DETAILED ACTION
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 Amendment
Applicant’s response filed 20 April 2026 has been received and entered. Claims 1-2 and 6 have been amended and claims 11, 20-32 and 39-40 have been canceled. Claims 1-10, 12-19, 33-38 are currently pending and under consideration in the instant Office action.
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Any objection or rejection of record which is not expressly repeated in this action has been overcome by Applicant's response and withdrawn.
Applicant's arguments filed 20 April 2026 have been fully considered but are not found to be persuasive.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 20 April 2026 has been considered by the examiner.
Specification
The disclosure remains objected to for the reasons stated in the Office action mailed 22 October 2025. A review of the Application file does not show any filing of a substitute specification as asserted by Applicant. Furthermore, there is no evidence of a substitute specification having been filed according to the Electronic filing receipt.
A substitute specification is still required which is entirely in black ink/font is required.
Appropriate correction is required.
Applicant’s amendment to the title has been received and entered. However, the title of the invention is not descriptive. A new title is required that is clearly indicative of the invention to which the claims are directed. The claims are not directed to treatment of respiratory disease generally as the claims are limited to ARDS..
Claim Rejections - 35 USC § 103
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 1-10, 12-19 and 33-38 is/are rejected under 35 U.S.C. 103 as being obvious over Zhou (WO 2017/073369) in view of any one of Beidler et al. (U.S. Pat. No. 9,290,570, 9,783,605, 10,093,727, 10,858,425) and further in view of Huang et al. (Lancet 395: 497-506, Jan. 24 2020). The specifications of each Beidler et al. patent are identical; the rejection only references ‘570 for the sake of simplicity but the disclosures cited are found in all of the Beidler et al. patents.
Zhou teaches an antibody, referred to as PanELR, which neutralizes human IL-8, Gro-alpha, Gro-beta, Gro-gamma, gcp-2 and ENA-78. These CXC chemokines are known to stimulate neutrophil chemotaxis by activation of the CXCR1 and CXCR2 receptors. PanELR decreases neutrophil chemotaxis through inhibition of CXCR1 and CXCR2 receptor activation by neutralizing the targets to which it binds. Specifically, the antibody suppresses the infiltration of neutrophils in a number of animal models including the LPS inhaled model of lung inflammation and the cantharidin skin blister model. 10 mg/Kg administered i.v. suppresses over 90% of neutrophil infiltration (see page 2, last 2 paragraphs). The inhibition of these CXC chemokines by the PanELR antibody can prevent inflammatory cells from infiltrating the lung tissue and therefore, prevent tissue damage.
Zhou teaches a method of treating a human with diseases or disorders characterized by elevated levels of one or more of human IL-8, Gro-alpha, Gro-beta, Gro-gamma, gcp-2 and ENA-78 with the PanELR antibody. Such conditions include COPD, asthma, acute lung injury, acute lung disease, sepsis, ARDS, neonatal respiratory distress syndrome, respiratory syncytial virus, flu, Bronchiolitis obliterans syndrome and diffuse panbronchiolitis (see page 4). Zhou teaches that the PanELR antibody can be used to treat or prevent the recited diseases/conditions (see page 15, lines 27-28).
Zhou does not teach prevention or treatment of ARDS with an antibody that additionally binds human neutrophil activating protein-2 (CXCL7) and has 6 CDRs with the amino acid sequences of SEQ ID NO:7-12 in a patient that has COVID-19 as recited in the instant claims.
Beidler et al. (U.S. Pat. No. 9,783,605) teach an antibody which binds and neutralizes human IL-8, Gro-alpha, Gro-beta, Gro-gamma, gcp-2, ENA-78 and NAP2 and has 6 CDRs with the amino acid sequences of SEQ ID NO:7-12 (aka Antibody 1). Beidler et al. teach that neutralization of all seven ELR+CXC chemokines inhibits the ability of CXCR1 and CXCR2 positive cells from migrating to sites of inflammation (see column 1). Beidler et al. teach that Antibody 1 neutralizes the chemotaxis ability of neutrophils in vitro (see column 12). The antibody comprises 6 CDRs which have the amino acid sequences of SEQ ID NO:7-12, heavy and light chain variable amino acid sequences of 2 and 4 or 14 and 16, respectively and heavy and light chain amino acid sequences of 1 and 13 or 3 and 15, respectively. See the disclosure of ‘570 at columns 1-2. The antibody of Beidler et al. is the same as the antibody of the instant application.
