)
Compound I-1 (see instant spec., pg. 30)
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488
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Compound I-194 and instant compound I-1 are very similar in structure. The main difference between the two structures is outlined with the dashed box and described below:
in compound I-194, the pyrazole ring is bonded to a fused bicyclic ring;
in instant compound I-1, the pyrazole ring is one part of a fused tricyclic ring core.
Moreover, Boezio does not teach nor suggest fusing the pyrazole ring with the bicyclic ring in compound I-194, for example, to arrive at the instant compound I-1.
Thus, the instant invention is considered nonobvious.
Claim Rejections – Improper Markush Grouping
Claims 1-30 and 33-41 are rejected on the judicially-created basis that it contains an improper Markush grouping of alternatives. See In re Harnisch, 631 F.2d 716, 721-22 (CCPA 1980) and Ex parte Hozumi, 3 USPQ2d 1059, 1060 (Bd. Pat. App. & Int. 1984). The improper Markush grouping includes species of the claimed invention that do not share both a substantial structural feature and a common use that flows from the substantial structural feature.
A Markush claim contains an “improper Markush grouping” if: (1) the species of the Markush group do not share a single structural similarity,” or (2) the species do not share a common use. Members of a Markush group share a "single structural similarity” when they belong to the same recognized physical or chemical class or to the same art-recognized class. Members of a Markush group share a common use when they are disclosed in the Specification or known in the art to be functionally equivalent (see Federal Register, Vol. 76, No. 27, Wednesday, February 9, 2011, p. 7166, left and middle columns, bridging paragraph).
The members of the improper Markush grouping do not share a substantial feature and/or a common use that flows from the substantial structural feature for the following reasons:
The claimed Markush group encompasses compounds having substantially different core structures. Some examples are depicted below:
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.
Clearly no ‘‘single structural similarity’’ can be seen amongst the different core structures described above which are fused ring systems made up of rings of different molecular geometries as well as electronic (and, therefore, chemical) properties.
In response to this rejection, Applicant should either amend the claim(s) to recite only individual species or grouping of species that share a substantial structural feature as well as a common use that flows from the substantial structural feature, or present a sufficient showing that the species recited in the alternative of the claims(s) in fact share a substantial structural feature as well as a common use that flows from the substantial structural feature. This is a rejection on the merits and may be appealed to the Board of Patent Appeals and Interferences in accordance with 35 U.S.C. § 134 and 37 CFR41.31 (a) (1) (emphasis provided).
Claim Rejections - 35 USC § 112(a)
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.
Scope of Enablement
Claims 1-30 and 33-41 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:
A compound of Formula I:
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or a pharmaceutically acceptable salt thereof, wherein:
R1 = H,
W = CH,
R2 =
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,
R3 =
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,
Z = CH,
X is N and Y is C; or X is C and Y is N,
n = 0 or 1,
LA = covalent bond,
Ring A is a 5-membered monocyclic heteroaryl having 1-4 heteroatoms wherein the heteroatom is a nitrogen atom,
RA = -C(O)ORA1 or -C(O)N(RA1)2 wherein
RA1 is independently selected from the group consisting of:
H, C1-6 aliphatic, 5-membered monocyclic heteroaryl having 1-4 heteroatoms wherein the heteroatom is a nitrogen atom,
Wherein the C1-6 aliphatic can be substituted with 1 RG1
Wherein RG1 = -OR (with R = C1-6 aliphatic) and
Wherein the 5-membered monocyclic heteroaryl can be substituted with 1 C1-6 aliphatic or
two RA1 when attached to the same nitrogen atom are taken together to form an optionally substituted ring selected from 5-6 membered saturated monocyclic heterocyclyl having 0-2 additional heteroatoms independently selected from nitrogen and oxygen
wherein the 5-6 membered saturated monocyclic heterocylclyl, if substituted, is substituted with C1-6 alkyl;
A pharmaceutical composition comprising a compound of point (1), as recited above, or a pharmaceutically acceptable salt thereof, and a pharmaceutically acceptable carrier;
A method of inhibiting PI3Kα, comprising administering to a subject a compound of point (1), as recited above, or a pharmaceutically acceptable salt thereof;
The method of point (3), wherein the method selectively inhibits PI3Kα over other PI3K isoforms;
The method of point (3), wherein the method selectively inhibits mutant PI3Kα over wild-type PI3Kα;
A method of treating breast cancer, comprising administering to a subject in need thereof a compound of point (1), as recited above, or a pharmaceutically acceptable salt thereof;
does not reasonably provide enablement for elements that are outside the scope of the enabling elements listed above. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention commensurate in scope with these claims.
