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 .
Status of the Claims
Claims 1 and 5-6 are pending in the instant application and subject to examination herein. Claims 2-4 and 8-16 are withdrawn pursuant to Applicant’s response to the Restriction/Election Requirement dated 05/7/2025, in which response letter, dated 05/27/2025, Applicant elected neurodegeneration as a single disclosed disease/disorder.
Claim Rejections - 35 USC § 112(b) – Withdrawn
The prior rejection of claim 5 under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention is withdrawn in response to Applicant’s amendment of claim 5.
Claim Rejections - 35 USC § 112(b) – Necessitated by Amendment
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claim 5 is rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Where applicant acts as his or her own lexicographer to specifically define a term of a claim contrary to its ordinary meaning, the written description must clearly redefine the claim term and set forth the uncommon definition so as to put one reasonably skilled in the art on notice that the applicant intended to so redefine that claim term. Process Control Corp. v. HydReclaim Corp., 190 F.3d 1350, 1357, 52 USPQ2d 1029, 1033 (Fed. Cir. 1999). The term “neurodegeneration associated with CLEC16A dysfunction” in claim 5 is used by the claim to mean an autoimmune disorder distinct from the separately listed autoimmune disorders of type-1 diabetes, multiple sclerosis and lupus, while the accepted meaning is “progressive loss of structure and/or function of neurons, including their death” in a condition associated with CLEC16A dysfunction, which would not be distinct from the conditions of type-1 diabetes, multiple sclerosis and lupus, as each of these conditions is inherently associated with CLEC16A dysfunction, as evidenced by the teachings of Schuster (Schuster, et al.; Immunity, v42, pp942-952; 2015): Schuster teaches that CLEC16A variation has been associated with multiple immune-mediated diseases, including type-1 diabetes, multiple sclerosis and systemic lupus erythematosus, and that T-cell selection and reactivity are impacted by CLEC16A variation in thymic epithelium cells (TECs), because CLEC16A has a role in TEC autophagy (Abstract). Schuster further teaches that CLEC16A silencing impacts thymic selection, consistent with prior studies that show that loss of autophagy in TECs alters the selection of major histocompatibility complex (MHC) class II restricted T cells, and that a change in autophagic flux, as caused by CLEC16A variation, can be predicted to broadly shape the T cell repertoire and modulate the risk of autoimmunity (page 949). The term “neurodegeneration associated with CLEC16A dysfunction” is indefinite because the specification does not clearly redefine the term in a manner that would render it distinct from type-1 diabetes, multiple sclerosis and lupus.
The instant Specification does not provide any definition for the term “neurodegeneration associated with CLEC16A dysfunction” or any specific listing of disorders intended to fall under this term. On page 11, the condition of “neurodegeneration” in mice studied as part of Example 1 is compared to “spinocerebellar ataxia”, suggesting that at least this one disorder is included in the term “neurodegeneration”; however, a person of ordinary skill in the art would not be able to discern whether claim 5 intends for the term “neurodegeneration associated with CLEC16A dysfunction” to mean “spirocerebellar ataxia” or to also include additional disorder(s), and what such additional disorder(s) could be.
Neurodegeneration is defined by Ahmad (Ahmad, S.I.; Neurodegenerative Diseases, Springer Science+Business Media, New York, New York; 2012) as “progressive loss of structure and/or function of neurons, including their death” (Preface, page vii) and goes on in the Preface to directly address multiple sclerosis (pages ix-x, bridging paragraph) and diabetes (page x) as examples of neurodegenerative diseases. Additionally, Sankowski (Sankowski, et al.; Frontiers in Cellular Neuroscience, v9, Article 28, pp.1-20; 2015) provides a review of systemic inflammation and the brain, with particular context of an association between neurodegenerative disorders and persistent immune activation (Abstract, page 1) and specifically addresses systemic lupus erythematosus (SLE) as a driver of neurodegeneration (page 6). As discussed above, each of these conditions is known to be associated with CLEC16A dysfunction, per the teaching of Schuster. Claim 5 is indefinite because a person of ordinary skill in the art would not understand what is meant by “neurodegeneration associated with CLEC16A dysfunction” as a particular autoimmune disorder or set of disorders that is somehow distinct from multiple sclerosis, type-1 diabetes and lupus, given that the Specification provides no definition of the term and prior art provides definition(s) and teaching that would include multiple sclerosis, type-1 diabetes and lupus within this term.
Claim Rejections - 35 USC § 101 – Withdrawn
The prior rejection of claim 7 under 35 U.S.C. 101, because the claimed invention is not directed to patent eligible subject matter, is withdrawn in response to Applicant’s cancellation of claim 7.
