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 .
Priority
This application is a national stage entry of PCT/IB2020/057316 Filed on August 3, 2020. Acknowledgment is made of applicant's claim for foreign priority based on an application filed in Italy on August 9, 2019. Receipt is acknowledged of certified copies of papers required by 37 CFR 1.55.
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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 July 6, 2026 has been entered.
Response to Amendment
By Applicant’s amendment filed July 6, 2026, claims 1 and 15 were amended and claim 4 was canceled.. Claims 2, 3, 9, 12-14 and 16 were previously canceled. Claims 1, 5-8, 10, 11, 15, 17 and 18 are currently pending and presented for examination.
Response to Arguments
Applicant's arguments filed July 6, 2026 have been fully considered but they are not persuasive.
Applicant argues that that Tavakkoli teaches that vitamin D deficiency is a potential consequence or clinical manifestation of celiac disease, rather than as a causal or pathogenetic factor contributing to the onset or progression of the disease. Therefore, Applicant argues that a person skilled in the art would not derive from this document any teaching that vitamin D deficiency plays a causal role in the pathogenesis of celiac disease, and consequently would not derive that correcting vitamin D deficiency would prevent, treat, or modify CD. Applicant argues that at most he/she would derive that treating Celiac Disease may restore Vitamin D levels. Applicant further argues that Tavakkoli does not suggest a link between Vitamin D deficiency and villous atrophy.
These arguments are found not persuasive since, in response to applicant's argument that Tavakkoli does not suggest a link between Vitamin D deficiency and villous atrophy, the fact that the inventor has recognized another advantage which would flow naturally from following the suggestion of the prior art cannot be the basis for patentability when the differences would otherwise be obvious. See Ex parte Obiaya, 227 USPQ 58, 60 (Bd. Pat. App. & Inter. 1985). In the instant case, the prior art of record provides a legitimate rationale for administering vitamin D3 to patients with celiac disease. Tavakkoli et al. specifically demonstrates that almost 60% of patients with celiac disease were found to be vitamin D deficient or insufficient (page 517). Thus Tavakkoli et al. identifies a problem in patients with celiac disease which is reduced vitamin D levels. Furthermore, Kimball specifically teaches how to treat patients that are vitamin D deficient or insufficient with Vitamin D3 (cholecalciferol). Thus the teachings of Kimball provide a solution to the problem identified in Tavakkoli et al. Accordingly, the teachings of the prior art demonstrate that celiac disease is associated with vitamin D deficiency or insufficiency since most patients with celiac disease are vitamin D deficient or insufficient and thus a person of ordinary skill in the art would have been motivated to administer Vitamin D3 (cholecalciferol) therapy to a patient with celiac disease with a reasonable expectation of treating celiac disease by treating vitamin D deficiency or insufficiency.
A reference is good not only for what it teaches by direct anticipation but also for what one of ordinary skill in the art might reasonably infer from the teachings. (In re Opprecht 12 USPQ 2d 1235, 1236 (Fed Cir. 1989); In re Bode 193 USPQ 12 (CCPA) 1976). "[I]n considering the disclosure of a reference, it is proper to take into account not only specific teachings of the reference but also the inferences which one skilled in the art would reasonably be expected to draw therefrom." In re Preda, 401 F.2d 825, 826, 159 USPQ 342, 344 (CCPA 1968); In re Lamberti, 545 F.2d 747, 750, 192 USPQ 278, 280 (CCPA 1976).
In the instant case, a skilled artisan would reasonably infer from the teachings of Tavakkoli et al. that patients with celiac disease would benefit from the administration of Vitamin D3 (cholecalciferol) since Tavakkoli et al. specifically demonstrates that almost 60% of patients with celiac disease were found to be vitamin D deficient or insufficient (page 517). Furthermore, Kimball specifically teaches administration of vitamin D3 in the amounts as claimed to treat vitamin D deficiency. Thus by following the teachings and suggestions of the prior art of record, a person of ordinary skill in the art would arrive at the instant invention of treating celiac disease by administering vitamin D3 (cholecalciferol).
