FINAL ACTION
Notice of Pre-AIA or AIA Status
1. The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Claim Status
2. The amendments and remarks filed April 20, 2026 are acknowledged. Claims 2-3 and 17-20 are canceled; claims 1 and 15-16 are amended. Claims 1 and 4-16 are pending and under examination.
Withdrawn Rejections
3. A. The rejection of claims 17-20 under 35 USC § 101, for being drawn to non-statutory subject matter, is withdrawn in light of Applicant’s cancelation of the claims. See section 3 of the previous Office action.
B. The rejection of claims 2-3 and 17-20 under 35 USC § 112(a) (written description) are withdrawn in light of Applicant’s cancelation of the claims. See sections 4-5 of the previous Office action.
C. The rejection of claims 15-20 under 35 USC § 112(b), for lack of antecedent basis or clarity, is withdrawn in light of Applicant’s amendments to claims 15-16 and the cancellation of claims 17-20. See sections 6-8 of the previous Office action.
D. The rejection of claims 2-3 and 17-19 under 35 USC § 102 (a)(1), for being anticipated by Zhang et al., are withdrawn in light of Applicant’s cancelation of the claims. See sections 9-10 of the previous Office action.
Maintained Rejections
4. The rejection of claims 1 and 4-16 under 35 USC §112(a) (written description) as set forth in the Nonfinal Office action, sections 4-5, is maintained.
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.
Claims 1 and 4-16 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 claims contain 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.
The MPEP states that the purpose of the written description requirement is to ensure that the inventor had possession, as of the filing date of the application, of the specific subject matter later claimed. The MPEP lists factors that can be used to determine if sufficient evidence of possession has been furnished in the disclosure of the application. These include “level of skill and knowledge in the art, partial structure, physical and/or chemical properties, functional characteristics alone or coupled with a known or disclosed correlation between structure and function, and the method of making the claimed invention.”
The written description requirement for a claimed genus may be satisfied through sufficient description of a representative number of species by actual reduction to practice, disclosure of drawings, or by disclosure of relevant identifying characteristics, for example, structure or other physical and/or chemical properties, by functional characteristics coupled with a known or disclosed correlation between function and structure, or by a combination of such identifying characteristics, sufficient to show the Applicants were in possession of the claimed genus.
The instant claims are directed to methods for treating movement disorders comprising administering a CCK-B receptor agonist; wherein the movement disorders are caused by a condition selected from the group consisting of a brain injury, a stroke, Chorea, Dystonia, Parkinson's disease, brain infarction, neuron death or loss of neuronal plasticity due to aging; and methods for regaining motor learning ability comprising administering a CCK-B receptor agonist (e.g., claim 10). The methods further recite various dosing regimens and timelines.
The specification provides examples of (i) characterizing CCK knockout or antagonism in the motor cortex (see FIGs. 1-5); (ii) treating movement disorders or motor learning defects caused by CCK knockout by administering a CCK-B receptor agonist (see FIGs. 6C-6E); and (iii) restoring neuronal plasticity defects caused by CCK knockout by administering a CCK-B receptor agonist (see FIGs. 6A-6B). No other experimental models suitable as a proxy for movement disorders were tested. However, the claims are directed to a genus of movement disorders far broader than single species of movement disorder (e.g., caused by CCK knockout or antagonism) supported by the examples.
The claims recite methods for treating a broad genera of movement disorders (including: brain injury, a stroke, Chorea, Dystonia, Parkinson's disease, brain infarction, neuron death or less of neuronal plasticity due to aging) and motor learning deficits. The specification only teaches a single example of treating a movement disorder, e.g., treating a movement disorder specifically caused by CCK knockout. However, the claims are not limited to a movement disorder or motor learning deficit caused by CCK knockout. The specification also provides no guidance as to what other movement disorders may be related to a CCK deficiency, and neither would a skilled person appreciate the claim-recited movement disorders to be related to a CCK deficiency. Therefore, the specification provides insufficient written description to support the genus encompassed by the claim. Vas-Cath Inc. v. Mahurkar, 19 USPQ2d 1111, makes clear that:
"applicant must convey with reasonable clarity to those skilled in the art that, as of the filing date sought, he or she was in possession of the invention. The invention is, for purposes of the 'written description' inquiry, whatever is now claimed." (See page 1117.) The specification does not "clearly allow persons of ordinary skill in the art to recognize that [he or she] invented what is claimed." (See Vas-Cath at page 1116.)
