DETAILED ACTION
This action is in response to papers filed on 08/21/2025. Claims 19 and 25-32 of Quitterer et al., 17/040,011 (09/21/2020) are pending examination on the merits: claims 19, 31 and 32 are amended, and claims 20-24 are cancelled. Claims 19 and 25-32 are rejected.
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 is a 371 of PCT/EP2019/056565 (03/15/2019) and claims foreign priority to EP 18162579.9 (03/19/2018). Acknowledgment is made of applicant's claim for foreign priority. It is noted, however, that applicant has not filed a certified copy of the EP 18162579.9 application as required by 37 CFR 1.55.
Information Disclosure Statement
The Information Disclosure Statements (IDS) submitted on 08/21/2025 are in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statements have been considered by the examiner.
Election/Restrictions
Applicant elected the following species in a reply filed on 4/11/22:
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241
211
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,
determined to read on Formula (Ia)
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202
256
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when:
a=0; R1=5-benzodioxolyl; R2=oxo; R3=-C(O)-R12, R12=cyclopropyl; R4=hydroxyl
R5= substituted (4-fluoro) C6-carbocycle (phenyl), and the corresponding species of “decline of male and female fertility”.
Applicant’s Amendment
Applicant’s amendment to claims 19, 31, and 32 is acknowledged. Regarding claim 19, Applicant has narrowed the general compound of formula (Ia), to four compounds, as well as narrowed the list of claimed diseases. Regarding claims 31 and 32, Applicant has further narrowed the compounds of claim 19.
The claimed compounds now consist of:
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953
742
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However, compounds three and four in the sequence do not reflect R4 as a hydroxyl group per formula (Ia) definition of R4 on pages 15-16 of the Specification. Moreover, nowhere in the Specification is R4 defined only as O.
New Claim Objection - 35 USC § 112Claims 19 and 25-32 are objected to because of the following informalities:
As described above, Applicant’s amendment to claims 19, 31, and 32 narrows the previously presented Markush grouping of formula (Ia) to four compounds. The definition per the Specification for R4 (c.f., pp. 15-16 of Specification), the definition of R4 is equivalent only to a hydroxyl group. Nowhere in the Specification is R4 presented solely as oxygen. Appropriate correction is required.
Maintained 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 19, and 25-32 are rejected under 35 U.S.C. 112(a).
Claims 19, and 25-32 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 the compounds identified as having activity with experimental data, does not reasonably provide enablement for the entirety of the claim scope. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims.
Particularly relevant to the instant case is the issue as to whether the specification provides embodiments allowing use of the claimed invention without requiring undue experimentation by one of ordinary skill in view of the highly unpredictable nature of affecting enzymes and the prevention of diseases such as Alzheimer’s and Parkinson’s diseases, where there is no proven cure let alone prevention of the diseases.
“[An inventor] must not be permitted to achieve . . . dominance by claims which are insufficiently supported and hence not in compliance with the first paragraph of 35 U.S.C. 112. That paragraph requires that the scope of the claims must bear a reasonable correlation to the scope of enablement provided by the specification to persons of ordinary skill in the art. In cases involving predictable factors, such as mechanical or electrical elements, a single embodiment provides broad enablement in the sense that, once imagined, other embodiments can be made without difficulty and their performance characteristics predicted by resort to known scientific laws. In cases involving unpredictable factors, such as most chemical reactions and physiological activity, the scope of enablement obviously varies inversely with the degree of unpredictability of the factors involved.” In re Fisher, 427 F.2d 833, 839, 166 USPQ 18, 24 (CCPA 1970).
Accordingly, the critical element here is how broad the claims are compared to the level of unpredictability in the art.
