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 .1 The petition to make Special Based on Age for Advancement of Examination under 37 CFR 1.102(c)(1) was granted on Sept 23 2024.
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on May 26 2026 has been entered.
Status of Claims and Prosecution
Claims 1-21 are pending and directed to the elected species of a patient suffering from Parkinson’s disease, mild traumatic brain injury and brain cancer remain under examination.
Claim Rejections - 35 USC § 103
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
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, 3, 4, 7-9, 11, 13-14 and 19-20 are rejected under 35 U.S.C. 103 as being unpatentable over MISCHLEY ET AL. Nature Partner Journals, 2016, 2, 16002, pages 1-6.
Initially, the specification is referenced for claim interpretation purposes. It defines N-acetylcysteine (NAC) and derivatives thereof as therapeutic agents, known to increase the concentration and bioavailability of the antioxidant glutathione (GSH). See paragraphs 18-19. In an embodiment, NAC derivative is GSH., i.e. a therapeutic agent. See paragraph 29.
Initially, the specification is referenced for claim interpretation purposes. It defines N-acetylcysteine (NAC) and derivatives thereof as therapeutic agents, known to increase the concentration and bioavailability of the antioxidant glutathione (GSH). See paragraphs 18-19. In an embodiment, NAC derivative is GSH., i.e. a therapeutic agent. See paragraph 29.
Mischley discloses treatment of PD (as per claim 1’s preamble, a) and b); and claims 3-4, 7 and 8 noting CNS disease Parkinson’s Disease (PD)), as defined by a lack of GSH. See abstract. Mischley teaches administration of therapeutically effective amounts of an agent are administered intranasally to a patient in need. See abstract.
While Mischley expressly teaches the limitations of the preamble, steps a) and b) of claim 1, it does not expressly disclose step c) of claim 1, the selection of a delivery parameter (dose, formulation and delivery device) for subsequent intranasal administration based on quantified glutathione (GSH) concentration.
However, based on the teachings of Mischley that its study was the first to demonstrate an increase an increase in CNS GSH levels with a noninvasive GSH augmentation, (See page 3, column 1, Discussion), a person having ordinary skill in the art (PHOSITA) would have routinely optimized the selection of a dose and/or formulation for any subsequent intranasal administration based on glutathione concentrations in said subject. MPEP 2144.05(II)
Mischley teaches previous obstacles to assess human CNS GSH concentrations in vivo and poor oral absorption of GSH were overcome by its H-MRS editing method to measure CNS GSH levels and a noninvasive (intranasal) GSH administration strategy as a therapeutic approach for PD as well as other CNS GSH deficiency disorders. Page 3, column 1. Thus Mischley teaches the selection of dose delivery formulation parameter for subsequent intranasal formulation for administration throughout its disclosure. See especially page 3, column 1. For example, Table 2 demonstrates changes in brain GSH levels (GSH/Cr peak ratios) relative to baseline after 200 mg nasally administered GSH. See page 3, top of page. Based off the Table 2 of Mischley, where a 200 mg intranasal dose of GSH resulted in various GSH/Cr peak ratios over time, a PHOSITA would routinely optimize the delivery parameter of dose with potential subsequent intranasal administration to optimize GSH levels based on resulting GSH levels measured. Optimization of dosing, whether higher or lower than the 200 mg intranasal taught be Mischley would be readily apparent to a PHOSITA clinician, who would lower or increase doses of GSH, based on teachings of Mischley (Table 2) to achieve desired clinical profiles to treat the subject in need via intranasal administration. Mischley teaches in Figure 3, GSH and GSH/Cr levels relative to baseline levels over time, which provide guidance to the PHOSITA to select the various delivery parameters specifically taught by Mischley in guiding subsequent intranasal administration based on these observations of Table 2 and Figure 3.
Prior to the filing of the present patent application, it would have been prima facie obvious to a PHOSITA following the teachings of Mischley that encompass steps a) and b) of claim 1 (administration of therapeutic agent (GSH) to a subject to treat a condition such as PD,) to modify with the secondary teachings of Mischley (selection of dose delivery formulation parameter per Table 2) so as to routinely optimize treatment based on quantified GSH concentrations in the subject.
The PHOSITA would have had a reasonable expectation of success because Mischley not only teaches treatment of PD subjects in need with GSH where patients under go MRIs to determine treatment effectiveness, but also Mischley teaches the effects of GSH dose as a delivery parameter administered in terms of GSH concentration quantified in the treated subjects.
Regarding claim 9, Mischley discloses a dose of 200 mg (therapeutically effective dose of about 100 to about 400 mg) was self-administered. See abstract.
Regarding claims 11 and 13-14, Mischley teaches where GSH was formulated as 200 mg GSH in 1cm3 of saline (claimed pharm. accept. excipient formulated as a solution), using a syringe attached to a Mucosal Atomization Device (claimed atomizer), see page 5, column 2, under Study Medication.
Regarding Claim 19, Mischley discloses determining GSH concentration changes in the brainer over time. “After baseline GSH measurement, 200 mg (in) GSH was self-administered inside the scanner without repositioning, then serial GSH levels were obtained over ~1h, Statistical significance was determined by one-way repeated measures analysis of variance.” See Abstract.
Regarding claim 20 Mischley discloses significantly higher than baseline GSH levels at all remaining time points (P<0.05; Figure 3a,b). Mischley discloses between the baseline and the 45-min scan, there was a mean 269% increase in GSH/Cr (240% increase in absolute GSH). See P. 4, Fig. 3) which reads upon the limitation of GSH increased concentration from about 20 to about 300%.
Claims 1-5, 7-14 and 19-20 are rejected under 35 U.S.C. 103 as being unpatentable over MISCHLEY ET AL. Nature Partner Journals, 2016, 2, 16002, Pgs. 1-6 in view of WO 2019/084543.
