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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 03/30/2026 has been entered.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 03/30/2026 in compliance with the provisions of 37 C.F.R. 1.97. All references cited in this IDS have been fully considered.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
Previous rejections under 35 U.S.C. § 103
The claims were rejected as obvious over Stringer in view of Goldenberg and Li. Applicant traverses this rejection and has provided a declaration by Dr. Jian Li (hereinafter “Li Declaration”). The Li Declaration presents the following arguments.
First, Li Declaration asserts that at the time of filing the application, there were a number of studies suggesting activating plasmin pathway can exacerbate inflammation including neuroinflammation. Li Declaration states that the plasminogen activation system was understood to be a tightly regulated proteolytic cascade and because components act at different levels of the pathway, interventions targeting each component were understood to produce distinct biological effects. And therefore, increasing plasmin activity through different mechanisms would not have been expected to yield predictable or interchangeable outcomes (Li Declaration, par. 5).
Second, Li Declaration provides Li et al. (American Journal of Pathology, 2005, Vol. 166(3), pages 783-792; Cited in IDS filed on 03/30/2026) which demonstrates that plasminogen may promote rather than suppress inflammation (Li Declaration, par. 6-7 and 11). Similarly, plasminogen activation was known to contribute to neuronal injury (Li Declaration, par. 9). Finally, plasmin was known to degrade proteins including components of myelin and the potential for direct degradation of myelin would have raised significant concerns when considering a treatment of multiple sclerosis (Li Declaration, par. 10). Li Declaration asserts that these references provide a well-recognized body of evidence indicating that activation of the plasminogen pathway could exacerbate inflammation and in the Inventor/Declarant’s opinion, this lack of clear consensus would have led to an unpredictable result and there would have not been a reasonable expectation of success when administering plasminogen.
Declarant’s arguments (and the arguments summarized in the Remarks dated 03/30/2026) have been fully considered but are not sufficient to overcome the rejection of record. The examiner agrees that there was a conflicting body of evidence surrounding the inflammatory/anti-inflammatory responses associated with administration of components of the plasminogen/plasmin pathways. In fact, such arguments were presented by the Examiner when considering the enablement of this invention when the breadth of the claims encompassed administration of inter alia any “component of plasminogen activation pathway”, “compound directly activating plasminogen” or “indirectly activating plasminogen by activating an upstream component of a plasminogen activation pathway”. And although there was conflicting evidence as to the role plasminogen pathway components played in the inflammatory process, this evidence does not outweigh the prima facie obviousness set forth in the rejection of record.
As discussed previously, Stringer teaches that multiple sclerosis can be treated by administering plasminogen activators and although it does not teach administration of plasminogen per se, plasminogen was known before the effective filing date as being capable of treating nerve tissue injury and neuroinflammation (as shown in Li). Accordingly, a person having ordinary skill in the art would have had a reasonable expectation of success when arriving at the claimed invention (such as by modifying Stringer’s methods so that they involve administration of plasminogen rather than plasminogen activator). When viewing a disclosure that multiple sclerosis can be treated by providing plasminogen activators, the reasonable conclusion is that administration of plasminogen would similarly be suitable for treatment because plasminogen per se was previously known to be suitable for treating neuroinflammation.
For at least these reasons, the rejection of record is proper and must be maintained.
Maintained rejection under 35 U.S.C. § 103
Claims 1 and 6-14 are rejected under 35 U.S.C. 103 as being unpatentable over Stringer et al. (US 6,497,877 B1) in view of Goldenberg (Pharmacy and Therapeutics, 2012, vol. 37(3), pages 175-184) and Li et al. (US 2018/0369345 A1; cited in IDS filed on 07/27/2023).
Regarding claim 1, Stringer teaches a method of treating an organism (i.e., a subject) afflicted by an inflammatory disease (col. 2, lines 64-65). Stringer teaches that inflammatory diseases include diseases such as multiple sclerosis (col. 9, lines 50-64). Accordingly, Stringer teaches a method for treating multiple sclerosis.
With respect to the method comprising administration of plasminogen, although Stringer teaches administration of plasminogen activators, it does not teach the administration of plasminogen per se.
Nonetheless, Li et al. (hereinafter Li) teaches methods for preventing or repairing diabetic nerve injury (e.g., nerve tissue injury or neuroinflammation) comprising administering a therapeutically effective amount of plasminogen or plasmin to a subject ([0010]-[0011]). Li teaches that plasmin is a key component of the plasminogen activation system and plasmin is formed by the proteolysis of plasminogen by plasminogen activators ([0005]). Finally, Li teaches that plasminogen has significant effects in nerve repair ([0009]).