As a general rule, enablement must be commensurate with the scope of claim language. MPEP 2164.08 states, “The Federal Circuit has repeatedly held that ‘the specification must teach those skilled in the art how to make and use the full scope of the claimed invention without undue experimentation.’ In re Wright, 999 F.2d 1557, 1561, 27 USPQ2d 1510, 1513 (Fed. Cir. 1993)” (emphasis added). The “make and use the full scope of the invention without undue experimentation” language was repeated in 2005 in Warner-Lambert Co. v. Teva Pharmaceuticals USA Inc., 75 USPQ2d 1865, and Scripps Research Institute v. Nemerson, 78 USPQ2d 1019 asserts: “A lack of enablement for the full scope of a claim, however, is a legitimate rejection.” The principle was explicitly affirmed more recently in Liebel-Flarsheim Co. v. Medrad, Inc., 481 F.3d 1371, 82 USPQ2d 1113; Auto. Tech. Int’l, Inc. v. BMW of N. Am., Inc., 501 F.3d 1274, 84 USPQ2d 1108 (Fed. Cir. 2007), Monsanto Co. v. Syngenta Seeds, Inc., 503 F.3d 1352, 84 U.S.P.Q.2d 1705 (Fed. Cir. 2007), and Sitrick v. Dreamworks, LLC, 516 F.3d 993, 85 USPQ2d 1826 (Fed. Cir. 2008).
The test of enablement is whether one skilled in the art could make and use the claimed invention from the disclosures in the specification coupled with information known in the art without undue experimentation (United States v. Telectronics, 8 USPQ2d 1217 (Fed. Cir. 1988)). Whether undue experimentation is needed is not based upon a single factor but rather is a conclusion reached by weighing many factors. These factors were outlined in Ex parte Forman, 230 USPQ 546 (Bd. Pat. App. & Int. 1986) and again in In re Wands, 8 USPQ2d 1400 (Fed. Cir. 1988) and include the following:
Nature of Invention.
The nature of the invention involves compounds of claim 19 i.e., GRK2-inhibitory compounds, c.f., Specification p. 50), for treating CNS- or neurodegenerative diseases in a patient (c.f., Specification p. 51-56). The claims also recite prevention, and prevention is suggested to include a level of protection against, up to and including complete protection against the development of a disease or condition, which is unsupported by the disclosure. Giving the claims their broadest reasonable interpretation, the term “prevention” includes any measure taken prior to the onset or occurrence of a disease or condition which precludes its coming into existence, absolutely and in all cases. Therefore, preventing diseases of a CNS or neurodegenerative diseases, such as Alzheimer’s and Parkinson’s disease render the scope of the claims unreasonably broad and not enabling by the disclosure as filed.
Scope of the Invention.
The claim breadth is vast in view of the generic nature of the claimed method and the limited disclosure. The claims encompass the treatment and prevention of a large number of disorders and diseases affecting the Central Nervous System (CNS), including Alzheimer’s and Parkinson’s diseases. Moreover, because the instant specification does not teach methods or models to determine the full scope of “CNS-or neurodegenerative disease in a patient” that is treatable and preventable by the compounds of claim 19, the full claim breadth of claim 19 cannot be ascertained in exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with the claims (c.f., Specification p. 51-56). (See discussion of “State of the Art” below). Additionally, the claim is broad with regard to patient, which is not defined in the specification or the rejected claims. However, it is noted that preferences that the patient is a mammal or human are stated on page 53 of the specification. Thus, patient given its broadest reasonable interpretation includes humans, mammals, and any other animal that has a CNS or is able to suffer from a neurogenerative disease.
State of the Art and Level of Skill in the Art.
There is no evidence in the prior art or Specification that the instant compounds would be usable as preventative therapeutics, particularly for preventing CNS and neurological diseases such as Alzheimer’s and Parkinson’s disease.
“Preventing” connotes an absolute absence of a condition which cannot reasonably be achieved with regard to infections, with few exceptions (such as vaccines to prevent the development of pathogen-borne illnesses). In addition, there is no definitive method by which to determine whether a patient will develop a particular condition and, thus, be in need of preventive therapy. This is distinguished from preventing the relapse or recurrence of certain conditions, in which case an objective basis may exist to identify patients at risk of disease or infection, and could reasonably be construed as treatment. Prior to the initial onset or occurrence, however, even if a patient can be identified as having known risk factors for a condition, there is no certainty that the patient would in fact develop the condition. Further, the failure of a disease, infection, or condition to develop cannot reliably be attributed to the claimed active agent(s). The non-development of a condition such as CNS or neurological may be due to other factors such as lifestyle. In this sense, in the context of preventing a disease, the level of unpredictability is extremely high.
