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 .
DETAILED ACTION
Response to Amendment
Acknowledgment is made of the amendment filed on 02/10/2026, wherein claim 1 is amended to remove “whereby the administration suppresses the expression of a Kca2.3 channel protein in a cell membrane” and recite “wherein the subject suffers from liver fibrosis and pulmonary fibrosis characterized by elevated KCa2.3 expression”.
Election/Restriction
Applicant elected the species: i) pulmonary fibrosis ii) compound species of Formula A: 2-(benzhydrylsulfinyl)acetamide (i.e. modafinil) without traverse on 06/10/2024.
Status of Claims
Claims 1, 6, 9 and 10 are pending.
Claims 6 and 9 remain withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a non-elected invention/species.
Claim 1 and 10 are currently under examination.
Response to Declaration
The Declaration under 37 CFR 1.132 by Suh filed 02/10/2026 is fully considered, but NOT persuasive to overcome the rejection of claims over Suh’412 in view of Roach and Organ under 35 U.S.C. 103.
Suh Declaration argues prior art emphasized Kca3.1 in pulmonary fibrosis and described "minimal if any evidence" for Kca 2.1-2.3 channels (including Kca2.3) in fibrosis, instant application discloses treatment of pulmonary fibrosis by suppressing Kca2.3 expression and modafinil decreases Kca2.3 expression in fibrogenic cellular contexts.
The Examiner does not dispute modafinil decreases Kca2.3 expression. However, it’s already known modafinil suppresses KCa 3.1 expression as taught by Suh’412, Kca3.1 is a well-supported ion-channel target in pulmonary fibrosis taught by Roach and Organ as Suh Declaration agrees, POSA would be motivated to explore modafinil for treating pulmonary fibrosis based on combined teaching of KCa 3.1 by prior art and reasonably expect modafinil exhibit efficacy in treating pulmonary fibrosis with elevated KCa 3.1. Although Kca2.3 alone is not well- known for causing pathological fibrosis as Suh Declaration argues, Kca2.3 and Kca 3.1 are closely related ion channel activated by increases in the concentration of Ca2+ and associated with fibrosis markers, both KCa 3.1 and Kca2.3 are expected to coexist in the subject suffering from pulmonary fibrosis, such that subjects with elevated Kca2.3 substantially overlaps with those having elevated KCa3.1. Accordingly, it would have been prima facie obvious for POSA to extend modafinil treatment for subjects with elevated KCa 3.1 to subjects with elevated KCa 2.3. A POSA would reasonably expect modafinil exhibit certain activity/efficacy in treating pulmonary fibrosis with elevated KCa 2.3 based on their close relationship in absence of evidence to the contrary.
Suh Declaration argues Li 2023 provides post-priority experimental evidence that pulmonary fibrosis is characterized by elevated Kca2.3 expression and that modafinil treatment reduces Kca2.3 (and Kca3.1) along with fibrosis markers.
Li 2023 provides data that both KCa 3.1 and KCa2.3 are associated with profibrotic growth factors (PDGF, TGF-B, VEGF) and both are elevated in the murine model of fibrotic disease ( liver or lung tissue) compared with control(See abstract; page 381 left column). Li 2023 does not provide evidence that liver or lung fibrosis is exclusively characterized/ associated with elevated KCa2.3 expression. Li discloses modafinil suppress both KCa3.1 and KCa2.3 in vitro and in vivo fibrotic response. Li 2023 does not provide conclusive evidence that efficacy of modafinil is exclusively by suppressing KCa2.3 or KCa 3.1 in the subject. Li 2023 is consistent with the known close relationship between KCa 3.1 and KCa 2.3 in overlapping subject population and further supports the reasonable expectation of success for modafinil treatment across overlapping population. Therefore, the 35 USC $103 is maintained.
Response to Arguments
Applicant’s Remarks filed 02/10/2026 have been fully considered, but NOT persuasive to overcome rejections of claims 1 and 10 over Suh’412 (US 9.259,412 B2) in view of Roach (2013) and Organ (2017) under 35 USC $103, and double patenting rejection over Suh’412 (US 9.259,412 B2) in view of Organ (2017).
