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 .
Detailed Action
Summary
This is the Final Office action based on the 17/602361 RCE response filed 02/02/2026.
Claims 1, 3-6, 13-14, & 17-24 are pending and have been fully examined.
Claims 2, 7-12, & 15-16.
Claim Rejections - 35 USC § 101
35 U.S.C. 101 reads as follows:
Whoever invents or discovers any new and useful process, machine, manufacture, or composition ofmatter, or any new and useful improvement thereof, may obtain a patent therefor, subject to theconditions and requirements of this title.
The claimed invention of Claims 1, 3-6, 13-14, & 17-24 are directed to non-statutory subject matter.
The invention of instant claims 1, 3-6, 13-14, & 17-24 are drawn towards a method of detecting and treating IL4I1 in a biological sample from a cell or subject and thereby detecting modulation of AHR.
Through 101, inquiry analysis:
Are the claims directed to a statutory category of invention?
Yes, independent claim 1 is drawn towards a statutory category of a method.
For independent Claim 14 the answer is also yes as it is drawn towards a kit/device or article of manufacture.
Step 2A, Prong One: Identify the law of nature/natural phenomenon/abstract ideas.
Independent claim 1, involves the judicial exception of a law of nature-- a natural correlation is a law of nature. The natural correlation which is claimed is the level of natural biomarker IL41 in a biological sample or cell, and its correlation with modulation of AHR (aryl hydrocarbon receptor), which is read as (or through broadest reasonable interpretation can be) the state/condition/whether there is a disease or condition associated with AHR modulation. The noticing of an increase or decrease in comparison to a control is also part of the judicial exception itself indicating the natural correlation. And further- the comparison to control is a mental process/abstract idea.
Though the instant claim is drawn towards “treating,” as claimed, mostly what is in the claim is implicit diagnostics. This is shown further in the analysis below as though by first glance, “administering AHR signaling inhibitor,” might read as particular and specific as claimed, when looking into the specification and claims in detail, it does not.
Further, the claimed “detecting,” for Claim 1 through broadest reasonable interpretation could just be an observation which is a mental process at most broad interpretation and therefore and abstract idea judicial exception. It is noted that no particular detection or sensing device is claimed, so at least broad reads as just data gathering to not particular practical application, and also well understood and routine and conventional so not significantly more. This is further shown in the analysis below.
Independent Claim 14 through broadest reasonable interpretation contains a natural biological sample (what is held in the container). Biological samples are products of nature.
Step 2A Prong Two: Has the abstract idea or natural correlation been integrated into a particular practical application?
For Claim 1 the answer is no.
For the instantly claimed, “detecting,” no specific sensor or detector is used. As generally claimed, the instant detecting can mean mentally detecting from looking at a chart. Even if the claimed analysis required an actual analysis device/sensor, then it would amount to mere data gathering which is then used in the abstract idea, if claimed generally. Note that data gathering to be used in an abstract idea is insignificant extra-solution activity, and not a particular practical application. See MPEP 2106.05(g).
After, “detecting,” the IL4I1 or AHR, no action which practically applies the judicial exception is taken.
Claim 1 requires that, “administering an AHR signaling inhibitor/ or activator compound to treat an AHR-related disease or condition, wherein an effective amount of the AHR signaling modulator compound is about 0.01 mg/kg to about 100 mg/kg,” and “wherein the AHR signaling inhibitor compound is a small molecule compound having a molecular weight of less than 2000 daltons,” and the same claimed for the AHR signaling activator. For a noticed increase when compared to a control the inhibitor is administered. For a noticed decrease when compared to a control an activator is administered.
As claimed, it seems the only time a treatment it not administered is when a detected level exactly matches the control level detected.
For the claimed AHR signaling activators and AHR signaling inhibitors, the instant specification first describes them both as AHR modulators.