Furthermore, the state of the prior art is that the pharmacological art involves screening in vitro and in vivo to determine which compounds exhibit the desired pharmacological activities (i.e. what compounds can treat which specific disease by what mechanism). There is no absolute predictability even in view of the seemingly high level of skill in the art. The existence of these obstacles establishes that the contemporary knowledge in the art would prevent one of ordinary skill in the art from accepting any therapeutic or preventative regimen on its face. No explicit data is found in Applicant’s Specification that would support the claims as presented.
While a full discussion of each disease which is encompassed by Applicant’s claim language will not be given, the following examples teach that the state of the prior art with respect to the claimed diseases has not advanced to the point of being predictive of the prevention of the breadth of diseases instantly claimed. Because of the known unpredictability of the art, and in the absence of experimental evidence, no one skilled in the art would accept the assertion the instantly claimed method could be predictably used for the prevention of Alzheimer’s and Parkinson’s disease. With regard to Alzheimer's disease, for example, it is the state of the art that there are no known and validated preventative treatment for Alzheimer’s disease. Some treatments include cholinesterase inhibitors and memantine, Lecanemab-irmb and Donanemab-azbt; however, even these well-established compounds do not fully cure or prevent the disease. Compounds of the present claims do not fall in either category (Mayo Clinic). Alzheimer’s disease has traditionally been very difficult or impossible to fully treat effectively. See e.g., the Journal of Alzheimer’s Disease, Vol. 29, Issue 2 wherein Korczyn states that “Attempts to find cures for Alzheimer’s disease (AD) have, however, failed so far, in spite of enormous investments, intellectual and financial,” (Abstract, line 1-2). Sparks et al. (2018), Mayo Clinic also teaches that Parkinson’s Disease, at least at the time, was not preventable as its cause was unknown at that time.
Number of Working Examples and Guidance Provided by Applicant.
The specification describes Compound-1 and -1F (differing only by a fluorine substituent), and third compound (i.e., compound-4). The specification has no other guidance regarding a correlation of structure with function, or therapeutic dosage required for the full treatment or prevention of diseases including Alzheimer’s and Parkinson’s disease.
Applicant’s Specification provides some experimental data in Examples 1-14, for example, where:
Example 1 describes the identification of Compound-1 and compound-4 in the retardation of Abeta plague formation in Tg2576 AD mice.
Example 2 describes the identification of Compound-1 and Compound-4 in the retardation of hippocampal neuronal loss and Tau hyperphosphorylation in AD mice.
Example 3 describes Compound-1 and Compound-4 in the retardation of hippocampal Tau hyperphosphorylation in a rat model with symptoms of sporadic AD, ageing and depression, wherein Applicant assessed depression by a decrease in the rats’ sucrose intake.
Example 4 describes the effects of Compound-1 and Compound-4 in decreased hippocampal content of hyperphosphorylated PHF Tau in a model of tauopathy.
However, support for enablement of the full scope of the claimed method for treatment or prevention of a CNS-or neurodegenerative disease in a patient comprising administering the claimed compounds is substantially lacking. Applicant asserts that the three experimental compounds of the Examples of the disclosure demonstrate retardation of cardiovascular disease-induced aging, retard plaque formation of Abeta plaques, Tau hyperphosphorylation, and hippocampal neuronal loss, and then formulates a grand conclusion that the “claimed compounds” have an effect on what Applicant calls the “hallmarks of neurodegenerative disease and tauopathies” (Applicant’s Specification at page 90), and thus can be used in the treatment and prevention of all the claimed diseases, including Alzheimer’s and Parkinson’s disease which no known cures are available. Moreover, Examples 10-14 describes Compound-1 and Compound-1F effects on aging-induced deterioration of male rats’ sperm quality, aging- induced decrease in female fertility and detection of a senescence marker MPP1 in peripheral blood mononuclear cells.
