DETAILED 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 .
Continued Examination Under 37 CFR 1.114
2. A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 10 January 2025 has been entered.
Status of Application, Amendments and/or Claims
3. The claims dated 1/10/2025 are under current examination. Claims 1-4, 6-15 and 18-22 are currently pending.
4. Claims 12-15 are withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to a nonelected invention, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 5 May 2021.
5. Claims 1-4, 6-11 and 18-22, drawn to a method of treating tremor and movement symptoms in an individual that has Parkinson’s disease, and a pharmaceutical composition comprising a Guanylate Cyclase 2C (GUCY2C) agonist as a sole active ingredient, are under examination in the instant application.
Rejections maintained
Claim Rejections - 35 USC § 103
6. The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
7. Claims 1, 3-4, 6-9, 11, and 19-21 are rejected under AIA 35 U.S.C. 103 as being unpatentable over Luo et al WO 2013/013338, 2013 (pages 1-10, Machine translation), as evidenced by Ganat et al (US 20150086481, 3/26/2015) and Kalia et al (Lancet 386: 896-912, 2015). The rejection is maintained for reasons of record in the Office Action dated 9/12/2024. Appropriate modifications are made to address the amendments.
8. The claims are drawn to a method of treating tremor and other movement symptoms in an individual having Parkinson’s disease (PD), comprising activating GUCY2C signaling by administering a GUCY2C agonist as a sole active pharmaceutical ingredient to the brain to increase dopamine production and ameliorate tremor and other movement symptoms, wherein the agonist is without an additional therapeutic moiety or an additional diagnostic moiety conjugated to it (claim 1); wherein: the individual has PD stage 1, 2, 3, or 4 (claim 3) and the agonist is guanylin or a functional derivative thereof (clam 4). Claims 6 and 7 are directed to increasing dopamine production by a dopaminergic cell, or increasing level of phosphorylation of Ser40 of tyrosine hydroxylase in a dopaminergic cell, comprising contacting the cell with a GUCY2C agonist as a sole active ingredient, wherein the agonist is without an additional therapeutic moiety or additional diagnostic moiety conjugated to it, to increase signaling and dopamine production/Ser40 phosphorylation of tyrosine hydroxylase in the cell; wherein: the agonist is guanylin or a functional derivative thereof (claims 8, 9), and the cell is a midbrain dopaminergic neuron (claims 11, 19). Claim 20 recites a pharmaceutical composition formulated for delivery to the brain by catheter or via epithelium of the nose comprising a GUCY2C agonist as a sole active pharmaceutical ingredient and a pharmaceutically acceptable carrier for treating an individual having PD, wherein the agonist is without an additional therapeutic moiety or additional diagnostic moiety conjugated to it; and the agonist is guanylin or a functional derivative thereof (claim 21).
9. Luo et al teach the use of substances or agents targeting guanylate cyclase – C (GC-C) (also known as GUCY2C) and protein kinase G (PKG) signaling pathway for treating midbrain dopamine neuronal diseases like PD (page 1, Title; Technical field; page 10, last para), wherein GC-C is specifically expressed on midbrain dopaminergic neurons (page 10, last para), and is a key receptor for intestinal hormones guanylin and uroguanylin, (page 1, last para). Luo et al also teach the making and using of a GC-C/PKG agonist or activator (or stimulator) as a drug for treating disorders like PD (page 2, last 2 lines; page 10, last 3 lines), suggesting GC-C agonist as the only therapeutic or a sole active pharmaceutical ingredient. The reference teaches a pharmaceutical product (composition) of guanylin or GC-C/PKG signaling pathway agonist (8-Br-cGMP) in pharmaceutical storage solutions, i.e., the presence of water and other components for storage (pharmaceutically acceptable excipient) (page 3, para 2; page 5, para 9) (instant claims 1, 20), indicating guanylin or GC-C/PKG agonist as the sole active pharmaceutical ingredient. Since the reference is silent about any additional therapeutic or diagnostic moiety conjugated to the agonist, the agonist is understandably without said moieties, absent any evidence to the contrary. Luo et al teach the addition of guanylin or uroguanylin in patch clamp recording of normal mouse midbrain dopamine neurons for testing GC-C activation (page 6, para 7, Example 2), suggesting that guanylin or uroguanylin can serve as GC-C agonist (instant claims 4, 8, 9, 21). The reference teaches that intracranial administration of PKG agonists (PKG mediates GC-C signaling (page 10, para 2 of Luo)) using indwelling drug delivery catheters, can reduce the elevated autonomous activity of GC-C knockout mice (page 5, para 4; page 10, para 2, 3; page 9, para 2), i.e., PKG agonists can correct the behavioral deficits of a GC-C knockout animal. Because Luo et al teach that PKG mediates GC-C signaling, and PKG agonists can correct deficits of GC-C deletion, PKG agonists can be considered to inherently function as a GC-C agonist. It is known that agonist peptides (like guanylin) target GUCY2C receptors on mDA neurons (mDA neurons are decreased in PD) as evidenced by Ganat et al (para 0002, 0003, 0040), therefore, administration of GC-C agonists, inherently implies that the agonist is contacting mDA neurons (instant claims 6, 7) upon administration, absent evidence to contrary (instant claims 1, 4, 8-9, 11, 19, 20-21).