Claim Rejections - 35 USC § 102 – Withdrawn
The prior rejection of claims 1 and 5-6 under 35 U.S.C. 102(a)(1) as being anticipated by NIAID (“Treating Multiple Sclerosis With Sirolimus, an Immune System Suppressor,” ClinicalTrials.gov, Identifier NCT00095329, Record History 20Sep2016, accessed 17Jun2025)1 is withdrawn in response to Applicant’s amendment of claim 1.
Claim Rejections - 35 USC § 102 – Necessitated by Amendment
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claims 1 and 5-6 are anticipated by NIAID.
Claims 1-2, 5-6 and 8-9 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by NIAID (“Treating Multiple Sclerosis With Sirolimus, an Immune System Suppressor,” ClinicalTrials.gov, Identifier NCT00095329, Record History 20Sep2016, accessed 17Jun2025)2.
Claim 1 is drawn to a method of treating a CLEC16A-associated autoimmune disorder associated with thymus degeneration or atrophy in a subject in need thereof, comprising administering an effective amount of one or more agents selected from a mitophagy suppressor/modulator, an ER suppressor, a JAK2 inhibitor and a SOCS1 inhibitor, wherein said one or more agents ameliorates symptoms associated with thymus degeneration or atrophy.
NIAID teaches a clinical trial designed to treat multiple sclerosis, a neurodegenerative autoimmune disorder, by administration of rapamycin (“sirolimus”), a mitophagy modulator. NIAID teaches that the purpose of the study is to determine the safety and tolerability of the drug sirolimus in patients with multiple sclerosis (MS) who have failed other treatments (Study Description, Brief Summary) and further teaches that sirolimus has been demonstrated to provide potent immunosuppression in recent clinical trials involving kidney transplantation, and may help people with autoimmune diseases like MS.
While NIAID does not teach that multiple sclerosis is a form of neurodegeneration, a person of ordinary skill in the art would at once recognize that the property of neurodegeneration is inherent in multiple sclerosis, as evidenced by Haider (Haider, et al.; Brain, v139, pp.807-815; 2016). Haider teaches an analysis of demyelination and neurodegeneration in a large series of multiple sclerosis brains, providing a map that displays the frequency of different brain areas to be affected by these processes. Two different patterns of neurodegeneration in the cortex were identified: oxidative injury of cortical neurons and retrograde neurodegeneration due to axonal injury in the white matter. (Abstract, page 807).
While NIAID does not teach that multiple sclerosis is a CLEC16A-associated autoimmune disorder, a person of ordinary skill in the art would at once recognize that the property of being a CLEC16A-associated autoimmune disorder is inherent in multiple sclerosis, as evidenced by van Luijn (van Luijn, et al.; Brain, v138, pp.1531-1547; 2015). van Luijn teaches a study of the potential contribution of the C-type lectin CLEC16A gene to human autoimmune diseases. Blood samples were taken from multiple sclerosis human patients as well as healthy control human subjects (page 1532) and were analyzed by DNA isolation and genotyping for single nucleotide polymorphism rs7200786 in CLEC16A (page 1533). The study showed that CLEC16A expression was strongly upregulated in peripheral blood mononuclear cells, and most abundant in monocyte-derived dendritic cells, and van Luijn identifies CLEC16A as a pivotal gene in multiple sclerosis that serves as a direct regulator of the human leukocyte antigen class II pathway in antigen-presenting cells (Abstract, page 1531).
While NIAID does not teach that thymus degeneration or atrophy is associated with multiple sclerosis, a person of ordinary skill in the art would at once recognize that the property of being associated thymus degeneration or atrophy is inherent in multiple sclerosis, as evidenced by Haegert (Haegert, D. G.; Journal of Neurology & Nephrology, v5, article 1000207; 2014). Haegert teaches that a unifying concept from cumulative data of various investigators, namely that premature thymic involution leads to a shift in peripheral T-cell homeostasis, which contributes to the pathogenesis of both relapsing-remitting multiple sclerosis (RRMS) and primary progressive multiple sclerosis (PPMS) (page 1). Thus Haegert teaches that thymic involution (i.e., atrophy) is associated to multiple sclerosis.
While NIAID does not teach that rapamycin is a mitophagy modulator, a person of ordinary skill in the art would at once recognize that the property of being a mitophagy modulator is inherent to rapamycin, as evidenced by Civiletto (Civiletto, et al.; EMBO Molecular Medicine, v10, Article e8799, pp.1-15; 2018). Civiletto teaches a study on rapamycin treatment of mice suffering from impaired autophagic flux due to genetic knockout of Cox-15 gene. According to Civiletto, prolonged rapamycin treatment of the Cox-15 knockout mice improved motor endurance, corrected morphological abnormalities of muscle, increased cytochrome c oxidase activity and reduced the number of damaged mitochondria which otherwise accumulated in untreated Cox-15 knockout mice. Rapamycin treatment also activated lysosomal biogenesis. The coordinated activation of autophagic flux and lysosomal biogenesis is proposed by Civiletto to contribute to the effective clearance of dysfunctional mitochondria (Abstract, page 1).