Huang et al. teach that 2019-nCoV (a.k.a. SARS-Co19; 2019 novel coronavirus which causes COVID19) caused a cluster of pneumonia cases in Wuhan, China. The patients all had pneumonia and complications included acute respiratory distress syndrome (see “Findings” in abstract).
It would have been obvious before the effective filing date of the instant application to prevent or treat ARDS in a subject in need thereof with an antibody that inhibits neutrophil chemotaxis through inhibition of CXCR1 and CXCR2 receptor activation as taught by Zhou. Further, it would have been obvious to treat a subject that has COVID-19 as taught by Huang et al. because complications of COVID-19 include ARDS and therefore, such subjects would necessarily be in need of treatment/prevention of ARDS. It would have been obvious to one of ordinary skill in the art practice the method of Zhou and to substitute the antibody of Beidler et al. for the antibody of Zhou because the antibody of Beidler et al. binds to seven chemokines while the antibody of Zhou only binds six of the chemokines which activate CXCR1 and CXCR2. The substitution would have been obvious to one of ordinary skill in the art because the antibody of Beidler et al. would inactivate more stimulatory chemokines and because Beidler et al. teach that Antibody 1 neutralizes all seven ELR+CXC chemokines and inhibits CXCR1 and CXCR2 positive cell migration. With regard to claims 2-5 which require that the patient have pneumonia, a respiratory insult, a respiratory disease or injury, the subjects of Huang et al. appear to meet these limitations as the subjects have pneumonia which meets these limitations. Additionally, one of ordinary skill in the art would be motivated to treat ARDS in any patient regardless of the degree of the condition (mild, moderate, severe) or the method of diagnosis or what condition precipitated the ARDS (viral infection) because ARDS is a life-threatening lung condition which damages the alveoli and can lead to fluid accumulation in the lungs which impairs oxygen exchange and can result in respiratory failure. It would have been obvious to one of ordinary skill in the art before the effective filing date to treat patients who had been diagnosed by any means, including according to the Berlin definition of ARDS because this definition has been widely adopted by healthcare professionals.
With regard to claims 17-19 and 36-38, neither reference specifically teaches dosages to be administered. However, determination of dosages is routine optimization because the prior art of Zhou and Beidler et al. teach that panELR antibodies are effective to inhibit neutrophil migration and infiltration and determining of optimum or workable ranges of doses would be characterized as routine experimentation in the relevant art as dosage is a result-effective variable. Therefore, the instant claims directed to dosage administration are obvious over the teachings of Zhou and Beidler et al. in view of Huang et al.
Response to Arguments
Applicant argues at page 8 of the response that neither Zhou nor Beidler et al. teach or suggest the claimed methods as claim 1 has been amended to recite a method of preventing ARDS in a patient that has COVID-19. Applicant’s arguments are persuasive. The grounds of rejection have been changed to reflect the nature of the amendment.
Applicant argues at the bottom of page 8 that Zhou does not teach preventing ARDS in patients with COVID-19, or in the context of any viral infection leading to ARDS and that Beidler does not teach or suggest treating any respiratory disease, let alone ARDS precipitated by a viral infection. Applicant asserts that there is nothing in the combined teachings that would have led a person of ordinary skill in the art to preventing ARDS in COVID-19 patients or treating ARDS in patients with a viral infection as recited in the claims.
Applicant’s argument has been fully considered, but is not found persuasive. Zhou teach at page 2 that CXC chemokines are known to stimulate neutrophil chemotaxis and that inhibition of these chemokines could prevent inflammatory cells from infiltrating the lung tissue and therefore, prevent tissue damage. One of ordinary skill in the relevant art would have been apprised of the fact that ARDS is caused by an uncontrolled systemic inflammatory response resulting from various clinical events, including severe infections including viral infections and that activated leukocytes and chemokines play a key role in the pathogenesis of ARDS (see Puneet et al. Am J. Physiol. Lung Cell Mol. Physiol. 288(1): 13-15, 2005). Therefore, one of ordinary skill in the art, having an understanding of the pathophysiology of ARDS would have reasonably concluded that administration of the PAN-ELR+ CXC chemokine antibodies of Beidler et al. would prevent ARDS in a patient with COVID-19, which patients are at risk of ARDS as taught by Huang et al., because Zhou teaches that CXC chemokines are known to stimulate neutrophil chemotaxis and that inhibition of these chemokines could prevent inflammatory cells from infiltrating the lung tissue and therefore, prevent tissue damage and therefore, prevent ARDS.
