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 .
Information Disclosure Statement
The information disclosure statements (IDS) submitted on 3/26/2024 and 6/23/2024 are in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statements are being considered by the examiner.
Claim Objections
Claims 2 and 3 are objected to because of the following identical informality: as one or more of the listed biomarkers may be used, it is recommended to have the lists of biomarker end with “and/or” before the final biomarker (i.e. “and/or CCL5” in claim 2 and “and/or CCL8” in claim 3). Appropriate correction is required.
Claim 4 is objected to because of the following informality: to better match the language used in claim 1, it is recommended that “the comparison of detected levels of one or more” in line 2 read “the comparison of the determined level of one or more.” Appropriate correction is required.
Claim 8 is objected to because of the following informality: in the final line “to the skin,” it is recommended that this read “to the skin of the patient” for better clarity. Appropriate correction is required.
Claim Rejections - 35 USC § 112(a)
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 1-8 rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for the use of some biological protein markers encompassed by the claims, does not reasonably provide enablement for the use of all biological protein markers encompassed by claim 1. Additionally, the specification does not provide enablement for the time requirements described in instant claims 5-6. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention commensurate in scope with these claims.
Factors to be considered in determining whether a disclosure meets the enablement requirement of 35 USC 112, first paragraph, have been described by the court in In re Wands, 8 USPQ2d 1400 (CA FC 1988). These factors include (1) the quantity of experimentation necessary, (2) the amount of direction or guidance presented, (3) the presence or absence of working examples, (4) the nature of the invention, (5) the state of the prior art, (6) the relative skill of those in the art, (7) the predictability or unpredictability of the art, and (8) the breadth of the claims. Each of these factors is discussed below.
Nature of the Invention
Claims 1-7 are drawn to a method of predicting atopic dermatitis (AD) relapse in a patient by determining biomarker protein expression in blood and predicting risk based on this expression and empirical data.
Claim 8 uses the method of claim 1 followed by the selection of an emollient.
Breadth of the Claims
Claims 1 and 4-8 are very broad in scope as they encompass the use of any biomarker protein that can be measured in blood.
Claims 2-3 do specifically recite narrower lists of biomarkers, though the list in claim 2 encompasses a large number of genes.
Claims 5-6 also note particular times to relapse. Claim 6 in particular recites a relapse time of “more than 7 days,” which does not have a strict upper limit other than that set by the lifespan of the patient, and thus is considered very broad in scope.
Level of Skill in the Art
The ordinary artisan typically holds at least a master’s degree has several years of experience.
State of the Prior Art & Unpredictability
Concerning the claimed invention, what was (and is) unpredictable in the art is whether any particular protein biomarker, or a combination of protein biomarkers, is associated with an AD relapse. In particular, biomarkers that may generally be associated with AD may not necessarily be associated with AD relapse. Additionally, it is unpredictable in the art how biomarker expression levels generally relate to time range for AD relapse. Therefore, it is not possible to know a priori that a particular biomarker, alone or in combination, will be correlated with AD relapse or time to AD relapse.
Regarding the encompassed biomarkers, the prior art has many examples of examining biomarkers associated with AD generally, but not many that are directly associated with any indication of relapse. Kou et al. (Arch Dermatol Res, 2012) teaches an analysis of atopic dermatitis and associated biomarkers (Abstract). In the section titled “Cyclosporine A treatment,” a protocol in which baseline levels of biomarkers (IL-18, TARC, IgE, and LDH) were taken, then a treatment was provided, biomarkers levels were remeasured, and after the stoppage of treatment, biomarker levels were measured as a metric of recurrence rates. Nikolaevna et al. (RU2603463C1; cited in Applicant’s IDS, English translation used for citations) measures biomarkers in association with AD (Abstract), and page 4 notes a formula which predicts the risk of relapse based on the expression of serum lactoferrin, alpha-1-antitrypsin, and 1 alpha-2-macroglobulin. Hoon (KR101512121B1; cited in Applicant’s IDS, English translation used for citations) provides a method and kit for diagnosing AD, and particularly noting if there is disease recurrence (Abstract). This recurrence metric is based on expression of Galectin-10 or S100A9 (page 8, second to last paragraph). Winqvist et al. (US 2014/0175018 A1) teaches that AD disease progression may be monitored based on the levels of increase in the biomarker CCR4, where disease progression may be indicated based on the degree of increase (para. 1008). This represents only a small group of biomarkers that are encompassed by instant claim 1.