In the instant specification—the modulators (which are the activators or inhibitors) are described as : “selected from a proteinaceous domain, a small molecule, a peptide, antibodies, an environmental substance, probiotic, toxin, aerosol, medicine, nutrient, galenic composition, plant extract, volatile compound, homeopathic substance, incense, pharmaceutical drug, vaccine, a compounds or compound mixture derived from animals, plants, fungi, bacteria, archaea, a chemical compound, a compound used in food or cosmetic industry, and a library of said compounds.” (See instant application specification, Claim 11).
Since the “AHR signaling activator,” and “AHR signaling inhibitor,” can be such a broad and general list of compounds---- which are not all solely specific to AHR activation, or AHR inhibition, the claimed treatment is not particular or specific treatment. This remains the same even with the claim amendment dated 02/02/2026 that the “AHR signaling inhibitor compound is a small molecule compound having a molecular weight of less than 2000 daltons,” and the “AHR signaling activator compound is a small molecule compound having a molecular weight of less than 2000 daltons.”
The instant application does contain disclosure of treatments which could be considered particular and specific, but due to the general claiming and the disclosure with respect for how these terms can be interpreted—just saying “AHR signaling activator,” and “AHR signaling inhibitor,” is not considered particular or specific.
In fact, many of the compounds described in the PGPub disclosure, Claim 11, as being IL4I1 or AHR inhibitors or modulators, such as plants, fungi, probiotics, small molecules, nutrients, peptides, chemical compounds are ingested by humans on a daily basis though a normal diet, so they are not considered particular and specific in light of “AHR-related disease or condition,” as claimed. Though only treatments in PGPub Claim 11 are called out--- all of the claimed treatment compounds in Claim 11 are not considered specific and are akin to, “administering a suitable treatment.”
Even further--- as instantly amended 02/02/2026, both the “AHR signaling activator,” and “AHR signaling inhibitor,” are described as exactly the same compound indicating that the claimed treatment is not particular and specific, nor even dependent at all on the claimed detection. Instead, it seems that the administered compound which is, a “compound is a small molecule compound having a molecular weight of less than 2000 daltons, ” and one which “ is about 01 mg/kg to 100 mg/kg,” for an effective dose is administered regardless of detection or measurement.
See MPEP 2106.04 (d)(2) a.
“Conversely, consider a claim that recites the same abstract idea and "administering a suitable medication to a patient." This administration step is not particular, and is instead merely instructions to "apply" the exception in a generic way. Thus, the administration step does not integrate the mental analysis step into a practical application.”
This the case for the instant claims, in that what is claimed is akin to merely “apply,” the judicial exceptions, for the reasons above.
Further, due to the fact that even if applicant claimed treatment with a particular and specific compound, applicant does not actually claim administration of an effective amount of the treatment, but instead only says in the claim what the effective amount of a treatment would be. The claims do not necessitate the using of the effective amount.
For Claim 14 the answer is also no. The claim requires a kit containing materials for performing the method of Claim 1, in one or separate containers. As seen in claim 1, all that is needed is a cell or biological fluid sample and some types of signaling inhibitor or activator which is a “small molecule”. Therefore, applicant is claiming a biological fluid sample and a very unspecific, general compound/molecule or reagent in a container. A container through BRI can be the human body, but even if not, a test tube. Putting a biological fluid in a test tube or them in a container does not make them “markedly different,” from what is found in nature, and as claimed the small molecule is also not markedly different from what is found in nature.
Therefore, there is no particular practical application.
Step 2B: Do the claims recite any elements which are significantly more than the natural correlation or abstract idea?
Here, we look to the elements other than the natural correlation or abstract idea to see if there is significantly more.
Claim 1 does not recite any other elements which are considered significantly more.
Comparison to a control is routine and conventional in the art so does not change the matters above.
The claimed detection is not claimed using and particular reagents or machines that are non-routine and conventional.
The treatments in Claim 1 are interpreted the same way as in the practical application step above. What is disclosed in the specification and what was amended to the claims 02/02/2026 for possible treatments /modulators is very general and broad. The “AHR signaling activator,” and “AHR signaling inhibitor,” are required to be a “compound is a small molecule compound having a molecular weight of less than 2000 daltons, ” and one which “ is about 01 mg/kg to 100 mg/kg,” for an effective dose is administered regardless of detection or measurement, though no dosing of an actual effective dose is claimed.