Applicant argues in the paragraph spanning pages 8-9 that ARDS can develop for many reasons and that the LPS model in Zhou differs mechanistically from viral entry and replication. Applicant’s argument has been fully considered, but is not found persuasive. While the initial insult which triggers the release of chemokines and inflammatory cytokines may differ, the resulting condition which is ARDS, is the same and is triggered by the same release of biological molecules that stimulate neutrophil chemotaxis and infiltration to the lung, which one of ordinary skill in the art would have reasonably recognized as evidenced by Puneet et al. (general knowledge in the art as of at least 2005).
Applicant argues at page 9 of the response that the rejection does not provide a reason to substitute the antibody of Beidler et al. for the antibody of Zhou. Applicant asserts that a person of ordinary skill in the art would not have had a reason to believe that the inclusion of NAP-2 neutralization would predictably lead to an effective therapy for ARDS. Applicant’s argument has been fully considered, but is not found persuasive. The rejection provides a clear motivation to substitute the antibody of Beidler et al. for the antibody of Zhou. The rejection does not rely on NAP-2 neutralization for treating ARDS but rather inhibition of the ability of CXCR1 and CXCR2 positive cells from migrating to sites of inflammation and resulting in ARDS. Zhou already teach using an antibody that inhibits 6 human ELR+CXC chemokines so it would be obvious to one of ordinary skill in the art to use an antibody that blocks 7 human ELR+CXC because it would be expected to inhibit CXCR1 and CXCR2 positive cells better because it blocks more of the ELR+CXC chemokines that activate CXCR1 and CXCR2.
Applicant argues at the bottom of page 9 that Beidler et al. does not teach or suggest using its antibody to treat or prevent any respiratory disease. Applicant is correct that Beidler et al. does not teach this aspect of the claimed invention and this was acknowledged in the rejection. However, Beidler et al. was not cited for such a teaching, but rather for the specific antibody that blocks 7 human ELR+CXC. Zhou et al. was cited for the teaching that PanELR antibodies could be used for treating respiratory disease and for preventing ARDS. Because Zhou et al. already teach that PanELR antibodies can be used for such, it would have been obvious to use the PAN-ELR+ CXC chemokine antibodies of Beidler et al. for the same purpose because the antibody of Beidler et al. inhibit all the same molecules of Zhou et al. with the additional inhibition of NAP-2.
Applicant argues at page 10 of the response that the Examiner has not established that a person of ordinary skill in the art would have had a reasonable expectation of success in preventing or treating ARDS with the claimed antibody.
Applicant asserts that Zhou’s inclusion of ARDS in a laundry list of more than thirty diseases and conditions does not amount to a meaningful teaching that any particular pan-ELR antibody would be effective in treating ARDS much less in preventing ARDS in a patient with COVID-19 and states “such an open-ended enumeration, without supporting data or specific guidance regarding ARDS, would not have given a person of ordinary skill confidence that the approach would succeed”.
Applicant’s argument has been fully considered, but is not found persuasive. The prior art before the effective filing date of the claimed invention has established the importance of inflammatory chemokines in the development of ARDS. In the Office action mailed 22 October 2025, Grommes et al. was cited as teaching that neutrophils are considered to play a key role in the progression of acute lung injury (ALI) and ARDS and that activation and transmigration of neutrophils is a hallmark event in the progression of ALI and ARDS. Boyle et al. was also cited as teaching that ARDS is an inflammatory condition characterized by neutrophil and macrophage-mediated injury, with excessive pro-inflammatory cytokine and protease activity in the alveolar space (see page 969, paragraph 2). Williams et al. (Thorax 72: 66-73, 2017) was cited as teaching that ARDS is characterised by the recruitment of neutrophils into the lung interstitium and alveolar space and that inflammatory chemokines are involved in regulating neutrophil migration and may have value as therapeutic targets for the treatment of ARDS. Puneet et al. (cited previously) teach that chemokines are a specific class of inflammatory mediators that play a key role in the pathogenesis of ARDS (see Figure 1 of Puneet). Also cited previously, US Pat. No. 8,496,932 (Clegg et al.) teach an antibody which binds human IL-8, Gro-alpha, Gro-beta, Gro-gamma and ENA-78 and its use for prevention/treatment of ARDS and other respiratory diseases (see columns 9-10).