10. The limitations of claims 6 and 7 respectively reciting “a method of increasing dopamine production...”, and “a method of increasing the level of phosphorylation of Ser40 of tyrosine hydroxylase…” in the preamble, recite an intended outcome of the claimed method steps and does not receive patentable weight. MPEP 2111.02(II) states that “If the body of a claim fully and intrinsically sets forth all of the limitations of the claimed invention, and the preamble merely states, for example, the purpose or intended use of the invention, rather than any distinct definition of any of the claimed invention's limitations, then the preamble is not considered a limitation and is of no significance to claim construction”. Here, the body of the claim sets forth all the steps and starting materials, and the preamble of the claim merely sets forth an intended use of the steps. Additionally, with respect to the conclusion, the "to increase signaling…" clause in claims 6 and 7 recites an intended result of the method, but not a step that is to be performed by the artisan. Upon performing the only step of administering a GC-C agonist as the only active ingredient to a subject (inherently resulting in “contacting... cell” for reasons stated earlier), one will necessarily have increased signaling, dopamine production and phosphorylation of tyrosine hydroxylase by GC-C in the cell.
11. Even though Luo et al do not teach administration to an individual that has PD, the reference explicitly states that the invention is directed to the use of GC-C and PKG signaling pathway as targets for treating midbrain dopamine neuronal diseases and presents a finite number (4) of such diseases, one of which is PD (page 1, background; page 10, last para). Luo et al therefore, clearly contemplate using the method for treating an individual having PD, absent evidence to contrary. It is noted that the limitation of claim 1 reciting “to increase dopamine production and ameliorate tremor and other movement symptoms” is directed to a result of the method of claim 1, but not a step that is to be performed by the artisan. Upon performing the only step of administering a GC-C agonist as the sole active ingredient to a subject having PD, one will necessarily have increased dopamine in mDA neurons as agonists like guanylin target GUCY2C receptors on mDA neurons, and treat symptoms of PD (like tremor, etc.). In considering the disclosure of a reference, it is proper to take into account not only specific teaching of the reference but also the inferences which one skilled in the art would be reasonably be expected to draw therefrom (In re Preda, 401 F.2d 825, 159 USPQ 342, 344 (CCPA 1968)). Also, a reference must be considered, under 35 U.S.C. 103, not only for what it expressly teaches but also for what it fairly suggests; all disclosures of prior art, including unpreferred embodiments, must be considered in determining obviousness (In re Burckel 201 USPQ 67 (CCPA 1979)).
12. Luo et al do not mention the stage of PD (instant claim 3). However, it is known that the onset of motor symptoms leads to diagnosis of PD with Lewy pathology that progresses through 4 stages, and that tremor is a major motor symptom of PD in these stages, as evidenced by Kalia et al (i.e., motor or movement symptoms are inherently present in all stages of PD or upon PD diagnosis) (page 900, Panel 4; Figure 2; page 896, col 2, last para; page 901, col 1, para 1).
13. Even though Luo et al teach that PKG mediates GC-C signaling and implicitly suggest that PKG agonist can inherently function as a GC-C activator, Luo et al do not teach the step of administering a GC-C agonist. Luo et al however, teach that GC-C agonists can be used for treating midbrain dopamine system diseases like PD (page 10, last 3 lines), obviously implying administration of a GC-C agonist.
