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 .
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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 11 May 2026 has been entered.
Claim 1 has undergone amendments. Claims 2, 3, 6, and 7 have been cancelled. Claim 14 is newly added. Thus, Claims 1, 4, 5, 9, 10, and 12-14, submitted 11 May 2026, represent all claims currently under consideration.
Response to Arguments
The 35 U.S.C. § 103 rejections of Claim 1-4, 9, and 13 over Bishop, Claims 1-4, 9 and 13 over Bishop in view of Chen and Wagner, and Claims 5-7 and 10-13 over Bishop in view of Chen, Wagner, and Xv are each withdrawn. Applicant argues that Bishop provides no specific motivation to select a combination of cholecalciferol, calcidiol, and calcitriol for the treatment of cancers, and specifically, non-melanoma skin cancer, and rather suggests combinations of any vitamin D analogue. This is very broad, and Bishop does not provide any particular motivation to select these three compounds. The Examiner finds these arguments to be persuasive.
Specification
The spacing of the lines of the specification is such as to make reading difficult. New application papers with lines 1 1/2 or double spaced (see 37 CFR 1.52(b)(2)) on good quality paper are required.
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 4, 9, 10, and 12-13 are rejected under 35 U.S.C. 101 because the claimed invention is directed to non-statutory subject matter. The claims do not fall within at least one of the four categories of patent eligible subject matter because the claimed invention is directed to a natural product (a pharmaceutical composition of vitamin D3 and metabolites with magnesium and vitamin K) without significantly more. The claims recite a pharmaceutical composition with an intended use (for treating cancer) comprising an effective amount of cholecalciferol, calcidiol, calcitriol, magnesium, and vitamin K2. Cholecalciferol is a natural product, which can be found in a variety of food products, and calcidiol and calcitriol are natural metabolites of cholecalciferol. Magnesium and vitamin K2 are both natural products as well which are found in a variety of food products. Thus, each of these components are natural products. The judicial exception is not integrated into a practical application because there is no indication that formulating these compounds have any characteristics that are different from the naturally occurring compounds. The claims do not impart any characteristics that are different from each of the individual naturally occurring compounds. The claims do not include additional elements that are sufficient to amount to significantly more than the judicial exception because the claimed compositions are not markedly different from their closest naturally occurring counterparts and thus are product of nature judicial exceptions. The claims do not include additional elements that are sufficient to amount to significantly more than the judicial exception because the claims do not recite any additional elements beyond the compositions themselves. Therefore, the claims do not recite something significantly more than a judicial exception and thus are deemed patent ineligible subject matter.
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, 5, and 14 are 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 treatment of non-melanoma skin cancers or other forms of cancer in which the vitamin D receptor is implicated, does not reasonably provide enablement for the treatment of all forms of cancer. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to practice the invention commensurate in scope with these claims. Consideration of the relevant factors sufficient to establish a prima facie case for lack of enablement is set forth below:
The nature of the invention and breadth of the claims:
The claims are directed towards a method of treating cancer, comprising administering to a patient in need a therapeutically effective amount of cholecalciferol, calcidiol, and/or calcitriol to a patient in need thereof. Thus, the claims are directed to a method which can be used to treat all forms of cancer using vitamin D3 and its metabolites.
The state of the prior art and the predictability or unpredictability of the art:
Trump (Cancer J. 2010; 16(1): 1-9) provides a review of the use of vitamin D in the treatment of cancers. Many preclinical studies indicate that exposing cancer cells to high concentrations of active metabolites of vitamin D halts progression through the cell cycle, induces apoptosis, and will slow or stop the growth of tumors in vivo. However, there are no data that one type of cancer is more or less susceptible to the effects of vitamin D. In view of the substantial preclinical and epidemiologic data supporting the potential role of vitamin D in cancer, careful studies to evaluate the impact of vitamin D replacement on the frequency of cancer and the impact of appropriate dose and schedule of calcitriol or other active vitamin D analogues on the treatment of established cancer are indicated (Abstract). In model systems of murine squamous cell carcinoma, and human carcinomas arising in the prostate, lung, ovary, breast, bladder, pancreas, as well as neuroblastoma, calcitriol or calcitriol analogues have significant anti-cancer effects. Calcitriol and its derivatives act through the vitamin D receptor to regulate differentiation, proliferation, apoptosis, and angiogenesis. (Antitumor Activity of Vitamin D).
