DETAILED ACTION
Notice of Pre-AIA or AIA Status
1. 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
2. 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 on January 13, 2026, 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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 November 12, 2025 has been entered.
Claim Status
3. Applicant’s correspondence filed November 12, 2025 is acknowledged; claim 1 has been amended to recite species “MST1 protein.” Claim 13 was amended for clarity and claims 35-44 have been canceled. Claims 1, 12-13, and 33-34 are pending examination and currently under consideration for patentability.
Maintained Rejection
Claim Rejections - 35 USC § 112
4. 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.
Enablement
5. Claims 1, 12-13 and 33-34 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the enablement requirement. The claims contain subject matter which was not described in the specification in such a way as to enable one skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention.
The enablement rejection of record has been modified below to address the instant agonist species comprising genus “MST1 protein” and repeated below for convenience:
Factors to be considered in determining whether a disclosure enables one skilled in the art to make and use the claimed invention in its full scope without resorting to undue experimentation 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 or complexity 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. See In re Wands, 8 USPQ2d. 1400 (Fed. Cir. 1988).
In the instant case, the nature of the invention is complex and unpredictable, involving the effects of biological molecules on an individual having diseased physiology. As was found in Ex parte Hitzeman, 9 USPQ2d 1821 (BPAI 1987), a single embodiment may provide broad enablement in cases involving predictable factors such as mechanical or electrical elements, but more will be required in cases that involve unpredictable factors such as most chemical reactions and physiological activity. This invention is in a class of invention which the CAFC has characterized as "the unpredictable arts such as chemistry and biology", Mycogen Plant Sci., Inc. V. Monsanto Co., 243 F.3d 1316, 1330 (Fed. Cir. 2001). See also In re Fisher, 427 F.2d 833, 839, 166 USPQ 18, 24 (CCPA 1970); Amgen Inc. V. Chugai Pharmaceutical Co. Ltd., 927 F.2d 1200, 1212, 18 USPQ2d 1016, 1026 (Fed. Cir.), cert. denied, 502 U.S. 856 (1991).
Specifically, the claimed invention is broadly directed to a method of treating a patient having inflammatory bowel disease (IBD) or primary sclerosing cholangitis (PSC), the method comprising administering to the patient an agonist of the Macrophage Stimulating 1 (MST1)/Macrophage Stimulating 1 Receptor (MST1R) pathway. The remaining species recited in the claims is agonist comprising “MST1 protein.” Dependent claims recite additional method steps of detecting the presence or absence of an MST1 and/or MST1R variant nucleic acid molecule or variant polypeptide associated with an increased risk of developing IBD and/or PSC. The claims are broad with respect to the agent being administered (agonist comprising genus “MST1 protein” with no additional structural limitations, which encompasses myriad MST1 fusion proteins having no support in the specification).
Conversely, the amount of detailed guidance and working examples provided by the application is decidedly narrower. The specification only demonstrates overexpression of MST1 by hydrodynamic delivery of expression construct comprising wild-type MST1 cDNA (i.e., Example 6), which is not equivalent to administering the protein directly as instantly claimed. However, the source of this agonist is not provided, nor are structures thereof other than wild-type MST1 (i.e., SEQ ID NO: 35). Accordingly, the ordinary skilled artisan is not taught how to make and use them within the entire scope of the claimed methods.
Furthermore, none of the potential therapeutic agents were tested for therapeutic activity in a patient, animal model, or in vitro. Six MST1R variants were shown to be associated with Crohn's Disease (a type of IBD) in Table 3. A prophetic example is provided about generating a mouse model of IBD wherein MST1R is knocked out (Example 2). However, the model was not generated and evaluated critically as a good or bad model of IBD. Also, no potential drugs were tested in the model. Example 3 provides data regarding two MST1 variants (rs3197999 and 3:49684379:G:A) that are been associated with increased risk of IBD and PSC, as well as reduced serum levels or activity of MST1. (Mutation rs3197999 is disclosed as being linked to IBD in Goyette et al., 2008, Mucosal Immunology 1(2):131-138; of record). Example 4 shows that induction of colitis in mice via administration of DSS resulted in increased expression of MST1 and MST1R. Human IBD, Crohn's, UC, and FGID subjects also had increased serum levels of MST1 and/or MST1R. Example 5 discloses generation of a variant MST1R construct. Example 6 postulates that increased MST1/MST1R signaling is protective and/or promotes tissue repair in IBD and PSC. The example discloses expression of WT and variant MST1 constructs in normal mice. Again, no effect on IBD and/or PSC was demonstrated.