Regarding the claim language of wherein the “one or more agents ameliorates symptoms associated with thymus degeneration or atrophy”, this aspect of claim 1 is understood to be a desired result of the method rather than any limitation on the structure of the claimed method.
Thus, claim 1 is anticipated by the teaching of NIAID.
Claim 5 further limits the method of claims 1 to a Markush group of autoimmune disorders that includes multiple sclerosis, and is met by the rejection above.
Claims 6 further limits the method of claims 1 to a Markush group of agents that includes rapamycin, and is met by the rejection above.
Thus, the limitations of claims 5-6 are anticipated by the teaching of NIAID.
Claim Rejections - 35 USC § 103 – Withdrawn
The prior rejection of claims 1 and 5-6 under 35 U.S.C. 103 as being unpatentable over van Luijn (van Luijn, et al.; Brain, v138, pp.1531-1547; 2015) in view of NIAID (“Treating Multiple Sclerosis With Sirolimus, an Immune System Suppressor,” ClinicalTrials.gov, Identifier NCT00095329, Record History 20Sep2016, accessed 17Jun2025)3, is withdrawn in response to Applicant’s amendment of claim 1.
Claim Rejections - 35 USC § 103 – Necessitated by Amendment
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.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 1 and 5-6 are unpatentable over van Luijn in view of NIAID.
Claims 1 and 5-6 are rejected under 35 U.S.C. 103 as being unpatentable over van Luijn (van Luijn, et al.; Brain, v138, pp.1531-1547; 2015) in view of NIAID (“Treating Multiple Sclerosis With Sirolimus, an Immune System Suppressor,” ClinicalTrials.gov, Identifier NCT00095329, Record History 20Sep2016, accessed 17Jun2025)4.
The limitations of claims 1 and 5-6 and the teachings of NIAID are discussed in the rejection above and hereby incorporated into the instant rejection.
van Luijn teaches a study of the potential contribution of the C-type lectin CLEC16A gene to human autoimmune diseases. Blood samples were taken from multiple sclerosis human patients as well as healthy control human subjects (page 1532) and were analyzed by DNA isolation and genotyping for single nucleotide polymorphism rs7200786 in CLEC16A (page 1533). The study showed that CLEC16A expression was strongly upregulated in peripheral blood mononuclear cells, and most abundant in monocyte-derived dendritic cells, and van Luijn identifies CLEC16A as a pivotal gene in multiple sclerosis that serves as a direct regulator of the human leukocyte antigen class II pathway in antigen-presenting cells (Abstract, page 1531). van Luijn further teaches that the increased expression of CLEC16A in multiple sclerosis points to an autoimmune model in which it promotes the biogenesis of the Major Histocompatibility Complex (MHC) class II-containing compartment (MIIC) to affect Human Leukocyte Antigen II (HLA-II) antigen presentation, and establishes that CLEC16A has a novel C-type lectin function by regulating the strongest genetic risk factor in multiple sclerosis, HLA-II (page 1545).
While van Luijn is silent on the relevance of neurodegeneration to CLEC16A and/or multiple sclerosis, a person of ordinary skill in the art would at once recognize that multiple sclerosis is a form of autoimmune neurodegeneration because neurodegeneration is an inherent property of multiple sclerosis, as evidenced by Haider (Haider, et al.; Brain, v139, pp.807-815; 2016). The teaching of Haider is discussed in the rejection above and hereby incorporated into the instant rejection.
While van Luijn is silent on the relevance of thymic degeneration or atrophy to multiple sclerosis, a person of ordinary skill in the art would at once recognize that the property of being associated thymus degeneration or atrophy is inherent in multiple sclerosis, as evidenced by Haegert (Haegert, D. G.; Journal of Neurology & Nephrology, v5, article 1000207; 2014). Haegert teaches that a unifying concept from cumulative data of various investigators, namely that premature thymic involution (i.e., atrophy) leads to a shift in peripheral T-cell homeostasis, which contributes to the pathogenesis of both relapsing-remitting multiple sclerosis (RRMS) and primary progressive multiple sclerosis (PPMS) (page 1). Thus Haegert teaches that thymic involution (i.e., atrophy) is associated to multiple sclerosis.
While van Luijn is silent on a method for treatment of a CLEC16A autoimmune disorder with agent that is a mitophagy suppressor/modulator, an ER suppressor, a JAK2 inhibitor and/or a SOCS1 inhibitor, a person of ordinary skill in the art would have a reasonable expectation of treating CLEC16A-associated multiple sclerosis with rapamycin, a known mitophagy modulator (as per the teaching of Civiletto), because the treatment of multiple sclerosis with rapamycin was already known in the art per the teaching of NIAID. The teaching of Civiletto is discussed in the rejection above and hereby incorporated into the instant rejection.