14. It would have been, therefore, obvious to the person of ordinary skill in the art before the effective filing date of the claimed invention to modify a method of treating midbrain dopamine disorders comprising intracranial administration of a PKG agonist by using a GC-C agonist for treating PD and its symptoms like tremor and movement disorders, in view of the teachings of Luo et al. Because of functional similarity between GC-C agonist and PKG agonist as set forth in Luo teachings, it would be obvious to one of ordinary skill in the art to have a simple substitution of equivalent elements, i.e., the substitution of a PKG agonist for a GC-C agonist with predictable results (MPEP 2143 (B)) in view of Luo et al. The person of ordinary skill would have been motivated to try treating PD using a GC-C agonist as the “activity of the midbrain dopamine neuron can be selectively regulated by controlling the GC-C/PKG signaling pathway”, and PD is one of the four disorders taught to be closely associated with the midbrain dopamine system (Luo et al, page 10, last para). The person of ordinary skill in the art would have had a reasonable expectation of success based on the cumulative disclosures of Luo et al.
15. Thus, the claimed invention as a whole was prima facie obvious over the combined teachings of the prior art.
16. Claims 1-4, 6-11 and 18-22 are rejected under AIA 35 U.S.C. 103 as being unpatentable over Luo et al (2013), in view of Garcia et al (Curr Med Chem 21: 1171-1187, 2014). The rejection is maintained for reasons of record in the Office Action dated 9/12/2024. Appropriate modifications are made to address the amendments.
17. Claims 2, 10, 18 and 22 recite further administering or providing the cell with a phosphodiesterase (PDE) inhibitor.
18. The teachings of Luo et al are set forth above.
19. Luo et al do not teach a PDE inhibitor.
20. Garcia et al teach that PDE (e.g., PDE10A) inhibitors are therapeutic targets and disease modifying drugs for PD treatment (abstract). Even though the reference does not teach administering a PDE inhibitor to an individual having PD, it teaches that the inhibitors are important pharmacological agents for modifying diseases like PD, which would obviously imply that the inhibitors are being administered for treating individuals having PD. The reference concludes that PDE inhibitors are a "new treatment approach to Parkinson's disease" (page 1185, concluding para). (instant claims 2, 10, 18, 22).
21. Neither Luo et al. nor Garcia et al teach both GC-C agonist and PDE inhibitor (as the only active pharmaceutical ingredients) to be administered to the subject having PD, or be present in a pharmaceutical composition (in the same manner) for treating an individual having PD. However, in the absence of unexpected results, it would have been prima facie obvious to one of ordinary skill in the art to combine the teachings of the references to have both GC-C agonist and PDE inhibitor in a method, or in a composition for treating subjects with PD. Each of these therapeutics had been taught by the prior art to be useful agents functioning as sole active ingredients, for the treatment of PD. The instant situation is amenable to the type of analysis set forth in In re Kerkhoven, 205 USPQ 1069 (CCPA 1980) wherein the court held that it is prima facie obvious to combine two compositions each of which is taught by the prior art to be useful for the same purpose in order to for a third composition that is to be used for the very same purpose since the idea of combining them flows logically from there having been individually taught in the prior art. Applying the same logic to the instant method and composition claims, given the teaching of the prior art of using GC-C agonist and PDE inhibitor individually, as sole active ingredients for treating PD, it would have been obvious to use both GC-C agonist and PDE inhibitor for the same purpose or in the same composition, because the idea of doing so would have logically followed from there having been individually taught in the prior art to be useful for the same purpose.
22. Thus, the claimed invention as a whole was prima facie obvious over the combined teachings of the prior art.
Applicant’s Remarks
23. Applicant disagrees with the 103 rejections for the same reasons provided in the 6.6.24 response, and specifically refers to arguments presented with regards to Figures 5-7 of the Luo reference. Applicant presents additional arguments to show that the Luo reference fails to teach or suggest administration of the agonist “alone to treat tremor and other movement symptoms as presently claimed”. Applicant alleges that Luo "teaches away from the claimed subject matter", as it requires "co-stimulation of guanylin or uroguanylin with a second therapeutic compound". Going over the experiments and results presented in Figure 8 of the reference, Applicant concludes that according to Luo, guanylin or uroguanylin "does not independently exhibit an effect on dopaminergic cells", i.e., "the observed effect is attributable to the combination of two therapeutic agents, rather than solely to guanylin or uroguanylin". Applicant adds that claim 1 of the reference also suggests a combination of two therapeutic compounds. Applicant alleges that there would be no motivation from Luo teachings to administer a GUCY2C agonist as a sole active agent to treat PD symptoms as instantly claimed, and no expectation that the agonist alone will have a therapeutic effect on dopaminergic cells.