Regarding instant claim 1 step a) and step b) and claims 3-4, 7-8, Mischley teaches step a), where it notes intranasally administered reduced GSH, (in)GSH (i.e., a therapeutic agent, per claims 1 and 3), augments CNS GSH concentrations, determined by magnetic resonance spectroscopy (teaching step b)’s GSH concentration quantification by MRI) to the claimed mid-stage Parkinson’s subjects in need (elected species of PD). See abstract. As defined by the specification, GSH is a NAC derivative. See paragraph 29.
As required by claims 1 (preamble), 3-4, 7-8, Mischley discloses treatment of PD, as defined by a lack of GSH. See abstract. Mischley teaches administration of therapeutically effective amounts of an agent are administered intranasally to a patient in need. See abstract.
While Mischley teaches the invention of main independent claim 1 as detailed above, it does not expressly teach the various species of the method of claim 1; the species of claims 2 (a species of N-acetylcysteine per se); claim 5 (species of treatment of mild traumatic brain injury); claim 10 (nasal pump for NAC or glutathione) and claim 12 (repeat doses). However a PHOSITA would have a reasonable expectation in arriving at the claimed invention because 1) NAC is known to treat subjects in need, 2) treatment of mild traumatic brain injury is known and 3) nasal pumps are art known.
With regard to claim 2, Mischley discloses “intravenous NAC repletion” is seen “as a therapeutic strategy in PD,” despite some issues. See page 1, column 2 bridging to page 2, column 1. While Mischley does not teach NAC administered intranasally, WO 543 teaches treating CNS disorders comprising intranasally administering at least one antioxidant compound. See paragraph 90. WO 543 discloses the antioxidant compound is, inter alia, NAC or glutathione. See paragraph 91. Because Mischley and WO 543 are in the same space of treatment of conditions (brain conditions) with NAC or glutathione, a PHOSITA would have rationale to combine them.
Regarding claims 5, WO 543 discloses the CNS disorder is traumatic brain injury (TBI). See paragraph 95.
Regarding claim 10, WO 543 teaches devices for intranasal delivery include, inter alia, “Aptar Pharma nasal spray pump.” See paragraph 52.
Prior to the filing of the present patent application, it would have been prima facie obvious to a PHOSITA following the teachings of steps a)-c) of claim 1 to modify with the second reference WO 543 teaching intranasal administration of NAC for the same patient population. The rationale to support a finding of obviousness are the prior art elements of Mischley combined with known methods, intranasal administration of therapeutic antioxidant agents such as NAC and NAC derivative GSH to subjects in need to treat brain conditions such Parkinson’s disease and mild traumatic brain injury.
With regard to claim 12 and the limitation of wherein the administering is repeated at least one time, Mischley teaches the treatment of Parkinson’s disease, a long term debilitating CNS disorder, requiring a lifetime of treatment. See abstract and paragraph 95 of WO 543. While not expressly reciting a repeat administration of GSH or NAC of at least once, one skill in the art would repeat the GSH or NAC treatment at least once due to the lifelong nature of Parkinson’s disease.
Claims 1, 3, 4, 6-9, 11, 13, 14, 19 and 20 are rejected under 35 U.S.C. 103 as being unpatentable over MISCHLEY ET AL. Nature Partner Journals, 2016, 2, 16002, Pgs. 1-6 in view of U.S. 2015/0148423 A1.
The teachings of Mischley are as applied supra (see 35 U.S.C. 103 rejection above), and are herein incorporated by reference in their entirety, rendering Claims 1 (steps a), b) and c) of claim 1) and dependent claims 3,4, 7-9, 11, 13, 14, 19 and 20 prima facie obvious. However, the claim 6 method species differs from Mischley as it doesn’t teach treating brain cancer.
Regarding claim 6, US Pub 423 discloses administering NAC intranasally to a subject’s brain cancer condition, see paragraphs 42, 44 and 15. The motivation to combine the cited prior art is the fact that Mischley discloses nasal administration of the “essential intracellular antioxidant GSH” and NAC, see above. Further, US Pub 423 discloses both NAC and GSH for its antioxidant activity (see paragraphs 2-4).
Prior to the filing of the present patent application, it would have been prima facie obvious to a PHOSITA following the teachings of Mischley (with regard to steps a)-c) of claim 1 and dependent claims) as modified by US 423 in order to treat species of brain cancer via intranasal administration of NAC. The rationale to support a finding of obviousness is the combination of prior art elements according to known methods to yield predictable results, i.e. intranasal administration of GSH or NAC to treat in injury (as per Mischley) and to treat brain cancer (as per US Pub 423).
Claims 1, 3, 4, 7-9, 11 and 13-21 are rejected under 35 U.S.C. 103 as being unpatentable over MISCHLEY ET AL. Nature Partner Journals, 2016, 2, 16002, Pgs. 1-6 in view of Duncan et al. (Movement Disorders Volume 28 Issue 4 April 2013). Duncan is listed on the PTO-892 form.
The teachings of Mischley are as applied supra (see 35 U.S.C. 103 rejection above), and are herein incorporated by reference in their entirety, rendering Claims 1 (steps a), b) and c) of claim 1) and dependent claims 3,4, 7-9, 11, 13, 14, 19 and 20 prima facie obvious. Claims 15-18 and 21 differ from the teachings of Mischley as it does not disclose treating the brain’s cerebrum, frontal lobe, occipital lobe, occipital cortex and substantia nigra
Regarding claims 15-18 and 21, it is known the cerebrum is divided into frontal, parietal, occipital and temporal lobes/cortex and substantia nigra. Duncan discloses MR imaging studies to investigate PD cognitive decline, outline study limitations, suggestions for future research. See abstract. Duncan discloses various MRI brain region scans of PD and cognitive impairment, including the frontal lobe (Beyer et al. (2007)); the left occipital lobe, (Burton et al. (2004); the occipital cortex, (Melzer et al. (2012)), see Table 1. See also page 426, column 1 noting the presence of PD-associated Lewy bodies in the substantia nigra.