Regarding relapse times for AD, the prior art generally does not show or describe the ability to predict relapse within a week of testing. Ertas et al. (J Allergy Clin Immunol, 2017) discusses relapse linked to medication cessation, and shows relapses from 1.5-30.5 weeks (see the confidence intervals for the time to relapse in Table 1). Koppelhus et al. (Frontiers in Medicine, 2014) shows relapses of 2-8 weeks after ending AD treatment (Abstract, Figure 1, and page 3, column 1, para. 1). Tang et al. (J Allergy Clin Immunol, 2014) is a review of various studies concerning AD (Abstract), and notes times to relapse that are 36 days or longer (page 1622, column 1, para. 4). Table II on page 1619 also notes time to first relapse in various studies, where some show numbers as high as 295 days. Granlund et al. (British Journal of Dermatology, 1995) investigates details related to cyclosporin treatment (Abstract). Patients with AD were treated with cyclosporin over various time periods, and relapse was measured (page 107, “Study protocol”). Relapse was around 50% two weeks after stopping cyclosporin treatment, and around 80% after 6 weeks after treatment, though it is noted that not all patients exhibited relapse during 6 months of follow up (page 108, “Follow-up”). No prior art could be found that alone discusses a particular time range for relapse based solely on biomarker expression and not associated with a treatment.
Guidance in the Specification and Examples
Regarding the protein biomarkers that may be used, the specification notes that “in certain embodiments,” the markers of Table 1 may be used, where these biomarkers are all those written in instant claim 2 (para. 20). Paras. 21-22 and 24 discuss those biomarkers written in claim 3. Para. 24 states that a “cut off point” for relapse within a week for each of these four biomarkers was established based on collecting blood samples from more than one individual, but this data is not specifically shown. Para. 22 also states, “For all of these markers IL-4, CCL27, CCL5 or CCL8, not one of them has been associated with atopic dermatitis relapse,” further supporting the finding of unpredictability in the art as described above. In the working example, only two patients were examined, which represents a small sample size, particularly in view of the fact that each “predicted time to relapse” category (7 days or less or more than 7 days) only has a single patient in it. Only IL-4, CCL27, CCL5 and CCL8 were tested, and these biomarkers were all examined together.
The empirical data conclusions were based on statistical tests, though it is unclear what precisely these tests were comparing. They appear to be based on expression levels of the four biomarkers examined, but it is unknown if any controls were used. “A range of individuals that had recently been affected by lesions” are said to be examined, and then these individuals are tested, and relapse relative to the time of testing is noted. It is unclear what criteria is then used to determine if relapse has occurred if the individuals have already been affected by lesions (para. 24 of the instant specification).
Thus, overall Applicant’s specification only specifically tests four potential biomarkers encompassed by the claims, and tests no biomarkers individually. The data presented is of a low sample size, lowering the power of the conclusions drawn, and the empirical data used for comparison is only vaguely described.
Therefore, in view of the unpredictability in the art discussed above, it is not clear that the results discussed by Applicant would extend over the full scope of the claimed invention.
Quantity of Experimentation
The ordinary artisan would have to conduct a very large quantity of highly unpredictable experimentation before being able to successfully practice the full scope of the claimed methods. Specifically, the ordinary artisan would have to determine that any particular biomarker encompassed by the claim is capable of functioning as a biomarker for AD relapse, and that this biomarker’s expression can determine a particular time to relapse. Based on the teachings in the art, this would be an inventive and unpredictable undertaking, requiring extensive experimentation in which there is no guarantee of success. The large quantity of experimentation and its unpredictability constitute undue experimentation.