24. Applicant argues that claims 9 and 10 of Luo are directed to “both an agonist and an inhibitor of the GC-C/PKG” pathway for treating a disease (from the 4 diseases, which includes PD). Applicant asserts that Luo teachings claiming both an agonist and an inhibitor indicate uncertainty over “which or even whether such a compound works”, thereby providing an “invitation to perform further research”. Applicant adds that since Luo mentions the effect of both agonists and inhibitors in disease, the reference fails to teach or suggest that the agonist would provide the desired effect “when administered on its own".
25. Applicant argues that the GC-C knockout mouse model of Luo exhibit symptoms of human ADHD and therefore, the skilled artisan “would not be convinced” that the GC-C receptor is also involved in PD or the other diseases of the reference, and that the GC-C agonist will have a therapeutic effect when administered alone. Applicant also argues that the Luo teachings with regards to guanylin/uroguanylin enhancing mesencephalic dopamine neurons, which is mediated by metabotropic glutamate or acetylcholine receptors, does not indicate a treatment of PD using the GC-C agonist as the sole active ingredient, rather “such treatment would require the co-administration of the GC-C agonist with…an agonist of one or both of the metabotropic receptors”. Applicant therefore, reasons that Luo “does not disclose the use of guanylin or uroguanylin, nor any other GC-C agonist as a sole active …...treatment of Parkinson’s disease”.
26. Applicant argues that the suggestion by Examiner stating that PKG agonists can inherently function as GC-C agonist "is taken out of context", as "it is the other way around". Citing para bridging pages 2 and 3 of the translation, Applicant asserts that GC-C produces cGMP, which activates PKG. Applicant reasons that "while the PKG activator may have an effect on downstream signaling, it does not have functional properties of GC-C agonist" or activate GC-C, and therefore, cannot be "considered as a GC-C agonist".
27. Applicant concludes by requesting reconsideration and withdrawal of the 103 rejections for the above stated reasons.
28. Applicant’s arguments are fully considered, but not found to be persuasive. With regards to Applicant’s comments about Figures 5-7 (Example 2) of the Luo reference in the previous response, it is reiterated that the figures, only state that GC-C activation by the stated agonist does not have a significant impact on specific electrophysiological parameters of DA neurons (opening of ion exchange, excitatory response, inhibitory response) in healthy cells of normal adult mice. However, none of these parameters are required by instant claims. The claims (claims 1, 6,7) only require that the agonist (G or its functional derivative like UG) activates or increases GUCY2C signaling in a dopaminergic cell. Additionally, Example 2 describes the effect of G or UG on excitatory responses mediated by metabolic receptors (glutamate or acetylcholine) (page 7, Section 4), which is neither what is required by instant claims, nor this provides any indication for the use of a combination of two agents (in the instant method of composition of instant claims), as alleged by Applicant. As stated in the rejection, Luo et al teach the addition of G or UG in patch clamp recording of normal mouse mDA neurons for testing GC-C activation, implicitly suggesting that G or UG can serve as a GC-C agonist. Luo et al teach that GC-C is expressed on mDA neurons, wherein GC-C is a key receptor for guanylin or UG, and suggests GC-C agonist as a therapeutic or an active pharmaceutical ingredient for PD. Applicant therefore, seems to be arguing teachings of the cited art, which are not pertinent to instant claims.
29. Applicant’s arguments pertaining to Figure 8, emphasizing that G or UG has an effect on DA neuronal cells only upon co-stimulation by other agents, is considered, but not found to be persuasive for the same reasoning provided in the preceding paragraph. Figures 8B-D show that GC-C activation by G significantly increases the excitatory response by the co-stimulating agents (pages 15 and 16 of Luo translation (presented in IDS dated 4/25/2022)). i.e. the experiments depict an enhancing effect of G/UG on responses by glutamate or acetylcholine receptors. The argued results are once again not pertinent to instant claims, which only require GC-C activation by an agonist, NOT the effect of G/UG on other receptors/molecules. It is repeated, that there is no indication whatsoever in the reference, implicitly or explicitly, that a co-stimulation or, a combination of ingredients is required for activating GC-C (in context with the present claims), and that such combination is necessary in a pharmaceutical composition or in a method for treating PD. Luo et al teach that G or UG is “an active” component that activates GC-C, therefore, are agonists to GC-C which can be the only therapeutic or pharmaceutical ingredient for PD, as required by instant claims. Since Luo teaches the development and use of GC-C agonists (only) as (PD) therapeutics, the reference does not teach away from the claimed subject matter, as alleged by Applicant.
