DETAILED ACTION
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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 04 March 2026 has been entered.
This Office Action is in response to Applicant’s Amendment and Remarks filed on 04 March 2026 in which claims 6-9, 20-23 and 60-63 were canceled, and claims 1, 4, 13, 14, 18, 26, and 52 were amended to change the scope and breadth of the claims.
Claims 1, 4, 10, 13, 14, 18, 24-26 and 52-59 are pending in the current application and are examined on the merits herein.
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 .
Response to Arguments
Applicant's arguments filed 04 March 2026 have been fully considered but they are not persuasive.
Applicant contends claims 1, 4, 13, 14, 18, 24 and 52 have been amended to recite an acute respiratory distress syndrome, treated by 5-aza-2’-deoxycytidine as the sole therapeutic agent.
While the amendment overcomes the rejection of claims 1, 4, 10, 13, 14, 18, 24-26, 52 and 53 under 35 U.S.C. §112(a), first paragraph, for lack of enablement, it does not overcome the rejection of claims 54-59 under 35 U.S.C. §112(a), first paragraph, for lack of enablement, because those claims are still drawn towards administering any DNA methyltransferase inhibitor.
The rejection is hereby maintained over claims 54-59.
Modified Rejections
The following are new ground(s) or modified rejections. Therefore, rejections from the previous Office Action, dated 03 February 2025, have been modified and are listed below.
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 54-59 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for lung injury by administering 5’-aza-2’-deoxycytidine as a sole therapeutic agent, does not reasonably provide enablement for treating any lung injury with any DNA methyltransferase inhibitor as a sole therapeutic agent. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims.
The Applicant’s attention is drawn to In re Wands, 8 USPQ2d 1400 (CAFC1988) at 1404 where the court set forth eight factors to consider when assessing if a disclosure would have required undue experimentation. Citing Ex parte Forman, 230 USPQ 546 (BdApls 1986) at 547 the court recited eight factors: (1) The nature of the invention; (2) the state of the prior art; (3) the relative skill of those in the art; (4) the predictability or unpredictability of the art; (5) the breadth of the claims; (6) the amount of direction or guidance presented; (7) the presence or absence of working examples; and (8) the quantity of experimentation necessary.
The nature of the invention: The nature of the invention is directed towards administering a DNA methyltransferase inhibitor to treat any lung injury.
The state of the prior art: According to Cleveland Clinic (cited in PTO-892), types of lung injury include asthma, bronchiectasis, COPD, cystic fibrosis, pneumonia, tuberculosis, pulmonary fibrosis, lung cancers (e.g. non-small cell lung cancer, small cell lung cancer, mesothelioma), lymphangioleiomyomatosis.
According to Cleveland Clinic, causes of lung disease include smoking, pathogens (viral, bacterial, fungal), inflammatory diseases like rheumatoid arthritis (RA), lupus, scleroderma and sarcoidosis, inhaling harmful substances like asbestos and radon, allergic reactions to inhaled substance, certain medications or treatments, and/or genetics.
Cleveland Clinic teaches treatments include corticosteroids, inhaled medications, oxygen therapy, anti-fibrotic and cytotoxic drugs, biologic drugs, positive airway pressure, and others.
Before the effective filing date of the claimed invention, Zhang et al. (Molecular Medicine Reports, 2013, vol. 7, pp. 1417-1424, cited in previous Office Action) recognize animals with acute lung injury have aberrant DNA methylation in their lung tissues (abstract). Thangaval et al. describe the use of 5’-aza-2’-deoxycytidine as part of a combination therapy in the treatment of lung injury. And Wu et al. found 5-azacytidine alleviated airway inflammation in an asthma mice model (cited in previous Office Action).
The relative skill of those in the art: The relative skill of those in the art is low. As noted above, animals with acute lung injury were known to have aberrant DNA methylation in their lung tissues.
The predictability or unpredictability of the art: From the combined teaching of the prior art (Zhang, Wu, Thangaval), one of ordinary skill would have recognized aberrant DNA methylation is present in animals with lung injury, such as in asthma, and the use of DNA methyltransferase inhibitors in treating lung inflammation was being investigated.
Thangaval et al. (cited in previous Office Action) found no improvement in mortality in LPS-challenged mice treated with 5’-aza-2’-deoxycytidine alone (p.2248, second para).
With the additional teaching of Thangaval et al., the ordinary artisan would have recognized treating acute lung inflammation with a DNA methyltransferase inhibitor is insufficient to improve outcome in vivo, making their therapeutic efficacy as a sole therapeutic agent unpredictable.