A skilled person would recognize CCK-B receptor agonism as effective for the treatment of Parkinson’s disease (e.g., Zhang et al. "Neuroprotective effects of a cholecystokinin analogue in the 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine Parkinson’s disease mouse model." Frontiers in neuroscience 16 (2022): 814430.) at abstract); and for enhancing some forms of memory (e.g., “encoding sound-sound, visuoauditory, fear, and spatial memory”; instant specification at paragraph [0113]). However, it would not have been apparent that successfully treating a movement disorder caused by the artificial reduction of CCK in the motor cortex and having no know relevance to a disease state with a CCK-B receptor agonist (i.e., as demonstrated in the specification) may also predict the treatment of movement disorders with etiologies that may originate wholly outside the motor cortex. For example, Parkinson’s disease is caused by a loss of dopaminergic neurons in the substantia nigra, and cerebellar/brainstem stroke or infarct will also cause movement disorders. Therefore, there is no nexus between the instantly demonstrated rescue of CCK deficiencies in the motor cortex and treating neurological disorders only tangentially related to the motor cortex, as encompassed by the instant claims. Applicant also has not established any nexus that CCK abnormalities specifically exist in the relevant subject populations, e.g., subjects suffering from a “cryptogenic stroke” (e.g., claim 8), to establish possession of the claimed invention. In other words, a skilled person would have no reason to believe the claim-recited CCK-B receptor agonist treatments may beneficially treat the broad genus of movement disorders instantly claimed since the specification only demonstrates a single species of movement disorder: the treatment of a motor disorder specifically caused by CCK knockout.
Therefore, neither the art nor the specification provides a sufficient representative number of movement disorders to meet the written description requirements.
MPEP § 2163.02 states, “[a]n objective standard for determining compliance with the written description requirement is, 'does the description clearly allow person of ordinary skill in the art to recognize that he or she invented what is claimed’”. The courts have decided: the purpose of the "written description" requirement is broader than to merely explain how to "make and use"; the Applicant must convey with reasonable clarity to those skilled in the art, that as of the filing date sought, he or she was in possession of the invention. The invention is for purposes of the “written description” inquiry, whatever is now claimed. See Vas-Cath, Inc v. Mahurkar, 935 F.2d 1555, 1563-64, 19 USPQ2d 1111, 1117 (Federal Circuit, 1991).
Furthermore, the written description provision of 35 USC §112 is severable from its enablement provision; and adequate written description requires more than a mere statement that it is part of the invention and reference to a potential method for isolating it. Fiers v. Revel, 25 USPQ2d 1601, 1606 (CAFC 1993). And Amgen Inc. v. Chugai Pharmaceutical Co. Ltd., 18 USPQ2d 1016. Moreover, an adequate written description of the claimed invention must include sufficient description of at least a representative number of species by actual reduction to practice, reduction to drawings, or by disclosure of relevant, identifying characteristics sufficient to show that Applicant was in possession of the claimed genus. However, factual evidence of an actual reduction to practice has not been disclosed by Applicant in the specification; nor has Applicant shown the invention was “ready for patenting” by disclosure of drawings or structural chemical formulas that show that the invention was complete; nor has the Applicant described distinguishing identifying characteristics sufficient to show that Applicant were in possession of the claimed invention at the time the application was filed.
Therefore, for all these reasons the specification lacks adequate written description, and one of skill in the art cannot reasonably conclude that Applicant had possession of the claimed invention at the time the instant application was filed.