Goldenberg reviews multiple sclerosis and teaches that multiple sclerosis is a chronic autoimmune, inflammatory neurological disease and goals of multiple sclerosis therapies include providing symptomatic relief, which is aimed at maintaining function and improving quality of life (p. 175, left col., par. 1 and p. 176, left col., par. 4-5).
Accordingly, because Stringer teaches the treatment of multiple sclerosis by administering a component of the plasminogen activation pathway (plasminogen activator) and because Li teaches that nerve tissue injury and neuroinflammation can be treated by administering plasminogen as “plasminogen has significant effects in nerve repair” ([0009]), it would have been obvious to have modified Stringer’s method such that Stringer’s plasminogen activator is substituted with plasminogen. There would have been a reasonable expectation of success when making this modification because Goldenberg teaches neuroinflammation to be a symptom of multiple sclerosis and Li teaches that plasminogen can be used to treat neuroinflammation. This obviousness is based upon the “Simple Substitution of One Known Element for Another to Obtain Predictable Results” rationale set forth in KSR Int'l Co. v. Teleflex Inc., 550 U.S. 398, 415-421, 82 USPQ2d 1385, 1395-97 (2007).
With respect to the composition being administered to a subject in a therapeutically effective amount, Stringer teaches that the compounds of the invention will contain an effective amount of the plasminogen activator or derivative thereof in order to prepare pharmaceutically acceptable compositions suitable for administration to a human or animal (col. 8, lines 30-37). More specifically, Stringer teaches administration of a therapeutically effective amount of the composition (claim 1). Additionally, Li teaches that plasminogen is administered in a therapeutically effective amount to a subject ([0010]). As such, it would have been obvious to have administered a therapeutically effective amount of plasminogen in the modified method.
Thus, claim 1 is obvious over Stringer in view of Li and Goldenberg.
Regarding claim 6, as discussed above, Stringer in view of Li and Goldenberg makes obvious the administration of plasminogen for the purpose of treating multiple sclerosis.
Li teaches that the plasminogen can be one which has at least 80% sequence identity with SEQ ID NO: 2 ([0036]). Applicant’s SEQ ID NO: 2 has 100% identity with Li’s SEQ ID NO: 2 (see attached “Sequence Comparison.pdf”). Thus, Li’s range (“at least 80%”) overlaps with the instantly claimed range (“at least 75%”). Because the sequences are identical, it is considered that Li’s composition has the proteolytic activity of plasminogen. This interpretation is supported by the fact that Li describes a human natural plasminogen and it therefore must have the activity of plasminogen ([0030]).
Regarding claim 7, as discussed above, Li teaches the same composition and therefore it must have the same activity (i.e., the lysine binding activity of plasminogen). This interpretation is supported by the fact that Li describes a human natural plasminogen and it therefore must have the activity of plasminogen ([0030]).
Regarding claim 8, Li teaches that the plasminogen of the present invention comprises a protein containing a plasminogen active fragment and still having plasminogen activity (i.e., the proteolytic activity of plasminogen)([0053]). Li defines this fragment as SEQ ID NO: 14 or an amino acid sequence having an amino acid sequence identity of at least 80% with SEQ ID NO: 14. Applicant’s SEQ ID NO: 14 has 100% identity with Li’s SEQ ID NO: 14 (see previously attached “Sequence Comparison.pdf”). Thus, Li’s range (“at least 80%”) overlaps with the instantly claimed range (“at least 75%”).
Regarding claim 9, as discussed above, Li envisions variants of SEQ ID NO: 2 such as those having at least 80% identity to SEQ ID NO: 2. Li teaches that the variant can be a conservatively substituted variant ([0020]).
Regarding claim 10, Li teaches that the plasminogen can be human natural plasminogen ([0020]). As discussed above, Li teaches variants of this natural plasminogen, which are considered to be synthetic human plasminogen.
Regarding claims 11-13, as discussed above, Stringer in view of Goldenberg and Li renders obvious the method of treating multiple sclerosis by administering plasminogen.