The state of the art establishes that a correlation between altered expression or function of a protein (or its encoding gene) and a disease state may be of interest diagnostically, but does not automatically or predictably indicate that treatment with an agonist or antagonist of the altered protein (or gene encoding such) would be beneficial. Specifically, markers can be elevated as a result of the disease, or as part of a body's response to a disease, and cannot be presumed to be causative or contributory to the disease without significant further research. For example, with respect to G-protein coupled receptor perturbations in the disease hypertension, "it has been difficult to determine whether they are the cause or consequence of the disease" (Feldman, 2002, Molecular Pharmacology. 61(4): 707-709; of record). With respect to temporal lobe epilepsy, Janigro (2008, Epilepsy Currents 8(1): 23-24) teaches that "[a]s with many pathological findings in neurodegenerative diseases, it is difficult to determine if the changes are a cause or consequence of epileptic seizures" (p. 23). The literature also speaks to GDF15 levels and cardiac disease, For example, Kempf et al. (2007, Clin. Chem. 53:284-291; of record) and Kempf et al. (2006, Cir. Res. 98:351-360; of record) show a correlation between elevated that GDF-15 levels and adverse cardiovascular events. Such may suggest that treatment with anti-GDF-15 would be beneficial to patients, as was postulated by US 7,919,084 (Breit et al., issued 05 April 2011; of record). However, it was also hypothesized that GDF-15 expression was elevated in response to the cardiovascular event as a way for the body to attempt to protect its tissues from ischemia/reperfusion injury, and data in support of this hypothesis were sound. See Xu et al. (2006, Circ. Res. 98:342-350); Tobin et al. (2006, Drug Discovery Today 11:405-411; of record); and Lajer et al. (2010, Diabetes Care 33:1567-1572; of record). In light of the contradictory findings in the prior art, the therapeutic effects of administering a MST1 or MST1R agonist to a subject—let alone genus “MST1 protein”—could not have been predicted without significant further research amounting to an act of further invention. Accordingly, discovery of a correlation alone is not enabling for a method of treatment.
Additionally, regarding the remaining recited therapeutic agent, the scientific literature provides evidence that significant optimization and undue experimentation is required to create an effective therapeutic “protein” as instantly claimed. For example, Binder et al. ("Strategies for extending the half-life of biotherapeutics: successes and complications." Expert Opinion on Biological Therapy 25.1 (2025): 93-118) shows that therapeutic proteins are often rapidly cleared from the subject’s body, and so additional modifications to the protein, requiring substantial trial and error to perfect, are typically required to generate a workable protein therapeutic. Goswami et al. ("Gene therapy leaves a vicious cycle." Frontiers in oncology 9 (2019): 297) summarizes the undue experimentation required well: “more than 5,000 critical steps are involved in developing a single therapeutic protein. Therefore, the quotient of unpredictability is very high in developing both chemical and protein-based therapies. Gene therapy, on the other hand, leads to long-lasting production of the desired therapeutic protein and can localize protein expression to an area of the body, fixing the problem at its source.” Goswami et al. at introduction.
Due to the large quantity of experimentation necessary to determine how to achieve a desired therapeutic effect on IBD and/or PSC via administration of a MST1 and/or MST1R agonist comprising “MST1 protein,” the lack of direction/guidance presented in the specification regarding the same, the absence of working examples directed to the same, the complex nature of the invention, the state of the prior art establishing the unpredictability of the effects of a drug targeted to a marker of a disease, and the breadth of the claims, undue experimentation would be required of the skilled artisan to make and/or use the claimed invention.
Applicant’s Arguments:
With the claim amendments of November 12, 2025, introducing species “MST1 protein,” Applicant argued that: “There is no reason to believe that one skilled in the art would be required to perform undue experimentation to treat IBD and/or PSC in a patient that is heterozygous or homozygous for an MST1 and/or MST1R variant nucleic acid molecule associated with an increased risk of developing IBD and/or PSC, and the patient is treated with an MST1 protein.”
Response to Arguments:
Applicant’s arguments have been carefully considered but are not persuasive. Specifically, the substantive issues raised in the 35 USC § 112(a) rejection of record are applicable to species “MST1 protein” and have not been addressed by Applicant. Therefore, the rejection under 112(a) is maintained.
New Rejections Necessitated by Amendment
Claim Rejections - 35 USC § 112
6. 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.
Written Description
7. Claims 1, 12-13, and 33-34 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claims contain subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
The MPEP states that the purpose of the written description requirement is to ensure that the inventor had possession, as of the filing date of the application, of the specific subject matter later claimed. The MPEP lists factors that can be used to determine if sufficient evidence of possession has been furnished in the disclosure of the application. These include “level of skill and knowledge in the art, partial structure, physical and/or chemical properties, functional characteristics alone or coupled with a known or disclosed correlation between structure and function, and the method of making the claimed invention.”
