DETAILED ACTION
All rejections and objections not mentioned below are withdrawn.
Continued Examination Under 37 CFR 1.114
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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 08/03/2026 has been entered.
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 .
Claim Objections
Claim 13 is objected to because of the following informalities: Streptococcus pneumoniae. Appropriate correction is required.
Claim Rejections - 35 USC § 112
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.
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.
Claims 16-17 are rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th 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. Claims 16-17 improperly broaden claim 1 from which they depend because MIS is associated with SARS-CoV-2 which has been removed from claim 1. 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.
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 (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 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.
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.
Claim(s) 1, 13 and 22 is/are rejected under 35 U.S.C. 103 as being unpatentable over DANESI (DANESI ET AL: "Clinical study on the efficacy of clofoctol in the treatment of infectious respiratory diseases", https://www.ncbi.nlm.nih.gov/pubmed/4018951, INT. J. CLIN. PHARM. RES. V(3) 175-179 (1985), IDS) in view of Mayo Clinic (Mayo Clinic, Pneumonia, June 13, 2020).
The reference DANESI teaches “The effectiveness and the safety of a new chemotherapeutic phenol derivative, clofoctol, was evaluated in adult hospitalized patients affected by infectious diseases of the bronchopulmonary tract. The clinical diagnosis included acute exacerbation of chronic bronchitis, acute bronchitis, bronchiectasis, pneumonia, bronchopneumonia and lung cavitary neoplasm. Expectoration, cough, dyspnoea, respiratory murmur and body temperature were considered as clinical factors to which an arbitrary score was given. Functional respiratory parameters including FVC, FEV1 and FEV1/FVC X 100 were also evaluated. All the patients were treated rectally with clofoctol 1500 mg daily for five days. Bacterial evidence of infection was obtained by sputum culture, which was repeated at the end of treatment. At that time, bacteriological results were 72.4% disappearance of baseline pathogens, 20.7% persistence of baseline pathogens and 6.9% presence of different organisms. Functional respiratory parameters were found to be significantly improved by treatment. Clinical results, arbitrarily evaluated on the basis of the overall assessment of laboratory and functional data, were excellent in 33.3%, good in 44.4%, fair in 5.6% and poor in 16.7% of patients. Tolerance was generally good; side-effects included maculopapular rash in 2 patients and rectal disturbances in 10 patients. In conclusion, for the treatment of bronchopulmonary diseases clofoctol offers an interesting alternative to antibiotic therapy”(page 175).
The reference Danesi teaches the following tables (page 178):
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This helps to teach claims 1, 13, 22.
The reference DANESI does not specifically teach lung inflammation but instead teaches treating diseases that cause lung inflammation (all claims).
The Mayo Clinic reference teaches that “Pneumonia is an infection that inflames the air sacs in one or both lungs. The air sacs may fill with fluid or pus (purulent material), causing cough with phlegm or pus, fever, chills, and difficulty breathing. A variety of organisms, including bacteria, viruses and fungi, can cause pneumonia”(page 1) and “Bacteria. The most common cause of bacterial pneumonia in the U.S. is Streptococcus pneumoniae. This type of pneumonia can occur on its own or after you've had a cold or the flu. It may affect one part (lobe) of the lung, a condition called lobar pneumonia(page 4).
This helps to teach claims 1, 13, and 22.
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the instant invention to have modified DANESI with the Mayo Clinic reference because DANESI teaches using clofoctol to treat bacterial lung infections in patients including pneumonia and the Mayo Clinic teaches that pneumonia is an infection that inflame the lungs often caused by bacteria. Thus it would be obvious to treat pneumonia inflammation by using the clofoctol anti-bacteria treatment. It would also be obvious to one of ordinary skill in the art to determine the effectiveness of treating the pneumonia inflammation by comparing the levels of lung inflammation after the administration of clofoctol since it is standard practice to determine the effectiveness of treatment by comparing before and after patient conditions. One would be motivated to do so to treat pneumonia and determine if the pneumonia inflammation is improving after treatment. One would have a reasonable expectation of success because the reference Danesi showed good clinical results in a patient with pneumonia.
Claim(s) 1, 9, 22 is/are rejected under 35 U.S.C. 103 as being unpatentable over Beghyn (Beghyn et al., US2023233483A1, effective filing date 2020-10-26) in view of Mayo Clinic (Mayo Clinic, Pneumonia, June 13, 2020).
The reference Beghyn teaches “The present invention relates to the use of clofoctol for the treatment of a disease caused by a coronavirus, in particular Covid-19”[0001] and “The method of claim 7, wherein the coronavirus is SARS-CoV, MERS-CoV or SARS-CoV2” (reference claim 8).
