DETAILED ACTION
Claims 1, 3, 5-10, 12-13 and 16-25 are currently pending in the instant application.
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/Arguments
Applicant’s amendments and arguments in a response filed 01/02/2026 have been fully considered and entered into the application. Applicant has overcome
The 35 U.S.C. 112(b) rejection of claims 1, 3, 5, 9, 21 and 25.
Regarding the 35 U.S.C. 103 rejections, Applicant argues that Snyder does not teach or suggest that a PDE1 inhibitor would promote M2 activation of macrophages other than microglia. Further Snyder does not teach or suggest a method of promoting resolution of inflammation and promoting macrophage activation from the M1 activation state to the M2 activation state for treatment of inflammation in a patient suffering from diseases recited in claim 1. Applicant further argues that Snyder teaches that PDE1 knockdown can inhibit transition from monocyte to activated macrophage which is a differentiation process that is biologically and mechanistically distinct from polarization of M1 macrophages to M2 macrophages. Applicant also argues that microglia have activation states “somewhat similar” to macrophages does not establish equivalence between M2 activation of microglia and M2 activation of macrophages and discloses that microglia and macrophages are developmentally, anatomically and functionally distinct. Applicant then states that Bannister does not cure deficiency of Snyder and discloses therapeutic compounds having anti-inflammatory activity without identifying which specific therapeutic compounds achieve each listed effect. Applicant argues that Bannister does not teach or suggest PDE1 inhibitors are capable of promoting the phenotypic change of M1 to M2. Applicant cites Rapoport v Dement case law stating that a PDE1 inhibitor has been taught to be administered to a broad population with inflammation does not suggest or make obvious administering a PDE1 inhibitor for purpose of promoting resolution of inflammation and promoting macrophage activation from the M1 activation state to the M2 activation state in patients suffering from the particular diseases or disorders listed in claim 1. Lastly, Applicant argues unexpected results stating that Examples 1 and 3 show claimed PDE 1 inhibitor promotes resolution of inflammation and promotes macrophage activation to M2 activation state using mouse zymosan pleurisy model and that the results demonstrate shift from M1 to M2 was a result of administering the tested PDE1 inhibitors, which is not taught by Snyder or Bannister.
In response, MPEP 2142 states "[t]o support the conclusion that the claimed invention is directed to obvious subject matter, either the references must expressly or impliedly suggest the claimed invention or the examiner must present a convincing line of reasoning as to why the artisan would have found the claimed invention to have been obvious in light of the teachings of the references." Ex parte Clapp, 227 USPQ 972, 973 (Bd. Pat. App. & Inter. 1985). As discussed, Snyder teaches “that inhibition of PDE1B may affect macrophage activation … in the blood so as to reduce M1 activation and the release of pro-inflammatory cytokines, and to enhance the action of M2 microglia, through the up-regulation of anti-inflammatory cytokines such as IL-10” - see paragraph [0024]. Snyder further teaches that microglia have activation states somewhat similar to macrophages and in response to IFN-γ or lipopolysaccharide (LPS), they will be activated to release pro-inflammatory cytokines such as TNF-, IL-1 γ, and reactive oxygen species/reactive nitrogen species (ROS/NOS). Under other circumstances, they can be activated to release anti-inflammatory cytokines, such as IL-10, and to participate in tissue repair. Thus, based on the statements of Snyder, inhibition of PDE1B could be expected to affect macrophage activation so as to reduce M1 activation. Snyder teaches that inhibition of PDE1B enhances the action of M2 microglia through the up-regulation of anti-inflammatory cytokines such as IL-10 and that microglia have activation states somewhat similar to macrophages. According to Liu et al (see Journal of Immunology, Volume 206, Issue 4, February 2021, Pages 883–891), in vitro studies frequently use LPS, IFN-γ, or LPS + IFN-γ treatment to induce the M1-like phenotype and IL-4 or IL-10 to induce the M2-like phenotype in mouse (see 2nd full paragraph under discussion). Thus, as Snyder teaches that action of M2 microglia is up-regulated through cytokines such as IL-10 which is enhanced by PDE1B inhibition, it would follow that PDE1B inhibition would also up-regulate M2-like macrophages. Thus, one of ordinary skill in the art would expect that a PDE1B inhibitor would also induce M2 macrophage, especially since Snyder teaches that microglia have activation states similar to macrophages. Snyder already explicitly teaches PDE1B inhibitors reduce M1 activation macrophage. Thus, it would be reasonable based on the teachings of Snyder to expect that inhibition of PDE1B affects macrophage activation by both reduction of M1 activation and induction of M2 activation.