As stated in the MPEP 2164.01(a), “There are many factors to be considered when determining whether there is sufficient evidence to support a determination that a disclosure does not satisfy the enablement requirement and whether any necessary experimentation is “undue.”
In evaluating the enablement question, several factors are to be considered. According to In re Wands, 8 USPQ2d 1400 (Fed. Cir. 1988), these factors include:
1) The nature of the invention,
2) the state of the prior art,
3) the predictability or lack thereof in the art,
4) the amount of direction or guidance present,
5) the presence or absence of working examples,
6) the breadth of the claims, and
7) the quantity of experimentation needed to make and use the invention based on the content of the disclosure, and
8) the level of the skill in the art.
In the instant case, the Wands factors are relevant for the following reasons:
The nature of the invention
The nature of the invention claims compounds, compositions, and methods useful for inhibiting PI3Kα, and/or treating a disease, disorder, or condition associated with PI3Kα, and/or treating cancer. The compounds of the present disclosure are represented by Formula I:
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. The variables of instant Formula I are described within the instant specification.
State of the prior art and the predictability or lack thereof in the art
Prior art referenced:
Krop et al. (Krop) (Krop, I. E. et al. Phase II Study of Taselisib in PIK3CA-Mutated Solid Tumors Other Than Breast and Squamous Lung Cancer: Results From the NCI-MATCH ECOG-ACRIN Trial (EAY131) Subprotocol I. JCO Precision Oncology 2022, 6, e2100424.; published online: February 9, 2022.)
Juric et al. (Juric) (Juric, D. et al. Phase I Dose-Escalation Study of Taselisib, an Oral PI3K Inhibitor, in Patients with Advanced Solid Tumors. Cancer Discovery 2017, 7, 704-715.)
Taselisib is known in the prior art to be a potent and selective PI3K inhibitor that displays greater sensitivity for mutant PI3Kα isoforms than wild-type PI3Kα (see Juric, pg. 705, right col., 1st paragraph, 1st sentence).
Krop teaches that “although taselisib has shown clinical activity in PIK3CA-mutant HR+ breast cancer as monotherapy and when added to antiestrogen therapy, in this study, very little activity was observed in other cancer types with PIK3CA mutations” (see Krop, pg. 8, right col., last paragraph, 1st sentence). Therefore, Krop demonstrates that therapeutic efficacy of a PI3Kα inhibitor in one cancer type does not necessarily predict efficacy of the same inhibitor in other cancer types.
Prior art referenced:
Madsen et al. (Madsen) (Madsen, R. R. et al. Cancer-Associated PIK3CA Mutations in Overgrowth Disorders. Trends in Molecular Medicine 2018, 24, 856-870.)
Madsen explains that although PI3K inhibitors are promising candidates for treatment of PROS (see abstract), “[f]aithful experimental models of PROS, ideally spanning a spectrum of mutations, are required to obtain mechanistic insight into the underlying disease pathology and to test proposed therapeutic regimens” (pg. 865, last sentence). Therefore, Madsen teaches that therapeutic efficacy of a PI3Kα inhibitor demonstrated in a cancer setting does not, by itself, establish therapeutic efficacy in PROS. Rather, Madsen explains that faithful experimental models of PROS are required to evaluate proposed therapeutic regimens.
The level of the skill in the art
The level of ordinary skill in the art is relatively high. A person of ordinary skill would typically have formal training in medicinal chemistry and organic synthesis and would be familiar with standard methods for evaluating therapeutic efficacy of compounds.
The breadth of the claims
The claims are extremely broad insofar as the instant claims recite a compound of instant formula I wherein the compound can possess a structurally diverse range of chemical substituents and substantially different core scaffolds.