However, not all cancers can be successfully treated in this manner, and there is currently no known treatment that can be used to treat all forms of cancer. Conquer Cancer (https://web.archive.org/web/20260507071106/https://www.conquer.org/news/why-havent-we-conquered-cancer-yet-understanding-complexities-curing-cancer) provides an overview of why there has not been a single treatment which can be used for all forms of cancer. Mutations which cause cancer are not the same in every body, and differ from person to person and even within the same tumor. This diversity makes developing a single, universal cure for cancer nearly impossible. Cancer cells are adaptable, allowing them to resist treatment, spread through the body and evolve. The biggest challenges to curing cancer include that it is not a single disease. It is hundreds of diseases. Each type of cancer behaves differently, responds to treatments differently, and requires unique approaches. Even within one cancer type, there can be multiple subtypes. Breast cancer includes HER-2 positive. HR-positive, and triple-negative subtypes, each requiring a tailored treatment strategy. Cancer is influenced by both genetics and the environment. Mutations can occur due to inherited genes, lifestyle choices, or exposure to carcinogens. Because there is no single cause, treatment requires multifaceted solutions. Cancer cells can adapt to survive even the most aggressive therapies, forcing reserachers to continually explore innovative treatments. A significant barrier to curing cancer is metastasis. Once a cancer becomes metastatic, it is far more difficult to treat. Cancer’s diversity is the most formidable obstacle in finding a single cure. Even within an individual patient’s tumor, there can be immense differences in cells, called tumor heterogeneity.
The relative skill of those in the art:
The artisan would generally have an advanced degree related to the treatment or study of various cancers; however, their high level of training and knowledge would not be sufficient to overcome the lack of understanding of how to use the claimed compounds to treat all forms of cancer, as there is no support in the current state of oncology for a panacea that can be used to treat all forms of cancer.
The amount of direction or guidance presented and the presence or absence of working examples:
The only working examples of the treatment of any form of cancer is a single sentence, which states that 12 non-melanoma skin cancers were resolved through oral intake of vitamin D3 at a moderate daily dose (Page 8). Thus, the specification enables the treatment of non-melanoma skin cancer. The specification references the inhibition of pancreatic cancer cells in vitro, as well as the inhibition of human melanoma cells (Page 7). Thus, the specification enables the treatment of these forms of cancer. However, there is no further data demonstrating the treatment of all forms of cancer, and there is no indication in the current state of oncology that a single therapeutic agent can be used to treat each and every form of cancer.
The quantity of experimentation necessary:
Considering the state of the art as described above, in particular with regards to the lack of a panacea for the treatment of cancer due to the heterogenous nature of the disease, and the high unpredictability of the art as evidenced therein, and the lack of guidance provided in the specification, one of ordinary skill in the art would be burdened with undue experimentation to practice the invention commensurate with the scope of the claims.
Claim Rejections - 35 USC § 102
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Claims 4 and 13 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Sherman (WO 2014/197680; Publication Date: 11 December 2014).