Applicant’s Arguments
A. Applicant argues that: the claimed method encompasses the treatment of movement disorders caused by a condition selected from the group consisting of a brain injury, a stroke, Chorea, Dystonia, Parkinson’s disease, brain infarction, neuron death or less of neuronal plasticity due to aging, and a combination thereof; and that “while all of these disorders have distinct etiologies, they share a common pathological mechanism: neuronal death or damage leading to disruption or dysfunction of neural circuit
B. Applicant argues that the “CCK knockout model employed in the specification is not limited to mimicking a single disease state.” Applicant urges that the “CCK knockout model serves as a representative model of the shared pathological basis [of the movement disorders encompassed by the claims]—i.e., the impairment of neuronal plasticity.” Applicant points to examples in the specification demonstrating that “CCK from the rhinal cortex may promote dexterous motor skill learning by regulating the activity of the motor cortex of mice, and CCK-B receptor agonist such as CCK4 is capable of rescuing neuroplasticity and promoting motor skill learning.” Applicant urges that “this mechanism of action is directly applicable to all claimed movement disorders, as each involves a need for plasticity-driven repair.” Applicant concludes that the “disclosure proves a reasonable basis to conclude that the therapeutic effect observed in the CCK knockout model can be extended across the entire genus of claimed movement disorders.”
Response to Arguments
A. Applicant’s arguments have been fully considered but they are not persuasive. With regards to the Applicant’s argument that that “while all of these disorders have distinct etiologies, they share a common pathological mechanism: neuronal death or damage leading to disruption or dysfunction of neural circuit connections. Recovery from these movement disorder by rehabilitation relies on neuroplasticity,” the Office disagrees because: the claims encompass movement disorders / motor learning defects such as Parkinson’s disease (PD) that do not rely upon neuroplasticity for recovery therefrom. As shown by Zhang et al., PD is caused by the death of dopaminergic neurons in the substantia nigra, and CCK treatment prevented this death (i.e., promoted PD recovery) by a neuroprotective mechanism, not by neuroplasticity. In other words, recovery from the PD movement disorder did not rely on neuroplasticity, and therefore it is not true that “Recovery from [all of these] these movement disorders by rehabilitation relies on neuroplasticity” as alleged by Applicant.
Zhang et al. explains that: “The typical pathological manifestations of PD include a progressive loss and death of dopaminergic neurons in the substantia nigra pars compacta (SNpc),” and does not suggest that neuronal plasticity impairments, plays a role in the pathology or recovery of PD. Zhang et al. at introduction. Zhang et al. explains that the CCK analog treated PD by its neuroprotective effects, not by enhancing neuroplasticity, e.g., “The CCK analogue administration also restored tyrosine hydroxylase (TH) positive dopaminergic neurons number and synapse number (synaptophysin levels) in the substantia nigra pars compacta (SNpc). The CCK analogue decreased glia activation and neuroinflammation in the SNpc, and regulated autophagy dysfunction induced by MPTP. CCK analogue protected against mitochondrial damage and ER stress, and also decreased the ratio of apoptosis signaling molecules Bax/Bcl-2. Importantly, the CCK analogue improved the decrease of p-CREBS133 growth factor signaling in the SNpc. Therefore, the CCK analogue promotes cell survival of dopaminergic neuron in the SNpc by activating the cAMP/PKA/CREB pathway that also inhibits apoptosis and regulates autophagy impairment.” Zhang et al. at abstract.
Therefore, both the art and the specification provide insufficient written description to support the genus of causes of movement disorder encompassed by the claims because: the art already of record indicates that at least the claim-recited PD cause of movement disorder does not rely upon neuroplasticity for recovery therefrom.
B. With regards to Applicant’s argument that: the CCK knockout model employed in the specification is not limited to mimicking a single disease state; the CCK knockout model employed in the specification is representative of pathological basis—impairment of neuronal plasticity [i.e., in the motor cortex]; and that CCK from rhinal cortex may promote motor skill learning by regulating the activity of the motor cortex, the Office agrees. However, as discussed above, this is not a shared pathological basis of all the claim-recited movement disorders, e.g., PD at claim 1, which has a pathological basis of “progressive loss and death of dopaminergic neurons in the substantia nigra pars compacta (SNpc)” wholly unrelated to neuronal plasticity in the motor cortex. Therefore, Applicant’s argument does not address the full breadth of the instant claims, e.g., that the instant claims encompass PD and fails to properly associate the neuronal plasticity demonstrated in the specification with the motor cortex.