Applicant argues claim 1 is amended by removing reliance on an intended-result framing with a positive patient limitation “The subject suffers from pulmonary fibrosis characterized by elevated KCa2.3 expression”, one of ordinary skill in the art would not have been motivated, with a reasonable expectation of success, to treat pulmonary fibrosis characterized by elevated KCa2.3 expression with modafinil according to Suh Declaration (Remarks, page 4-6/9 ).
RESPONSE: It’s acknowledged that claim 1 is amended to recite a patient population. However, the recitation “ subject suffers from liver fibrosis and pulmonary fibrosis characterized by elevated KCa2.3 expression” is ambiguous, because KCa2.3 and KCa3.1 are closely related and both are elevated in the same or overlapping subject population suffering from pulmonary fibrosis. The subject suffers from pulmonary fibrosis characterized by elevated KCa2.3 expression does not exclude subject with elevated KCa3.1. There is no criteria to clearly distinguish the subject with elevated KCa2.3 from the subject with elevated KCa3.1. Wherein a claimed patient population overlaps with or is not meaningfully distinct form a population disclosed in the prior art, the claimed limitation does not necessarily confer patentability. Further, it’s common practice to explore/extend different population for active drug.
Applicant argues inherency property rationale does not supply the missing limitations of amended claim 1, and relies on Suh Declaration that KCa2.3 was not an established fibrosis target and would not have been treated as an assumed or inevitable feature of pulmonary fibrosis therapies investigated in the KCa3.1-focused art.
RESPONSE: Please see above response to Suh Declaration. As explained during the interview on 01/07/2026, both K Ca3.1 and K Ca2.3 channels would be present at lung tissue of the subject with lung/pulmonary fibrosis. By administering modafinil for treating fibrotic disease in a subject with elevated KCa3.1 expression, one might also be treating a subject with elevated KCa 2.3 even though the prior art was not aware of it. Choi (2021) on the record discloses both KCa2.3- and KCa3.1 coexist in nonalcoholic hepatitis suggesting inhibiting both KCa2.3- and KCa3.1-mediated signaling may serve as a therapeutic approach for inflammatory and fibrotic liver. Even if KCa2.3-elevated subject characterization/ suppression might not flow from KCa3.1 suppression in all disease/disorder, KCa2.3 and KCa3.1 are closely related KCa channels, cyclic adenosine monophosphate (cAMP) are associated with both KCa 3.1 and KCa 2.3 for treating variety disease/conditions (e.g. vascular disease, fibrotic disease, etc.) as shown in Suh’412, Organ (2017). Roach (2013, 2015, 2020), etc. Olivan-Viguera (2013) on the record teaches KCa3.1/KCa2.3 channels are key players in the proliferation of some cell types as well as in endothelial function and natural phenols inhibit/suppress both KCa3.1 and KCa2.3. Oliva´n-Viguera also teaches modafinil (2-benzhydrylsulfinylacetamide) block KCa3.1 by increasing cAMP-mediated phosphorylation (See Table 2; Page 4, left column). It’s common practice to repurpose drugs and explore different pharmaceutical use of active compound in different population as shown by Suh’ 412 repurposing narcolepsy drug modafinil for treating KCa3.1 channel-mediated disease, e.g. fibrotic disease and vascular disease including pulmonary hypertension which is a frequent co-morbidity with pulmonary fibrosis. A skilled artisan would have been motivated to extend modafinil treatment to subject with elevated KCa2.3 based on the close relationship of KCa3.1 and KCa2.3, and reasonably expect modafinil would exhibit certain activity in treating fibrosis with elevated KCa2.3 in absence of evidence to the contrary.
Applicant argues again about reasonable expectation of success for the claimed method as a whole, which is limited by a KCa2.3-defined patient population (Remarks, page 6-9).