Sherman methods of treating and preventing pancreatitis by administration of a vitamin D receptor agonist (such as vitamin D, vitamin D analogs, vitamin D precursors, and vitamin D receptor agonist precursors) (Abstract). This application relates to methods of treating or preventing diseases, such as pancreatitis and cancers in which there is activation of juxtaposed stellate cells by administration of one or more vitamin D receptor (VDR) agonists (Page 1, Lines 15-17). The disclosure provides methods for treating a cancer, such as cancer of the pancreas, liver, kidney, lung, bile duct, or prostate (Page 3, Lines 28-30). The specification defines vitamin D as a group of fat-soluble secosteroid prohormones, the two major forms of which are ergocalciferol and cholecalciferol, which are converted to calcitriol, the physiologically active form of vitamin D. Vitamin D agonist or analogs are any compound that binds to and activates the vitamin D receptor such as a VDR ligand (e.g., calcitriol), VDR agonist precursor, vitamin D analog, and vitamin D precursor. Specific non-limiting examples of vitamin D precursors include vitamin D3 (cholecalciferol) and calcidiol (Page 14, Lines 6-30). Provided herein are methods of using a therapeutically effective amount of one or more VDR agonists (including calcitriol or a precursor analog thereof) for the treatment of pancreatitis (Page 20, Lines 4-7). In one embodiment, precursors of calcitriol (such as calcidiol) are administered to a subject, and are then converted within the target cell population to calcitriol. This approach has the advantage that the local intestinal as well as the systemic effects of calcitriol on calcium homeostasis can be significantly avoided, even when large doses of the precursors are administered (Page 23, Lines 15-18). The disclosed methods of treating cancer include administering one or more VDR agonists, such as calcitriol, vitamin D precursors (for instance, calcidiol, cholecalciferol, or vitamin D2) to a subject in a pharmaceutically acceptable carrier. The present disclosure contemplates the administration of a therapeutic composition comprising more than one VDR agonist. The vehicle in which the VDR agonist is delivered can include pharmaceutically acceptable compositions of the compounds, using methods well known to those with skill in the art (Page 25, Lines 5-15). Claim 16 claims the use of a VDR agonist selected from vitamin D, vitamin D precursor, vitamin D analog, a vitamin D receptor ligand, a vitamin D receptor agonist precursor, or combinations thereof. Claim 17 claims the method of claim 16 wherein the vitamin D precursor is calcidiol, cholecalciferol, ergocalciferol, or combinations thereof. Claim 18 claims the method of claim 16 wherein the vitamin D receptor ligand is calcitriol. Claim 21 is drawn to the method of any of the previous claims wherein administering the one or more VDR agonists comprises oral, intraperitoneal, or intravenous administration of the one or more VDR agonists.
Sherman directly claims a composition comprising calcidiol, cholecalciferol, ergocalciferol, or combinations thereof. Claims 4 and 13 are written as a composition with an intended use (the treatment of cancer, specifically, non-melanoma skin cancer). As Sherman teaches these compositions, and further claims their use in methods in the treatment of cancer, this renders Claims 4 and 13 as anticipated as the intended use of the claimed invention does not result in a structural difference between the claimed invention and the prior art (See MPSP § 2112.02 (II)).
Claim Rejections - 35 USC § 103
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Claims 4, 9-10, and 12-13 are rejected under 35 U.S.C. 103 as being unpatentable over Sherman (WO 2014/197680; Publication Date: 11 December 2014) in view of Uwitonze (Journal of the American Osteopathic Association, March 2018, Vol. 118, No. 3) and Xv (Oncology Letters, 15, 8926-8934, 2018).
The teachings of Sherman are described previously and are fully incorporated into this rejection.
Uwitonze teaches the role of magnesium in ensuring the biological activity of vitamin D. Magnesium assists in the activation of vitamin D. All of the enzymes that metabolize vitamin D require magnesium, which acts as a cofactor in the enzymatic reactions in the liver and kidneys. It is therefore essential to ensure that the recommended amount of magnesium is consumed to obtain the optimal benefits of vitamin D (Abstract). Vitamin D, either D3 or D2, does not have significant biological activity. It needs to be processed further in the liver and kidneys to generate its biologically active forms. The enzymatic activity of both the hepatic and renal enzymes are magnesium dependent. The activity of vitamin D-binding protein is also a magnesium dependent process (Page 184). The potential associations of serum 25(OH)D with mortality, particularly due to cardiovascular disease and colorectal cancer were found to be modified by magnesium ingestion (Page 185). Magnesium potentiates vitamin D activities, possibly by increasing its absorption and endogenous activation (Page 186). Studies have shown that magnesium supplementation can increase the effectiveness of vitamin D activity (Page 186).