Furthermore, Cleveland Clinic shows causes of lung disease vary, and treatments vary as well. There is no single therapy designed to treat all causes of lung injury. Thus, there is no reasonable expectation that a single DNA methyltransferase inhibitor could treat any and all forms of lung injury as presently claimed.
The breadth of the claims: The breadth of the claims includes treating any lung injury with any DNA methyltransferase inhibitor as the sole therapeutic agent.
The amount of direction or guidance presented: Example 1 demonstrates the effects of 5’-aza-2’-deoxycytidine (DAC) in a lung injury model. Example 4 showed improved mortality among injured mice treated with DAC. Example 10 exhibited a smaller magnitude of weight loss and decreased BAL protein, cell count, neutrophil count and histologic injury in influenza-induced mice.
(8) The quantity of experimentation necessary: In order to practice the invention with the full range of all possible treatment methods beyond those known in the art, one skilled in the art would undertake a novel and extensive research program to show that any DNA methyltransferase inhibitor was sufficient, as a sole therapeutic agent for treating any lung injury.
In order to determine the efficacy of the claimed therapies in the absence of existing in vivo data, one skilled in the art would undertake animal testing in order to practice the invention. Animal experiments include, induction of the disease state, administration of the potential pharmaceutical compound and collection and analysis of data, additional burdens associated with compliance with animal welfare regulations, care, feeding and other maintenance of the animals, dissection of dead animals to collect data, and dispose of the dead animals after the research is finished. These trials would need to be run separately and repeatedly for each disorder to be treated, and success in treating each and every disorder would still not be definitive. The experimentation involved would therefore be significant, undue and unpredictable.
Genentech, 108 F.3d at 1366, sates that, “a patent is not a hunting license. It is not a reward for search, but compensation for its successful conclusion.” And “patent protection is granted in return for an enabling disclosure of an invention, not for vague intimations of general ideas that may or may not be workable.”
Therefore, in view of the Wands factors, as discussed above, particularly the scope of the claims, Applicants fail to provide information sufficient to practice the claimed invention for treating any lung injury wherein DNA methyltransferase is administered as a sole therapeutic agent.
Response to Arguments
Applicant's arguments filed 04 March 2026 have been fully considered but they are not persuasive.
Applicant contends the submitted Rule 130 Declaration includes a statement that covers Venkataraman K. Sidhaye.
A screenshot of the 130 Declaration submitted 08 April 2024 is provided below:
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Paragraph 6 of the 130 Declaration does not mention Venkataraman K. Sidhaye.
Applicant contends the Singer reference (published October 2014) is disqualified as prior art under 35 U.S.C. §102(b)(1)(A), because the cited reference is the inventors’ own work published less than one year before the effective filing date of the claimed invention.
The statement made in the Response and Declaration filed 23 January 2023 and most recently 08 April 2024 is insufficient to disqualify the Singer reference, because Applicant has not provided a reasonable explanation of the presence of Venkataramana K. Sidhaye listed on the Singer reference.
Applicant must provide a reasonable explanation of their role in the cited disclosure.
See MPEP 717.01(a):
(B) Whether the affidavit or declaration shows sufficient facts, in weight and character, to establish that
(1) the disclosure was made by the inventor or a joint inventor, or
(2) the subject matter disclosed was obtained directly or indirectly from the inventor or a joint inventor.
Some factors to consider are the following:
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Where the authorship of the prior art disclosure includes the inventor or a joint inventor named in the application, an "unequivocal" statement from the inventor or a joint inventor that he/she (or some specific combination of named joint inventors) invented the subject matter of the disclosure, accompanied by a reasonable explanation of the presence of additional authors, may be acceptable in the absence of evidence to the contrary. See In re DeBaun, 687 F.2d 459, 463, 214 USPQ 933, 936 (CCPA 1982).
(2) A mere statement from the inventor or a joint inventor, without any accompanying reasonable explanation, may not be sufficient where there is evidence to the contrary, such as a contrary statement from another named author that was filed in another application on behalf of another party. See Ex parte Kroger, 219 USPQ 370 (Bd. App. 1982) (affirming rejection notwithstanding declarations by the alleged actual inventors as to their inventorship in view of a non-applicant author submitting a letter declaring the non-applicant author’s inventorship).
The rejections are hereby 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 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.
Claim(s) 1, 4, 13, 18, 26, 52, 54 and 55 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Singer et al. (Am. J. Respir. Cell Mol. Biol., October 2014, vol. 52, iss 5, pp.641-652, cited in previous Office Action).