In addition, it is not necessary that the prior art suggests the same advantage or result discovered by applicant when the steps of the claim are the same as those described or suggested by the prior art. See, e.g., In re Kahn, 441 F.3d 977, 987 (Fed. Cir. 2006) (motivation question arises in the context of the general problem confronting the inventor rather than the specific problem solved by the invention); Cross Med. Prods., Inc. v. Medtronic Sofamor Danek, Inc., 424 F.3d 1293, 1323 (Fed. Cir. 2005) (“One of ordinary skill in the art need not see the identical problem addressed in a prior art reference to be motivated to apply its teachings.”); In re Lintner, 458 F.2d 1013 (CCPA 1972); In re Dillon, 919 F.2d 688 (Fed. Cir. 1990), cert. denied, 500 U.S. 904 (1991). The mere recognition of latent properties in the prior art does not render nonobvious an otherwise known invention. In re Prindle, 297 F.2d 251, 254 (CCPA 1962). Here, the latent property identified by Applicant is reduction of intestinal villous atrophy by the administration of cholecalciferol. However, since the prior art renders obvious administering cholecalciferol to treat patients with celiac disease, in the same amounts as claimed that treat intestinal villous atrophy, reduction of intestinal villous atrophy will necessarily result by following the teachings and suggestions of the prior art and administering cholecalciferol in patients with celiac disease.
Applicant further argues that the skilled person would have disregarded the use of Vitamin D supplementation in a CD patient, recognizing that villous atrophy can lead to malabsorption, potentially hindering the improvement of Vitamin D levels. Thus Applicant argues that the skilled person would have no expectation to improve Vitamin D levels in CD patients and even less to treat CD and thus even improvement of Vitamin D levels would have been discouraged. Applicant argues that in Kimball the only mention of celiac disease regards a subgroup of participants (n = 285) in the study, with substantial intakes of vitamin D supplements (> 4,000 IU/d), which did not experience an increase in serum 25(OH)D concentrations. Kimball suggests that this result could be due to disorders of intestinal absorption including celiac disease. Thus Applicant argues that given that CD patients have intestinal malabsorption and that some patients don't experience an increase in serum 25(OH)D concentrations after Vitamin D supplementation, a skilled person would have been discouraged from using Vitamin D, even for treating Vitamin D deficiency, let alone for treating celiac disease. Therefore, the fact that the present application demonstrates that Vitamin D can reduce intestinal villous atrophy is even more surprising in view of the content of Tavakkoli and Kimball.
These arguments are found not persuasive since the state of the art prior to the effective filing date of the claimed invention supports vitamin D supplementation in patients with celiac disease and having vitamin D deficiency in spite of intestinal malabsorption in these patients. For example, Komlosy and Jagger (Arnold A 2017 Primary hyperparathyroidism: molecular genetic insights and clinical implications. Presented at Society for Endocrinology BES 2017, Harrogate, UK. Endocrine Abstracts 50 PL1) teach that vitamin D deficiency is especially prevalent in Coeliac disease as the intolerance to absorb gluten reduces not only the absorption of calcium, but can also further induce secondary hyperparathyroidism, infertility and a small increased risk of bowel carcinoma and osteoporosis. A cohort of 50 Coeliac patients were tested for vitamin D deficiency at their routine appointment and forty patients were found to be deficient in varying ranges. Twenty were treated with 40,000 IU cholecalciferol daily for 10 days and the remainder where prescribed 20,000 IU to be taken weekly for 12 weeks. The patients bloods were rechecked after 12 weeks, to ensure that they were vitamin D replete and most patients preferred the 40,000 IU over 10-day regime and reported a positive health benefit such as reduced bone pain and lethargy. In addition, Caruso et al. (Annals of Medicine, 2013; 45: 522–531) teaches that Vitamin D and calcium levels normalize and bone mineral density (BMD) significantly improves following 1–2 years of a strict Gluten Free Diet (GFD), however, some Celiac Disease (CD) patients on a GFD, particularly post-menopausal women, exhibit persistently low BMD and in these subsets of patients, long-term vitamin D and calcium supplementation prevents further bone loss and improves BMD (page 527). Caruso further teaches that severe vitamin D deficiency in adults may cause osteomalacia, and there is also evidence that a combination of a GFD and vitamin D supplementation is effective in improving osteomalacia-related symptoms and normalizing calcium levels (page 527). In addition, Duerksen et al. (Journal of Clinical Densitometry, Volume 15, Issue 1, January–March 2012, Pages 120-123) also teaches Low bone mineral density (BMD) and osteoporosis are frequent findings in patients with celiac disease (CD), affecting up to 70% of individuals (page 120). The effects of a gluten-free diet (GFD) have been evaluated in CD patients, and many have shown modest improvements in BMD (page 120). Duerksen et al. describes a case of CD with dramatic BMD improvement with a GFD, calcium, and vitamin D supplementation (page 120). Finally Sgaramella et al. (Abstracts / Digestive and Liver Disease 47S (2015) e237–e27) teaches that supplementation of vitamin D in patients with celiac disease increases vitamin D levels. Sgaramella et al. teaches that children with celiac disease (CD) have low bone mineral content and density at diagnosis and after 12 months, the gluten-free diet (GFD) normalizes bone metabolism and bone mass. However, supplementation with vitamin D can result in increased vitamin D levels in less time which support vitamin D supplementation to treat patients with celiac disease. Thus Applicant’s arguments are found not persuasive since the art as provided for by the references detailed above, supports vitamin D supplementation in patients with CD with the expectation of increasing vitamin D levels despite intestinal malabsorption.