The reference Beghyn teaches “Three coronaviruses have crossed the species barrier to cause deadly pneumonia in humans since the beginning of the 21st century: Severe Acute Respiratory Syndrome coronavirus (SARS-CoV), Middle East Respiratory Syndrome coronavirus (MERS-CoV), and SARS-CoV-2 (also known as 2019-nCoV)”[0003].
This helps to teach claims 1, 9, 22.
The reference Beghyn does not specifically teach lung inflammation but instead teaches treating diseases that cause lung inflammation (all claims).
The Mayo Clinic reference teaches that “Pneumonia is an infection that inflames the air sacs in one or both lungs. The air sacs may fill with fluid or pus (purulent material), causing cough with phlegm or pus, fever, chills, and difficulty breathing. A variety of organisms, including bacteria, viruses and fungi, can cause pneumonia”(page 1) and “Bacteria. The most common cause of bacterial pneumonia in the U.S. is Streptococcus pneumoniae. This type of pneumonia can occur on its own or after you've had a cold or the flu. It may affect one part (lobe) of the lung, a condition called lobar pneumonia(page 4).
This helps to teach claims 1, 9, 22.
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the instant invention to have modified Beghyn with the Mayo Clinic reference because Beghyn teaches using clofoctol to treat viral lung infections in patients that cause pneumonia and the Mayo Clinic teaches that pneumonia is an infection that inflame the lungs often caused by viruses. Thus it would be obvious to treat pneumonia inflammation by using the clofoctol anti-viral treatment. It would also be obvious to one of ordinary skill in the art to determine the effectiveness of treating the pneumonia inflammation by comparing the levels of lung inflammation after the administration of clofoctol since it is standard practice to determine the effectiveness of treatment by comparing before and after patient conditions. One would be motivated to do so to treat pneumonia and determine if the pneumonia inflammation is improving after treatment. One would have a reasonable expectation of success because the reference Beghyn suggested treatment of disease that cause inflammation.
Claim(s) 1, 13 and 18 is/are rejected under 35 U.S.C. 103 as being unpatentable D'ANGELO (D'ANGELO ET AL: "Identification of FDA-Approved Drugs as Antivirulence Agents Targeting the pqs Quorum-Sensing System of Pseudomonas aeruginosa", ANTIMICROBIAL AGENTS AND CHEMOTHERAPY, vol. 62, no. 11, 2018-11-01, IDS) further in view of Cantin (Cantin et al., Inflammation in cystic fibrosis lung disease: Pathogenesis and therapy, Journal of Cystic Fibrosis Volume 14, Issue 4, July 2015, Pages 419-430).
The reference D'ANGELO teaches “Here, we describe the identification of new inhibitors of the pqs QS system of the human pathogen Pseudomonas aeruginosa by screening a library of 1,600 U.S. Food and Drug Administration-approved drugs. Phenotypic characterization of ad hoc engineered strains and in silico molecular docking demonstrated that the antifungal drugs clotrimazole and miconazole, as well as an antibacterial compound active against Gram-positive pathogens, clofoctol, inhibit the pqs system, probably by targeting the transcriptional regulator PqsR. The most active inhibitor, clofoctol, specifically inhibited the expression of pqs-controlled virulence traits in P. aeruginosa, such as pyocyanin production, swarming motility, biofilm formation, and expression of genes involved in siderophore production. Moreover, clofoctol protected Galleria mellonella larvae from P. aeruginosa infection and inhibited the pqs QS system in P. aeruginosa isolates from cystic fibrosis patients. Notably, clofoctol is already approved for clinical treatment of pulmonary infections caused by Gram-positive bacterial pathogens; hence, this drug has considerable clinical potential as an antivirulence agent for the treatment of P. aeruginosa lung infections”(abstract).
This helps to teach claim 18.
The reference D'ANGELO does not teach inflammation(claim 18) or detecting a reduced level of fibrosis .
The specification defines inflammation-induced fibrosis as fibrosis developing during inflammatory diseases including pathogen infections.