The method claims are also broad insofar as they encompass treatment of a wide range of diseases, including any cancer and any disease, disorder, or condition associated with PI3Kα. In other words, the instantly claimed methods also encompass treating diseases, disorders, or conditions that are currently not established as being associated with PI3Kα, but may be discovered to be associated with PI3Kα upon future scientific investigations.
The presence or absence of working examples
The instant specification only provides 15 specific examples of compounds encompassed by instant claim 1 (see pg. 31-32 for structures). The working examples do not adequately represent the full breadth of the claimed genus which was established to be extremely broad (see “4. The breadth of the claims” subsection above). For example, according to instant claim 1, the compound of Formula I can possess many different core structures, wherein each of these core structures can be substituted with structurally diverse substituents. However, in the instant case, all 15 specific examples possess the following structural features:
R1 = H,
W = CH,
R2 =
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,
R3 =
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,
Z = CH,
n = 0 or 1,
X is N and Y is C; or X is C and Y is N,
LA = covalent bond.
Accordingly, significant portions of the claimed structural space remain unexplored by the working examples. The examples, therefore, provide very limited information regarding how variations in Ring A and RA affect PI3Kα inhibitory activity within breast cancer cell lines (see Table 3 on pg. 61 for data).
Additionally, the working examples do not adequately represent the full breadth of the claimed methods of treatment. The instant specification demonstrates that selected compounds have PI3Kα inhibitory activity in the context of breast cancer cell lines (see Table 3 on pg. 61 for data). However, the instant specification does not provide working examples demonstrating therapeutic activity in other cancer types or any other disease, disorder, or condition associated with PI3Kα, such as CLOVES syndrome or PIK3CA-related overgrowth syndrome [i.e., PROS] (as recited in instant claim 39).
The amount of direction or guidance present and the quantity of experimentation needed to make and use the invention based on the content of the disclosure
Although the specification provides synthetic procedures for the 15 specific examples, it provides limited direction and guidance regarding which structural features of the PI3Kα inhibitors of instant formula I are responsible for PI3Kα inhibitory activity and how modifications to the PI3Kα inhibitors (such as modifications of the R1, R2, and R3 groups with the modification of Ring A) affect such activity. In the instant case, all 15 specific examples have the same R1, R2, R3, W, LA, and Z. Furthermore, in all 15 examples:
n is 0 or 1 and
X is N and Y is C; or X is C and Y is N.
The only variables that are being varied amongst the 15 working examples are Ring A and RA. The specification does not provide guidance regarding the effect of modifying R1, R2, R3, W, LA, Z, n, X, and Y in PI3Kα inhibitory activity. The instant specification also does not provide a structure-activity relationship that would allow a POSITA to predict which structural features of a compound of instant claim 1 would retain or improve PI3Kα inhibitory activity of the compound and which features would destroy such activity. Recall that the compounds of the instant claim set are part of a novel and nonobvious compound genus (see the “Examiner’s note on novelty and nonobviousness” section above for details).
Because the claims encompass numerous variables, the required experimentation would involve not mere routine verification of activity but extensive exploration of the claimed genus to identify operative species which involves undue experimentation. Although a POSITA possesses expertise in medicinal chemistry and organic synthesis, such expertise cannot substitute for the absence of guidance in the specification. The issue is not whether a POSITA is capable of synthesizing and testing compounds encompassed by the claims. Rather, the issue is that the specification provides insufficient information to identify which structural modifications (e.g., which combinations of R1, R2, R3, W, LA, Z, n, X, Y, Ring A, and RA) preserve or improve PI3Kα inhibitory activity and which modifications destroy such activity. Consequently, a POSITA would be required to undertake a substantial medicinal chemistry research program to establish the relevant structure-activity relationships before the full scope of the claimed novel and nonobvious genus could be practiced.
The instant specification also provides insufficient direction and guidance regarding the full scope of the claimed therapeutic methods. The working examples demonstrate that selected compounds have PI3Kα inhibitory activity in the context of breast cancer cell lines (see Table 3 on pg. 61 for data). However, the specification does not provide sufficient guidance demonstrating how these results can be extrapolated to the full scope of claimed methods including the treatment of any cancer or any disease, disorder, or condition associated with PI3Kα. PI3Kα inhibitory activity in the context of breast cancer cell lines does not establish that the claimed genus of compounds would provide therapeutic benefit across all cancers having different genetic drivers and mechanisms of disease progression. This is consistent with the prior art teaching of Krop which demonstrated that therapeutic efficacy of a PI3Kα inhibitor (i.e., taselisib) in one cancer type does not necessarily predict efficacy of the same inhibitor in other cancer types (see the “2. State of the prior art and the predictability or lack thereof in the art” subsection above for details).