It is noted that the instant claims state a method of “promoting macrophage activation from the M1 activation state to the M2 activation state”. According to Merriam-Webster, the term “promoting” refers “to help growth or development of”. Thus, it appears that administering a PDE inhibitor merely needs to further the progress rather than necessitate the particular outcome of macrophage activation from M1 activation state to the M2 activation state. As Snyder teaches inhibition of PDE1B affects macrophage activation and M1 activation is reduced and the action of M2 microglia is enhanced, through the up-regulation of anti-inflammatory cytokines such as IL-10 which are known to induce M2-like phenotypes, the prior art clearly teaches or suggests PDE1 inhibitor promoting macrophage activation from M1 activation to M2 activation since M1 activation is reduced and cytokines that activate M2 phenotypes are released. Further Snyder teaches the claimed compounds as inhibitors of PDE1B for treatment and prophylaxis of inflammation and/or disease or disorders related to inflammation.
MPEP 2145, Section X(B) states that an "obvious to try" rationale may support a conclusion that a claim would have been obvious where one skilled in the art is choosing from a finite number of identified, predictable solutions, with a reasonable expectation of success. " [A] person of ordinary skill has good reason to pursue the known options within his or her technical grasp. If this leads to the anticipated success, it is likely that product [was] not of innovation but of ordinary skill and common sense. In that instance the fact that a combination was obvious to try might show that it was obvious under § 103." KSR Int'l Co. v. Teleflex Inc., 550 U.S. 398, 421, 82 USPQ2d 1385, 1397 (2007). What was ‘obvious to try’ was to explore a new technology or general approach that seemed to be a promising field of experimentation, where the prior art gave only general guidance as to the particular form of the claimed invention or how to achieve it." In re O’Farrell, 853 F.2d 894, 903, 7 USPQ2d 1673, 1681 (Fed. Cir. 1988) (citations omitted) (The court held the claimed method would have been obvious over the prior art relied upon because one reference contained a detailed enabling methodology, a suggestion to modify the prior art to produce the claimed invention, and evidence suggesting the modification would be successful.).
Bannister is used to teach that PDE1 inhibitors as well as compounds that promoting phenotypic change of M1 to M2 are used in clinically effective treatment of chronic inflammation (see paragraph [0192]). Thus, BANNISTER teaches PDE1 inhibitors and compounds that promote the resolving phenotypic change of M1 to M2 in methods of treating inflammation and having an anti-inflammatory activity. Further BANNISTER teaches treating inflammation may include treating of a chronic inflammation in both allergic reactions and some myopathies and include diseases such as pleuritis (see paragraph [0166]). Specifically, a pharmaceutical composition comprising said PDE1 inhibitor (see claim 35, paragraph [0232]) is administered to an individual with chronic inflammation, resulting in reduction of a symptom associated with the chronic inflammation (see claim 80, paragraph [0277]) with pleuritis named as associated with the chronic inflammation (see claim 83, paragraph [0280]). Thus Bannister is used to teach examples of diseases mediated by macrophages that are disclosed in the instant claims.
Regarding Applicant’s citation of Rapoport v Dement case law to support the argument that a PDE1 inhibitor has been taught to be administered to a broad population with inflammation does not suggest or make obvious administering a PDE1 inhibitor for purpose of promoting resolution of inflammation and promoting macrophage activation from the M1 activation state to the M2 activation state in patients suffering from the particular diseases or disorders listed in claim 1. According to Rapoport: The anxiolytic amount of buspirone taught by the FPR publication still inherently anticipates in view of the fact that the Dement et al. application contains disclosures that anxiolytic amounts of buspirone overlap the preferred therapeutically effective amounts of buspirone disclosed in the Dement et al. application for reducing the frequency and severity of the apnea episodes during sleep.
It appears that Applicant references the case law of Rapoport since Snyder does not teach the particular diseases of claim 1. However, Snyder is relied upon for teaching a method of promoting resolution of inflammation and promoting macrophage activation from the M1 activation state to the M2 activation state for treatment of inflammation, the method comprising administering a PDE1 inhibitor as well as specific PDE1 inhibitors while Bannister is relied upon for teaching of examples of inflammatory diseases mediated by macrophages that could be reasonably be expected to be treated, which includes the diseases found in the instant claims. Thus, based upon applicant's arguments against the references individually, one cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986).