Applicant’s remaining arguments with respect to the Agardh reference and with respect to the Deltius reference for claim 11 are found not persuasive for the same reasons as detailed above. Accordingly, the previous rejections under 35 USC 103 are hereby maintained, however the rejections have been modified upon further search and consideration. This action is NON-final.
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.
Claims 1, 5-8, 10, 17 and 18 are rejected under 35 U.S.C. 103 as being unpatentable over Tavakkoli et al. (J Clin Gastroenterol 2013;47:515–519) in view of Duerksen et al. (Journal of Clinical Densitometry, Volume 15, Issue 1, January–March 2012, Pages 120-123) and Kimball et al. (Dermato-Endocrinology, April 13, 2017, Vol. 9, No. 1, e1300213). The cited claims of the instant application claim a method for treating celiac disease in a subject in need thereof, said method consisting of administering a therapeutically effective amount of cholecalciferol as an active agent to said subject in need thereof, wherein cholecalciferol is in the form of a pharmaceutical composition or food supplement consisting essentially of cholecalciferol and at least one suitable excipient.
Claim 7 of the instant application claims administration of a dose of 0.4 mg/kg/day to 11 mg/kg/day which is equivalent to 1120 IU to 30,800 IU per day in a 70 kg person. Claim 17 of the instant application claims a dose of 0.8 mg/kg/day to 11 mg/kg/day which is equivalent to 2240 IU to 30,800 IU per day in a 70 kg person. Claim 18 of the instant application claims a dose of 4 mg/kg/day to 11 mg/kg/day which is equivalent to 11,200 IU to 30,800 IU per day in a 70 kg person or in a dose of 160 IU/kg/day to 430 IU/kg/day.
Tavakkoli et al. teaches that celiac disease (CD) is an autoimmune disorder induced by the ingestion of gluten in genetically predisposed individuals who carry the HLA-DQ2 or DQ-8 alleles, wherein CD commonly affects the gastrointestinal tract, classically causing diarrhea and malabsorption; in addition, it has multiple extraintestinal manifestations, including iron-deficiency anemia, osteoporosis, and dermatitis herpetiformis (page 515).
Tavakkoli et al. teaches that vitamin D deficiency or insufficiency (commonly defined as levels less than 20 and 20 to 30 mg/dL, respectively) has been estimated to affect up to 80% of the general US population and has been shown to be prevalent across all age groups, both sexes, and multiple geographic locations (page 515). Tavakkoli et al. teaches that common causes of vitamin D deficiency include reduced skin synthesis from skin pigmentation, increased catabolism from medications such as anticonvulsants and antiretroviral therapy, nutritional deficiencies, and malabsorptive disorders including celiac disease (page 515). Tavakkoli et al. teaches that a total of 530 patients were identified who had both celiac disease and a 25-hydroxyvitamin D level on record (Table 1 on page 516). Tavakkoli et al. teaches that among the 530 patients, 133 (25%) were vitamin D deficient and 180 (34%) were vitamin D insufficient (page 516). Tavakkoli et al. further teaches that the degree of villous atrophy was recorded in 191 patients, 36% of the cohort and of these 191 patients, 80 (42%) had Marsh 3C lesions, or total villous atrophy, whereas the remaining 111 patients had lesser degrees of villous atrophy (page 517). Among the 80 patients with total villous atrophy on diagnosis, 16 (20%) had a 25-hydroxyvitamin D level less than 20 mg/dL, as compared with 30 of the 111 (27%) patients with lesser degrees of villous atrophy (P = 0.34). Thus Tavakkoli et al. teaches that this study demonstrates that almost 60% of patients with celiac disease were found to be vitamin D deficient or insufficient (page 517).