Prior to the filing of the present patent application, it would have been prima facie obvious to a PHOSITA following the teachings of Mischley (with regard to steps a)-c) of claim 1 and dependent claims) as modified by US 423 in order to investigate the claimed regions of the brain via MRI, as they are associated with PD as per Duncan, where Mischley discloses MRI use measuring GSH levels to treat PD. The rationale to support a finding of obviousness is the combination of prior art elements according to known methods to yield predictable results, i.e. intranasal administration of GSH or NAC to treat an injury (per Mischley in combination with Duncan, where MRIs are used to research, diagnose, and evaluate brain areas for PD).
RESPONSE TO ATTORNEY ARGUMENTS:
The Attorney response states if Mischley fails to teach or suggest step c) of claim 1, all four pending rejections must fail.
The Attorney response states Mischley is a single-dose, proof-of-concept study that expressly identifies the optimization contemplated by Applicant claim 1 as future work that remains to be done, not as something Mischley itself performed or taught per step c). Applicant argues its previous statement of its five point deliberate, multi-step feedback process of step c) do not reading the specification’s details into the claims, but rather reflect step c)’s requirement of selecting a delivery parameter for a subsequent intranasal administration based on the quantified concentration of GSH.
In response, based on the teachings of Mischley that its study was the first to demonstrate an increase an increase in CNS GSH levels with a noninvasive GSH augmentation, (See page 3, column 1, Discussion), a PHOSITA would have routinely optimized the selection of a dose and/or formulation for any subsequent intranasal administration based on glutathione concentrations in said subject. MPEP 2144.05(II).
Mischley teaches previous obstacles to assess human CNS GSH concentrations in vivo and poor oral absorption of GSH were overcome by its H-MRS editing method to measure CNS GSH levels and a noninvasive (intranasal) GSH administration strategy as a therapeutic approach for PD as well as other CNS GSH deficiency disorders. Page 3, column 1. Thus Mischley teaches the selection of dose delivery formulation parameter for subsequent intranasal formulation for administration throughout its disclosure. See especially page 3, column 1. For example, Table 2 demonstrates changes in brain GSH levels (GSH/Cr peak ratios) relative to baseline after 200 mg nasally administered GSH. See page 3, top of page. Based off the Table 2 of Mischley, where a 200 mg intranasal dose of GSH resulted in various GSH/Cr peak ratios over time, a PHOSITA would routinely optimize the delivery parameter of dose with potential subsequent intranasal administration to optimize GSH levels based on resulting GSH levels measured. Optimization of dosing, whether higher or lower than the 200 mg intranasal taught be Mischley would be readily apparent to a PHOSITA clinician, would lower or increase doses of GSH, based on teachings of Mischley (Table 2) to achieve desired clinical profiles to treat the subject in need via intranasal administration.
The Attorney response states quotes Mischley to state “[f]further dose-response and steady-state administration studies will be required to optimize the dosing schedule for future trials to evaluate therapeutic efficacy”, which Applicant argues that Mischley did not itself perform but only identifies optimization as future work.
The Attorney response argues Mischley is limited in scope (Discussion) section due to a single dose 1h observation period and lack of placebo arm (proof of concept study); study designed to demonstrate (in) GSH increases its signal in brain (not generating a pharmacokinetic profile); and provides guidance towards optimizing delivery techniques, dosing schedules, product stability and intranasal formulations.
In response, as detailed above, Mischley expressly states its proof of concept study does “provide direction for follow-up studies” (emphasis added). See Mischley, page 3, column 1.
The Attorney argues to characterize that GSH could elevate brain GSH levels, making the Attorney argument that Mischley’s object is not to use that data to optimize subsequent treatment parameters.
In response, per MPEP 2145.I. attorney argument does not replace evidence where evidence is necessary. The rejections are based on data from Table 2 demonstrates changes in GSH brain levels upon administration of GSH to a subject. The Attorney response rebuts the rejection with statements from Mischley to formulate an argument that this demonstration of data is insufficient to routinely optimize step c) selection of a delivery parameter in terms of dose, formulation and a delivery device. However, as detailed in the rejections, all three parameters of quantifying concentration of GSH in a subject, doses, a formulation and a delivery device are spelled out Mischley, see above rejection. Further, Mischley teaches in Figure 3, GSH and GSH/Cr levels relative to baseline levels over time, which provide guidance to the PHOSITA to select the various delivery parameters specifically taught by Mischley in guiding subsequent intranasal administration based on these observations of Table 2 and Figure 3.
The Attorney response states Table 2 from Mischley merely reports observed GSH/Cr peak ratios at various time points after a single fixed 200 mg dose.
The Attorney response states Table 2 is merely observation of a single administration and does not teach or suggest parameters for a subsequent administration’s delivery parameters.
In response, Mischley spells out parameters doses, formulation and delivery device as claimed by step c) with particular data from Table 2. In fact, these details from Mischley’s study teaches doses (200 mg), the intranasal formulation administered in Table 2 (200 mg GSH in 1cm3 of saline solution) and delivery device (syringe attached a Mucosal Atomization Device) specifically (see section Study Medication on page 5, column 2), in contrast to step c) of claim 1, which merely generically lists these parameters. See the data of Fig. 3 of GSH and GSH/Cr relative to baseline levels over time, which provide guidance to the PHOSITA to select the various delivery parameters specifically taught by Mischley in guiding subsequent intranasal administration based on these observations of Table 2 and Figure 3.
The Attorney response states routine optimization only applies where the general conditions of a claim are disclosed in the prior art.2 The Attorney response states Mischley does not teach general conditions such as GSH concentrations to selected deliver parameters for subsequent treatment, citing from Mischley such as further dose-response and steady state admin. studies are required to optimize the dosing schedule.
In response, between Table 2, Figures 3, and the Study Medication section, Mischley teaches delivery parameters recited in claim 1, step c), a specific dose, a specific formulation and delivery device. Data points from Table 2 and Figure 3 noting GSH and GSH/Cr values over time would be reasonably relied upon PHOSITA to predictably arrive at a dosing regimen with subsequent administration as claimed. The teaching of a single dose of drug to a patient and subsequent monitoring over time provides guidance for subsequent dosing, especially where Mischley already teaches the claimed parameters of dose, formulation and a delivery device.