Xv provides an overview of the use of Vitamin K2 in the treatment of cancer. Vitamin K2 (VK2) exerts anticancer effects on a number of cancer cell lines, and is considered to be a prospective novel agent for the treatment of cancer. The combination of VK2 and established chemotherapeutics may achieve better results with fewer side effects (Abstract). Previous reports have demonstrated that VK2 can inhibit several neoplastic cell lines at different levels by inducing apoptosis and cell cycle arrest of cancer cells. Hence VK2 is a potential chemotherapeutic candidate for the treatment of cancer (Introduction). Vitamin D3 is another micronutrient capable of restricting the growth of cancer cells by inhibiting proliferation and stimulating differentiation. However, an adverse effects of vitamin D3 treatment is hypercalcemia, which can lead to vascular calcification. VK2 regulates the calcium deposition between bone tissue and other tissue, and inhibits the formation of vascular calcified foci. The combination of vitamin D3 with VK2 on cancer cells can synergistically improve the reduction of cellular differentiation and also significantly reduces the risk of hypercalcemia and vascular calcification (Synergistic Effect of VK2 in combination with other chemotherapeutics, Page 8931). VK2 can positively inhibit cancer cells, and appears to be an extremely promising agent with limited toxicity with can be a useful option for the clinical therapy of cancer (Page 8932).
Sherman, Uwitzone, and Xv are considered analogous to the claimed invention as all are involved in the use of vitamin D as a therapeutic agent. Therefore, it would have been prima facie obvious to one of ordinary skill in the art the time of the effective filing date of the instant application to modify the composition of Sherman which contains cholecalciferol and calcidiol to include both magnesium and vitamin K2. Sherman states that cholecalciferol and calcidiol function as “pro-drugs”, and are converted in the body to the active form of vitamin D, calcitriol. The enzymes required for this metabolic conversion require magnesium, as taught by Uwitzone. Thus, it is known in the art that magnesium is useful for enhancing the transformation of cholecalciferol and/or calcidiol into its biologically active form, calcitriol. Xv indicates that vitamin K2 is known to be an anticancer agent, and states that the combination with Vitamin D3 may not only enhance anticancer properties of each component, but can also help to reduce hypercalcemia which is brought about by high doses of vitamin D3. Sherman states that administration of calcitriol can impact calcium homeostasis, and thus, incorporating vitamin K2 can help to mitigate this. The combination of these teachings is prima facie obvious use of a known technique to improve similar products in the same way (See MPEP § 2143 (C)), wherein the known product is an oral or injectable formulation of vitamin D, calcidiol, and calcitriol, with added magnesium and vitamin K, which, as Uwitzone and Xv teach, will allow for higher doses of the compounds to be delivered safely. Further, as vitamin K2 is known to be an anticancer agent, and has been shown to work synergistically with Vitamin D3, it would be prima facie obvious to one of ordinary skill in the art to combine these agents which individually are known to be useful for the treatment of cancer, to form a third composition for the treatment of cancer (See MPEP § 2144.06 I).
Regarding the incorporation of calcitriol into the composition, Sherman states that compositions can include calcitriol, and further indicates that this is the pharmacologically active ingredient as this has the highest affinity for the VDR. Thus, it would be obvious to include all three forms (cholecalciferol, calcidiol, and calcitriol) in a single formulation to have form of extended release of calcitriol, allowing for an extended period of time where the active ingredient is at a therapeutically effective concentration within the body. The artisan would understand that the body converts cholecalciferol into calcidiol, which is then converted into the active calcitriol, at a consistent rate, and this would allow for a longer time period between administration of doses to the patient.
Claims 1, 4, 5, 9, 10, and 12-14 are rejected under 35 U.S.C. 103 as being unpatentable over Albert (Chapter 18 of Sunlight, Vitamin D and Skin Cancer, Second Edition, 2014, Interaction of Hedgehog and Vitamin D Signaling Pathways in Basal Cell Carcinomas) in view of Uhmann (Molecular Medicine in Practice, Volume 10, Issue 11, 1 November 2011), Trump (Cancer J. 2010; 16(1): 1-9), Uwitonze (Journal of the American Osteopathic Association, March 2018, Vol. 118, No. 3) and Xv (Oncology Letters, 15, 8926-8934, 2018).