Applicant’s conclusion that the “disclosure proves a reasonable basis to conclude that the therapeutic effect observed in the CCK knockout model can be extended across the entire genus of claimed movement disorders” because “each involves a need for plasticity-driven repair” lacks merit because, as discussed above, Zhang et al. shows that at least PD does not involve a need for plasticity-driven repair; rather PD involves a need for neuroprotection of dopaminergic neurons in the SNpc. Accordingly, both the art and the specification provide insufficient written description to support the genus of causes of movement disorder encompassed by the claims
5. The rejection of claims 1, 4-7, 10-14, and 16 under 102 (a)(1) as set forth in the Nonfinal Office action at sections 9-10 is maintained.
Claim Rejections - 35 USC § 102
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.
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.
6. Claims 1, 4-7, 10-14, and 16 are rejected under 35 U.S.C. 102 (a)(1) as being anticipated by Zhang et al. (Zhang, Zijuan, et al. "Neuroprotective effects of a cholecystokinin analogue in the 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine Parkinson’s disease mouse model." Frontiers in neuroscience 16 (2022): 814430.)
Zhang et al. teaches the treatment of a MPTP Parkinson’s disease mouse model (i.e., a movement disorder) with a CCK8 analog (Abstract). The CCK8 analog is a CCK-B receptor agonist, e.g., “CCKR-2 [i.e., the CCK-B receptor] is predominantly expressed in the brain and is activated by short fragments such as CCK-8” (page 2, left column, first paragraph). Accordingly, Zhang et al teaches a method for treating movement disorders comprising a step of administrating a CCK-B receptor agonist to a subject in need thereof, wherein the movement disorders are caused by a condition selected from the group consisting of a brain injury, a stroke, Chorea, Dystonia, Parkinson's disease, brain infarction, neuron death or less of neuronal plasticity due to aging, and a combination thereof.
Zhang et al. teaches a CCK8 analog. however, a CCK8 analog is also a CCK4 analog. Applicant’s specification at paragraph [0052] describes CCK4 analogs as:
The CCK4 analogues may have structures similar to CCK4, and thus we can expect similar functions. It is believed that the main structure of CCK4 (Trp-Met-Asp-Phe-NH2) is the most critical part, some modifications for C-terminal, N-terminal or both to protect the stability or activity, or replacement of the sulfhydryl in Met with other radical without changing the backbone of the molecule may lead to analogues having similar functions as CCK4 itself. In some embodiment, the CCK-B receptor agonist is CCK4. Without intending to be bound by theory, it is believed that CCK4 can pass through the brain-blood barrier, may have fewer side effects and high efficiency with low dosage. In contrast, it is believed that other types of CCK peptides including CCK58, CCK32, and CCK8 cannot pass through the brain-blood barrier.
The specification therefore defines CCK4 analogs as having similar structure (especially the main structure) to CCK4 and by having similar functions to CCK4 (e.g., CCK-B receptor agonism and able to pass through the blood-brain barrier). The CCK8 of Zhang et al. definitively meets all of these criteria.
CCK8 is a CCK4 analog within the meaning of Applicant’s specification because (i) it shares the same main structure (Trp-Met-Asp-Phe-NH2) with CCK4 (see Zhang et al. at page 2, “Peptides and Chemicals”); (ii) it is an agonist of the CCK-B receptor like CCK4 (see above); and it can pass through the brain-blood barrier contrary to Applicant’s assertion in the specification, e.g., “[t]he CCK[8] analogue carboxyfluorescein can cross the BBB and is abundantly expressed in the substantia nigra and striatum” (page 4, “Assessment of CCK Analogue”). Therefore, Zhang et al. anticipates the claim-recited CCK4 analog (claim 1).
Zhang et al. further teaches administering the CCK-B receptor agonist intraperitoneally, e.g., “CCK-AC were injected at 50 nmol/kg ip” (page 2, “Assessment of Cholecystokinin”) (claim 4). Zhang et al. further teaches administering the CCK-B receptor agonist over a period of two weeks (Figure 2A) (claim 5). Zhang et al. further teaches administering the CCK-B receptor agonist at 50 nmol/kg (page 2, “Assessment of Cholecystokinin”). The common Trp-Met-Asp-Phe-NH2 sequence of Applicant’s CCK4 and Zhang’s CCK8 analog has a peptide molecular weight of about 596.71 g/mol, and so 50 nmol/kg converts1 to a dosage of about 0.0298 mg/kg of the CCK4 Trp-Met-Asp-Phe-NH2 sequence (claim 6).