30. Applicant's pointing to claims 1, 9 and 10 of the reference to show that Luo suggests a combination comprising an agonist and an inhibitor of GC-C/PKG pathway for treating a disease, is not found to be persuasive. The claims, in particular claim 9, clearly recite "agonists or inhibitors of the GC-C/PKG signaling pathway" (emphasis added) in drug preparation for treating diseases related to "midbrain dopamine system". Contrary to Applicant’s argument, the same (agonists or inhibitors…) is also stated in the last 2 lines of page 2 of the machine translation (Luo). The reference exemplifies (Example 4) that intracranially administering the PKG stimulator/activator 8-Br-cGMP (sole ingredient) to a GC-C knockout mice (having low dopamine levels and high activity), results in reduced autonomous activity. The reference teaches that “the agonist of the GC-C/PKG signaling pathway is specifically an activator of protein kinase G 8-Br-cGMP” (page 3, para 2). Applicant's repetitive assertion that the reference suggests using a combination of two or more therapeutic agents therefore, has no basis and is taken out of context.
31. Applicant’s arguments that the GC-C knockout mouse model of Luo exhibit symptoms of human ADHD and therefore, it will not be convincing that this would be applicable to other diseases, are considered. The reference teaches that extracellular DA levels of GC-C knockout mice are significantly lower than wild type mice (page 9, para 9; Figure 22), and demonstrates that administration of an agonist of the GC-C/PKG signaling pathway like 8-Br-cGMP (alone) can reverse behavioral symptoms of the knockout model. Even though the GC-C knockout mouse is a model for human ADHD, Luo et al teach that “GC-C knockout mice provide a good opportunity for further study of the correlation and mechanism of action between GC-C and midbrain dopamine neuron-related diseases” (page 10, last para), thereby suggesting that the model can be applied to the four stated diseases associated with the midbrain dopamine system - ADHD, schizophrenia, PD and drug addiction, wherein mDA (midbrain dopamine neurons (mDA)) neurons are decreased in PD.
32. Applicant’s questioning as to whether the agonist will have a therapeutic effect when administered alone, is not found to be persuasive for reasons mentioned above. Applicant's repeated argument that Luo does not teach administration of GC-C agonist as the sole active ingredient for treating PD, rather implies a co-administration of the GC-agonist with other agonists of metabolic receptors, is not persuasive for reasons provided in the preceding paragraphs. Applicant seems to be picking on the teachings of the reference out of context. Nowhere, the reference teaches or even suggests that both an agonist and an inhibitor of the GC-C/PKG pathway are required, or a combination of active ingredients/other agonists is needed, either to be administered for treating any of the four diseases of the reference, or in a pharmaceutical composition for treating the same.
33. Applicant’s argument that a PKG activator is not a GC-C agonist is considered. As stated in the rejection, PKG mediates GC-C signaling (even if it is downstream as asserted by Applicant) and a PKG stimulator (agonist) corrects the behavioral deficits of a GC-C knockout animal. As noted above Luo et al teach that “the agonist of the GC-C/PKG signaling pathway is specifically an activator of protein kinase G 8-Br-cGMP”, which indicates that a PKG agonist can reasonably be equated with a GC-C agonist in terms of function. PKG agonists can therefore, be considered to have the functional properties of GC-C (or its agonists), as also derived from Example 4 of the reference (by reducing the autonomous activity of GC-C knockout mice).
34. Applicant’s remarks on each experiment in the Luo reference have been considered, however, are not found to be pertinent or persuasive for reasons explained above. Applicant's argument that Luo teachings "by no means suggest treating of PD nor whether the tested PKG activator would have an actual effect in treating of PD", seem to question the teachings of the reference. Applicant’s remarks about uncertainty in effectiveness of the compound that would only provide an “invitation to perform further research”, seem to allege that Luo et al is not enabled for the instant method claims. However, a non-enabling disclosure is prior art for all it teaches for purposes of determining obviousness under 35 U.S.C. 103. Symbol Techs. Inc. v. Opticon Inc., 935 F.2d 1569, 1578, 19 USPQ2d 1241, 1247 (Fed. Cir. 1991); Beckman Instruments v. LKB Produkter AB, 892 F.2d 1547, 1551, 13 USPQ2d 1301, 1304 (Fed. Cir. 1989) [MPEP 2158].