While Zhou does identify a number of different inflammatory conditions in which members of the EXRCXC subfamily of CXCL chemokines are elevated, Zhou specifically states that CXC chemokines are known to stimulate neutrophil chemotaxis by engaging and activating the CXCR1 and CXCR2 receptors and thus “the inhibition of these chemokines could prevent inflammatory cells from infiltrating the lung tissue and thus preventing tissue damage” (see page 2, lines 22-25). This teaching taken with the knowledge of the prior art which clearly establishes neutrophil infiltration stimulated by chemokines as being a key part of the pathogenesis of ARDS would provide an expectation of success that inhibition of such would prevent ARDS because it would prevent inflammatory cells from infiltrating the lung tissue and thus preventing tissue damage.
Applicant asserts that Zhou does not provide any data or experimental evidence to support the asserted method of preventing ARDS. However, it is noted that the only experiment which is disclosed in the instant application is a single-ascending dose study to evaluate the safety, tolerability, pharmacokinetics and pharmacodynamics of the disclosed antibody in healthy subjects. The antibody was administered subcutaneously to assess bioavailability. Additionally skin blisters were induced and the antibody was administered via IV to assess neutrophil chemotaxis and accumulation (see page 10 of the specification). Example 2 at page 11 of the specification is a prophetic example which was not undertaken and therefore, no data regarding prevention/treatment of ARDS was ever obtained. Therefore, the instant specification does not provide any more data or evidence than is found in the prior art. If Applicant is asserting that data is required for there to be a reasonable expectation of success, it is noted that no such data is found in the instant specification.
Applicant argues that the instant application addresses a long-felt but unmet need in the art. Applicant’s argument has been fully considered, but is not found persuasive. COVID-19 was only first recognized in late 2019 and the instant application was filed in April of 2021 with a priority date of April 2020 (provisional application). Considering the patients who are to be treated were only known to exist for 4-5 months before the earliest effective filing date of the instant invention, one would not consider the instant claims to address a long-felt need.
Establishing a long-felt need requires objective evidence that an art recognized problem existed in the art for a long period of time without solution. There is no showing that others of ordinary skill in the art were working on the problem and if so, for how long. In addition, there is no evidence that if persons skilled in the art who were presumably working on the problem knew of the teachings of the above cited references, they would still be unable to solve the problem. See MPEP § 716.04.
Applicant asserts at page 11 of the response that the specification describes a clinical study design for evaluating the claimed invention and that this “clinical development program is directed to demonstrating efficacy in the specific context of the amended claims, further supporting the non-obvious nature of the claimed invention”. Applicant’s argument has been fully considered, but is not found persuasive. Example 2 of the specification is prophetic and has not been undertaken. Therefore, there is no data or evidence to be obtained from this example. It is not clear how this prophetic disclosure supports a conclusion of non-obviousness.
Claims 1, 6, 17-19 and 36-38 is/are rejected under 35 U.S.C. 103 as being obvious over Zhou (WO 2017/073369) in view of Beidler et al. (U.S. Pat. No. 9,783,605) and Huang et al. (Lancet 395: 497-506, Jan. 24 2020) and further in view of U.S. Pat. No. 12,037,387 (Kikly et al.).
The teachings of Zhou, Beidler et al. and Huang et al. are as provided above. None of the references disclose the dosages which are recited in claims 17-19 and 36-38.