The reference Cantin teaches “Lung disease is the major cause of morbidity and mortality in patients with cystic fibrosis (CF). Although CF lung disease is primarily an infectious disorder, the associated inflammation is both intense and ineffective at clearing pathogens. Persistent high-intensity inflammation leads to permanent structural damage of the CF airways and impaired lung function that eventually results in respiratory failure and death. Several defective inflammatory responses have been linked to cystic fibrosis transmembrane conductance regulator (CFTR) deficiency including innate and acquired immunity dysregulation, cell membrane lipid abnormalities, various transcription factor signaling defects, as well as altered kinase and toll-like receptor responses. The inflammation of the CF lung is dominated by neutrophils that release oxidants and proteases, particularly elastase. Neutrophil elastase in the CF airway secretions precedes the appearance of bronchiectasis, and correlates with lung function deterioration and respiratory exacerbations. Anti-inflammatory therapies are therefore of particular interest for CF lung disease but must be carefully studied to avoid suppressing critical elements of the inflammatory response and thus worsening infection. This review examines the role of inflammation in the pathogenesis of CF lung disease, summarizes the results of past clinical trials and explores promising new anti-inflammatory options”(abstract) and “Persistent bronchopulmonary infections with Staphylococcus aureus, Pseudomonas aeruginosa and several other pathogens ensue, leading to chronic airway and systemic inflammation, tissue destruction, and respiratory insufficiency [10–12]. But why is the inflammation so severe? The link between CFTR deficiency and inflammation likely involves several CFTR-related abnormalities (Fig. 1) that are discussed in the paragraphs below”(page 420).
This helps to teach claim 18.
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the instant invention to have modified D'ANGELO with Cantin because D'ANGELO suggests using clofoctol to treat bacteria from cystic fibrosis patients and Cantin teaches cystic fibrosis inflammation caused by the same bacteria is dangerous to the patient and anti-inflammatory therapies are a promising new option for treatment. One would be motivated to treat the bacterial infection in cystic fibrosis patients to decrease damaging inflammation with clofoctol because it inhibited the pqs QS system in P. aeruginosa isolates from cystic fibrosis patients. One would have a reasonable expectation of success because clofoctol is already approved for clinical treatment of pulmonary infections. It is implicit to one of ordinary skill in the art when considering new therapies to determine if the therapy is working by determining the condition of the patient before and after the treatment. It would be obvious to check the level of fibrosis when treating cystic fibrosis at the start and end of treatment. This is considered inflammation-induced fibrosis as defined on page 11 of the specification.
Claim(s) 1 and 15 is/are rejected under 35 U.S.C. 103 as being unpatentable over D'ANGELO (D'ANGELO ET AL: "Identification of FDA-Approved Drugs as Antivirulence Agents Targeting the pqs Quorum-Sensing System of Pseudomonas aeruginosa", ANTIMICROBIAL AGENTS AND CHEMOTHERAPY, vol. 62, no. 11, 2018-11-01, IDS) in view of Martin (Martin et al., Gram-Negative Sepsis and the Adult Respiratory Distress Syndrome, Clinical Infectious Diseases 1992;14:1213-28, previously provided) further in view of Cantin (Cantin et al., Inflammation in cystic fibrosis lung disease: Pathogenesis and therapy, Journal of Cystic Fibrosis Volume 14, Issue 4, July 2015, Pages 419-430).
The D'ANGELO and Cantin have been discussed supra and do not disclose respiratory distress syndrome (claims 15).
The reference Martin teaches “Gram-negative sepsis has dramatically increased in frequency throughout the twentieth century in the United States. Currently, —200,000 patients develop gram-negative sepsis each year in this country. Of these, about one-quarter develop the adult respiratory distress syndrome (ARDS). Among these critically ill patients, mortality is estimated at 60%-90%. In the complex series of events leading to acute lung injury in gram-negative sepsis, endotoxin is the proximal mediator. Although endotoxin may be capable of causing direct injury to the pulmonary endothelium, its primary role is as a trigger activating inflammatory agents, including complement, neutrophils, and platelets, and inducing the production of cytokines and arachidonic acid metabolites. The end results are impairment of the endothelial barrier, diffusely increased capillary permeability, and adherence of neutrophils to the endothelium with subsequent migration into the tissues. The consequent clinical syndrome is one of acute respiratory distress with pulmonary edema, poorly compliant lungs, and refractory hypoxemia”(abstract) and “Although our review focuses on acute lung injury occurring during the course of gram-negative sepsis, ARDS can also develop as a consequence of sepsis caused by gram-positive bacteria or even fungi”(page 1214).
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the instant invention to have modified D'ANGELO and Cantin with Martin because D'ANGELO teaches an antibacterial compound active against Gram-positive pathogens, clofoctol, and Martin teaches Gram-positive pathogens may trigger ARDS. One would be motivated to combine the references to treat ARDS and one would have a reasonable expectation of success because clofoctol is a well-known antibacterial.
Claim(s) 1 and 11 is/are rejected under 35 U.S.C. 103 as being unpatentable over D'ANGELO (D'ANGELO ET AL: "Identification of FDA-Approved Drugs as Antivirulence Agents Targeting the pqs Quorum-Sensing System of Pseudomonas aeruginosa", ANTIMICROBIAL AGENTS AND CHEMOTHERAPY, vol. 62, no. 11, 2018-11-01, IDS) in view of Sriskandan (Sriskandan et al., GRAM-POSITIVE SEPSIS: Mechanisms and Differences from Gram-Negative Sepsis, Infectious Disease Clinics of North America Volume 13, Issue 2, 1 June 1999, Pages 397-412, previously provided) further in view of Cantin (Cantin et al., Inflammation in cystic fibrosis lung disease: Pathogenesis and therapy, Journal of Cystic Fibrosis Volume 14, Issue 4, July 2015, Pages 419-430).