Tavakkoli et al. does not teach the administration of vitamin D3 also known as cholecalciferol.
Duerksen et al. teaches vitamin D deficiency is frequently identified in patients with celiac disease (CD) (page 122). Duerksen et al. teaches that individuals who are vitamin D deficient may require large doses of vitamin D to normalize their serum 25(OH) vitamin D levels and in our case, 400 IU of vitamin D3 supplementation was insufficient to normalize these levels (page 122). Duerksen et al. teaches that CD may be associated with osteomalacia and profoundly low bone mineral density (BMD) and that major improvement in BMD occurs with vitamin D supplementation (page 122). Duerksen et al. teaches that serum 25(OH)-vitamin D levels should be measured in all patients with newly diagnosed CD and aggressive supplementation is required in patients with vitamin D deficiency (page 122).
Kimball et al. teaches the amount of vitamin D3 supplementation required to achieve a serum 25(OH)D above 100 nmol/L is on average 5,000 IU/d and 2–3 times more for overweight and obese individuals (page 2). Kimball et al. teaches that Natural levels of 25(OH)D achieved through sun exposure in Maasai herdsman that is in the range of 100–150 nmol/l can also be achieved with oral intake of 5,000–10,000 IU/d (page 2). Kimball et al. teaches that the Endocrine Society Practice Guidelines recommend that up to 10,000 IUs daily was safe for adults (page 2). For an individual with a high body mass index (BMI), doses over 10,000 IU/d may be necessary to achieve a 25(OH)D of at least 100 nmol/L (page 2). Kimball et al. evaluated vitamin D supplementation at intakes up to 15,000 IU/d in a community setting on various parameters of calcium metabolism and potential toxicity (pages 2-3).
Kimball et al. demonstrates the effect of vitamin D supplementation at doses up to 15,000 IU/d in a community-based program on vitamin D status, calcium homeostasis as well as on kidney, liver and immune function (abstract). Kimball et al. teaches that participants were supplemented with a wide range of vitamin D doses (1,000-15,000 IU/d) aimed at achieving serum 25-hydroxyvitamin D [25(OH) D] levels of at least 100 nmol/L wherein serum 25(OH)D concentrations up to 300 nmol/L were achieved without perturbation of calcium homeostasis or incidence of toxicity and hypercalcemia and hypercalciuria were not related to an increase in 25(OH)D concentrations nor vitamin D dose (abstract). Kimball et al. teaches that to achieve serum 25(OH)D levels >100 nmol/L on average, required vitamin D intakes of 6,000 IU/d for normal Body Mass Index (BMI), 7,000 IU/d for overweight and 8,000 IU/d for obese and thus doses of vitamin D in excess of 6,000 IU/d were required to achieve serum 25(OH)D concentrations above 100 nmol/L, especially in individuals who were overweight or obese without any evidence of toxicity.
Kimball et al. teaches that the Endocrine Society concluded that ingestion of up to 10,000 IUs daily was not associated with any significant alteration in calcium metabolism and recommended that circulating levels of 25(OH)D to be at least 75 nmol/L with a preferred range of 100-150 nmol/L for maximum bone and muscle health (page 6). Kimball et al. teaches that the amount of vitamin D required to achieve serum 25(OH)D concentrations of at least 100 nmol/L, particularly in overweight and obese individuals was between 6,000-8,000 IU/d on average and some of the participants were taking as much as 15,000 IUs of vitamin D daily without any untoward toxicity (page 6). Kimball et al. teaches that the Endocrine Society recommended that a blood level of 25(OH)D up to 250 nmol/L was not associated with toxicity and that vitamin D toxicity is usually observed when the blood level is above 375 nmol/L and their data are consistent with this recommendation since some of the participants achieved serum 25(OH)D levels up to 300 nmol/L without any evidence of hypercalciuria or hypercalcemia and there was no significant reduction in the PTH levels in those participants who had the highest intakes of vitamin D and achieved blood levels of 25(OH)D above 250 nmol/L (page 6).