Kikly et al. teach the administration of the same antibody of Beidler et al. for the treatment of hidradenitis suppurativa wherein the dose is administered either intravenously or subcutaneously in the range of about 100 mg to about 1000 mg, or 150 mg to about 1500 mg, 100-600mg, 300-600mg, 100-150mg, 150-900mg, 450-900mg, 250-450mg, 600-1000mg, 900-1500mg, about 300mg, about 600mg, and about 900mg as well as including a loading dose and administration includes multiple administrations (see claims 4-22 of Kikly et al.).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to practice the method of Zhou for the treatment/prevention of ARDS with the antibody of Beidler et al. in subjects with COVID-19 as taught by Huang et al. because administration of the antibody of Beidler et al. neutralizes seven chemokines rather than the six of Zhou and to further administer the antibody subcutaneously or intravenously at doses in the range of about 100mg to about 1500mg as taught by Kikly et al. because Kikly et al. teach that these dosages are safe and well-tolerated in patients as well as the dosages being effective to inhibit neutrophil chemotaxis and accumulation in a skin blister model (see columns 9-10 beginning at line 32). As the dosages of Kikly et al. were determined to be safe and effective to inhibit neutrophil chemotaxis, it would have been obvious to one of ordinary skill in the art to treat/prevent ARDS as taught by Zhou with the antibody of Beidler et al. using the dosages of Kikly et al. with a reasonable expectation of success because administration with the dosages of Kikly et al. inhibit neutrophil chemotaxis and neutrophil infiltration is the hallmark of ARDS.
Response to Arguments
Applicant argues that Kikly et al. teaches dosing regimens of the same antibody in the treatment of hiradenitis suppurativa and not for the treatment of ARDS. Applicant asserts that ARDS and hiradenitis suppurativa are different diseases with different pathophysiology, etc. Applicant asserts that the Examiner has not “articulated why a person of ordinary skill in the art would have looked to dosing regimens developed and validated for a chronic inflammatory skin condition and applied them to an acute respiratory emergency. Applicant’s arguments have been fully considered, but are not found persuasive.
As stated above, Kikly et al. teach dosages of the antibody (subcutaneously in the range of about 100 mg to about 1000 mg, or 150 mg to about 1500 mg, 100-600mg, 300-600mg, 100-150mg, 150-900mg, 450-900mg, 250-450mg, 600-1000mg, 900-1500mg, about 300mg, about 600mg, and about 900mg as well as including a loading dose and administration includes multiple administrations) are safe and well-tolerated in patients as well as the dosages being effective to inhibit neutrophil chemotaxis and accumulation in a skin blister model (see columns 9-10 beginning at line 32). The skin blister model appears to be the same model which is relied upon in the instant application (see page 10 of the specification). As pointed out in the rejection above, neutrophil infiltration is the hallmark of ARDS, therefore, the ability of the antibody to inhibit neutrophil chemotaxis using the dosages taught be Kikly et al. provide a reasonable expectation of success in treating/preventing ARDS because such dosages would inhibit neutrophil chemotaxis into the lung tissue. Again, the instant application uses the exact same experimental model for determining effective dosages which is based on a skin blister model which is clearly not an acute condition such as ARDS.
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 1-10, 12-19 and 33-38 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-5 and 10-12 of U.S. Patent No. 9,290,570 in view of Zhou (WO 2017/073369) and Huang et al. Although the claims at issue are not identical, they are not patentably distinct from each other because the claimed method of preventing/treating ARDS with an antibody which binds and neutralizes human IL-8, Gro-alpha, Gro-beta, Gro-gamma, gcp-2, ENA-78 and NAP2 and has 6 CDRs with the amino acid sequences of SEQ ID NO:7-12 (aka Antibody 1) in a subject with COVID-19 would have been obvious over the claims of ‘570 directed to the same antibody in view of the teachings of Zhou (WO 2017/073369) and Huang et al.
The antibody recited in the methods of the instant claims is identical to that of ‘570. The claims of ‘570 are directed to the PAN-ELR+CXC chemokine antibody called Antibody 1.
The teachings of Zhou are provided above. Briefly, Zhou teach the prevention/treatment of ARDS with a PanELR antibody (neutralizes human IL-8, Gro-alpha, Gro-beta, Gro-gamma, gcp-2 and ENA-78). It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to practice the method of Zhou with the antibody of ‘570 because the antibody of ‘570 neutralizes all of the same chemokines as that of Zhou and additionally neutralizes NAP2, an additional chemokine that activates CXCR1 and CXCR2 which are responsible for neutrophil chemotaxis and infiltration of the lungs in ARDS. Additionally, it would have been obvious to practice the method of Zhou in a subject with COVID-19 because Huang et al. teach that COVID-19 patients have complications that include ARDS.
One would have had a reasonable expectation of success in practicing the method of Zhou with the antibody of ‘570 in patients with COVID-19 because the antibody of ‘570 neutralizes human ELR+CXC chemokines and inhibits neutrophil chemotaxis (see columns 11-12 of ‘570) and neutrophil chemotaxis is the hallmark of ARDS.