Conclusion
In view of the foregoing, it is clear that the specification fails to enable the full scope of the claimed methods, and claims 1-8 are rejected under 35 U.S.C. 112(a) for failing to comply with the enablement requirement.
In terms of what is considered to be enabled in light of the In re Wands analysis conducted above, the teachings of the prior art do render the use of a single biomarker for predicting AD relapse enabled, and the biomarkers discussed in the prior art references cited above are considered to be enabled for use. Additionally, based on Applicant’s empirical data and working examples, the use of the four biomarkers that appear in instant claim 3, either individually or in combination, are considered to be enabled, as the empirical data conclusions were based on statistical tests related to biomarker expression. As noted above however, it is unclear how the testing and statistics are specifically evaluated relative to relapse in the individuals examined. In light of this and the teachings regarding AD relapse in the prior art, which do not teach evaluations of relapse of 7 days or less, only the time range described in instant claim 6 is considered enabled.
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 of matter, or any new and useful improvement thereof, may obtain a patent therefor, subject to the conditions and requirements of this title.
Claims 1-8 are rejected under 35 U.S.C. 101 because the claimed invention is directed to judicial exceptions without significantly more. The claims recite an abstract idea and a natural law.
Claim 1 is directed to a method for predicting atopic dermatitis (AD) patient relapse based on protein biomarker expression. The natural law recited is the biomarker expression and its correlation with AD relapse risk. The predicting in the claim is done by comparing expression levels with empirically determined data, with no particular limit to how this comparison may be performed. Thus, this predicting/comparing can encompass comparing expression values to one another, which would be possible to perform in the human mind, and would therefore be considered a mental process. The judicial exceptions are not integrated into a practical application because there is no required active treatment step or other step that integrates the judicial exception into a practical application. See MPEP 2106.04(d). The claim does not include additional elements that are sufficient to amount to significantly more than the judicial exception because they do not amount to more than well-understood, routine, and conventional activity in view of Kou et al. (Arch Dermatol Res, 2012).
Kou teaches an analysis of atopic dermatitis and associated biomarkers (Abstract). These biomarkers comprised IL-8 and TARC (also known as CCL17). Serum levels from both AD patients and controls were collected (page 306, “Subjects and assessments of clinical conditions”). In the section titled “Cyclosporine A treatment,” a protocol in which baseline levels of biomarkers were taken, then a treatment was provided, additional biomarkers levels were measured, and after the stoppage of treatment, biomarker levels were measured as a metric of recurrence rates. Biomarker levels were measured from the serum samples via an ELISA protocol (pages 306-307, “ELISAs for serum IL-18, TARC, and total IgE”). Figure 1 shows the results associated with the cyclosporine treatment. For both TARC and IL-8, expression increased with AD exacerbation after treatment, with IL-8 expression significantly increasing compared to the week 8 treatment condition. Table 1 also notes a generally significant increase in both IL-18 and TARC levels in AD patients compared to controls.
Thus, claim 1 is directed to judicial exceptions without significantly more.
Claims 2-3 depend on claim 1 and describe specific biomarkers that may be used in the method of claim 1. These claims only serve to further narrow the judicial exceptions of claim 1. The judicial exceptions are not integrated into a practical application because there is no required active treatment step or other step that integrates the judicial exception into a practical application. See MPEP 2106.04(d). The claims do not include additional elements that are sufficient to amount to significantly more than the judicial exceptions because they do not amount to more than well-understood, routine, and conventional activity for the same reasons described above for claim 1.
Thus, claims 2-3 are directed to judicial exceptions without significantly more.
Claims 4-6 depend on claim 1 and require that the comparison of claim 1 indicate a time to relapse. Because the comparison may still encompass comparing expression values to one another, where particular expression is simply associated with a time to relapse, the comparison step is still considered to encompass a mental process. Thus, these claims only serve to further narrow the judicial exceptions of claim 1. The judicial exceptions are not integrated into a practical application because there is no required active treatment step or other step that integrates the judicial exception into a practical application. See MPEP 2106.04(d). The claims do not include additional elements that are sufficient to amount to significantly more than the judicial exceptions because they do not amount to more than well-understood, routine, and conventional activity for the same reasons described above for claim 1.