Kimball et al. further teaches that there was a subgroup of participants (n=285) that reported substantial intakes of vitamin D supplements (> 4,000 IU/d) that did not experience an increase in serum 25(OH)D concentrations (page 3). Kimball et al. teaches that conditions that could cause intestinal absorption [including Crohn’s disease, celiac disease, inflammatory bowel disease (IBD), irritable bowel syndrome (IBS), ulcerative colitis, gastrointestinal esophageal reflux disease (GERD)] were present in 38% of these participants, which increased to 60% of the 285 participants when we included whether participants reported stomach issues (including bloating, stomach pain, indigestion, upset stomach) (page 3).
Accordingly, prior to the effective filing date of the claimed invention, it would have been obvious to a person of ordinary skill in the art to combine the teachings of Tavakkoli et al. which demonstrates that a majority of patients with celiac disease are vitamin D deficient or insufficient, with the teachings of Duerksen et al. which also teaches that vitamin D deficiency is frequently identified in patients with celiac disease and that individuals who are vitamin D deficient may require large doses of vitamin D to normalize their serum 25(OH) vitamin D levels and aggressive supplementation is required in patients with vitamin D deficiency, and with the teachings of Kimball et al. which teaches that the recommended circulating levels of 25(OH)D to be at least 75 nmol/L with a preferred range of 100-150 nmol/L for maximum bone and muscle health and that the amount of vitamin D3 required to achieve serum 25(OH)D concentrations of at least 100 nmol/L, particularly in overweight and obese individuals was between 6,000-8,000 IU/d on average and some needing as much as 15,000 IUs of vitamin D daily. Thus, a person of ordinary skill in the art would have been motivated to optimize the daily dosage of vitamin D3 for a subject that is vitamin D deficient or insufficient based on dosages well-known in the art as taught in Kimball et al, that are necessary in order to maintain the recommended levels for maximum bone and muscle health. Since Duerksen et al. teaches that individuals who are vitamin D deficient require large doses of vitamin D to normalize their serum 25(OH) vitamin D levels and aggressive supplementation is required in patients with vitamin D deficiency, and Kimball et al. teaches that in patient with intestinal disorders such as celiac disease, substantial intakes of > 4,000 IU/d vitamin D supplementation did not result in an increase in serum 25(OH)D concentrations, an ordinary skilled artisan would have been motivated to administer higher amount of vitamin D3 since 15,000 IUs of vitamin D daily was not shown to have toxic effects. Thus Kimball et al. teaches and suggests administration of vitamin D3 within the claimed range in order to treat a patient with celiac disease and having vitamin D deficiency or insufficiency in order to achieve and maintain the recommended levels for maximum bone and muscle health.
In the case where the claimed ranges "overlap or lie inside ranges disclosed by the prior art" a prima facie case of obviousness exists. In re Wertheim, 541 F.2d 257, 191 USPQ 90 (CCPA 1976); In re Woodruff, 919 F.2d 1575, 16 USPQ2d 1934 (Fed. Cir. 1990); In re Geisler, 116 F.3d 1465, 1469-71, 43 USPQ2d 1362, 1365-66 (Fed. Cir. 1997).
Therefore, since Tavakkoli et al. in view of Duerksen et al. and Kimball et al. render obvious treating a subject with celiac disease with the same amount of cholecalciferol as claimed, reduction of intestinal villous atrophy and the other effects achieved by administering cholecalciferol to a subject with celiac disease as claimed in claims 5-6 are also rendered obvious. This is because administration of the same compound in the same amount to the same patient will necessarily have the same effects absent a showing to the contrary. "Products of identical chemical composition cannot have mutually exclusive properties." A chemical composition and its properties are inseparable. Therefore, if the prior art teaches the identical chemical structure, the properties applicant discloses and/or claims are necessarily present. In re Spada, 911 F.2d 705,709, 15 USPQ2d 1655, 1658 (Fed. Cir. 1990). Thus, administration of the same cholecalciferol compound in the same amount to the same subject will necessarily result in the reduction of intestinal villous atrophy, protection and regeneration of the intestinal epithelium as claimed.
Thus the cited claims of the instant application are rendered obvious in view of the cited prior art teachings.