Lastly, Applicant argues unexpected results stating that Examples 1 and 3 show claimed PDE 1 inhibitor promotes resolution of inflammation and promotes macrophage activation to M2 activation state using mouse zymosan pleurisy model. The results demonstrate shift from M1 to M2 was a result of administering the tested PDE1 inhibitors. However, it is unclear why the data from Examples 1 and 3 would be considered unexpected in view of the prior art teachings which suggest that the tested PDE1 inhibitors would promote resolution of inflammation and macrophage activation from M1 activation state to the M2 activation state. This would be considered an expected result as the prior art teaches that inhibition of PDE1B may affect macrophage activation … in the blood so as to reduce M1 activation. According to MPEP 716.02(b)(II), "[A]ppellants have the burden of explaining the data in any declaration they proffer as evidence of non-obviousness." Ex parte Ishizaka, 24 USPQ2d 1621, 1624 (Bd. Pat. App. & Inter. 1992). Applicant appear to be merely stating the results of experiments without explanation as to why the results are unexpected and significant. MPEP 716.02(b)(I) - BURDEN ON APPLICANT TO ESTABLISH RESULTS ARE UNEXPECTED AND SIGNIFICANT. The evidence relied upon should establish "that the differences in results are in fact unexpected and unobvious and of both statistical and practical significance." Ex parte Gelles, 22 USPQ2d 1318, 1319 (Bd. Pat. App. & Inter. 1992) (Mere conclusions in appellants’ brief that the claimed polymer had an unexpectedly increased impact strength "are not entitled to the weight of conclusions accompanying the evidence, either in the specification or in a declaration."); Ex parte C, 27 USPQ2d 1492 (Bd. Pat. App. & Inter. 1992) (Applicant alleged unexpected results with regard to the claimed soybean plant, however there was no basis for judging the practical significance of data with regard to maturity date, flowering date, flower color, or height of the plant.). See also In re Nolan, 553 F.2d 1261, 1267, 193 USPQ 641, 645 (CCPA 1977) and In re Eli Lilly, 902 F.2d 943, 14 USPQ2d 1741 (Fed. Cir. 1990) as discussed in MPEP § 716.02(c).
Applicant argues that the data in the Specification found in Examples 1 and 3 are not taught by the ‘666 patent and Bannister. However, this is not found persuasive because: (1) such a shift is suggested to occur with the administration of PDE1B inhibitors by Snyder and was thus predictable from the prior art and (2) Applicants have not met their burden of demonstrating the shift M1 to M2, which occurs naturally, is the result of administering the tested PDE1 inhibitor and that the tested PDE1 inhibitor is representative of all PDE1 inhibitors. See MPEP 716.02.
Thus all the prior 103 rejection and double patenting rejections have been maintained.
Maintained 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.
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 nonobviousness.
Claims 1, 3, 5, 9, 21 and 25 are rejected under 35 U.S.C. 103 as being unpatentable over Snyder (see WIPO Pub. No. 2018/049417, pub. 03/15/2018 and filed 09/12/2017, cited in IDS filed 06/09/2022) in view of BANNISTER (see U.S. 2016/0317482, pub. 11/03/2016).
Snyder teaches inhibitors of PDE1 for treatment and prophylaxis of inflammation and/or disease or disorders related to inflammation (see paragraph [0001], p. 1). Snyder teaches an inhibitor of PDE1 as
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(see paragraph [0084], p. 68 and claims 5-6), which corresponds to the elected species.
Snyder teaches PDE1 inhibitors are administered to a patient with increased levels of one or more pro-inflammatory cytokines (e.g., IL1β, TNF-α, and Ccl2, or combination thereof) in an amount effective to (i) reduce or inhibit activation of M1 microglia, and/or (ii) and amount effective to reduce levels of one or more pro-inflammatory cytokines (e.g., IL1β, TNF-α, and Ccl2, or combination thereof); to a patient in need thereof with disease. Additionally, Snyder teaches that the patient has elevated levels of one or more pro-inflammatory cytokines (e.g., selected from IL1β, TNFα, Ccl2, IL-6, and combinations thereof); reduced levels of one or more anti-inflammatory cytokines (e.g., IL-10) (see paragraph [0064], p.64). This corresponds to limitations of claim 3.
Snyder teaches that an PDE1 inhibitor is administered in combination with a PDE4 inhibitor, specifically rolipram (see claim 9). This reads on claims 9 and 25.