The written description requirement for a claimed genus may be satisfied through sufficient description of a representative number of species by actual reduction to practice, disclosure of drawings, or by disclosure of relevant identifying characteristics, for example, structure or other physical and/or chemical properties, by functional characteristics coupled with a known or disclosed correlation between function and structure, or by a combination of such identifying characteristics, sufficient to show the Applicants were in possession of the claimed genus.
Vas-Cath Inc. v. Mahurkar, 19 USPQ2d 1111, makes clear that:
"applicant must convey with reasonable clarity to those skilled in the art that, as of the filing date sought, he or she was in possession of the invention. The invention is, for purposes of the 'written description' inquiry, whatever is now claimed." (See page 1117.) The specification does not "clearly allow persons of ordinary skill in the art to recognize that [he or she] invented what is claimed." (See Vas-Cath at page 1116.)
The claims are drawn to methods of treating a patient having IBD or PSC comprising administering a MST1/MST1R pathway agonist comprising “MST1 protein,” wherein the patient has a MST1 and/or MST1R variant associated with increased risk of developing IBD and/or PSC. The dependent claims recite various MST1 and MST1R variants related to IBD and/or PSC.
The claimed agonist comprising genus “MST1 protein” must possess specific functions, including treating IBD or PSC. There is no structure presented that corelates with this function. The specification only sets forth protein expression constructs having nucleotides encoding wild-type MST1 (i.e., SEQ ID NO: 35) as potentially having the required function, but the expression construct is not representative of the genus of agonists comprising “MST1 protein” instantly claimed.
Applicant is also not in possession of the breadth of subject populations treatable by species “MST1 protein” recited in instant claim 1.
A. No Written Description for agonists comprising genus “MST1 protein”
The claimed invention recites “wherein the agonist of the MST1/MST1R pathway comprises MST1 protein,” and the broadest reasonable interpretation for this recitation is: the claim language reads on directly administering not only wild-type MST1 protein (i.e., SEQ ID NO: 35), but also fusion proteins comprising the wild-type MST1 protein. The specification also indicates “MST1 protein” includes fusion proteins comprising the MST1 protein, and fragments thereof. However, the specification only discloses administering an expression construct comprising cDNA encoding wild-type MST1 protein (i.e., Example 6), as set out below.
Example 6 shows: “Hydrodynamic delivery (HDD) was used to deliver WT MST1 cDNA packaged in an expression construct to mice, leading to overexpression of WT MST1. Mice injected with MST1 HDD construct survived the course of experiment, indicating that MST1 overexpression is not lethal (data not shown).” Specification at page 36, lines 9-12. No other agonists of the MST1/MST1R pathway are administered in the specification, let alone administration of members of the genus “MST1 protein”.
The specification teaches regarding MST1 protein: “In some embodiments, the MST1 agonist is a protein, such as recombinant MST1. In some embodiments, the recombinant MST1 is a fusion protein comprising MST1 or a fragment thereof fused to a heterologous protein, for example an antibody or a fragment thereof, such as Fc fragment (e.g., Mst1-Fc).” Specification at page 13, lines 9-13.
The (i) broadest reasonable interpretation of the claim-recited term “MST1 protein,” and (ii) the specification, suggests that “MST1 protein” encompasses an unbounded genus MST1 fusion proteins, but the specification does not define any structural features commonly possessed by the member of the genus. The claims recite functional language of the proteins, such as that the proteins treat IBD and PSC, however a definition by function does not suffice to define the genus because it is only an indication of what the protein does, rather than what it is; therefore, it is only a definition of a useful result rather than a definition of what achieves that result. In addition, because the genus of MST1 protein is highly variable (i.e., each MST1 protein would necessarily have a unique structure; see MPEP 2434), the generic description of the substance is insufficient to describe the genus. Thus, the encompassed MST1 proteins have no correlation between their structure and function. To address this issue, a brief assessment of the state of the art regarding the unpredictability of fusion proteins, e.g., Fc fusions, is made herein.