As broadly and generally claimed, these treatments are considered well understood, routine and conventional in the art (WURC) and therefore are not significantly more. Even though they are claimed at the broad concentration of, an effective amount of the AHR signaling modulator compound is about 0.01 mg/kg to about 100 mg/kg,” this remains the case since the treatments themselves, which are now also required to include “small molecule compound,” which have a molecular weight of “less than 2000 daltons,” can be things that are so broad including food type things.
Paragraph 0047 of the instant specification indicates that the, “AHR modulator,” can be “dietary components,” such as resveratrol or curcumin (which is found in foods and drinks many consume daily) or toxic compounds such as cigarette smoke, fuel emissions, or pesticides (which again many people are exposed to daily). This again, is not a particular and specific treatment as most people do this every day. These treatments include small molecule compounds having the claimed size.
Especially at the level of generality claimed, all of these claimed treatments are routine and conventionally used in the art. This is true even at the level of concentration recited--- of, “about .01 mg/kg to about 100 mg/kg,” as many of them are ingested by humans on a regular basis in small amounts, among other reasons. See MPEP 2106.05 (d) for example what the courts have found to be well understood routine and conventional (WURC) in the art.
For Claim 14 the answer is also no. The claim requires a kit containing materials for performing the method of Claim 1, in one or separate containers. As seen in claim 1, all that is need is a cell or biological fluid sample and some type of signaling inhibitor or activator which is a “small molecule”. Therefore, applicant is claiming a biological fluid sample in a container. A contained through BRI can be the human body, but even if not, a test tube. Test tubes are so routinely and conventionally used in the art that this does not move the claims to be a significantly more. Small molecules having the claimed size of less than 2000 daltons are also not markedly different or something which is significantly more or different from what is found in nature.
For the claimed treatments, see MPEP 2106.04 (b) and Vanda memorandum.
Nothing in any of the dependent claims change the matters above:
Claims 3-5 state where the biological state is detected from and what the subject and sample are/are from. All claimed products the state is detected from are natural compounds/products of nature so this does nothing to change the above.
Claim 6 states that the control sample is from a healthy subject. Again- a sample from a healthy subject is still a natural sample. Further, using controls from healthy populations is well understood, routine and conventional in the art and therefore does nothing to change the above.
Claim 21 states that the modulator is an inhibitor or inducer of IL4I1, or the metabolites are modulated by IL4I1. At the level of generality claimed- this could be almost anything through broadest reasonable interpretation. Further – samples that are modulate by IL4I1 are natural samples as is IL4I1 itself. Therefore-none of this is particular or specific treatment, nor does it change the claims from something that naturally occurs into a practical application or significantly more.
Claims 13 & 22 do not change the above. Claim 13 specifies that clustering happen or classification. This is math and also could be a mental process which are abstract ideas themselves.
Claims 17-18 state where the metabolite is detected from and what the metabolite is. All claimed products are natural compounds/products of nature so this does nothing to change the above.
Claims 19, states what the condition is. This is part of the claimed natural correlation itself and therefore does not change the above.
Claim 20 specifies that the state with the modulator is compared to the state without the modulator. Again- this is just viewing of the natural correlation--- and adds no specificity or particularity to the claimed treatment (modulator)—therefore does not change the matters above.
Claim 23 does not change the above. Claim 23 specifies stratification into groups. This is a mental process which is an abstract idea itself.
Claim 24 does not change the above. Claim 24 depends on Claim 1, and describing what the AHR signaling modulator does, does not make the treatment particular or specific. Also see comments on how AHR signaling modulator is disclosed for Claim 11, as the same applies here.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
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, 3-6, 13-14, & 17-24 are rejected under U.S.C. 103 as being obvious over SULLIVAN in WO 2017/189353 (cited on IDS dated 10/08/2021) in view of BOWLES in US 20140213638 and further in view of KRUTMANN in US 20090028804.