Thus, claims 4-6 are directed to judicial exceptions without significantly more.
Claim 7 depends on claim 1 and specifies the type of sample that must be used in the method of claim 1. The judicial exceptions are not integrated into a practical application because there is no required active treatment step or other step that integrates the judicial exception into a practical application. See MPEP 2106.04(d). The claims do not include additional elements that are sufficient to amount to significantly more than the judicial exceptions because they do not amount to more than well-understood, routine, and conventional activity in view of Kou, which measures expression levels in serum, as described above in the rejection of claim 1.
Thus, claim 7 is directed to judicial exceptions without significantly more.
Claim 8 utilizes the method of claim 1 “followed by selecting an emollient to apply to the skin.” As this method includes the method of claim 1, the same judicial exceptions recited in claim 1 would apply here. The judicial exceptions are not integrated into a practical application because there is no required active treatment step or other step that integrates the judicial exception into a practical application. Though a particular emollient may be “selected,” no particular emollient is actually applied, and thus no active treatment step is recited. See MPEP 2106.04(d)(2). The claims do not include additional elements that are sufficient to amount to significantly more than the judicial exceptions because they do not amount to more than well-understood, routine, and conventional activity in view of Kou, which does recite the use of moisturizers for AD patients (page 306, column 1, para. 4).
Thus, claim 8 is directed to judicial exceptions without significantly more.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
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 1-2 and 7 are rejected under 35 U.S.C. 103 as being unpatentable over Kou et al. (Arch Dermatol Res, 2012).
Kou teaches an analysis of atopic dermatitis and associated biomarkers (Abstract). These biomarkers comprised IL-8 and TARC (also known as CCL17; instant claim 2). Serum levels from both AD patients and controls were collected (page 306, “Subjects and assessments of clinical conditions”). In the section titled “Cyclospotine A treatment,” a protocol in which baseline levels of biomarkers were taken, then a treatment was provided, additional biomarkers levels were measured, and after the stoppage of treatment, biomarker levels were measured as a metric of recurrence rates. Biomarker levels were measured from the serum samples via an ELISA protocol (pages 306-307, “ELISAs for serum IL-18, TARC, and total IgE”; instant claim 7). Figure 1 shows the results associated with the cyclosporine treatment. For both TARC and IL-8, expression increased with AD exacerbation after treatment, with IL-8 expression significantly increasing compared to the week 8 treatment condition. Table 1 also notes a generally significant increase in both IL-18 and TARC levels in AD patients compared to controls.
The information provided by Kou renders the invention of claim 1 prima facie obvious in light of the ordinary artisan’s skill, knowledge, and creativity in the art. Specifically, Figure 1 shows that with cyclosporine A treatment, AD symptoms were significantly reduced over the course of treatment, as evidenced by a significant decrease in SCORAD, which measured AD disease severity (page 306, column 2, para. 3). This decrease was then reversed upon cessation of treatment, representing a relapse in symptoms and an increase in disease severity. This decrease and increase in disease severity is accompanied by respective significant decreases and increases in IL-18 protein expression, as also shown in Figure 1. Thus, the ordinary artisan would recognize that the onset on more severe symptoms is associated with an increase in IL-18. Kou supports this conclusion, stating that, “Our findings also highlight the potential of serum IL-18 as a biomarker of AD, suggesting that an anti IL-18 antibody may be useful in future AD treatment,” (page 311, column 2, para. 1). Thus, the ordinary artisan would recognize that IL-18 expression could be used as a biomarker to non-invasively monitor AD disease progression, and thus could be used to predict when exacerbation of disease symptoms (i.e. a relapse) is likely. As obtaining serum samples is generally possible within a typical clinical setting (e.g. no specialized equipment or facilities is necessary), and is relatively safe and quick for both the patient and practitioner, utilizing these samples to monitor patient disease progression would be an attractive option for the ordinary artisan, and given this and Kou’s teachings regarding IL-18, the ordinary artisan would be motivated to use this biomarker to monitor disease progression. This monitoring could aid in determining treatment efficacy, as well as disease severity increases and decreases during routine clinical visits. This would provide more information to inform treatment plans and aid in patient decision-making. As the expression and use of IL-18 in conjunction with AD is readily shown in Kou, there would be a reasonable expectation of success.