Binder et al. ("Strategies for extending the half-life of biotherapeutics: successes and complications." Expert Opinion on Biological Therapy 25.1 (2025): 93-118), teaches that many therapeutic proteins have short half-lives when administered directly and that Fc fusion proteins can extend half-life. Binder et al. at Table 1. Regarding Fc fusion technology, Binder et al. teaches that Fc and linker selection/optimization is critical to preserving the activity of the protein: “[a] critical component of Fc fusion proteins is the linker, which can significantly affect the binding activity of the fusion partner, as shown for dulaglutide (Trulicity®)[… .] Whereas fusion of the GLP-1 derivative via the natural hinge region to an IgG1 Fc reduced potency in vitro by 95% in comparison to the free peptide, optimization of linker length and sequence, together with the choice of an Fc from the IgG4 subclass, led to a four-fold improvement.” Binder et al. at page 104, right col. In other words, a person of skill in the art would readily appreciate that significant unpredictability exists around how to construct Fc fusion proteins suitable as therapeutics. No MST1 fusion proteins are provided in the specification, let alone MST1-Fc fusion proteins and/or fusion proteins comprising fragments of MST1. Therefore, neither the art nor the specification provides a sufficient representative number of MST1 proteins that are therapeutically effective to meet the written description requirement for instant claims directed to the genus “MST1 protein.”
The claims also lack written description for administering the species unmodified “MST1 protein,” e.g., SEQ ID NO: 35. The specification only discloses administering an expression construct comprising WT MST1 cDNA via hydrodynamic delivery, not administering the protein directly. To address this issue, a further brief assessment of the art regarding challenges with converting gene therapies to protein therapies is made herein.
Binder et al. further teaches that “[e]ngineering of the drug half-life in vivo has become an integral part of modern biopharmaceutical development due to the fact that many proteins/peptides with therapeutic potential are quickly cleared by kidney filtration after injection and, thus, circulate only a few hours in humans (or just minutes in mice).” Binder et al. at Abstract. Binder et al. teaches therapeutic effects are unlikely by administering an unmodified therapeutic protein, as presently encompassed by the claims, e.g., “[c]ompared to the unmodified protein/peptide, the concentration of the [modified] drug with prolonged plasma half-life remains much longer within the therapeutic window. This cannot be achieved by higher dosing [of the unmodified protein], which poses the risk of eliciting side effects[.]” Binder et al. at FIG. 2. Various techniques to extend half-life have been successfully applied to different proteins, e.g., PEGylation, FC fusion, hyper glycosylation, albumin fusion, and lipidation. Binder et al. at Table 1. However, significant research and development is required to obtain a solution that extends the half-life while retaining the functionality of the protein; it is unpredictable what modification will work. For example, regarding possible PEGylation solutions: “examples underline that there is no universal plug-and-play solution for PEGylation of biopharmaceuticals. Rather, the coupling chemistry, choice of linker, type of PEG macromolecule – branched, linear, short or long chain – and the conjugation site(s) within the pharmacologically active protein or peptide must be optimized individually[.]” Binder et al. at page 98, left col.
Goswami et al. ("Gene therapy leaves a vicious cycle." Frontiers in oncology 9 (2019): 297) summarizes the unpredictability of converting the hydrodynamic delivery of an expression construct expressing MST1 demonstrated in the specification to the protein therapy instant claimed well: “more than 5,000 critical steps are involved in developing a single therapeutic protein. Therefore, the quotient of unpredictability is very high in developing both chemical and protein-based therapies. Gene therapy, on the other hand, leads to long-lasting production of the desired therapeutic protein and can localize protein expression to an area of the body, fixing the problem at its source.” Goswami et al. at introduction. Therefore, neither the art nor the specification provides a sufficient number of MST1 proteins suitable as therapeutic proteins to meet the written description requirement for instant claims directed to the species unmodified “MST1 protein.”
It is therefore unknow how either the species unmodified “MST1 protein” or the genus “MST1 protein” in general would work for treating IBD or PSC, especially considering the specification provides no examples of treating any disease, let alone IBD or PSC, with any MST1R agonist. Applicant has not shown possession of a representative number of species that have the claimed function(s). The specification therefore proves insufficient written description to support the “MST1 proteins” encompassed by the claims. Given all the above, Applicant does not have written description for MST1 protein.
B. No Written Description for Breadth of Genus: “Patient Heterozygous or Homozygous for an MST1 and/or MST1R Variant Nucleic Acid Molecule Associated with an Increased Risk of Developing IBD and/or PSC.”
Claim 1 also recites treating a patient of the genus “heterozygous of homozygous for an MST1 and/or MST1R variant nucleic acid molecule associated with an increased risk of developing IBD and/or PSC.” Dependent claims 12-13 and 33-14 further specify species of MST1 and MST1R variants associated with the risk of developing IBD and/or PSC. Claim 1 is therefore very broad as to MST1 and MST1R variants associated with increased risk of developing IBD and/or PSC that may be treatable with the claimed invention; however, Applicant has only demonstrated possession of the variants included in the dependent claims. Additionally, Egen et al. (US20160032013A1, published February 4, 2016) discloses the treatment of a patient heterozygous or homozygous for MST1 variant rs3197999 with MST1 protein agonist, as discussed in the 35 USC 102 rejection below. See e.g., Egen et al. at para. [0004]. Therefore, Applicant is not in possession of the breadth of subject populations treatable by species “MST1 protein” recited in instant claim 1.