With respect to Claim 1 & 20 SULLIVAN teach of a method of detecting, and treating disease by reducing or inhibiting IL4I1 activity (abstract). Specifically, SUILLIVAN teach of detecting association between two substances (Page 6, lines 17- Page 7, end of first paragraph), and of screening for an antagonist of IL4I1 (Page 2, line 30-31) and of monitoring the biological state with respect treatments (Page 12, last paragraph, Page 13, first paragraph). SULLIVAN teaches that the sample is contacted with a candidate modulator compound (inhibitor or activator)/at least one compound (treatment) in a course of treatments and of detecting IL4I1 after and that the treated samples can be compared to the untreated samples (Page 11, line 19-23, Page 12, last paragraph).
SULLIVAN teaches of comparison to a healthy volunteer (control)(Page 7, last paragraph). SUILLIVAN teach of detecting association between two substances (Page 6, lines 17- Page 7, end of first paragraph), and of screening for an antagonist of IL4I1 (Page 2, line 30-31).
SULLIVAN further teach that the samples are compared to a control (Page 12, line 25-35). Since as claimed, IL411 detection indicates IL4I1 modulation of AHR as instantly claimed (activation or repression)- this makes it obvious that SULLIVAN teaches of “detecting modulation of AHR,” through the claimed method of detecting IL4I1. However, if this is not clear to one of ordinary skill, BOWLES is used to remedy this.
BOWLES teaches of a method to measure biomarkers for inflammatory conditions (paragraph 0177, abstract), and of specifically measuring AHR (paragraph 0046, 0174, 0260, 0268), and also of treating the subject with a substance that modulates the detected compounds (paragraph, 0268, 0020-0028, 0034, 0037). It would have been obvious to one of ordinary skill in the art before the effective filing date of the instant invention to detect modulation in AHR as is done in BOWLES in the method of SULLIVAN and one would have had reasonable expectation of success due to the potential modulating AHR has shown for modulating failing heart diseases (BOWLES, paragraph 0268).
Neither SULLIVAN or BOWLES call out specific treatment with an AHR modulator (activator or inhibitor) which is a small molecule having a molecular weight of under 2000 daltons.
KRUTMANN is used to remedy this. KRUTMANN teaches of a method of assessing and using AHR agonists and antagonists (this reads on both activators and inhibitors) (abstract), and even more specifically KRUTMANN teaches of treating with AHR agonists, antagonists, and modulators (Table 1, paragraph 0047, 0044).
KRUTMANN teaches that AHR modulators have a sign lightening or darkening affect (abstract) and that these molecules can be kojic acid (which has a molecular weight of around 142.11 Daltons--- this is a material property), or beta-arbutin (which has a molecular weight of 272.5 Daltons (paragraph 0065). These compounds are small compounds and have the claimed molecular weight of “less than,” “2000 Daltons.”
KRUTMANN teaches of treatments for conditions such as cancer (paragraph 0044, 0075). KRUTMANN further teaches that the use of AHR antagonists and that in certain situations concentrations of 10 to 20 times the minimum concentration is used (paragraph 0063). KRUTMANN teaches that in other situations only two times the minimum concentration is used (paragraph 0061-0062). KRUTMANN further teaches of determining the minimum effective concentration of the AHR agonists and antagonists by carrying out the methods repeatedly using different concentrations (paragraph 0064).
Though KRUTMANN does not call out the exact claimed concentration for treatment with the AHR modulator, it would have been obvious to one of ordinary skill in the art to determine the effective concentration through repeatedly trying different concentration as is done in KRUTMANN above and result in the claimed concentration through routine optimization. See. MPEP 2144.05, II, A. Routine optimization.