Consistent with this reasoning, Applicant’s Specification does not reasonably provide enablement for the full scope of the claimed invention. The Specification does not provide sufficient guidance on the manner and process using the claimed invention, 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. The Specification also does not set forth a best mode of the method for the treatment and prevention of the claimed CNS-or neurodegenerative diseases in a patient, comprising administering the full scope of the claimed compounds as per instant claim 1. Again, there is no data to support or even a method contemplated regarding the actual prevention of any of the claimed disease in a patient, wherein the patient is a mammalian or human patient.
Unpredictability of the Art and Amount of Experimentation.
The art of using pharmaceuticals to affect enzymes is highly unpredictable as described by Kubinyi, Waldschmidt and Wermuth also cited on the PTO-892 mailed on April 22, 2025. In nearly every case, the skilled artisan could not predict a priori whether a given compound would affect GRK2, let alone prevent a disease. When small variations in structure such as the addition of a methyl group has radical effects on the binding, without specific guidance or correlations indicating how the structure of species affects its activity, the scope of enablement is constrained to compounds showing substantial similarity to those actually demonstrated to be useful. Furthermore, there would be a huge amount of undue experimentation required in order to determine dosage for example in the treatment and prevention of the claimed diseases including Alzheimer’s disease and Parkinson’s disease. Furthermore, the conclusions drawn in Applicant’s Specification at pages 95 are not commensurate in scope with the invention as claimed. The claims are far broader in scope than what is presented as disclosed above in “Number of Working Examples and Guidance Provided by Applicant”. Applicant relies on generic animal model data to support a broad claim scope directed to the treatment and prevention of CNS-or neurodegenerative disease in a human; however, McGonigle et al., Biochemical Pharmacology 87 (2014), 162–171 for example, states that, “some of the challenges associated with the evaluation and predictive validation of animal models, as well as methodological flaws in both preclinical and clinical study designs that may contribute to the current translational failure rate. The testing of disease hypotheses and NCEs (new chemical entities) in multiple disease models necessitates evaluation of pharmacokinetic/pharmacodynamic (PK/PD) relationships and the earlier development of validated disease-associated biomarkers to assess target engagement and NCE efficacy…” (Abstract). Thus, “The predictive value of an animal model is thus only as useful as the context in which it is interpreted...” as disclosed by McGonigle.
Considering the above factors, the claims are clearly not enabled for the full scope of the diseases or compounds claimed especially in terms of the prevention of CNS-or neurodegenerative diseases. The rejection is maintained.
Applicant’s Arguments
Applicant contends that claim 19 has been amended to narrow the scope of CNS diseases and to limit the scope of compounds. Applicant also contends that Examples 1-14 of the disclosure sufficiently supports the enablement of claim 19. Applicant’s Remarks at pages 10-12. Applicant argues against the terms “preventing” and “prevention”, and claims that the term prevention encompasses different stages of diseases, not solely the prevention of primary disease. Applicant argues that the compounds of the claimed invention have anti-depressant activities, and depression is associated with Alzheimer’s disease; therefore, anti-depressant activity qualifies for preventative treatment of Alzheimer’s disease. Applicant’s Remarks at pages 14-15.
Examiner’s Response
Applicant’s arguments are acknowledged, but are not found to be persuasive in view of the arguments discussed above. Applicant argues that the claims are sufficiently enabled by the specification such that a person of skill in the art could practice the claimed invention.