RESPONSE: Again, obviousness does not require absolute predictability, only a reasonable expectation of success, i.e., a reasonable expectation of obtaining similar properties. See, e.g., In re O’Farrell, 853 F.2d 894, 903, 7 USPQ2d 1673, 1681 (Fed. Cir. 1988). As MPEP 2143.02.I. stated : “Conclusive proof of efficacy is not required to show a reasonable expectation of success. OSI Pharm., LLC v. Apotex Inc., 939 F.3d 1375, 1385, 2019 USPQ2d 379681 (Fed. Cir. 2019) ("To be clear, we do not hold today that efficacy data is always required for a reasonable expectation of success. Nor are we requiring ‘absolute predictability of success.’"); Acorda Therapeutics, Inc. v. Roxane Lab., Inc., 903 F.3d 1310, 1333, 128 USPQ2d 1001, 1018 (Fed. Cir. 2018) ("This court has long rejected a requirement of ‘[c]onclusive proof of efficacy’ for obviousness." (citing to Hoffmann-La Roche Inc. v. Apotex Inc., 748 F.3d 1326, 1331 (Fed. Cir. 2014); PharmaStem Therapeutics, Inc. v. ViaCell, Inc., 491 F.3d 1342, 1364 (Fed. Cir. 2007); Pfizer, Inc. v. Apotex, Inc., 480 F.3d 1348, 1364, 1367–68 (Fed. Cir. 2007) (reasoning that "the expectation of success need only be reasonable, not absolute"))”.
As elaborated above, both teachings of Choi 2021 and Li 2023 are consistent with the known close relationship between KCa 3.1 and KCa 2.3 in overlapping subject population and further supports the reasonable expectation of success for modafinil treatment across overlapping population.
Specification
The substitute specification filed 04/25/2025 is objected to because it does not conform to 37 CFR 1.125(b) and (c) because: the statement as to a lack of new matter under 37 CFR 1.125(b) is missing and a marked-up copy of the substitute specification has not been supplied in addition to the clean copy.
A substitute specification must not contain new matter. The substitute specification must be submitted with markings showing all the changes relative to the immediate prior version of the specification of record. The text of any added subject matter must be shown by underlining the added text. The text of any deleted matter must be shown by strike-through except that double brackets placed before and after the deleted characters may be used to show deletion of five or fewer consecutive characters. The text of any deleted subject matter must be shown by being placed within double brackets if strike-through cannot be easily perceived. An accompanying clean version (without markings) and a statement that the substitute specification contains no new matter must also be supplied. Numbering the paragraphs of the specification of record is not considered a change that must be shown.
Claim interpretation
Instant claims are amended to a method of treating fibrotic disease comprising administering to a subject in need thereof an effective amount of 2-(benzhydrylsulfinyl)acetamide, wherein the fibrotic disease is selected from liver fibrosis and pulmonary fibrosis, wherein the subject suffers from liver fibrosis and pulmonary fibrosis characterized by elevated KCa2.3 expression.
Please note biological/pharmaceutical activities are the properties of modafinil and its derivative, The function of suppressing expression of a KCa3.1 channel, KCa2.3 channel and/or other KCa channels/biomarkers is the property of modafinil and its derivative. MPEP 2112.01 Il states: "Products of identical chemical composition cannot have mutually exclusive properties." /n re Spada, 911 F.2d 705, 709, 15 USPQ2d 1655, 1658 (Fed. Cir. 1990). A chemical composition and its properties are inseparable. Therefore, if the prior art teaches the identical chemical structure, the properties applicant discloses and/or claims are necessarily present. KCa2.3 and KCa3.1 are closely related KCa channels and commonly coexist in a subject. By administering modafinil for treating fibrotic disease in a subject with elevated KCa3.1 expression, one might also be treating a subject with elevated KCa 2.3 expression even though one might not be aware of it.