It would have been obvious to one of ordinary skill in the art before the effective filing date of the instant invention to use the AHR agonist/antagonist/modulator with the claimed small molecule size as a treatment as is done in KRUTMANN in the methods of SULLIVAN and BOWLES due to the disadvantage that virtually no compounds are known which act as AhR antagonists on human skin and due to the advantages the instant methods offer for determining AHR modulators (KRUTMANN, paragraph 0029, 0031).
With respect to Claim 2, SULLIVAN teaches of detecting inflammatory lung disease by the method of claim 1, which is, “inflammation,” (Page 10, lines 19-30).
With respect to Claims 3-5, SULLIVAN teaches of detecting a biological component (such as an IL4I1 protein, antibody, or nucleic acid molecule) has been substantially separated, produced apart from, or purified away from other biological components in the cell of the organism in which the component occurs, such as other chromosomal and extrachromosomal DNA and RNA, and proteins. Nucleic acids molecules and proteins which have been "isolated" thus include nucleic acids and proteins purified by standard purification methods. The term also embraces nucleic acid molecules and proteins prepared by recombinant expression in a host cell as well as chemically synthesized nucleic acids. A purified or isolated cell, antibody, protein, or nucleic acid molecule can be at least 70%, at least 80%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99% pure (Page 9, lines 18-26). SULLIVAN further teach that the sample can be from a mammal and that this term includes both human and non-human mammals. Similarly, the term "subject" includes both human and veterinary subjects (such as cats, dogs, horses, cows, and pigs) and rodents (such as mice and rats) (Page 9, line 27-30).
With respect to Claim 13, SULLIVAN teaches the above as shown for claim 1, but does not teach of clustering or classification as claimed.
BOWLES is used to remedy this and teaches of claim 1 as shown above. BOWLES further teaches of performing hierarchial clustering for all peptides (paragraph 0044, 0169, 0252). It would have been obvious to one of ordinary skill in the art to perform clustering on the obtained measurements and data as is done in BOWLES in the method of SULLIVAN and one would have had reasonable expectation of success due to the advantage it offers in being able to group data in order to observe overall expression patterns (BOWLES, paragraph 0252).
With respect to Claim 14, SULLIVAN teaches of using carriers, binding agonists (Page 10, last paragraph and second paragraph), and of containing the parts in plates/containers (Page 17, line 10- bottom). Though this makes containing all components claimed in a kit obvious, since SUILLIVAN does not call out the use of a kit, BOWLES is used to remedy this. BOWLES further teaches of using a kit for determination of the biomarkers (paragraph 0014). It would have been obvious to one of ordinary skill in the art to use a kit for determination and diagnosis of the disease as is done in BOWLES in the method of SULLIVAN and one would have had reasonable expectation of success with biomarkers due to the advantage this would offer in ease of use.
With respect to Claim 17, SULLIVAN teaches of the metabolites which are measured being produced by IL4I1(such as IL4I1 protein, antibody, or nucleic acid molecule) (Page 9, line 18026).
With respect to Claim 18, SULLIVAN teaches of the cells being myeloid- cells or B- cells among other cell types (Page 9, lines 5-17).
With respect to Claim 19, SULLIVAN teaches of Claim 5 as shown above, but does not teach of AHR. BOWLES is used to remedy this.
BOWLES teaches of a method to measure biomarkers for inflammatory conditions (paragraph 0177, abstract), and of specifically measuring AHR (paragraph 0046, 0174, 0260, 0268), and also of treating the subject with a substance that modulates the detected compounds (paragraph, 0268, 0020-0028, 0034, 0037). It would have been obvious to one of ordinary skill in the art to detect modulation in AHR as is done in BOWLES in the method of SULLIVAN due to the potential modulating AHR has shown for modulating failing heart diseases (BOWLES, paragraph 0268 ).
With respect to Claim 21, SULLIVAN teaches of the metabolites which are measured being produced by/modulate by IL4I1(such as IL4I1 protein, antibody, or nucleic acid molecule) (Page 9, line 18026).
With respect to Claim 22, SULLIVAN teaches the above as shown for claim 1, but does not teach of clustering or classification as claimed.