The Attorney response further argues the alleged deficiencies of Mischley with regard to claim 1, step c) are not corrected by the teachings of Duncan, WO 543 or US 423. In response, Mischley nonetheless teaches the amended claim 1 with regard to step c) and in particular the dose delivery parameters as detailed previously.
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.
RESPONSE TO ATTORNEY ARGUMENTS OF THE ODP REJECTIONS:
The Attorney response states each of the provisional double patenting rejections relies on Mischley to supply the limitation of step c) of claim 1, which requires "selecting a delivery parameter for a subsequent intranasal administration based on the quantified concentration of glutathione." The Examiner has acknowledged that the reference patents and co-pending applications do not teach quantifying glutathione by MRI as required by claim 1, and has relied on Mischley to cure this deficiency. In response, Mischley nonetheless teaches the amended claim 1 with regard to step c) and in particular the dose delivery parameters as detailed previously. Note the provisional ODP rejection over 18/792,836 has been converted to an ODP rejection over US Patent 12414929, see below. Also note the new rejection over Application 19328413.
Claims 1-5 and 9-21 remain provisionally rejected on the ground of nonstatutory obviousness-type double patenting as being unpatentable over claims 1-15 and 19-20 of copending Application No. 18/509,935 in view of MISCHLEY et al. Nature Partner Journals, 2016, 2, 16002, Pgs. 1-6.
Examined claims 1-5 disclose administration of therapeutic agent to a subject in need, with a brain/CNS condition such, mild traumatic brain injury where the agent is NAC or derivative, where claim 1 requires quantifying glutathione in the brain by magnetic spectroscopy (such as MRI).
The reference application generally claims treating traumatic brain injury in a subject, the method comprising intranasally administering a dose of N-acetylcysteine (NAC). See reference claim 1, in humans as per reference claim 2. Reference claim 3 discloses a condition such as a concussion. It is noted that the reference application does not teach quantifying glutathione by MRI as per claim 1.
However one of ordinary skill in the art would do so with a reasonable expectation of success as such technique is known in the art. As required by claim 1, Mischley discloses its objective was to evaluate whether intranasally administered reduced GSH, (in)GSH, is capable of augmenting central nervous system GSH concentrations, as determined by magnetic resonance spectroscopy in 15 participants with mid-stage PD, see abstract. As defined by the specification, GSH is a NAC derivative. See paragraph 29. Also Mischley teaches in Figure 3, GSH and GSH/Cr levels relative to baseline levels over time, which provide guidance over time to the PHOSITA to select the various delivery parameters specifically taught by Mischley in guiding subsequent intranasal administration based on these observations of Table 2 and Fig. 3.
Regarding claim 9 (dose about 100-400mg), reference claim 15 discloses an overlapping dose of about 50-350 mg.
Regarding claims 10-11, the reference application teaches a nebulizer (a form of nasal pump claim 19) and atomizer (claim 20).
With regard to claim 12, the reference claims while not expressly reciting a repeat administration of GSH or NAC of at least once, a PHOSITA would have a rationale to repeat the GSH or NAC treatment at least once due to traumatic brain injury likely requiring repeat dosing to cure the subject.
Regarding claim 13, reference claims 4-14 teach a composition comprising pharmaceutically acceptable excipient(s).
Regarding claim 14, Mischley teaches where GSH was formulated as 200 mg GSH in 1cm3 of saline (claimed pharm. accept. excipient formulated as a solution), using a syringe attached to a Mucosal Atomization Device (claimed atomizer), see page 5, column 2, under Study Medication.
Claims 15-18 and 21 are directed to regions of the brain, the cerebrum, frontal lobe, occipital lobe, occipital cortex and substantia nigra. While not expressly claimed by the reference patent, it would be obvious to scan these regions of the brain via magnetic resonance spectroscopy as the mild traumatic brain injury of traumatic brain injury (concussion) would affect these brain regions.
Regarding claim 19 and measurement of changes of glutathione in the brain over time, Mischley discloses “After baseline GSH measurement [followed by]. . . . then serial GSH levels were obtained over~ 1 h. . . .” See Abstract. . With regard to the amendment of claim 19, wherein the selected delivery parameter is based on the determined change in the concentration of GSH, it would be routine for a PHOSITA to optimize the selection of the delivery parameter of dosages of GSH based on determined changes of GSH concentration, where Table 2 and Fig. 3 discloses corresponding GSH levels in response to a given dose of GSH administered intranasally, over time.
Regarding claim 20 wherein the administering increases the concentration of glutathione from about 20% to about 300%, Mischley discloses between the baseline and the 45-min scan, there was a mean 269% increase in GSH/Cr (240% increase in absolute GSH). See P. 4, Fig.3).
This is a provisional obviousness-type double patenting rejection because the conflicting claims have not in fact been patented.
Claims 1-5, 7-8 and 7-21 are provisionally rejected on the ground of nonstatutory obviousness-type double patenting as being unpatentable over claims 1-20 of copending Application No. 19/328413 in view of MISCHLEY et al., Nature Partner Journals, 2016, 2, 16002, Pgs. 1-6.
Claims 1-5 and 7-8 disclose administration of therapeutic agent to a subject in need, with a brain/CNS condition such as Parkinson’s, mild traumatic brain injury and cancer where the agent is NAC or derivative, where claim 1 requires quantifying glutathione in the brain by magnetic spectroscopy (such as MRI).
Regarding claims 1-5 and 7-8, the reference application teaches treatment of brain disorder in a subject with GSH (a known NAC derivative) where doses are administered via first the olfactory pathway and second the trigeminal pathway of the subject. See claims 1, 5 and 18. Reference application claims 2-5, 12-13 and 17-18 disclose disorders such as mild traumatic brain injury, Parkinson’s disease, etc. Mischley teaches in Figure 3, GSH and GSH/Cr levels relative to baseline levels over time, which provide guidance over time to the PHOSITA to select the various delivery parameters specifically taught by Mischley in guiding subsequent intranasal administration based on these observations of Table 2 and Figure 3, so as to routinely optimize and arrive at step c), claim 1.