While neither Zhou nor ‘570 specifically discusses patients at risk of ARDS, one of ordinary skill in the art would have known that patients with respiratory insults, disease or injury are those patients at risk of developing ARDS because is an inflammatory lung condition. Additionally, Huang et al. teach that subjects with COVID-19 have complications that include ARDS. Additionally, one of ordinary skill in the art would be motivated to treat ARDS as taught in Zhou in any patient regardless of the degree of the condition (mild, moderate, severe) or the method of diagnosis or what condition precipitated the ARDS (viral infection) because ARDS is a life-threatening lung condition which damages the alveoli and can lead to fluid accumulation in the lungs which impairs oxygen exchange and can result in respiratory failure. It would have been obvious to one of ordinary skill in the art before the effective filing date to treat patients who had been diagnosed by any means, including according to the Berlin definition of ARDS because this definition has been widely adopted by healthcare professionals.
With regard to claims 17-19 and 36-38, neither Zhou nor ‘570 specifically teaches dosages to be administered. However, determination of dosages is routine optimization because the prior art of Zhou and ‘570 teach that panELR antibodies are effective to inhibit neutrophil migration and infiltration and determining of optimum or workable ranges of doses would be characterized as routine experimentation in the relevant art as dosage is a result-effective variable. The instant claims directed to dosage administration are obvious over the teaching of Zhou, Huang et al. and the claims of ‘570. Therefore, the instant claims are not patentably distinct from those of ‘570 because the claimed method of treating/preventing ARDS would have been an obvious use in view of Zhou and Huang et al.
Response to Arguments
Applicant argues that the claims of ‘570 are directed to compositions of matter while the instant claims are directed to methods of treating/preventing ARDS. Applicant asserts that these method-of-treatment claims with specific disease indications and patient populations are entirely absent from the ‘570 patent claims. Applicant is correct but such a distinction does not negate the obviousness-type double patenting rejection. If the methods recited such elements, the rejection may have been made as a statutory double patenting rejection and not as an obviousness-type double patenting rejection.
Applicant argues at page 13 of the response that neither the ‘570 patent nor Zhou teach or suggest treating/preventing ARDS in COVID-19 patients. Applicant’s arguments have been fully considered, but are not found persuasive as the rejection now includes Huang et al. which has a publication date of Jan. 2020.
Applicant argues that Zhou includes ARDS in a laundry list of over thirty diseases/conditions without providing any data, specific guidance or teaching related to ARDS treatment. Applicant’s argument has been fully considered, but is not persuasive. While Zhou does identify a number of different inflammatory conditions in which members of the EXRCXC subfamily of CXCL chemokines are elevated, Zhou specifically states that CXC chemokines are known to stimulate neutrophil chemotaxis by engaging and activating the CXCR1 and CXCR2 receptors and thus “the inhibition of these chemokines could prevent inflammatory cells from infiltrating the lung tissue and thus preventing tissue damage” (see page 2, lines 22-25). This teaching taken with the knowledge of the prior art which clearly establishes neutrophil infiltration stimulated by chemokines as being a key part of the pathogenesis of ARDS would provide an expectation of success that inhibition of such would prevent ARDS because it would prevent inflammatory cells from infiltrating the lung tissue and thus preventing tissue damage. With regard to Zhou not providing any data or experimental evidence to support the asserted method of preventing ARDS it is noted that Zhou provides the same experimental evidence that the instant application relies upon for the instant claims (a skin blister model).
Applicant argues that there is not a reasonable expectation of success in using the antibody of the ‘8 patent to prevent or treat ARDS. Applicant’s arguments have been fully considered and are not found persuasive for the reasons applied above with regard to expectation of success.
Applicant argues that dosage determination is not routine and requires extensive clinical investigation and cannot be dismissed as routine optimization. Applicant’s arguments are not found to be persuasive. Applicant has not provided anything more than a mere allegation which is not supported by any facts. In the absence of such, and in light of the instant disclosure which also lacks extensive clinical investigation, the determination of dosage ranges is considered routine optimization for the reasons of record.
Conclusion
No claim is allowed.
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/Christine J Saoud/Primary Examiner, Art Unit 1645
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