In response to Applicant’s Remarks, nothing in the disclosure as filed enables one of skill in the art to utilize the invention in a way that is commensurate in scope with the claims, especially in regard to the prevention of the claimed diseases. It is important to note that the claimed method is not limited to treating depression associated with or caused by Alzheimer’s disease per Applicant’s response. The claims encompass the treatment or prevention of disorders, and diseases affecting the Central Nervous System (CNS) including Alzheimer’s disease and Parkinson’s disease; however, the instant specification does not teach methods or models to treat or even to support the prevention of the full scope of “CNS-or neurodegenerative disease in a patient”, including the prevention of Alzheimer’s and Parkinson’s disease by compounds of claim 19. The Specification further includes multiple other diseases that Applicant claims to be treatable and preventable using the claimed compounds without any definitive support to the claim (c.f., Specification p. 51-56). Moreover, as discussed above, because of the known unpredictability of the art, and in the absence of experimental evidence, no one skilled in the art would accept the assertion the instantly claimed method could be predictably used for the prevention of Alzheimer’s and Parkinson’s disease per claim 19.
There is no evidence in the prior art or Specification that the instant compounds would be usable as preventative therapeutics, particularly for preventing CNS and neurological diseases such as Alzheimer’s and Parkinson’s disease. “Preventing” connotes an absolute absence of a condition which cannot reasonably be achieved with regard to infections, with few exceptions (such as vaccines to prevent the development of pathogen-borne illnesses). In addition, there is no definitive method by which to determine whether a patient will develop a particular condition and, thus, be in need of preventive therapy. This is distinguished from preventing the relapse or recurrence of certain conditions, in which case an objective basis may exist to identify patients at risk of disease or infection, and could reasonably be construed as treatment. Prior to the initial onset or occurrence, however, even if a patient can be identified as having known risk factors for a condition, there is no certainty that the patient would in fact develop the condition. Further, the failure of a disease, infection, or condition to develop cannot reliably be attributed to the claimed active agent(s). The non-development of a condition such as CNS or neurological may be due to other factors such as lifestyle. In this sense, in the context of preventing a disease, the level of unpredictability is extremely high.
Furthermore, the state of the prior art is that the pharmacological art involves screening in vitro and in vivo to determine which compounds exhibit the desired pharmacological activities (i.e. what compounds can treat which specific disease by what mechanism). There is no absolute predictability even in view of the seemingly high level of skill in the art. The existence of these obstacles establishes that the contemporary knowledge in the art would prevent one of ordinary skill in the art from accepting any therapeutic or preventative regimen on its face. No explicit data is found in Applicant’s Specification that would support the claims as presented.
While a full discussion of each disease which is encompassed by Applicant’s claim language will not be given, the following examples teach that the state of the prior art with respect to the claimed diseases has not advanced to the point of being predictive of the prevention of the breadth of diseases instantly claimed. Because of the known unpredictability of the art, and in the absence of experimental evidence, no one skilled in the art would accept the assertion the instantly claimed method could be predictably used for the prevention of Alzheimer’s and Parkinson’s disease.
With regard to Alzheimer's disease, for example, it is the state of the art that there are no known and validated preventative treatment for Alzheimer’s disease. Some treatments include cholinesterase inhibitors and memantine, Lecanemab-irmb and Donanemab-azbt; however, even these well-established compounds do not fully cure or prevent the disease. Compounds of the present claims do not fall in either category (Mayo Clinic). Alzheimer’s disease has traditionally been very difficult or impossible to fully treat effectively. See e.g., the Journal of Alzheimer’s Disease, Vol. 29, Issue 2 wherein Korczyn states that “Attempts to find cures for Alzheimer’s disease (AD) have, however, failed so far, in spite of enormous investments, intellectual and financial,” (Abstract, line 1-2).
The specification describes Compound-1 and -1F (differing only by a fluorine substituent), and third compound (i.e., compound-4). The specification has no other guidance regarding a correlation of structure with function, or therapeutic dosage required for the full treatment or prevention of diseases including Alzheimer’s and Parkinson’s disease. Applicant’s Specification provides some experimental data in Examples 1-14, for example, where:
Example 1 describes the identification of Compound-1 and compound-4 in the retardation of Abeta plague formation in Tg2576 AD mice.
Example 2 describes the identification of Compound-1 and Compound-4 in the retardation of hippocampal neuronal loss and Tau hyperphosphorylation in AD mice.