Regarding claim 9, the reference application teaches a therapeutically effective amount from about 100-400 mg. See claim 19.
Regarding claims 10-11, the reference application teaches a nasal pump and atomizer. See claim 20.
With regard to claim 12 wherein the administering is repeated at least one time, while not expressly reciting a repeat administration of GSH or NAC of at least once, one skilled in the art would have a rationale to repeat the GSH or NAC treatment at least once due to the nature of traumatic brain injury and/or Parkinson’s disease likely requiring repeat dosing to cure the patient.
Regarding claim 13 and the limitation of a pharmaceutical composition that further comprises a pharmaceutically acceptable excipient, these limitations are taught by reference claims 1-20, as the methods of the application administering a therapeutic agent to a subject in need, by virtue of this method by its nature, requires a pharmaceutical composition that must pharmaceutically acceptable excipients.
Regarding claim 14 and the limitation of an aqueous solution administered, reference claim 20 discloses an atomizer. By their nature, atomizers administer liquid formulations, such as aqueous solutions. Therefore, it would be routine for one skilled in the art optimize and formulate an aqueous therapeutic agent composition as claimed.
Also, Mischley teaches where GSH was formulated as 200 mg GSH in 1cm3 of saline (claimed pharm. accept. excipient formulated as a solution), using a syringe attached to a Mucosal Atomization Device (claimed atomizer), see page 5, column 2, under Study Medication.
Claims 15-18 and 21 are directed to regions of the brain, the cerebrum, frontal lobe, occipital lobe, occipital cortex and substantia nigra. While not expressly claimed by the reference patent, it would be obvious to scan these regions of the brain via magnetic resonance spectroscopy as the mild traumatic brain injury of traumatic brain injury (concussion) would affect these brain regions.
Regarding claim 19 and measurement of changes of glutathione in the brain over time, Mischley discloses “After baseline GSH measurement [followed by]. . . . then serial GSH levels were obtained over~ 1 h. . . .” See Abstract. . With regard to the amendment of claim 19, wherein the selected delivery parameter is based on the determined change in the concentration of GSH, it would be routine for a PHOSITA to optimize the selection of the delivery parameter of dosages of GSH based on determined changes of GSH concentration, where Table 2 and Fig. 3 discloses corresponding GSH levels in response to a given dose of GSH administered intranasally, over time.
Regarding claim 20 wherein the administering increases the concentration of glutathione from about 20% to about 300%, Mischley discloses between the baseline and the 45-min scan, there was a mean 269% increase in GSH/Cr (240% increase in absolute GSH). See P. 4, Fig.3). This is a provisional obviousness-type double patenting rejection because the conflicting claims have not in fact been patented.
RESPONSE TO ATTORNEY ARGUMENTS OVER THE ‘278, ‘939 ‘130 PATENTS:
The Attorney response argues the newly amended claim 1 render the invention patentably distinct from the claims of the conflict patents.
In response, Mischley nonetheless teaches the amended claim 1 with regard to step c) and in particular the dose delivery parameters as detailed previously.
Claims 1-5, and 9-21 are rejected on the ground of nonstatutory obviousness-type double patenting as being unpatentable over claims 1-16 of US 11,660,278 B2 in view of MISCHLEY et al., Nature Partner Journals, 2016, 2, 16002, Pgs. 1-6.
Although the claims at issue are not identical, they are not patentably distinct from each other because they are directed to treating a subject in need with NAC and/or an NAC derivative.
Examined Claims 1-5 disclose administration of therapeutic agent to a subject in need, with a brain/CNS condition such, mild traumatic brain injury where the agent is NAC or derivative, where claim 1 requires quantifying glutathione in the brain by magnetic spectroscopy (such as MRI).
The reference patent generally claims treating post-concussion syndrome in a brain of a subject in need thereof, the method comprising intranasally administering to the subject a dose of N-acetylcysteine (NAC), wherein the intranasal administration provides a therapeutically-effective amount of the NAC to the brain through a nasal cavity of the subject, wherein the dose is about 50 mg to about 350 mg. See reference claim 1, in human as per claim 2. It is noted that the reference patent does not teach quantifying glutathione by MRI as per claim 1.
Mischley discloses its objective was to evaluate whether intranasally administered reduced GSH, (in)GSH, is capable of augmenting central nervous system GSH concentrations, as determined by magnetic resonance spectroscopy in 15 participants with mid-stage PD, see abstract. As defined by the specification, GSH is a NAC derivative. See paragraph 29.
Mischley teaches in particular, the selection of dose delivery parameter for subsequent intranasal administration throughout its disclosure. See Abstract and page 3, column 1 Discussion. For example, Table 2 demonstrates changes in brain GSH levels (GSH/Cr peak ratios) relative to baseline after 200 mg nasally administered GSH. See page 3, top of page.
Mischley teaches in Figure 3, GSH and GSH/Cr levels relative to baseline levels over time, which provide guidance over time to the PHOSITA to select the various delivery parameters specifically taught by Mischley in guiding subsequent intranasal administration based on these observations of Table 2 and Figure 3. Based off the teachings of Mischley, for example Table 2, where a 200 mg intranasal dose of GSH resulted in various GSH/Cr peak ratios over time, a PHOSITA would routinely optimize the delivery parameter of dose with potential subsequent intranasal administration to optimize GSH levels based on resulting GSH levels measured. Optimization of dosing, whether higher or lower than the 200 mg intranasal taught be Mischley would be readily apparent to a PHOSITA, as a clinician of ordinary skill in the art would no doubt lower or increase doses of GSH, based on teachings of Mischley (Table 2) to achieve desired clinical profiles to treat the subject in need via intranasal administration.