BOWLES is used to remedy this and teaches of claim 1 as shown above. BOWLES further teaches of performing hierarchical clustering for all peptides (paragraph 0044, 0169, 0252). It would have been obvious to one of ordinary skill in the art to perform clustering on the obtained measurements and data as is done in BOWLES in the method of SULLIVAN and one would have had reasonable expectation of success due to the advantage it offers in being able to group data in order to observe overall expression patterns (BOWLES, paragraph 0252).
With respect to Claim 23, SULLIVAN teaches of the claimed invention as shown above for Claim 13, but does not teach of stratification or placement into groups. BOWLES teaches this (paragraph 0160, 0169, 0241 among others). It would have been obvious to group the results as is done in BOWLES in the method of SULLIVAN and one would have had reasonable expectation of success due to the advantage this offers in determination of disease state (paragraph 0252).
With respect to Claim 24, SULLIVAN and BOWLES do not teach of the AHR modulator as claimed in Claim 24.
KRUTMANN is used to remedy this. KRUTMANN teaches of a method of assessing and using AHR agonists and antagonists (abstract), and even more specifically KRUTMANN teaches of treating with AHR agonists, antagonists, and modulators (Table 1, paragraph 0047, 0044). KRUTMANN further teaches that the use of AHR antagonists and that in certain situations concentrations of 10 to 20 times the minimum concentration is used (paragraph 0063). KRUTMANN teaches that in other situations only two times the minimum concentration is used (paragraph 0061-0062). KRUTMANN further teaches of determining the minimum effective concentration of the AHR agonists and antagonists by carrying out the methods repeatedly using different concentrations (paragraph 0064). KRUTMANN further shows that AHR modulator can be an inhibitor of the AHR signal pathway (paragraph 0060).
It would have been obvious to one of ordinary skill in the art to use the AHR agonist/antagonist/modulator as a treatment of KRUTMANN in the methods of SULLIVAN and BOWLES due to the disadvantage that virtually no compounds are known which act as AhR antagonists on human skin and due to the advantages the instant methods offer for determining AHR modulators (KRUTMANN, paragraph 0029, 0031).
Response to Arguments
Applicant's arguments filed 02/02/2026 have been fully considered but they are not persuasive.
Applicant argues that the instantly claimed treatment added to the claims as amended 02/02/2026 should overcome the 101 rejection. The examiner disagrees. The claimed, very general treatment of and “AHR signaling inhibitor compound is a small molecule compound having a molecular weight of less than 2000 daltons,” and an “AHR signaling activator compound is a small molecule compound having a molecular weight of less than 2000 daltons,” is particular and specific treatment and non-routine and conventional. The examiner disagrees.
It is noted in the instant specification that these “small molecule compound/s,” can be an organic chemical compound having the claimed size. With respect to this--- using compounds that can be considered “small molecule compounds,” that fit the claimed size specification are commonly used in the prior art, and therefore are routine and conventional, and not significantly more at step 2B. Also- as claimed, the treatment does not practically apply, as shown in the above 101 rejection.
Since this subject matter was newly added, this is addressed in the rejection above instead of in the response to arguments.
With respect to the prior art, applicant argues that none of the pieces of prior art teach of the newly amended claim limitations with respect to the AHR inhibitor or activator treatment and concentration and claimed small molecule size in Daltons as amended 02/02/2026.
The examiner disagrees. KRUTMANN teaches that AHR modulators of using kojic acid or beta-arbutin, which have a sign lightening or darkening affect (abstract) and that these molecules can be kojic acid (which has a molecular weight of around 142.11 Daltons--- this is a material property), or beta-arbutin (which has a molecular weight of 272.5 Daltons (paragraph 0065).
Therefore—this reads on the newly amended claim subject matter, which is really the only substantive thing applicant argues about with respect to the prior art in arguments dated 02/02/2026.
In response to 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).
Therefore all claims remain rejected.
Conclusion
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). 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.
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/REBECCA M FRITCHMAN/Primary Examiner, Art Unit 1758