It is noted that the AD patient population treated with cyclosporine A initially had moderate to severe AD (page 309, column 1, para. 1). Table 1 states that a SCORAD score of <30 represents mild AD, 30-60 represents moderate AD, and 60 or greater is severe AD. After cyclosporine A treatment, many of the patients examined and shown in Figure 1 had only mild symptoms of disease based on the SCORAD values. Thus, the teachings of Kou were used on patients experiencing only mild symptoms of AD, as required in instant claim 1.
Thus, claims 1-2 and 7 are prima facie obvious over Kou.
Claim 3 is rejected under 35 U.S.C. 103 as being unpatentable over Kou et al. (Arch Dermatol Res, 2012) and further in view of Holm et al. (Dermatology, 2021), Bottari et al. (Allergy, 1999), and Hijnen et al. (J Allergy Clin Immunol, 2004).
Kou teaches the method of claims 1-2 and 7, as described above. However, the reference does not measure any of the biomarkers described in instant claim 3.
Holm teaches the measurement of various biomarkers that are associated with disease severity in AD (Abstract). SCORAD was measured, as was done in Kou, and the biomarkers utilized are shown in Table 1. These include IL-4 and CCL27. Table 2 shows serum biomarker expression correlations with each other and with SCORAD, where IL-4 is shown to be positively correlated with both SCORAD and CCL17 (TARC as described in Kou), and CCL27 is shown to be significantly positively correlated with both SCORAD and CCL17.
Bottari teaches biomarker levels in associated with cyclosporin treatment in AD patients (Abstract). Figure 1 shows that cyclosporin treatment reduces IL-4 serum expression, in some cases bringing it into a normal range.
Hijnen teaches an analysis of TARC and CTACK (also known as CCL27), and looks at serum expression of these biomarkers with cyclosporin treatment (Abstract). Cyclosporine treatment specifically given to patients who had AD (page 335, column 1, para. 5). Figure 4 details that the expression of both biomarkers decreased with treatment (see figure caption).
Prior to the effective filing date of the claimed invention, it would have been prima facie obvious for one of ordinary skill in the art to use the teachings of Holm, Bottari, and Hijnen to add the biomarkers IL-4 and CCL27 to the methods of Kou described above in the rejection of claim 1. Specifically, these secondary references together provide nearly the same information detailed for IL-18 in Kou – namely, that IL-4 and CCL27 are positively correlated with SCORAD, and that both biomarkers have reduced expression when an AD patient is treated with cyclosporin. Kou makes a point to note that panels of biomarkers are more reliable for monitoring than any single biomarker (page 306, column 1, para. 3), and states that, “a single biomarker alone is probably not adequate to reflect the complex pathophysiology of AD,” (page 311, column 1, para. 4). Thus, the ordinary artisan would recognize that the inclusion of additional informative biomarkers would capture more data concerning AD patients, and would thus be a more accurate monitoring system. IL-4 and CCL27 would be used in the same manner as IL-18 in terms of being predictive, as the general expression patterns for these biomarkers are all the same. As Holm, Bottari, and Hijnen teach the successful measurement of IL-4 and CCL27 in serum, there would be a reasonable expectation of success.
Thus, claim 3 is prima facie obvious over Kou, and further in view of Holm, Bottari, and Hijnen.
Claims 4 and 6 are rejected under 35 U.S.C. 103 as being unpatentable over Kou et al. (Arch Dermatol Res, 2012) and further in view of Granlund et al. (British Journal of Dermatology, 1995).