Zhang et al. further teaches the CCK-B receptor agonist is effective in regaining motor learning ability in adulthood. More specifically, Zhang et al. teaches that a CCK-B receptor agonist “significantly reversed” the “impairments in muscular strength and movement balance” induced by the MPTP Parkinson’s disease model (page 4, right column, first paragraph). The specific methodology employed demonstrates that this reversal is an improvement in motor learning rather than mere physical recovery because the rotarod test “was used to assess the balance and motor coordination ability of mice,” and notably, the “mice were trained for 3 min every day, lasting for three consecutive days” (page 3, Behavioral Tests, Rotarod). Per the experimental timeline in Figure 2A, this training occurred between days 12 and 14, subsequent to the administration of MPTP. Because the subjects acquired the coordination necessary for the rotarod test only after the establishment of the movement disorder, their performance represents the successful acquisition of a new motor skill. The CCK-B receptor agonist-treated mice therefore regained motor learning ability because the loss of such ability was “significantly reversed” (Figure 2D) relative to the MPTP-only control. Finally, Zhang et al. teaches this effect in maturity, as the “subjects” were 2-month-old adult mice (page 2) (claim 7). The aforementioned passages also teach the method of claims 10-14 and 16, directed to methods of regaining motor learning ability having the same limitations as claims 1 and 4-7.
Applicant’s Arguments
Applicant summarizes the rejection:
Zhang et al. teaches the treatment of a MPTP Parkinson's disease mouse model (i.e., a movement disorder) with a CCK8 analog (Abstract). The examiner further contends that the CCK8 analog is also a CCK4 analog as defined in the present application. On this basis, the examiner thinks the claimed invention is anticipated by Zhang et al. The Applicant respectfully disagrees for the following reasons.
The specification of this application at paragraph [0053] provides (with emphasis by the Office included):
[0053] ... The CCK4 analogues may have structures similar to CCK4, and thus we can expect similar functions. It is believed that the main structure of CCK4 (Trp-Met-Asp- Phe-NH2) is the most critical part, some modifications for C-terminal, N-terminal or both to protect the stability or activity, or replacement of the sulfydryl in Met with other radical without changing the backbone of the molecule may lead to analogues having similar functions as CCK4 itself. In some embodiment, the CCK-B receptor agonist is CCK4. Without intending to be bound by theory, it is believed that CCK4 can pass through the brain-blood barrier, may have fewer side effects and high efficiency with low dosage. In contrast, it is believed that other types of CCK peptides including CCK58, CCK32, and CCK8 cannot pass through the brain-blood barrier. After citing the foregoing, the Office states that (with emphasis by the Office included):
The specification therefore defines CCK4 analogs as having similar structure (especially the main structure) to CCK4 and by having similar functions to CCK4 (e.g., CCK-B receptor agonism and able to pass through the blood-brain barrier). The CCK8 of Zhang et al. definitively meets all of these criteria.
Applicant asserts the Office overlooked a critical limitation in para. [0053] regarding permissible backbone modifications:
Regarding the Office’s position that para. [0053] of the instant specification shows that the CCK8 analog of Zhang et al. is a CCK4 analog (i.e., para. [0053] defines CCK4 analogs as having similar structure (especially the main structure) to CCK4 and by having similar functions to CCK4 (e.g., CCK-B receptor agonism and being able to pass through the blood-brain barrier) and therefore the CCK8 of Zhang et al. definitively meets all of these criteria by disclosing the main structure of CCK4, being able to pass through the BBB, and having CCK-B receptor agonism), Applicant asserts that the Office appears to have overlooked a critical limitation regarding permissible modifications to the CCK4 structure. Specifically, Applicant asserts that any modification to the main structure of CCK4 must not alter the backbone of the molecule. Therefore, Applicant submits that the limitation in para. [0053] which allows for "some modifications for C-terminal, N-terminal or both to protect the stability or activity, or replacement of the sulfhydryl in Met with other radical without changing the backbone of the molecule" serves to preclude the CCK8 analog disclosed in Zhang et al. because the compound in Zhang allegedly constitutes a backbone-modified analog, placing it outside the scope of the claimed invention.