Singer et al. disclose “sterile direct lung injury using gram-negative bacterial cell wall component LPS-is a well-characterized system to study lung inflammation and recapitulates many ARDS features, including neutrophilic aveolitis, modest mortality, and spontaneous resolution in survivors. Our sterile inflammatory model has relevance for many ARDS causes, including aspiration of gastric contents, ventilator-induced lung injury, near drowning, and collateral lung injury associated with treated bacterial infection. Moreover, our data using an influenza model broaden the applicability of epigenetic manipulation as a therapeutic strategy for ARDS” (p.647, penultimate para).
Singer et al. disclose Treg DNA methyltransferase inhibition by 5-aza-2’-deoxycytidine (Aza) augmented Treg expression and accelerated resolution of direct lung injury (p.642, fourth paragraph). Singer et al. disclose inducing a state of acute inflammatory lung inflammation by injecting C57BL/6 WT and Foxp3DTR mice with diphtheria toxin (p.642, fifth and sixth paragraph).
Singer et al. teach administering 1 mg/kg Aza 24 hours after lung injury with LPS (p.642, sixth paragraph). Singer et al. found that Aza increased the expression of Treg in the lungs (p.643, second and third paragraph); and accelerated resolution of lung injury (p.643, fourth paragraph). Singer et al. also found that Aza increased the expression of Foxp3 in CD4+CD25- cells; as well as increased the expression of Foxp3 expression in Tregs (CD4+CD25+ cells), (p.644-645, bridging paragraph). Singer et al. further disclose Aza facilitated recovery of lung injury in WT mice with influenza-induced lung inflammation (abstract; figure 7).
Singer et al. disclose an adoptive transfer method in which T cells were cultured with Aza and administered to mice 1 hour after having a lung injury event (p.642, last para; p.647, left col.). Singer et al. found lung injury resolved in mice that received Aza-treated T-cells. Singer et al. teach exogenous lung Treg cells increased in mice that received Aza-treated Treg cells compared with vehicle-treated Treg cells. Singer et al. suggests systemic administration of a DNMT inhibitor coupled with T cell transfer could result in improved therapeutic efficacy (p.647, right col).
As explained in the above rejection, the recitation “treating an acute inflammatory disease or disorder in a subject” and recitation “treating a lung injury in a subject” in present claim 2 is broadly and reasonably interpreted to include a reduction in any symptoms of the injury. As noted above, Singer et al. disclose Aza treatment in mice having acute inflammatory lung injury accelerated resolution of lung injury. Thus, Singer et al. disclose treating the acute inflammatory disease and treating the lung injury (present claim 1).
By inducing inflammatory lung injury, Singer et al. identifies a subject having an acute inflammatory disease or disorder, or lung injury.
The recitation “wherein the DNA methyltransferase inhibitor is administered in an amount sufficient to increase Treg frequency in the subject” in present claim 1 is broadly and reasonably interpreted to include administering 1 mg/kg Aza (as explained in the above rejection).
Singer et al. expressly administered 1 mg/kg Aza. Thus, Singer et al. necessarily disclose administering Aza in an amount sufficient to increase Treg frequency per present claim 4.
Thus, the disclosure of Singer et al. anticipates claims 1, 4, 13, 18, 26, 52, 54 and 55 of the present application.
Claim(s) 54 and 55 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Bae et al. (Inflammation, 2010, vol. 33, no. 2, pp. 82-91, cited in previous Office Action as Relevant Prior Art).
Bae et al. disclose treating mice having acute lung injury induced by LPS (p.84, In Vivo Experiments). The mice were treated with epigallocatechin 3 gallate (EGCG), as the sole active agent, at a dose of 10 mg/kg by IP injection. Bae et al. found EGCG attenuated LPS-induced lung injury (abstract).
According to the present Specification, DNA methyltransferase inhibitor includes EGCG (p.2-3, bridging para).
Thus, Bae et al. disclose a method of treating a lung injury in a subject, the method comprising identifying a subject having a lung injury, and administering a DNA methyltransferase inhibitor as the sole therapeutic agent to the subject, thereby treating the lung injury in the subject.
Thus, the disclosure of Bae et al. anticipates claims 54 and 55 of the present application.
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.
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.
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.
Claims 1, 4, 10, 13, 14, 18, 24-26, 52, 54, 55, 57 and 58 are rejected under 35 U.S.C. 103 as being unpatentable over Singer et al. (cited above).
Singer et al. teach as discussed above.