Applicant’s invention is unpatentable over the teaching of van Luijn in view of the teaching of NIAID, because a person of ordinary skill in the art, at the effective time of filing, would have a reasonable expectation of success in treating CLEC16A-associated multiple sclerosis neurodegeneration with the mitophagy modulator rapamycin, because van Luijn teaches the prominence and role of CLEC16A in multiple sclerosis, a disorder for which neurodegeneration is an inherent property as per the teaching of Haider, and a disorder that is inherently associated to thymic degeneration or atrophy, per the teaching of Haegert, because NIAID teaches the treatment of multiple sclerosis with rapamycin, a compound that is known as a mitophagy modulator per the teaching of Civiletto.
Thus, the invention was prima facie obvious at the time of filing.
Double Patenting – Maintained
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.
The prior provisional rejection of claims 1 and 5-6 on the ground of nonstatutory double patenting as being unpatentable over claims 1, 3-4 and 7-8 of copending Application No. 19/107,920 (reference application) is maintained. Applicant has traversed the rejection on the grounds that Application No. 19/107,920 requires the use of a mitophagy enhancer which can be selected from probucol, quercetin or acipimox, and further traverses the rejection on the grounds that instant claim 1 recites a “mitophagy suppressor/regulator” which is patentably distinct from the “mitophagy enhancer” required for claim 1 of Application No. 19/107,920.
Applicant’s traverse has been considered, but is not found persuasive, because claim 1 of Application No. 19/107,920 does not in fact recite any Markush group of mitophagy enhancers consisting of probucol, quercetin or acipimox, and because instant claim 1 does not in fact recite any “mitophagy suppressor/regulator” but rather recites a “mitophagy suppressor/modulator” which, per the instant disclosure, is understood to encompass both mitophagy suppressors and mitophagy enhancers because the instant Specification establishes that “modulate” can include “increasing/promoting” (page 9).
Reiterated Rejection:
Claims 1 and 5-6 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 3-4 and 7-8 of copending Application No. 19/107,920 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of 19/107,920 are not patentably distinct from instant claims 1 and 5-6.
Reference claim 1 is drawn to a method for treating a CLEC16A-associated disorder or ameliorating a symptom in a subject in need thereof, comprising administering at least one mitophagy enhancer, thereby overlapping with the method of instant claim 1 that is drawn toward treating a CLEC16A-associated autoimmune disorder comprising administering an agent that fulfills any one of a Markush group of roles including “mitophagy suppressor/modulator” wherein the instant Specification establishes that “modulate” can include “increasing/promoting” (page 9), as well as overlapping with instant claim 5 that specifies a Markush group of CLEC16A-associated autoimmune disorders.
Reference claim 3 further limits reference claim 1 to wherein the CLEC16A-associated disorder is any of a Markush group of classes of disorder, including autoimmune disorders, thereby maintaining overlap with instant claims 1 and 5.
Reference claim 4 further limits reference claim 1 to wherein the mitophagy enhance enhances the clearance of mitochondria, a limitation that is internally redundant given that mitophagy is the clearance of mitochondria, as evidenced by Tolkovsky (Tolkovsky, A. M.; Biochimica et Biophysica Acta, v1793, pp.1508-1515; 2009).
Reference claim 7 further limits claim 1 to wherein the method further comprises an additional agent selected from a Markush group of roles including ER stress modulator. Reference claim 8 further limits claim 7 to wherein the ER stress modulator is selected from a Markush group that includes rapamycin. Instant claim 6 discloses rapamycin as an agent within the scope of instant claim 1. Additionally, as discussed in the rejections above rapamycin is a known mitophagy modulator (“enhancer”); thus rapamycin fulfills both the roles of mitophagy enhancer and ER stress modulator simultaneously in the reference claims while also qualifying as the agent for treatment in the instant claims.
This is a provisional nonstatutory double patenting rejection.
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 W. JUSTIN YOUNGBLOOD whose telephone number is (703)756-5979. The examiner can normally be reached on Monday-Thursday from 8am to 5pm. The examiner can also be reached on alternate Fridays.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Jeffrey S. Lundgren, can be reached at telephone number (571) 272-5541. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/W.J.Y./Examiner, Art Unit 1629
/JEFFREY S LUNDGREN/Supervisory Patent Examiner, Art Unit 1629
1 https://clinicaltrials.gov/study/NCT00095329
2 https://clinicaltrials.gov/study/NCT00095329
3 https://clinicaltrials.gov/study/NCT00095329
4 https://clinicaltrials.gov/study/NCT00095329