Response to Arguments
Applicant’s arguments have been fully considered but they are not persuasive. With regards to Applicant’s argument that “the Office overlooked a critical limitation in para. [0053] regarding permissible backbone modifications,” and that “any modification to the main structure of CCK4 must not alter the backbone of the molecule” the Office disagrees because: no modifications to the backbone of CCK4 are required to arrive at CCK8, as discussed below.
As highlighted by Applicant, the specification at para. [0053] states that CCK4 analogs allow for: “[i] some modification for C-terminal, N-terminal or both [ii] to protect the stability or activity, or replacement of the sulfhydryl in Met with other radical [iii] without changing the backbone of the molecule.” The CCK8 analog of Zhang et al. represents (i) “some modification” to the N-terminal of CCK4; that (ii) protects the stability or activity of the molecule as evidenced by Irwin et al. ("Beneficial effects of the novel cholecystokinin agonist (pGlu-Gln)-CCK-8 in mouse models of obesity/diabetes." Diabetologia 55.10 (2012): 2747-2758; cited by Zhang et al. as the source of the CCK8 analog); and (ii) does not change the backbone of CCK4, as discussed below. Therefore, the CCK8 analog of Zhang et al. is a CCK4 analog within the meaning of the instant specification because it meets all of points (i)-(iii) discussed at para. [0053] of the instant specification:
(i) CCK4’s sequence is WMDF-NH2 as indicated at para. [0053]; and the sequence of Zhang et al.’s CCK8 is H-pEQDYTGWMDF-NH2. Zhang et al. at peptides and chemicals. Therefore, “some modification,” e.g., H-pEQDYTG, is added to the N-terminal of WMDF-NH2 (CCK4) to obtain the CCK8 analog.
(ii) Furthermore, Irwin et al. (cited by Zhang et al. as the source of the CCK8 analog) indicates the N-terminal modification (H-pEQ) protects the stability (e.g., resistance to enzymatic degradation) of the molecule. Irwin et al at. at abstract.
(iii) This addition does not modify the backbone of WMDF-NH2 because the backbone of CCK4 (WMDF-NH2) is atomically identical to the WMDF-NH2 sequence in Zhang et al.’s CCK8 (pEQDYTGWMDF-NH2). Additionally, H-pEQDYTG is added to backbone WMDF-NH2, as would be required for any of the “some modifications for C-terminal, N-terminal, or both” encompassed by the CCK4 analogs of para. [0053]. Accordingly, Zhang et al. does not modify the backbone of CCK4 to obtain the CCK8 analog because the CCK8 analog comprises the exact same CCK4 / backbone.
Therefore, the Office has not overlooked a critical limitation regarding permissible modifications to the CCK4 structure as alleged by Applicant, and the CCK8 analog of Zhang et al. definitively meets all the criteria of a CCK4 “analog” as specified at para. [0053] of the instant specification, thereby anticipating the CCK “analog” recited at instant claim 1.
Conclusion
10. No claim is allowed.
11. THIS ACTION IS MADE FINAL. Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any 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.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to BRANDON R SCHWECHTER whose telephone number is (571)272-1270. The examiner can normally be reached M-Th 7-5 EST.
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/BRANDON R SCHWECHTER/
Examiner, Art Unit 1674
/VANESSA L. FORD/ Supervisory Patent Examiner, Art Unit 1674
1 To convert a dose of 50 nmol/kg for a peptide having a molecular weight of 596.71 g/mol into mg/kg, the molar concentration is multiplied by the molecular weight and adjusted for unit scale. Specifically, the dose of 50 x 10-9 mol/kg is multiplied by 596.71 g/mol, resulting in a mass of 2.98355 x 10-5 g/kg. To convert this value from grams to milligrams, it is multiplied by 1,000, which yields a final mass-based concentration of 0.0298 mg/kg.
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