Singer et al. do not expressly disclose administering 5’-Aza-2’-deoxycytidine to a human (present claims 10 and 24). Singer et al. do not expressly disclose using adoptive T-cell transfer to treat a subject having influenza (present claim 14). Singer et al. do not expressly disclose waiting at least 24 hours to treat a subject with treated cells (present claim 25).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to administer 5’-Aza-2’-deoxycytidine (Aza) to a human to treat an inflammatory lung injury; ARDS; use adoptive T-cell transfer to treat a subject having influenza; and wait at least 24 hours to treat a subject after a lung injury event.
The skilled artisan would have been motivated to administer Aza to a human to treat an inflammatory lung injury and ARDS because the in vitro experiments performed by Singer et al. demonstrated that treatment with Aza significantly increased the expression of Tregs after LPS injury, wherein Tregs are intricately involved in resolving lung injury. Furthermore, Singer et al. demonstrated in vivo Aza accelerated the resolution of lung injury in mice. The LPS model was expressly selected by Singer et al. to study lung inflammation and because it recapitulates many ARDS features, including neutrophilic aveolitis, modest mortality, and spontaneous resolution in survivors.
The ordinary artisan would have been motivated to use adoptive T-cell transfer to treat a subject having influenza because Singer et al. found lung injury resolved in mice that received Aza-treated T-cells 1 hour after injury, and suggests systemic administration of a DNMT inhibitor coupled with Treg cell transfer could result in improved therapeutic efficacy. Singer et al. teach using an influenza model broadens the applicability of epigenetic manipulation as a therapeutic strategy for ARDS.
One having ordinary skill in the art would have been motivated to wait 24 hours after a lung injury event to treat a subject with treated cells because Singer et al. found that Aza administration 24 hours after lung injury increased the expression of Treg in the lungs.
The ordinary artisan would have had a reasonable expectation of success in treating humans with an acute inflammatory lung injury, ARDS or influenza by administering Aza because it was demonstrated to have in vitro activity in protecting lung cells from inflammation, and it was demonstrated to be effective in protecting the lungs of mice in LPS-induced lung injury.
Thus, the claimed invention as a whole is prima facie obvious over the combined teaching of the prior art.
Claim(s) 54-56 are rejected under 35 U.S.C. 103 as being unpatentable over Bae et al. (cited above) in view of Reagan-Shaw et al. (The FASEB Journal, 2007, vol. 22, pp. 659-661, cited in PTO-892).
Bae et al. teach as discussed above.
Bae et al. do not expressly disclose administering the EGCG in an amount of 50-300 mg/day to a human (claim 56).
Reagan-Shaw et al. teach the conversion from a mouse to a human equivalent dose follows the formula of figure 1,
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. The Km factor of mice is 3, and the Km factor of an adult human is 37 (Table 1). The human Km assumes the human weighs 60 kg (Table 1).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to administer EGCG to a human in an amount of about 50 mg/day.
According to Reagan-Shaw et al., a mouse dosage of 10 mg/kg can be converted to a human equivalent dose by multiplying the Animal Km over the Human Km. In this case, 10 mg/kg is multiplied by 3/37 to give 0.81 mg/kg. Assuming an adult weighs 60 kg, the daily dose of EGCG would be 48.6 mg/day, which is close to the lower limit of 50 mg/day presently claimed. One having ordinary skill in the art would have routinely optimized the dose after determining the human equivalent dose.
Thus, the claimed invention as a whole is prima facie obvious over the combined teaching of the prior art.
Response to Arguments
Applicant's arguments filed 04 March 2026 have been fully considered but they are not persuasive.
Applicant contends the present claims are directed to a sole therapeutic agent.
The above argument is not found persuasive because the claims of the ‘706 Patent are directed towards a composition consisting essentially of AZA. A composition consisting essentially of AZA reads on a sole therapeutic agent, since no other agent is recited in the ‘706 Patent.
The rejection is hereby maintained.
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 USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The 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/process/file/efs/guidance/eTD-info-I.jsp.
Claims 1, 4, 10 and 52-56 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6 of U.S. Patent No. 10,905,706. Although the claims at issue are not identical, they are not patentably distinct from each other because claims are drawn towards a method of treating an acute inflammatory disorder, a lung injury or ARDS in a human subject comprising identifying a human subject having those disorders and administering a pharmaceutical composition consisting essentially of a DNA methyltransferase inhibitor in an amount of 50-300 mg/day to the subject.
The claims of the ‘706 Patent anticipate the present claims.
Conclusion
In view of the rejections to the pending claims set forth above, no claim is allowed.
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/BAHAR CRAIGO/
Primary Examiner
Art Unit 1699
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