The D'ANGELO and Cantin have been discussed supra and do not disclose sepsis (claims 11).
The reference Sriskandan teaches “In modern intensive care settings, gram-positive bacteria account for up to 50% of severe sepsis or septic shock cases, yet the pathogenesis of gram-positive shock is poorly understood”(abstract). This helps to teach claim 11.
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the instant invention to have modified D'ANGELO and Cantin with Sriskandan because D'ANGELO teaches an antibacterial compound active against Gram-positive pathogens, clofoctol, and Sriskandan teaches Gram-positive pathogens may trigger sepsis. One would be motivated to combine the references to treat sepsis and one would have a reasonable expectation of success because clofoctol is a well-known antibacterial.
Claim(s) 1 and 23 /are rejected under 35 U.S.C. 103 as being unpatentable DANESI (DANESI ET AL: "Clinical study on the efficacy of clofoctol in the treatment of infectious respiratory diseases", https://www.ncbi.nlm.nih.gov/pubmed/4018951, INT. J. CLIN. PHARM. RES. V(3) 175-179 (1985), IDS) in view of Mayo Clinic (Mayo Clinic, Pneumonia, June 13, 2020) further in view of Barnes (Barnes et al., How corticosteroids control inflammation: Quintiles Prize Lecture 2005, British Journal of Pharmacology (2006) 148, 245–254).
The DANESI and Mayo Clinic have been discussed supra and do not disclose corticosteroid (claim 23).
The reference Barnes teaches “Corticosteroids (also known as glucocorticosteroids, gluco corticoids or just steroids) are among the most widely used drugs in the world and are effective in many inflammatory and immune diseases”(page 245) and “The predominant effect of corticosteroids is to switch off multiple inflammatory genes (encoding cytokines, chemokines, adhesion molecules, inflammatory enzymes, receptors and proteins) that have been activated during the chronic inflammatory process”(page 245).
This helps to teach claim 23.
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the instant invention to have modified DANESI and the Mayo Clinic reference with Barnes because DANESI teaches using clofoctol to treat bacterial lung infections in patients including pneumonia and the Mayo Clinic teaches that pneumonia is an infection that inflame the lungs often caused by bacteria. Thus it would be obvious to treat pneumonia inflammation by using the clofoctol anti-bacteria treatment. It would also be obvious to one of ordinary skill in the art to determine the effectiveness of treating the pneumonia inflammation by comparing the levels of lung inflammation after the administration of clofoctol since it is standard practice to determine the effectiveness of treatment by comparing before and after patient conditions. One would be motivated to do so to treat pneumonia and determine if the pneumonia inflammation is improving after treatment. One would have a reasonable expectation of success because the reference Danesi showed good clinical results in a patient with pneumonia. It would then be obvious to combine other anti-inflammatory drugs for the same purpose of treating the pneumonia inflammation. Since Barnes teaches corticosteroids are well known anti- inflammatory drugs it would be obvious to one of ordinary skill in the art to use them in combination to treat a disease that has inflammation. One would have a reasonable expectation of success because they are well known to treat inflammation and one would be motivated to do so to treat pneumonia.
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.
Claim 1, 9, 22 provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6, 8-14 and 16-7 of copending Application No. 19/475,774 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because:
The application ‘774 claims:
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It is implicit to one of ordinary skill in the art when considering new therapies to determine if the therapy is working by determining the condition of the patient before and after the treatment.
This anticipates claims 1, 9, 22.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Response to Arguments
Applicant’s arguments with respect to all claim(s) have been considered but are moot because the new ground of rejection does not rely on any reference applied in the prior rejection of record for any teaching or matter specifically challenged in the argument.
Allowable Subject Matter
Claims 14 are objected to as being dependent upon a rejected base claim, but would be allowable if rewritten in independent form including all of the limitations of the base claim and any intervening claims.
Conclusion
Claims 1, 9, 11, 13, 15-18 and 22-23 are rejected.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to ALISON AZAR HASTINGS whose telephone number is (703)756-4584. The examiner can normally be reached Mon-Thurs 7:30am-5pm EST Friday 7:30-4pm EST (every other Friday off).
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/A.A.H./ Examiner, Art Unit 1627
/Kortney L. Klinkel/ Supervisory Patent Examiner, Art Unit 1627
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