As MPEP 2112.I.states: "[T]he discovery of a previously unappreciated property of a prior art composition, or of a scientific explanation for the prior art’s functioning, does not render the old composition patentably new to the discoverer." Atlas Powder Co. v. IRECO Inc., 190 F.3d 1342, 1347, 51 USPQ2d 1943, 1947 (Fed. Cir. 1999). Thus the claiming of a new use, new function or unknown property which is inherently present in the prior art does not necessarily make the claim patentable. In re Best, 562 F.2d 1252, 1254, 195 USPQ 430, 433 (CCPA 1977)”. MPEP 2145 II states: “ Mere recognition of latent properties in the prior art does not render nonobvious an otherwise known invention. In re Wiseman, 596 F.2d 1019, 201 USPQ 658 (CCPA 1979)”.
Priority
The instant application 16/964,752 filed on 05/17/2021 is a 371 of PCT/KR2019/011834 09/11/2019 and claims benefit of Korean patent application No. KR 10-2018-0110442 filed on 09/14/2018.
Acknowledgment is made of applicant’s claim for foreign priority under 35 U.S.C. 119 (a)-(d). The certified copy of foreign Application No. KR 10-2018-0110442 is filed on 07/24/2020 in Korean , no English translation is included in the certified copy of foreign Application No KR 10-2018-0110442 .
It’s noted the substitute specification filed 04/25/2025 contains information related to foreign application, but it’s not clear if it’s English translation copy of KR 10-2018-0110442 or other related document.
Claim Rejections - 35 USC § 103
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 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 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or non-obviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 1 and 10 are rejected under 35 U.S.C. 103 as being unpatentable over Suh et al. (US 9.259,412 B2, hereafter Suh’ 412 ), in view of Roach et al.( hereafter “Roach 2013”, PLOS ONE 2013, Volume 8, Issue 12, e85244, , "The K+ Channel KCa3.1 as a Novel Target for Idiopathic Pulmonary Fibrosis") and Organ et al. (American Journal of Respiratory Cell and Molecular Biology Volume 56 Number 4, April 2017 “Inhibition of the KCa3.1 Channel Alleviates Established Pulmonary Fibrosis in a Large Animal Model”)(reiterated as necessitated by amendment).
Suh’ 412 teaches method of treating K Ca3.1 channel (Ca activated K channel) mediated diseases (e.g. fibrotic disease) with modafinil or derivatives thereof (See abstract, Col. 3, lines 41-48, claim 1). Suh’ 412 teaches modafinil is also called 2-(benzhydrylsulfinyl)acetamide, having following structure (See Col. 6, lines 5-15).
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Suh’ 412 also teaches modafinil derivatives having following structures (See Col. 6, lines 22-65)(which read on other compound species of instant claim 1).
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Suh’ 412 teaches modafinil is used for treating sleep disorders such as narcolepsy since 2006 and has been extensively studied for different mechanism of modafinil on histamine, norepinephrine, serotonin, dopamine, and orexin, etc. (See Col. 2, lines 37-67; Col. 3, lines 1-24).
Regarding K Ca3.1 channel, Suh’ 412 teaches K Ca3.1 channel (Ca activated K channel) mediated diseases refers to any disease regulated by the activity of KCa3.1 channel which is distributed to various cells(e.g. immune cells, proliferating vascular smooth muscle cells, endothelial cells, secreting epithelial cells, etc.)(See Col. 12, lines 15-22, 58-60). Suh’ 412 and its incorporated references teaches KCa3.1 channel inhibitors are known to inhibit proliferation of immune cells (T cells and B cells), fibroblasts, vascular smooth muscle cells, etc. and suppress the progression of renal fibrosis (See Col. 2, lines 14-26). Suh’ 412 teaches modafinil and derivatives thereof inhibit KCa3.1 channel in cultured NIH-3T3 fibroblasts and maybe useful for treatment or prevention of K Ca3.1 channel (Ca activated K channel) mediated diseases including new fibrosis (Col. 4, lines 1-3; Col 18, lines 15-20; Col. 19, lines 8-30). Suh’ 412 teaches modafinil activating cAMP/PKA at similar degree as that of iloprost, indicating modafinil may also be used as a treatment for pulmonary arterial hypertension (See Col. 19, lines50-54). Please note pulmonary hypertension is a frequent co-morbidity with pulmonary fibrosis.