Likewise, the demonstration of PI3Kα inhibition for selected compounds in different breast cancer cell lines does not establish that all diseases, disorders, or conditions associated with PI3Kα (including CLOVES syndrome or PIK3CA-related overgrowth syndrome [i.e., PROS] as recited in instant claim 39) would be responsive to treatment with the claimed compounds, especially in view of the teachings disclosed by Madsen.
Specifically, Madsen teaches that therapeutic efficacy of a PI3Kα inhibitor demonstrated in a cancer setting does not, by itself, establish therapeutic efficacy in PROS. Rather, Madsen explains that faithful experimental models of PROS are required to evaluate proposed therapeutic regimens (see the “2. State of the prior art and the predictability or lack thereof in the art” subsection above for details).
Therefore, practicing the full scope of the instant compound and method claims extends beyond routine optimization and would require a substantial medicinal chemistry research program to identify operative species within the claimed genus, thereby amounting to undue experimentation.
Written Description
Claims 1-30 and 33-41 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.
Currently, the claims are extremely broad insofar as the instant claims recite a compound of instant formula I wherein the compound can possess a structurally diverse range of chemical substituents and substantially different core scaffolds.
The method claims are also broad insofar as they encompass treatment of a wide range of diseases, including any cancer and any disease, disorder, or condition associated with PI3Kα. In other words, the instantly claimed methods also encompass treating diseases, disorders, or conditions that are currently not established as being associated with PI3Kα, but may be discovered to be associated with PI3Kα upon future scientific investigations.
Although the instant claims are extremely broad, the instant specification provides very limited working examples.
According to MPEP § 2163:
“Satisfactory disclosure of a ‘representative number’ depends on whether one of skill in the art would recognize that the inventor was in possession of the necessary common attributes or features possessed by the members of the genus in view of the species disclosed. For inventions in an unpredictable art, adequate written description of a genus which embraces widely variant species cannot be achieved by disclosing only one species within the genus. See, e.g., Eli Lilly, 119 F.3d at 1568, 43 USPQ2d at 1406. Instead, the disclosure must adequately reflect the structural diversity of the claimed genus, either through the disclosure of sufficient species that are ‘representative of the full variety or scope of the genus,’ or by the establishment of ‘a reasonable structure-function correlation.’ Such correlations may be established ‘by the inventor as described in the specification,’ or they may be ‘known in the art at the time of the filing date.’ See AbbVie, 759 F.3d at 1300-01, 111 USPQ2d 1780, 1790-91 (Fed. Cir. 2014).
The instant specification only provides 15 specific examples of compounds encompassed by instant claim 1 (see pg. 31-32 for structures). The working examples do not adequately represent the full breadth of the claimed genus which was established to be extremely broad. For example, according to instant claim 1, the compound of Formula I can possess many different core structures, wherein each of these core structures can be substituted with structurally diverse substituents. However, in the instant case, all 15 specific examples possess the following structural features:
R1 = H,
W = CH,
R2 =
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,
R3 =
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,
Z = CH,
X is N and Y is C; or X is C and Y is N,
n = 0 or 1, and
LA = covalent bond.
As such, significant portions of the claimed structural space remain unexplored by the working examples. According to MPEP § 2163 (see above), a very narrow subgenus of compounds does not adequately reflect a claimed genus that is structurally diverse. In the instant case, the instant claims are extremely broad. Accordingly, the disclosed species do not adequately reflect the structural diversity of the claimed genus and do not demonstrate possession of the full scope of compounds recited in instant claims 1-30 and 33-41.