It would have been prima facie obvious to a PHOSITA following the teachings of the primary reference in Mischley teachings steps a) and b) of claim 1 (administration of therapeutic agent (GSH) to a subject to treat a condition such as PD,) to modify with the secondary teachings of Mischley (selection of dose delivery parameter) so as to routinely optimize treatment based on quantified GSH concentrations in the subject.
The PHOSITA would have had a reasonable expectation of success because Mischley not only teaches treatment of PD with GSH in subjects in need where patients under go MRIs to determine treatment effectiveness but also Mischley teaches the effects of GSH dose as a delivery parameter administered in terms of GSH concentration quantified in the treated subjects.
Regarding claim 9 (dose about 100-400mg), reference claim 1 discloses an overlapping dose of about 50-350 mg.
Regarding claims 10-11, the reference application teaches a nebulizer (a form of nasal pump claim 16) and atomizer (claim 21).
With regard to claim 12, the reference claims while not expressly reciting a repeat administration of GSH or NAC of at least once, a PHOSITA would have a rationale to repeat the GSH or NAC treatment at least once due to traumatic brain injury likely requiring repeat dosing to cure the subject.
Regarding claim 13, reference claims 3-15 teach a composition comprising pharmaceutically acceptable excipient(s).
Regarding claim 14, Mischley teaches where GSH was formulated as 200 mg GSH in 1cm3 of saline (claimed pharm. accept. excipient formulated as a solution), using a syringe attached to a Mucosal Atomization Device (claimed atomizer), see page 5, column 2, under Study Medication.
Claims 15-18 and 21 are directed to regions of the brain, the cerebrum, frontal lobe, occipital lobe, occipital cortex and substantia nigra. While not expressly claimed by the reference patent, it would be obvious to scan these regions of the brain via magnetic resonance spectroscopy as the mild traumatic brain injury of traumatic brain injury (concussion) would affect these brain regions.
Regarding claim 19 and measurement of changes of glutathione in the brain over time, Mischley discloses “After baseline GSH measurement [followed by]. . . . then serial GSH levels were obtained over~ 1 h. . . .” See Abstract. . With regard to the amendment of claim 19, wherein the selected delivery parameter is based on the determined change in the concentration of GSH, it would be routine for a PHOSITA to optimize the selection of the delivery parameter of dosages of GSH based on determined changes of GSH concentration, where Table 2 and Fig. 3 discloses corresponding GSH levels in response to a given dose of GSH administered intranasally, over time.
Regarding claim 20 wherein the administering increases the concentration of glutathione from about 20% to about 300%, Mischley discloses between the baseline and the 45-min scan, there was a mean 269% increase in GSH/Cr (240% increase in absolute GSH). See P. 4, Fig.3).
Claims 1-4, 8-10, and 12-21 are rejected on the ground of nonstatutory obviousness-type double patenting as being unpatentable over claims 1-21 of US Patent 11,963,939 in view of MISCHLEY et al., Nature Partner Journals, 2016, 2, 16002, Pgs. 1-6.
Although the conflicting claims are not identical, they are not patentably distinct from each other because both inventions are directed towards treatment of a brain condition with a therapeutic agent.
Examined claims 1-4 and 8 disclose administration of therapeutic agent to a subject in need, with a brain/CNS condition such, mild traumatic brain injury where the agent is NAC or derivative, where claim 1 requires quantifying glutathione in the brain by magnetic spectroscopy (such as MRI).
The reference patent generally claims treating Parkinson’s disease in a subject in need thereof, the method comprising intranasally administering to the subject a dose of N-acetylcysteine (NAC), wherein administering to the subject’s brain through the nasal cavity a dose of about 100 mg to about 350 mg. See reference claim 1, in human as per claim 2. See also reference 19. It is noted that the reference patent does not teach quantifying glutathione by MRI as per claim 1.
Mischley discloses its objective was to evaluate whether intranasally administered reduced GSH, (in)GSH, is capable of augmenting central nervous system GSH concentrations, as determined by magnetic resonance spectroscopy in 15 participants with mid-stage PD, see abstract. As defined by the specification, GSH is a NAC derivative. See paragraph 29.
Mischley teaches in particular, the selection of dose delivery parameter for subsequent intranasal administration throughout its disclosure. See Abstract and page 3, column 1 Discussion. For example, Table 2 demonstrates changes in brain GSH levels (GSH/Cr peak ratios) relative to baseline after 200 mg nasally administered GSH. See page 3, top of page.
Mischley teaches in Figure 3, GSH and GSH/Cr levels relative to baseline levels over time, which provide guidance over time to the PHOSITA to select the various delivery parameters specifically taught by Mischley in guiding subsequent intranasal administration based on these observations of Table 2 and Figure 3. Based off the teachings of Mischley, for example Table 2, where a 200 mg intranasal dose of GSH resulted in various GSH/Cr peak ratios over time, a PHOSITA would routinely optimize the delivery parameter of dose with potential subsequent intranasal administration to optimize GSH levels based on resulting GSH levels measured. Optimization of dosing, whether higher or lower than the 200 mg intranasal taught be Mischley would be readily apparent to a PHOSITA, as a clinician of ordinary skill in the art would no doubt lower or increase doses of GSH, based on teachings of Mischley (Table 2) to achieve desired clinical profiles to treat the subject in need via intranasal administration.
It would have been prima facie obvious to a PHOSITA following the teachings of the primary reference in Mischley teachings steps a) and b) of claim 1 (administration of therapeutic agent (GSH) to a subject to treat a condition such as PD,) to modify with the secondary teachings of Mischley (selection of dose delivery parameter) so as to routinely optimize treatment based on quantified GSH concentrations in the subject.
The PHOSITA would have had a reasonable expectation of success because Mischley not only teaches treatment of PD with GSH in subjects in need where patients under go MRIs to determine treatment effectiveness but also Mischley teaches the effects of GSH dose as a delivery parameter administered in terms of GSH concentration quantified in the treated subjects.