Suh’ 412 teaches various amount/concentration of modafinil and derivative in different assay (e.g. 10nM, 30nM, 1uM, etc.)(See Figures1-10). Suh’ 412 teaches the effective amount for treating different disease could be readily determined by those skilled in the related arts according to the elements well known in medical fields and active substance in general could be administered in a dose of about 0.01 mg/kg/day to 1000 mg/kg/day(See Col. 11, lines 4-19). Where the general conditions of a claim are disclosed in the prior art, it is not inventive to discover the optimum or workable ranges by routine experimentation. MPEP 2144.05.
Suh’ 412 collectively teaches a method of treating fibrotic disease mediated by Ca activated K channel (KCa 3.1) with modafinil and derivatives thereof.
Suh’ 412 is silent about modafinil and derivatives thereof treating liver or pulmonary fibrosis characterized by elevated KCa3.1 or KCa2.3 channel.
Roach 2013 teaches KCa3.1 currents were increased in human myofibroblasts and KCa3.1 activity promotes pro-fibrotic human lung myofibroblast function(See Abstract, Results). Roach teaches KCa3.1 pharmacological blockade attenuated human myofibroblast proliferation and blocking KCa3.1 may offer a novel approach to treating idiopathic pulmonary fibrosis (IPF) with the potential for rapid translation to the clinic( See conclusions).
Organ teaches Ca2+ activated KCa3.1 potassium channels have been shown to play a key role in the aberrant activation and responses to injury in both epithelial cells and fibroblasts which both are considered key drivers in the fibrotic process of idiopathic pulmonary fibrosis IPF (See abstract) . Organ teaches inhibiting the KCa3.1 ion channel is able to attenuate the early fibrogenic phase of fibrosis and inhibits profibrotic behavior of primary lung fibroblasts in sheep model, which supports the in-vitro research conducted in human IPF-derived fibroblasts by Roach 2013 and further establish that inhibiting KCa3.1 signaling may provide a novel therapeutic approach for idiopathic pulmonary fibrosis (IPF) ( See abstract, Discussion, page 546 right column; page 549, middle column).
It’s common practice to repurpose drugs and explore different pharmaceutical use of active compound as shown by Suh’ 412 repurposing narcolepsy drug modafinil for treating KCa3.1 channel-mediated disease, e.g. fibrotic disease and vascular disease including pulmonary hypertension which is a frequent co-morbidity with pulmonary fibrosis. The normal desire of scientists or artisans to improve upon what is already generally known provides the motivation to further explore the use of modafinil for treating other fibrotic disease. It would have been obvious for one of the ordinary skill in the art before the effective filing date of instant invention to explore the use of modafinil and derivative thereof taught by Suh’ 412 for the treatment of pulmonary fibrosis associated with KCa3.1 channel as taught by Roach 2013 and Organ. At the time of the instant invention, it was known that modafinil and derivative thereof can suppress the expression of KCa 3.1 channel and was used for treating disease associated with KCa channel (e.g. fibrotic disease, renal fibrosis, fibroblast for new fibrosis, etc.). It was also known that pulmonary fibrosis is a fibrotic disease associated with KCa3.1 channel and blockade of KCa3.1 attenuated human myofibroblast proliferation and may offer a novel approach to treating idiopathic pulmonary fibrosis IPF as taught by Roach 2013 and Organ. A skilled artisan would be motivated to explore the use of modafinil and derivative thereof in treating pulmonary fibrosis based on the combined teachings of prior art because KCa3.1 pharmacological blockade attenuated human myofibroblast proliferation and blocking KCa3.1 may offer a novel approach to treating idiopathic pulmonary fibrosis (IPF) as taught by Roach 2013 and Organ.