Kou teaches the method of claims 1-2 and 7, as described above. However, Kou does not specify the time period between the stoppage of cyclopsorin treatment and the exacerbation of AD symptoms.
Granlund investigates details related to cyclosporin treatment (Abstract). Patients with AD were treated with cyclosporin over various time periods, and relapse was measured (page 107, “Study protocol”). Relapse was around 50% two weeks after stopping cyclosporin treatment, and around 80% after 6 weeks after treatment, though it is noted that not all patients exhibited relapse during 6 months of follow up (page 108, “Follow-up”).
Prior to the effective filing date of the claimed invention, it would have been prima facie obvious for one of ordinary skill in the art to use the guidance provided by Granlund to aid in the predictive value of the teachings of Kou described above for claim 1. Specifically, Granlund teaches that generally, time to relapse from the cessation of cyclosporin treatment is 2-6 weeks, though such relapse is not necessarily a forgone conclusion for every patient. Thus, this same time period for relapse would be used to inform the analyses of Kou. Specifically, if a patient is monitored after stopping cyclosporin treatment and IL-18 expression begins to rise, then a range for time to relapse would be predictable based on the IL-18 expression levels obtained following treatment and during exacerbation of Kou. By determining this time period for relapse, practitioners may recommend more aggressive treatments to prevent full relapse into moderate or severe disease, which may improve patient outcomes, and would thus be motivated to the ordinary artisan. There would be a reasonable expectation of success as incorporating the teachings of Granlund into the method of Kou would not change any of the methodology of Kou, it would simply inform the conclusions drawn from the data of Kou.
Thus, claims 4 and 6 are prima facie obvious of Kou in view of Granlund.
Claim 8 is rejected under 35 U.S.C. 103 as being unpatentable over Kou et al. (Arch Dermatol Res, 2012) and further in view of Hon et al. (Drugs in Context, 2018).
Kou teaches the methods of claims 1-2 and 7, as described above. Kou also states that all AD patients in their study were treated with topical corticosteroids, along with moisturizers as needed, but does not specify any particular emollient choices (page 306, column 1, para. 4).
Hon reviews emollient treatment for atopic dermatitis and considerations for emollient choice (Abstract). The reference states that emollients in AD can, “provide an occlusive barrier for AD skin, retain moisture and protect it from irritants,” (page 1, column 1, para. 1). Table 1 describes various types of emollients, notes whether there is clinical evidence related to AD improvement, and notes the specific effects of each emollient. In patient preference for emollients, doctor preference is particularly important, and Hon urges physicians to provide evidence-based information (page 10, “Review of studies and patient preferences,” and “Conclusion”). Emollients when used in combination with topical corticosteroids can reduce the amount of steroid needed (page 10, column 2, para. 1), and emollients are frequently used with other topical medications in AD (page 1, column 1, para. 1).
Prior to the effective filing date of the claimed invention, it would have been prima facie obvious for one of ordinary skill in the art to use the teachings of Hon to aid in the specific choice of emollient/moisturizer in Kou. Hon provides specific evidence-based information on a variety of emollients, as well as ingredient and biophysical effect information, which would prompt the ordinary artisan to choose an emollient that has a noted clinical efficiency, taking into account potential patient ingredient preferences and allergies, as well as overall skin moisture levels before product use. By choosing a moisturizer that has a known clinical benefit, it would be more likely that the patient will show improvement in AD symptoms, which would prevent financial and time waste on products that would be ineffective. There would be a reasonable expectation of success in using the teachings of Hon as the emollients taught in Table 1 of the reference are all commercially available, and the evidence provided by Hon would be accessible for review by the ordinary artisan.
Thus, claim 8 is prima facie obvious over Kou in view of Hon.
Conclusion
No claims are currently allowable.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to FRANCESCA F GIAMMONA whose telephone number is (571)270-0595. The examiner can normally be reached M-Th, 7-5pm.
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/F.F.G./Examiner, Art Unit 1681
/SAMUEL C WOOLWINE/Primary Examiner, Art Unit 1681
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