The instant specification also fails to demonstrate possession of the full scope of the claimed therapeutic methods The instant specification demonstrates that selected compounds have PI3Kα inhibitory activity in the context of three cancer cell lines (see Table 3 on pg. 61 for data). However, the cancerous cell lines experimented with represent different breast cancer cell lines and do not adequately represent the broad genus of diseases encompassed by instant claims 37, 38, and 40. Note: PI3Kα inhibitory activity in the context of breast cancer cell lines does not establish that the claimed genus of compounds would provide therapeutic benefit across all cancers having different genetic drivers and mechanisms of disease progression. This is consistent with the prior art teaching of Krop which demonstrated that therapeutic efficacy of a PI3Kα inhibitor (i.e., taselisib) in one cancer type does not necessarily predict efficacy of the same inhibitor in other cancer types (see the “2. State of the prior art and the predictability or lack thereof in the art” subsection in the “Scope of Enablement” section above for details).
Likewise, the demonstration of PI3Kα inhibition for selected compounds in different breast cancer cell lines does not establish that all diseases, disorders, or conditions associated with PI3Kα (including CLOVES syndrome or PIK3CA-related overgrowth syndrome [i.e., PROS] as recited in instant claim 39) would be responsive to treatment with the claimed compounds, especially in view of the teachings disclosed by Madsen.
Specifically, Madsen teaches that therapeutic efficacy of a PI3Kα inhibitor demonstrated in a cancer setting does not, by itself, establish therapeutic efficacy of the same PI3Kα inhibitor in PROS. Rather, Madsen explains that faithful experimental models of PROS are required to evaluate proposed therapeutic regimens (see the “2. State of the prior art and the predictability or lack thereof in the art” subsection in the “Scope of Enablement” section above for details).
Accordingly, the disclosure of PI3Kα inhibitory activity in breast cancer cell lines does not adequately represent the full therapeutic breadth of the claimed therapeutic methods recited in instant claims 37-41. Therefore, the specification does not reasonably convey that Applicant was in possession of methods of treating the full scope of cancers and disease, disorder, or condition associated with PI3Kα encompassed by claims 37-41.
Furthermore, the recitation of “a disease, disorder, or condition associated with PI3Kα” and “disease, disorder, or condition is associated with mutant PI3Kα” creates a “reach-through” aspect to the claim. Specifically, the claim is not limited to diseases presently recognized as associated with PI3Kα, but, instead, potentially reaches through to diseases whose relationship to PI3Kα may only be discovered or established through future scientific investigation. In the instant case, the specification does not demonstrate possession of methods of treating diseases, disorders, or conditions whose association with PI3Kα was unknown or unrecognized at the time of filing, nor does it provide representative disclosure sufficient to show possession of such subsequently identified members of the claimed genus. Accordingly, the “reach-through” scope of the claim further demonstrates that the instant specification does not reasonably convey possession of the full scope of “a disease, disorder, or condition associated with PI3Kα” or “disease, disorder, or condition is associated with mutant PI3Kα” as presently claimed.
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 37 and 38 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.
The limitations “a disease, disorder, or condition associated with PI3Kα” and “disease, disorder, or condition is associated with mutant PI3Kα” render the scope of the claims indefinite because the claim defines the disease only by its functional relationship to PI3Kα, without identifying which diseases are encompassed or providing an objective standard for determining when a disease is sufficiently “associated” to PI3Kα to fall within the scope of the claim. It is therefore unclear whether the limitation only encompasses diseases that were established to be directly driven by PI3Kα activity as of the effective filing date, or does it also encompass diseases that may subsequently be discovered or later determined to involve PI3Kα activity. It is further unclear whether the limitation encompasses diseases in which PI3Kα activity contributes to pathogenesis or does the limitation encompass any disease for which PI3Kα inhibition produces some biological or therapeutic effect. For these above reasons, the boundaries of claims 37 and 38 are rendered vague and indefinite.
Allowable Subject Matter
Claims 31 and 32 are objected to as being dependent upon a rejected base claim.
Conclusion
Claims 1-30 and 33-41 are rejected. Claims 31 and 32 are objected. Any inquiry concerning this communication or earlier communications from the examiner should be directed to KRISTEN ROMERO whose telephone number is (571)272-6478. The examiner can normally be reached M-F 9:30 AM - 6:00 PM ET.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, JEFFREY H. MURRAY can be reached at (571) 272-9023. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/KRISTEN W ROMERO/Examiner, Art Unit 1624
/JEFFREY H MURRAY/Supervisory Patent Examiner, Art Unit 1624
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