Suh’ 412, Roach 2013 and Organ are silent about treating fibrotic disease (e.g. pulmonary disease) characterized by elevated KCa2.3 expression, However, KCa2.3 and KCa3.1 are closely related KCa channels and commonly coexist in a subject. By administering modafinil for treating fibrotic disease in a subject with elevated KCa3.1 expression, one might also be treating a subject with elevated KCa 2.3 even though the prior art was not aware of it. Even if the subject suffering from fibrotic disease with elevated KCa 2.3 is different from subject with elevated KCa 3.1, a skilled artisan would have been motivated to extend modafinil treatment to subject with elevated KCa2.3 based on their close relationship and reasonably expect modafinil would exhibit certain activity in treating fibrosis with elevated KCa2.3 in absence of evidence to the contrary.
Applicant might have discovered a new property or advantage of suppressing K2.3.by modafinil or derivatives thereof . MPEP 2145 II states: "The fact that Applicant has recognized another advantage which would flow naturally from following the suggestion of the prior art, cannot be the basis for patentability when the differences would otherwise be obvious". Ex parte Obiaya, 227 USPQ 58, 60. (FP 7.37.07, MPEP 707.07(f)).
One of ordinary skill in the art would have had a reasonable expectation of success in producing the claimed invention based on the combined teachings of prior art and general knowledge of KCa channels and treatment for fibrotic disease. Therefore, the invention as a whole is prima facie obvious to one of ordinary skill in the art at the time the invention was made, as evidenced by the references, especially in the absence of evidence to the contrary.
Double Patenting
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).
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).
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.
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.
Claims 1 and 10 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-4 of U.S. Patent No. US 9.259,412 B2 in view of Organ et al. (American Journal of Respiratory Cell and Molecular Biology Volume 56 Number 4, April 2017 “Inhibition of the KCa3.1 Channel Alleviates Established Pulmonary Fibrosis in a Large Animal Model”).
Although the claims at issue are not identical, they are not patentably distinct from each other. Reference claims are directed to method of treating KCa3.1 channel-mediated disease with modafinil or derivatives thereof, whereby modafinil or derivatives thereof increases intracellular cAMP
concentration and inhibits KCa3.1 channel.
Reference claims do not explicitly teach the KCa3.1 channel-mediated disease is pulmonary fibrosis. The collective teachings of Organ are elaborated in preceding 103 rejections. Organ teaches inhibiting the KCa3.1 ion channel is able to attenuate the early fibrogenic phase of fibrosis and inhibits profibrotic behavior of primary lung fibroblasts in sheep model, which supports the in-vitro research conducted in human IPF-derived fibroblasts and further establish that inhibiting KCa3.1 signaling may provide a novel therapeutic approach for idiopathic pulmonary fibrosis (IPF).
It’s common practice to repurpose drugs and explore different pharmaceutical use of active compound. It would have been prima facie obvious for one of the ordinary skill in the art to explore the use of modafinil and derivative thereof taught by reference claims for treatment of more fibrotic disease associated with KCa3.1 channel, e.g. pulmonary fibrosis taught by Organ.
Reference claims are silent about KCa 2.3 subject population. KCa2.3 and KCa3.1 are closely related KCa channels and commonly coexist in a subject. By administering modafinil for treating fibrotic disease in a subject with elevated KCa3.1 expression, one might also be treating a subject with elevated KCa 2.3 even though one might not be aware of it. A skilled artisan would have been motivated to extend modafinil treatment to subject with elevated KCa2.3 based on their close relationship and reasonably expect modafinil would exhibit certain activity in treating fibrosis with elevated KCa2.3 in absence of evidence to the contrary.
The instant application shares at least one common inventor /applicant with the reference patent. Furthermore, the instant application is not related to the reference patent based on the record, thus no 35 USC 121 shield exists.
Conclusion
No claims are allowed.
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 LIYUAN MOU whose telephone number is (571)270-1791. The examiner can normally be reached Mon-Fri 9:00-5:30.
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/LIYUAN MOU/Examiner, Art Unit 1628
/JARED BARSKY/Primary Examiner, Art Unit 1628
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