Example 3 describes Compound-1 and Compound-4 in the retardation of hippocampal Tau hyperphosphorylation in a rat model with symptoms of sporadic AD, ageing and depression, wherein Applicant assessed depression by a decrease in the rats’ sucrose intake.
Example 4 describes the effects of Compound-1 and Compound-4 in decreased hippocampal content of hyperphosphorylated PHF Tau in a model of tauopathy.
However, support for enablement of the full scope of the claimed method for treatment or prevention of a CNS-or neurodegenerative disease in a patient comprising administering the claimed compounds is substantially lacking. Applicant asserts that the three experimental compounds of the Examples of the disclosure demonstrate retardation of cardiovascular disease-induced aging, retard plaque formation of Abeta plaques, Tau hyperphosphorylation, and hippocampal neuronal loss, and then formulates a grand conclusion that the “claimed compounds” have an effect on what Applicant calls the “hallmarks of neurodegenerative disease and tauopathies” (Applicant’s Specification at page 90), and thus can be used in the treatment and prevention of all the claimed diseases, including Alzheimer’s and Parkinson’s disease which no known cures are available. Moreover, Examples 10-14 describes Compound-1 and Compound-1F effects on aging-induced deterioration of male rats’ sperm quality, aging- induced decrease in female fertility and detection of a senescence marker MPP1 in peripheral blood mononuclear cells.
Applicant also asserts that the guidance provided in the Examples featuring animal models of Alzheimer’s Disease is sufficient enough; however, McGonigle et al., Biochemical Pharmacology 87 (2014), 162–171 for example, states that, “some of the challenges associated with the evaluation and predictive validation of animal models, as well as methodological flaws in both preclinical and clinical study designs that may contribute to the current translational failure rate. The testing of disease hypotheses and NCEs (new chemical entities) in multiple disease models necessitates evaluation of pharmacokinetic/pharmacodynamic (PK/PD) relationships and the earlier development of validated disease-associated biomarkers to assess target engagement and NCE efficacy…” (Abstract). Thus, “The predictive value of an animal model is thus only as useful as the context in which it is interpreted...” as disclosed by McGonigle. Again, this echoes the lack of predictability in the art of using pharmaceuticals to affect enzymes, as described above by Kubinyi, Waldschmidt and Wermuth.
In view of the present disclosure, it is clear that there would be a significant amount of undue experimentation necessary to determine the full scope of the CNS-or neurodegenerative diseases treatable by the compounds of claim 19 based on the generic nature of the experimental data.
Consistent with this reasoning, Applicant’s Specification does not reasonably provide enablement for the full scope of the claimed invention. The Specification does not provide sufficient guidance on the manner and process using the claimed invention, 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. The Specification also does not set forth a best mode of the method for the treatment and prevention of the claimed CNS-or neurodegenerative diseases in a patient, comprising administering the full scope of the claimed compounds as per instant claim 1. Again, there is no data to support or even a method contemplated regarding the actual prevention of any of the claimed disease in a patient, wherein the patient is a mammalian or human patient. The rejection is maintained.
Noted Prior Art
Larbig et al. (J. Comb. Chem. 2006, 8, 480-490)
most active β-secretase (BACE-1) inhibitor compound:
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170
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represents a therapeutic for Alzheimer’s disease, and a close prior art compound
Godel et al. (US PG-PUB 2005/0119329)
[0267]: Some exemplary IC50 inhibition data for the β-secretase inhibition are given in Table 2 below:
TABLE 2
Example No.
IC50 in vitro (μM)
Example No.
IC50 in vitro (μM)
C12
12
G29
85
C9
13
C33
11
C19
15
I7
31
D2
33
J4
41
E7
57
K38
16
F5
14
K46
36
Godel claim 22:
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287
825
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.
Conclusion
No claims are allowed.
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). 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 nonprovisional extension fee (37 CFR 1.17(a)) 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.
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/C A/ Examiner, Art Unit 1622
December 20, 2025
/JAMES H ALSTRUM-ACEVEDO/Supervisory Patent Examiner, Art Unit 1622