Claim 15 is rejected under 35 U.S.C. 103 as being unpatentable over Tavakkoli et al. (J Clin Gastroenterol 2013;47:515–519) in view of Duerksen et al. (Journal of Clinical Densitometry, Volume 15, Issue 1, January–March 2012, Pages 120-123) and Kimball et al. (Dermato-Endocrinology, April 13, 2017, Vol. 9, No. 1, e1300213) and as applied to claims 1, 5-8, 10, 17 and 18 above and further in view of Agardh et al. WO 2018/130667 A1.
Claim 15 of the instant application claims further administering at least one probiotic.
Tavakkoli et al. in view of Duerksen et al. and Kimball et al. is as set forth above.
Tavakkoli et al. in view of Duerksen et al. and Kimball et al. does not teach further administering at least one probiotic.
Agardh et al. teaches that probiotics are useful for the treatment of celiac disease (see abstract).
Accordingly, prior to the effective filing date of the claimed invention, it would have been obvious to a person of ordinary skill in the art to combine the teachings of Tavakkoli et al. in view of Duerksen et al. and Kimball et al. which render obvious treating a subject having celiac disease comprising the administration of cholecalciferol with the teachings of Agardh et al. with teaches that probiotics are also useful in the treatment of celiac disease. Thus a person of ordinary skill in the art would have been motivated to combine probiotics with the vitamin D3 supplement with a reasonable expectation of improved success in treating celiac disease.
"It is prima facie obvious to combine two compositions each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose ....[T]he idea of combining them flows logically from their having been individually taught in the prior art." In re Kerkhoven, 626 F.2d 846, 850,205 USPQ 1069, 1072 (CCPA 1980).
Thus claim 15 of the instant application is rendered obvious in view of the cited prior art teachings.
Claim 11 is rejected under 35 U.S.C. 103 as being unpatentable over Tavakkoli et al. (J Clin Gastroenterol 2013;47:515–519) in view of Duerksen et al. (Journal of Clinical Densitometry, Volume 15, Issue 1, January–March 2012, Pages 120-123) and Kimball et al. (Dermato-Endocrinology, April 13, 2017, Vol. 9, No. 1, e1300213) as applied to claims 1, 5-8, 10, 17 and 18 above and further in view of Deltius (10,000 IU/ml oral drops solution of cholecalciferol (vitamin D3) Package leaflet, November 2014).
Claim 11 of the instant application claims the pharmaceutical composition or food supplement is in the form of a solution, suspension, gel emulsion or tincture and comprises cholecalciferol in a concentration of 10,000 IU/ml to 20,000 IU/ml.
Tavakkoli et al. in view of Duerksen et al. and Kimball et al. is as set forth above.
Tavakkoli et al. in view of Duerksen et al. and Kimball et al. does not teach the pharmaceutical composition or food supplement is in the form of a solution, suspension, gel emulsion or tincture and comprises cholecalciferol in a concentration of 10,000 IU/ml to 20,000 IU/ml.
Deltius teaches that prior to the effective filing date of the claimed invention, a suitable form of Cholecalciferol (vitamin D3) was available as a 10,000 I.U. /ml oral drops, solution (title). DELTIUS oral drops are used to prevent vitamin D3 deficiency in children and adults with problems in absorbing food (malabsorption) defined by doctor (page 1).
Accordingly, prior to the effective filing date of the claimed invention, it would have been obvious to a person of ordinary skill in the art to combine the teachings of Tavakkoli et al. in view of Duerksen et al. and Kimball et al. which render obvious treating a subject having celiac disease comprising the administration of cholecalciferol with the teachings of Deltius which teaches that prior to the effective filing date of the claimed invention, a suitable form of Cholecalciferol (vitamin D3) was available as a 10,000 I.U. /ml oral drops, solution used to prevent and treat vitamin D3 deficiency in children and adults with problems in absorbing food (malabsorption) defined by doctor (page 1). Thus a person of ordinary skill in the art would have been motivated to administer the Cholecalciferol oral drops, solution as a suitable form to a patient with celiac disease and thus having malabsorption, with a reasonable expectation of similar or improved results as compared to other oral dosage forms.
Thus claim 11 of the instant application is rendered obvious in view of the prior art teachings.
Conclusion
Claims 1, 5-8, 10, 11, 15, 17 and 18 are rejected. Claims 2-4, 9, 12-14 and 16 are canceled. No claims are allowed.
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/KARA R. MCMILLIAN/Primary Examiner, Art Unit 1623
KRM