Regarding claim 9 and the dose therein, the reference application teaches an overlapping dose of about 100 mg to about 350 mg. See claims 1 and 19.
Examined claim 10 claim a nasal pump. Reference patent claims 20-21 teach a nasal sprayer comprising a spray pump.
With regard to claim 12, the reference claims while not expressly reciting a repeat administration of GSH or NAC of at least once, a PHOSITA would have a rationale to repeat the GSH or NAC treatment at least once due to traumatic brain injury likely requiring repeat dosing to cure the subject.
Regarding claim 13, reference claims 3-18 teach a composition comprising pharmaceutically acceptable excipient(s).
Regarding claim 14 and the limitation of an aqueous solution, this taught by claims 16-18, noting liquid compositions, where it one of ordinary skill in the art would routinely optimize formulation of aqueous solutions where the art teaches liquid formulations.
Claims 15-18 and 21 are directed to regions of the brain, the cerebrum, frontal lobe, occipital lobe, occipital cortex and substantia nigra. While not expressly claimed by the reference patent, it would be obvious to scan these regions of the brain via magnetic resonance spectroscopy as the mild traumatic brain injury of traumatic brain injury (concussion) would affect these brain regions.
Regarding claim 19 and measurement of changes of glutathione in the brain over time, Mischley discloses “After baseline GSH measurement [followed by]. . . . then serial GSH levels were obtained over~ 1 h. . . .” See Abstract. . With regard to the amendment of claim 19, wherein the selected delivery parameter is based on the determined change in the concentration of GSH, it would be routine for a PHOSITA to optimize the selection of the delivery parameter of dosages of GSH based on determined changes of GSH concentration, where Table 2 and Fig. 3 discloses corresponding GSH levels in response to a given dose of GSH administered intranasally, over time.
Regarding claim 20 wherein the administering increases the concentration of glutathione from about 20% to about 300%, Mischley discloses between the baseline and the 45-min scan, there was a mean 269% increase in GSH/Cr (240% increase in absolute GSH). See P. 4, Fig.3).
Claims 1-5 and 7-21 are rejected on the ground of nonstatutory obviousness-type double patenting as being unpatentable over claims 1-24 of US Patent 12,090,130 in view of MISCHLEY et al., Nature Partner Journals, 2016, 2, 16002, Pgs. 1-6.
Although the claims at issue are not identical, they are not patentably distinct from each other because they are both directed to methods of treating brain disorders with NAC and/or derivatives thereof.
Claims 1-5 and 7-8 disclose administration of therapeutic agent to a subject in need, with a brain/CNS condition such as Parkinson’s, and mild traumatic brain injury where the agent is NAC or derivative, where claim 1 requires quantifying glutathione in the brain by magnetic spectroscopy (such as MRI).
Regarding claims 1-5 and 7-8, the reference patent teaches treatment of brain disorders, including concussion, post-concussion syndrome, mild traumatic brain injury athletic injury brain injury, dementia, neurodegenerative disease, Parkinson’s disease and stroke. See reference claims 1-11. It is noted that the reference patent does not teach quantifying glutathione by MRI as per claim 1.
Mischley discloses its objective was to evaluate whether intranasally administered reduced GSH, (in)GSH, is capable of augmenting central nervous system GSH concentrations, as determined by magnetic resonance spectroscopy in 15 participants with mid-stage PD, see abstract. As defined by the specification, GSH is a NAC derivative. See paragraph 29.
Mischley teaches in particular, the selection of dose delivery parameter for subsequent intranasal administration throughout its disclosure. See Abstract and page 3, column 1 Discussion. For example, Table 2 demonstrates changes in brain GSH levels (GSH/Cr peak ratios) relative to baseline after 200 mg nasally administered GSH. See page 3, top of page. Mischley teaches in Figure 3, GSH and GSH/Cr levels relative to baseline levels over time, which provide guidance over time to the PHOSITA to select the various delivery parameters specifically taught by Mischley in guiding subsequent intranasal administration based on these observations of Table 2 and Figure 3. Based off the teachings of Mischley, for example Table 2, where a 200 mg intranasal dose of GSH resulted in various GSH/Cr peak ratios over time, a PHOSITA would routinely optimize the delivery parameter of dose with potential subsequent intranasal administration to optimize GSH levels based on resulting GSH levels measured. Optimization of dosing, whether higher or lower than the 200 mg intranasal taught be Mischley would be readily apparent to a PHOSITA, as a clinician of ordinary skill in the art would no doubt lower or increase doses of GSH, based on teachings of Mischley (Table 2) to achieve desired clinical profiles to treat the subject in need via intranasal administration.
It would have been prima facie obvious to a PHOSITA following the teachings of the primary reference in Mischley teachings steps a) and b) of claim 1 (administration of therapeutic agent (GSH) to a subject to treat a condition such as PD,) to modify with the secondary teachings of Mischley (selection of dose delivery parameter) so as to routinely optimize treatment based on quantified GSH concentrations in the subject.
The PHOSITA would have had a reasonable expectation of success because Mischley not only teaches treatment of PD with GSH in subjects in need where patients under go MRIs to determine treatment effectiveness but also Mischley teaches the effects of GSH dose as a delivery parameter administered in terms of GSH concentration quantified in the treated subjects.
Regarding claim 9, the reference patent discloses an overlapping range of about 100 mg to about 400 mg. See claim 18.
Regarding claims 10-11, the reference patent teaches a nasal pump (claim 19) and an atomizer (claim 20).
With regard to claim 12 and the limitation of wherein the administering is repeated at least one time, while not expressly reciting a repeat administration of GSH or NAC of at least once, one skill in the art would have a rationale to repeat the GSH or NAC treatment at least once due to nature of brain disorders (concussion, dementia, Parkinson’s disease, traumatic brain injury, etc.) likely requiring repeat dosing to cure the subject.