Albert provides an overview of vitamin D in basal cell carcinoma (a form of non-melanoma skin cancer). Most basal cell carcinomas are caused by mutational inactivation of the tumor suppressor Patched (PTCH), which results in activation of Smoothened (SMO) and of the Hedgehog (HH) signaling pathways. Recent studies indicate that BCC progression involves a crosstalk between Hh signaling, vitamin D derivatives and the vitamin D receptor (VDR) signaling pathway. This has been demonstrated in BCC-bearing Ptch mutant mice and BCC cell lines, in which both vitamin D3 and its active metabolite calcitriol exert antitumor effects. The antitumor effects are mainly ascribed to an inhibition of Hh signaling. As evident from studies in Vdr deficient mice, calcitriol may also repress the activity of Hh signaling in a Vdr-dependent fashion thereby establishing an additional inhibitory feedback on Hh signaling activity (Abstract). Vitamin D3 is synthesized in keratinocytes, or comes from dietary sources. It is then transported in the blood to the liver, where it is hydroxylated to form calcidiol, which is then transported to the kidney and is hydroxylated to the hormonally active calcitriol, which binds to and activates the VDR in many tissues. The amount of calcidiol and calcitriol is limited by the enzyme 24-hydroxylase. Therefore, 24-hydroxylase limits the amount of calcitriol by both accelerating catabolism of calcitriol and by decreasing the amount of calcidiol available for calcitriol synthesis. The concentrations of calcitriol are regulated by several feedback loops. Furthermore, calcitriol (through binding of the VDR) represses the transcription of Cyp27b1, which results in inhibition of its own production. Calcitriol enhances VDR expression at the mRNA and protein levels, due to an increased transcription of the VDR gene and/or an increased receptor protein lifetime. In the skin, calcitriol has been shown to inhibit proliferation of keratinocytes by changing the expression of cell cycle regulators, and to induce differentiation markers. Data has shown that Vdr deficiency increases the susceptibility to BCCs. (Vitamin D Signaling in BCCs, Page 332-333). Anti-Hh effects of Vitamin D3 and calcitriol were also reported by Banerjee and colleagues, who conducted a structure-activity relationship survey to elucidate the role of Vitamin D3 derivatives in Hh pathway inhibition. The experiments showed that calcitriol as well as vitamin D3 and calcidiol inhibited Hh signaling, and that calcitriol was more potent than vitamin D3 (Page 337, first paragraph). Both vitamin D3 and its hormonally active form calcitriol inhibit Hh signaling probably by a direct interaction with Smo, which is followed by restrained BCC growth. Calcitriol activates Vdr signaling in BCC cells, further intensifying anti-Hh activity due to suppression of protein levels of several Hh pathway members. These findings have important implications for BCC therapy. Because vitamin D has relatively moderate side effects and is tolerated quite well, it could be a new option for treatment of BCCs (Conclusion).
Uhmann studied the activation of the Hedgehog (Hh)-signaling pathway due to deficiency in the Hh receptor Patched1 (Ptch) is the pivotal defect leading to formation of basal cell carcinoma (BCC). Recent reports provided evidence of Ptch-dependent secretion of vitamin D3-related compounds, which functions as endogenous inhibitor of Hh signaling by repressing the activity of the signal transduction partner of Ptch, Smoothened (Smo). This suggests that Ptch-deficient tumor cells are devoid of this substance, which in turn results in activation of Hh-signaling. The authors show that application of the physiologically active form of vitamin D3, calcitriol, inhibits proliferation and growth of BCC of Ptch mutant mice in vitro and in vivo. This is accompanied by the activation of the vitamin D receptor and induction of BCC differentiation. Calcitriol inhibits Hh signaling at the level of Smo in a Vdr-independent manner. The concomitant antiproliferative effects on BCC growth are stronger than those of the Hh-specific inhibitor cyclopamine. Taken together, the results show that exogenous supply of calcitriol controls the activity of 2 independent pathways, Hh and Vdr signaling, which are relevant to tumorigenesis and tumor treatment. The data suggest that calcitriol could be a therapeutic option in the treatment of BCC, the most common tumor in humans (Abstract).