35. For reasons stated, the 103 rejections are maintained.
New Rejections
Claim Rejections - 35 USC § 112, 4th paragraph
36. The following is a quotation of 35 U.S.C. 112(d):
(d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
37. The following is a quotation of pre-AIA 35 U.S.C. 112, fourth paragraph:
Subject to the following paragraph [i.e., the fifth paragraph of pre-AIA 35 U.S.C. 112], a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
38. Claims 2, 10, 18 and 22 are rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, fourth paragraph, as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends.
39. Claims 2, 10, 18 and 22 further broadens the limitations of claims 1, 6, 7 and 20 respectively. Claims 2, 10, 18 and 22 recite that the “GUCY2C agonist and the PDE inhibitor are the only active pharmaceutical ingredients”. However, claims 1, 6, 7 and 20 recite “GUCY2C agonist as a sole active pharmaceutical ingredient”. Since dependent claims 2, 10, 18 and 22 recite “further comprising/comprises …a PDE inhibitor”, wherein the PDE inhibitor is also an “active pharmaceutical ingredient”, claims 2, 10, 18 and 22 are broadening the scope of corresponding independent claims 1, 6, 7 and 20.
40. Applicant may cancel the claim(s), amend the claim(s) to place the claim(s) in proper dependent form, rewrite the claim(s) in independent form, or present a sufficient showing that the dependent claim(s) complies with the statutory requirements.
Double Patenting
41. The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
42. A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
43. The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
44. The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
45. Claims 1-4, 6-11 and 18-22 are provisionally rejected on the ground of nonstatutory obviousness-type double patenting as being unpatentable over claims 8-24 of co-pending application number 17/271,978 in view of Luo et al (2013).
Although the conflicting claims are not identical, they are not patentably distinct from each other because in each case the claims are drawn to a method of treating an individual suffering from PD, comprising administering GUCY2C agonist like guanylin, and a PDE inhibitor.
The only differences between the two sets of claims are:
(i) Instant claims recite comprising GUCY2C agonist as an active pharmaceutical ingredient, and a pharmaceutical composition, along with PDE inhibitor, while ‘978 claims do not recite a pharmaceutical composition. However, the ‘978 claims reciting treating PD (a human disease) using PDE inhibitor and GUCY2C agonist, are obviously contemplating a pharmaceutical composition as a therapeutic, as also taught on page 14, lines 40-42 of the ‘978 specification.
(ii) Instant claims recite modes of administration of the pharmaceutical composition, while the ‘978 claims do not have this recitation. However, this would be obvious as the same formulation is being administered to the same population for treating PD, which is also taught on page 17, lines 35-42 of the ‘978 specification.
(iii) Instant claims 1, 6-7 and 20 recite the use of GUCY2C agonist as the sole ingredient, while the ‘978 claims do not have this limitation. However, the use of said agonist alone for treating PD would be obvious in view of the teachings of Luo et al for reasons stated above. Also, the ‘978 specification contemplates the use of a GUCY2C agonist (alone) for treating an individual having PD, since it is “active on its own” and can be the “only pharmaceutically active ingredient” (page 4, lines 17-18; page 14, lines 23-26).
46. This is a provisional obviousness-type double patenting rejection because the conflicting claims have not in fact been patented.
Applicant’s Remarks:
47. Applicant requests that the provisional double patenting rejection be held in abeyance until allowable subject matter is indicated.
48. Applicant’s argument is considered, however, is not found to be persuasive. The rejection has not been overcome by amendment or the filing of an approved terminal disclaimer. The rejection is therefore, restated.
Conclusion
49. No claims are allowed.
50. Any inquiry concerning this communication or earlier communications from the examiner should be directed to Aditi Dutt whose telephone number is (571)272-9037. The examiner can normally be reached on M-F 9:00am-5:00pm.
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52. If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Jeffrey Stucker, can be reached on 571-272-0911. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/A. D./
Examiner, Art Unit 1675
18 April 2026
/KIMBERLY BALLARD/Primary Examiner, Art Unit 1675
Prosecution Insights