Snyder teaches the PDE1 is induced in inflammatory monocyte-to-activated macrophage transition mediated by GM-CSF (see paragraph [0003]) and PDE1 inhibitor vinpocetine has been shown to be anti-inflammatory. Additionally, inhibition of PDE1B may affect macrophage activation in the blood and/or microglial activation in the CNS, so as to reduce M1 activation and release of pro-inflammatory cytokines, and to enhance the action of M2 microglia, through the up- regulation of anti-inflammatory cytokines such as IL-10 (see paragraph [0024]). Further microglia have activation states somewhat similar to macrophages (see paragraph [0088]. Although Snyder teaches treatment of inflammation comprising administering a PDE1 inhibitor corresponding to the same compound as the instant claims, Snyder does not teach treating of pleurisy as the inflammatory disease.
BANNISTER teaches a method of treating individual with chronic inflammation by administering a composition and further discusses different embodiments through which therapeutic compounds may have anti-inflammatory activity and reduce levels of an inflammation inducing molecule. Specifically, BANNISTER teaches one method by which a therapeutic compound may have anti-inflammatory activity is by promoting the resolving phenotypic change of M1 to M2 – see (see paragraphs [0056]-[0057]). Other therapeutic compounds disclosed herein may be a Phosphodiesterase inhibitor. Examples of a suitable Phosphodiesterase inhibitor include, without limitation, a PDE 1 selective inhibitor” (see paragraph [0078]) and a therapeutic compound of the pharmaceutical composition disclosed herein is delivered to a macrophage. Macrophages are one of the key cell types believed to be involved in the control of the inflammation response. The resultant high level of a therapeutic compound having anti-inflammatory activity present in the macrophages results in a clinically effective treatment of chronic inflammation (see paragraph [0192]). Thus, BANNISTER teaches PDE1 inhibitors and compounds that promote the resolving phenotypic change of M1 to M2 in methods of treating inflammation and having an anti-inflammatory activity. Further BANNISTER teaches treating inflammation may include treating of a chronic inflammation in both allergic reactions and some myopathies and include diseases such as pleuritis (see paragraph [0166]). Specifically, a pharmaceutical composition comprising said PDE1 inhibitor (see claim 35, paragraph [0232]) is administered to an individual with chronic inflammation, resulting in reduction of a symptom associated with the chronic inflammation (see claim 80, paragraph [0277]) with pleuritis named as associated with the chronic inflammation (see claim 83, paragraph [0280]).
Thus, it would be prima facie obvious to one of ordinary skill in the art to utilize the compound of Snyder, which is taught to be a PDE1 inhibitor and treat diseases associated with inflammation by promoting macrophage activation in the blood so as to reduce M1 activation and release of pro-inflammatory cytokines and to enhance the action of M2 microglia, through the up- regulation of anti-inflammatory cytokines such as IL-10 (see paragraph [0024]). Snyder teaches microglia have activation states somewhat similar to macrophages (see paragraph [0088]). Snyder teaches wide application for treating inflammatory disease (see paragraph [0023]) and focuses on neuroinflammatory diseases rather than naming other specific inflammatory or disease associated with inflammation. BANNISTER teaches compounds such as PDE1 inhibitors and those that have anti-inflammatory activity by promoting the resolving phenotypic change of M1 to M2 may be used to treat a wide variety of inflammatory diseases, which includes diseases such as pleuritis (Applicant’s elected species) as well as other inflammatory diseases (see paragraph [0166]).
The Supreme Court in KSR International Co. v. Teleflex Inc., 550 U.S. 398, 127 S. Ct. 1727, 82 USPQ2d 1385, 1395-97 (2007) identified a number of rationales to support a conclusion of obviousness which are consistent with the proper “functional approach” to the determination of obviousness as laid down in Graham. The key to supporting any rejection under 35 U.S.C. 103 is the clear articulation of the reason(s) why the claimed invention would have been obvious. The Supreme Court in KSR noted that the analysis supporting a rejection under 35 U.S.C. 103 should be made explicit.