Trump provides a review of vitamin D in the treatment of cancer. Many preclinical studies indicate that exposing cancer cells- as well as vascular endothelial cells derived from tumors- to high concentrations of active metabolites of vitamin D halts progression through cell cycle, induces apoptosis, and will slow or stop the growth of tumors in vivo. Vitamin D analogues initiate signaling through a number of important pathways, but the pathways essential to the antitumor activities of vitamin D are unclear. Clinical studies of vitamin D as an anti-tumor agent have been hampered by lack of a suitable pharmaceutical preparation for clinical study. All commercially available formulations are inadequate because of the necessity to administer large numbers of caplets and the poor bioavailability of calcitriol (the most carefully studied analogue) at these high doses. Preclinical data suggests that very high exposures to calcitriol are necessary for the antitumor effects. Clinical data indicates that very high doses of calcitriol can be given safely. The maximum tolerated dose of calcitriol is unclear (Abstract).
Albert, Uhmann, and Trump fail to teach the use of Vitamin K2 or magnesium in combination with cholecalciferol, calcidiol, and calcitriol.
The teachings of Uwitonze and Xv are previously described and are fully incorporated into this rejection.
Albert, Uhmann, Trump, Uwitonze, and Xv are considered analogous to the claimed invention as all are involved in the use of vitamin D in the treatment of disease. Therefore, it would have been prima facie obvious to one of ordinary skill in the art the time of the effective filing date of the instant application to utilize cholecalciferol, calcidiol, and calcitriol, in combination with vitamin K2 and magnesium, for the treatment of basal cell carcinoma as Albert and Uhmann demonstrate that it is known in the art that each of cholecalciferol, calcidiol, and calcitriol display anti-cancer properties in BCC and act through a known receptor pathway known to inhibit the growth of this cancer. Trump further states that a limiting factor for the use of calcitriol, which is the most potent form of vitamin D, is its low bioavailability. It is known that cholecalciferol and calcidiol are precursors to the active calcitriol, and require metabolism via enzymes. Uwitonze states that these enzymes require magnesium. Thus, it would be obvious to further incorporate magnesium to ensure that the conversion of the pro-drug forms of calcitriol is not limited by enzyme saturation or lack of co-factors. Further, it is known that there is some risk of impact to calcium homeostasis with high doses of calcitriol. Xv establishes that Vitamin K2 is both beneficial for regulating this calcium homeostasis, and states that it may work synergistically with vitamin D in the treatment of cancer. In view of these teachings, it would be prima facie obvious to one of ordinary skill in the art to combine these agents which individually are known to be useful for the treatment of cancer, to form a third composition for the treatment of cancer (See MPEP § 2144.06 I).
Regarding Claim 14, Albert states that each form of vitamin D (cholecalciferol, calcidiol, and calcitriol) are effective at inhibiting Hh signaling, and thus would be effective at treating BCC. Thus, it would be obvious to utilize cholecalciferol on its own for the treatment of BCC as the artisan would recognize that on its own it is effective for inhibiting these pathways, and would also understand that following metabolism, it would be converted into forms which are known to have more potency in inhibiting these pathways.
Regarding Claims 4, 9-10, and 12-13, it would be obvious to generate a pharmaceutical composition comprising these ingredients in order to improve patient compliance by making dosing easier for the patient, ensuring consistent delivery of each therapeutic. Pharmaceutical formulation is also known in the art to enhance the delivery of the therapeutic, improving properties such as solubility, absorption, and bioavailability.
Conclusion
Claims 1, 4, 5, 9, 10, and 12-14 are rejected.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to PHILLIP MATTHEW RZECZYCKI whose telephone number is (703)756-5326. The examiner can normally be reached Monday Thru Friday 730AM-5PM EST.
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Andrew Kosar can be reached at 571-272-0913. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
/P.M.R./Examiner, Art Unit 1625 /Andrew D Kosar/Supervisory Patent Examiner, Art Unit 1625
Prosecution Insights