Regarding claim 13 and the limitation of a pharmaceutical composition comprising a pharmaceutically acceptable carrier, it is pointed out that claims 1-24 are methods of administering NAC/congeners/derivatives, etc. to a subject in need suffering from a brain disorder. By the very nature of such a method, active pharmaceutical ingredients, such as NAC, require formulation into pharmaceutical compositions which must be formulated with excipients to administer them to subjects. Therefore, the reference patent claims 1-24 render claim 13 obvious.
Regarding claim 14 and the limitation of an aqueous solution administered, reference claim 19 discloses a nasal pump. By their nature, nasal pumps administer liquid formulations, such as aqueous solutions. Therefore, it would be routine for one skilled in the art optimize and formulate an aqueous therapeutic agent composition as claimed.
Claims 15-18 and 21 are directed to regions of the brain, the cerebrum, frontal lobe, occipital lobe, occipital cortex and substantia nigra. While not expressly claimed by the reference patent, it would be obvious to scan these regions of the brain via magnetic resonance spectroscopy as the mild traumatic brain injury of traumatic brain injury (concussion) would affect these brain regions.
Regarding claim 19 and measurement of changes of glutathione in the brain over time, Mischley discloses “After baseline GSH measurement [followed by]. . . . then serial GSH levels were obtained over~ 1 h. . . .” See Abstract. . With regard to the amendment of claim 19, wherein the selected delivery parameter is based on the determined change in the concentration of GSH, it would be routine for a PHOSITA to optimize the selection of the delivery parameter of dosages of GSH based on determined changes of GSH concentration, where Table 2 and Fig. 3 discloses corresponding GSH levels in response to a given dose of GSH administered intranasally, over time.
Regarding claim 20 wherein the administering increases the concentration of glutathione from about 20% to about 300%, Mischley discloses between the baseline and the 45-min scan, there was a mean 269% increase in GSH/Cr (240% increase in absolute GSH). See P.4, Fig. 3).
Claims 1-5 and 7-21 are rejected on the ground of nonstatutory obviousness-type double patenting as being unpatentable over claims 1-23 of US 12414929 B2 in view of MISCHLEY et al., Nature Partner Journals, 2016, 2, 16002, Pgs. 1-6.
Claims 1-5 and 7-8 disclose administration of therapeutic agent to a subject in need, with a brain/CNS condition such as Parkinson’s, mild traumatic brain injury and cancer where the agent is NAC or derivative, where claim 1 requires quantifying glutathione in the brain by magnetic spectroscopy (such as MRI).
Regarding claims 1-5 and 7-8, the reference patent teaches treatment of brain disorder in a subject with GSH (a known NAC derivative) where doses are administered via first the olfactory pathway and second the trigeminal pathway of the subject. See claim 1. Reference patent claims 2-9 and 20 disclose disorders such as mild traumatic brain injury, Parkinson’s disease, etc. Mischley teaches in Figure 3, GSH and GSH/Cr levels relative to baseline levels over time, which provide guidance over time to the PHOSITA to select the various delivery parameters specifically taught by Mischley in guiding subsequent intranasal administration based on these observations of Table 2 and Figure 3, so as to routinely optimize and arrive at step c), claim 1.
Regarding claim 9, the reference application teaches a therapeutically effective amount from about 100-400 mg. See claim 17.
Regarding claims 10-11, the reference application teaches a nasal pump and atomizer. See claim 18.
With regard to claim 12 wherein the administering is repeated at least one time, while not expressly reciting a repeat administration of GSH or NAC of at least once, one skilled in the art would have a rationale to repeat the GSH or NAC treatment at least once due to the nature of traumatic brain injury and/or Parkinson’s disease likely requiring repeat dosing to cure the patient.
Regarding claim 13 and the limitation of a pharmaceutical composition that further comprises a pharmaceutically acceptable excipient, these limitations are taught by reference claims 1-23, as the methods of the application administering a therapeutic agent to a subject in need, by virtue of this method by its nature, requires a pharmaceutical composition that must pharmaceutically acceptable excipients.
Regarding claim 14 and the limitation of an aqueous solution administered, reference claim 18 discloses a nasal pump. By their nature, nasal pumps administer liquid formulations, such as aqueous solutions. Therefore, it would be routine for one skilled in the art optimize and formulate an aqueous therapeutic agent composition as claimed.
Claims 15-18 and 21 are directed to regions of the brain, the cerebrum, frontal lobe, occipital lobe, occipital cortex and substantia nigra. While not expressly claimed by the reference patent, it would be obvious to scan these regions of the brain via magnetic resonance spectroscopy as the mild traumatic brain injury of traumatic brain injury (concussion) would affect these brain regions.
Regarding claim 19 and measurement of changes of glutathione in the brain over time, Mischley discloses “After baseline GSH measurement [followed by]. . . . then serial GSH levels were obtained over~ 1 h. . . .” See Abstract. . With regard to the amendment of claim 19, wherein the selected delivery parameter is based on the determined change in the concentration of GSH, it would be routine for a PHOSITA to optimize the selection of the delivery parameter of dosages of GSH based on determined changes of GSH concentration, where Table 2 and Fig. 3 discloses corresponding GSH levels in response to a given dose of GSH administered intranasally, over time.
Regarding claim 20 wherein the administering increases the concentration of glutathione from about 20% to about 300%, Mischley discloses between the baseline and the 45-min scan, there was a mean 269% increase in GSH/Cr (240% increase in absolute GSH). See P. 4, Fig.3).
Conclusion and Correspondence
No claims are allowed. Any inquiry concerning this communication or earlier communications from the examiner should be directed to WILLIAM LEE whose telephone number is (571)270-3876. The examiner can normally be reached M-F.
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/WILLIAM Y LEE/Examiner, Art Unit 1623
/ADAM C MILLIGAN/Supervisory Patent Examiner, Art Unit 1623
1 This Application is a CON of 17089192, abandoned, and earliest claims priority to USSN 62/930,473 filed on 11/04/2019.
2 MPEP § 2144.05(II ) and In re Aller, 220 F .2d 454, 456, 105 USPQ 233,235 (CCPA 1955)
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