The cited references therefore demonstrate that the treatment of IBD or PSC with an “MST1 protein” is highly unpredictable, if even possible.
MPEP § 2163.02 states, “[a]n objective standard for determining compliance with the written description requirement is, 'does the description clearly allow person of ordinary skill in the art to recognize that he or she invented what is claimed’”. The courts have decided: the purpose of the "written description" requirement is broader than to merely explain how to "make and use"; the Applicant must convey with reasonable clarity to those skilled in the art, that as of the filing date sought, he or she was in possession of the invention. The invention is for purposes of the “written description” inquiry, whatever is now claimed. See Vas-Cath, Inc v. Mahurkar, 935 F.2d 1555, 1563-64, 19 USPQ2d 1111, 1117 (Federal Circuit, 1991).
Furthermore, the written description provision of 35 USC §112 is severable from its enablement provision; and adequate written description requires more than a mere statement that it is part of the invention and reference to a potential method for isolating it. Fiers v. Revel, 25 USPQ2d 1601, 1606 (CAFC 1993). And Amgen Inc. v. Chugai Pharmaceutical Co. Ltd., 18 USPQ2d 1016. Moreover, an adequate written description of the claimed invention must include sufficient description of at least a representative number of species by actual reduction to practice, reduction to drawings, or by disclosure of relevant, identifying characteristics sufficient to show that Applicant was in possession of the claimed genus. However, factual evidence of an actual reduction to practice has not been disclosed by Applicant in the specification; nor has Applicant shown the invention was “ready for patenting” by disclosure of drawings or structural chemical formulas that show that the invention was complete; nor has the Applicant described distinguishing identifying characteristics sufficient to show that Applicant were in possession of the claimed invention at the time the application was filed.
Therefore, for all these reasons the specification lacks adequate written description, and one of skill in the art cannot reasonably conclude that Applicant had possession of the claimed invention at the time the instant application was filed.
Claim Rejections - 35 USC § 102
8. 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 the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claims 1 and 33 are rejected under 35 U.S.C. 102 (a)(1) and 102(a)(2) as being anticipated by Egen et al. (US20160032013A1, published February 4, 2016).
Claim 1 is drawn to method of treating a patient having inflammatory bowel disease (IBD) or primary sclerosing cholangitis (PSC), the method comprising administering to the patient an agonist of the Macrophage Stimulating 1 (MST1)/Macrophage Stimulating 1 Receptor (MST1R) pathway, wherein the agonist of the MST1/MST1R pathway comprises MST1 protein; and wherein the patient is heterozygous or homozygous for an MST1 and/or MST1R variant nucleic acid molecule associated with an increased risk of developing IBD and/or PSC.
Claim 33 is drawn to the method according to claim 1, wherein the MST1 variant nucleic acid molecule associated with an increased risk of developing IBD and/or PSC does not encode Arg703Cys.
Egen et al. is directed to methods of treating disease with RON (i.e., MST1R) agonists. Egen et al. at Abstract (RON is an alternative name for instant MST1R, and MSP is an alternative name for instant MST1, see instant specification at page 2, lines 9-11). Therefore, Egen et al. discloses methods of treating a disease related to the MST1/MST1R pathway with MST1R agonist.
Egen et al. discloses the disease can be IBD or PSC (see e.g., Egen et al. at paragraph [0011]). Egen et al. discloses the MST1R agonist can be MST1 protein (see e.g., Egen et al. at claim 2).
Egen et al. discloses wherein the patient is heterozygous or homozygous for an MST1 and/or MST1R variant nucleic acid molecule associated with an increased risk of developing IBD and/or PSC (see e.g., Egen et al. at claim 21 and paragraph [0004]; claim 1).
The rs3197999 MST1 variant of Egen et al. encodes Arg689Cys, not Arg703Cys (see e.g., Egen et al at paragraph [0004]; claim 33).
Accordingly, Egen et al. anticipates instant claims 1 and 33.
Conclusion
9. No claim is allowed.
10. Any inquiry concerning this communication or earlier communications from the examiner should be directed to BRANDON R SCHWECHTER whose telephone number is (571)272-1270. The examiner can normally be reached M-Th 7-5 EST.
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/BRANDON R SCHWECHTER/
Examiner, Art Unit 1674
/VANESSA L. FORD/ Supervisory Patent Examiner, Art Unit 1674