Exemplary rationales that may support a conclusion of obviousness include:
(A) Combining prior art elements according to known methods to yield predictable results;
(B) Simple substitution of one known element for another to obtain predictable results;
(C) Use of known technique to improve similar devices (methods, or products) in the same way;
(D) Applying a known technique to a known device (method, or product) ready for improvement to yield predictable results;
(E) “Obvious to try” – choosing from a finite number of identified, predictable solutions, with a reasonable expectation of success;
(F) Known work in one field of endeavor may prompt variations of it for use in either the same field or a different one based on design incentives or other market forces if the variations are predictable to one of ordinary skill in the art;
(G) Some teaching, suggestion, or motivation in the prior art that would have led one of ordinary skill to modify the prior art reference or to combine prior art reference teachings to arrive at the claimed invention.
Note that the list of rationales provided is not intended to be an all-inclusive list. Other rationales to support a conclusion of obviousness may be relied upon by Office personnel.
The motivation to utilize the compounds of Snyder, taught to be PDE1 inhibitors to promote resolution of inflammation to treat other inflammatory diseases such as pleurisy, which is taught by BANNISTER to be an example of a chronic inflammatory disease would derive from (A) or (G) from KSR. In the instant case, Snyder explicitly names compounds as PDE1 inhibitors as having anti-inflammatory activity and used in treatment of inflammation. Snyder further teaches these compounds may affect macrophage activation in the blood so as to reduce M1 activation and the release of pro- inflammatory cytokines and to enhance the action of M2 microglia, through the up- regulation of anti-inflammatory cytokines such as IL-10 (see paragraph [0024]) and microglia have activation states somewhat similar to macrophages (see paragraph [0088]. BANNISTER teaches that both PDE1 inhibitors and therapeutic compounds having an anti-inflammatory activity capable of promoting resolving phenotypic change of M1 to M2 compounds can be used to treatment inflammation and names pleurisy as a chronic inflammatory disease. Thus, a skilled artisan would have had a reasonable expectation of success in to applying the anti-inflammatory compounds of Snyder for the treatment of the inflammatory diseases taught by BANNISTER.
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 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, 3, 5, 9, 21 and 25 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-2 and 4-7 of U.S. Patent No. 11,291,666 (‘666) in view of BANNISTER (see US 2016/0317482, pub. 11/03/2016). Although the claims at issue are not identical, they are not patentably distinct from each other because ‘666 is drawn to a method of treatment or propylaxis of inflammation and/or an inflammatory disease or disorder comprising administering of a PDE1 inhibitor to a patient in need thereof, wherein the PDE1 inhibitor is of formula VIII. Although ‘666 is drawn to a different scope of compounds than the instant application, ‘666 teaches the compound that corresponds to the elected species – see claims 5 and 6. One of ordinary skill in the art would be motivated to treat inflammatory diseases such as those taught in BANNISTER based upon the teachings of ‘666 as ‘666 teaches methods of treatment or prophylaxis of inflammation and/or an inflammatory disease comprising administration of the same compounds as found in the instant claims. BANNISTER teaches a method of treating individual with chronic inflammation by administering a composition and further discusses different embodiments through which therapeutic compounds may have anti-inflammatory activity and reduce levels of an inflammation inducing molecule. Specifically, BANNISTER teaches one method by which a therapeutic compound may have anti-inflammatory activity is by promoting the resolving phenotypic change of M1 to M2 – see (see paragraphs [0056]-[0057]). Other therapeutic compounds disclosed herein may be a Phosphodiesterase inhibitor. Examples of a suitable Phosphodiesterase inhibitor include, without limitation, a PDE 1 selective inhibitor” (see paragraph [0078]) and a therapeutic compound of the pharmaceutical composition disclosed herein is delivered to a macrophage. Macrophages are one of the key cell types believed to be involved in the control of the inflammation response. The resultant high level of a therapeutic compound having anti-inflammatory activity present in the macrophages results in a clinically effective treatment of chronic inflammation (see paragraph [0192]). Thus, BANNISTER teaches PDE1 inhibitors and compounds that promote the resolving phenotypic change of M1 to M2 in methods of treating inflammation and having an anti-inflammatory activity. Further BANNISTER teaches treating inflammation may include treating of a chronic inflammation in both allergic reactions and some myopathies and include diseases such as pleuritis (see paragraph [0166]). As a result, one of ordinary skill in the art would be motivated to utilize the compounds of ‘666 to treat other inflammatory diseases, specifically those mediated by macrophages.
Conclusion
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 KAREN CHENG whose telephone number is (703)756-4699. The examiner can normally be reached M-F, 9AM-6PM PST.
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/KAREN CHENG/Primary Examiner, Art Unit 1623
/ADAM C MILLIGAN/Supervisory Patent Examiner, Art Unit 1623