And although Stringer does not teach that the compound is used in combination with one or more other therapeutic methods or medicaments, Goldenberg reviews the therapeutic regimens typically employed in the treatment of multiple sclerosis and teaches that there are eight FDA-approved therapeutic agents to reduce disease activity and progression in patients with MS (p. 176, left col., par. 5). Among these are beta interferons, glatiramer acetate, mitoxantrone, natalizumab, and fingolimod (p. 176, Table 1). Goldenberg teaches that laquinimod, teriflunomide, BG-12, daclizumab, alemtuzumab, rituximab, and ocrelizumab may be potential medications for multiple sclerosis (p. 179, Table 2) and teaches the off-label use of azathioprine, methotrexate, and cyclophosphamide, mycophenolate mofetil, and cladribine (p. 179, left col., par. 1 through right col., par. 2). Finally, Goldenberg teaches that “a combination of drugs, and physical, speech, and occupational therapies” may relieve symptoms and promote a satisfactory quality of life (p. 183, left col., par. 1).
Since Stringer in view of Goldenberg and Li renders obvious the administration of plasminogen to treat multiple sclerosis and Goldenberg teaches a litany of therapeutic options which may be combined to relive symptoms and promote a satisfactory quality of life, it would have been obvious to have further modified the method of Stringer such that it involves the administration of one or more other therapeutic methods or medicaments (claim 11) such as physical therapy (claim 12) or an immunosuppressant (claim 13) such as azathioprine or methotrexate (p. 178, right col., par. 9 through p. 179, left col., par. 1). There would have been a reasonable expectation of success because Goldenberg teaches therapies as combinable and the modification would have been expected to more effectively treat the symptoms of multiple sclerosis. This obviousness is based upon the “Some Teaching, Suggestion, or Motivation in the Prior Art That Would Have Led One of Ordinary Skill To Modify the Prior Art Reference or To Combine Prior Art Reference Teachings To Arrive at the Claimed Invention” rationale set forth in KSR Int'l Co. v. Teleflex Inc., 550 U.S. 398, 415-421, 82 USPQ2d 1385, 1395-97 (2007). See MPEP 2143(I)(G).
Thus, claims 11-13 are obvious over Stringer in view of Goldenberg and Li.
Regarding claim 14, Stringer teaches administration of the composition through oral, topical, inhalation, or parental administration routes (claims 4-7). Stringer gives specific examples such as intravascular infusion (i.e., intravenous administration or intraarterial administration)(col. 9, lines 7-9), aerosol inhalation (col. 9, lines 17-19).
Li teaches that plasminogen can be administered intranasally (i.e., through nasal inhalation), through aerosol, intravenously, intraperitoneally, subcutaneously, intracranially, intrathecally, intraarterially, and intramuscularly ([0079]).
As such, it would have been obvious to have administered plasminogen through one of the routes listed above.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Previous double patenting rejections
RE: Rejection of claims 1 and 6-14 on the ground of nonstatutory double patenting as being unpatentable over claims 1-20 of U.S. Patent No. 11,400,142 B2 in view of Goldenberg (Pharmacy and Therapeutics, 2012, vol. 37(3), pages 175-184).
Applicant traverses the double patenting rejection by arguing the following.
First, applicant argues that the claims of ‘142 are patentably distinct from the instant claims. Specifically, applicant argues that neuroinflammation oversimplifies the underlying biology and a person having ordinary skill in the art would not have reasonably equated the conditions or assumed that a therapy effective in one context would be effective in the other.
Second, applicant argues that the Li Declaration demonstrates that the effects of plasminogen with MS were unpredictable and potentially detrimental and therefore there would not have been a reasonable expectation of success when applying the methods of the ‘142 patent to multiple sclerosis.
Applicant’s arguments have been fully considered but are not sufficient to overcome the rejection of record.
First, it is noted that applicant’s definition of “treatment” includes treating the disease or symptoms of the disease either completely or partially (Specification, p. 21, par. 6). As discussed by Goldenberg, multiple sclerosis is a neuroinflammatory disease (i.e., a symptom of multiple sclerosis is neuroinflammation). Therefore, because ‘142 teaches plasminogen as being suitable for treating nerve injuries such as neuroinflammatory disease, it would have been obvious to have modified ‘142 such that it is directed to treating multiple sclerosis.
Second, as discussed in the response to the Li Declaration above, it is accepted that there was conflicting information with respect to the effect of plasminogen components on inflammation but that evidence does not outweigh the direct teachings of ‘142 with respect to plasminogen’s capability to treat neuroinflammation, which is (as taught by Goldenberg), a symptom shared with multiple sclerosis (claim 18).
For at least these reasons, the rejection of record is proper and has been maintained.
RE: Provisional Rejections
Applicant has requested abeyance of the provisional rejections over 17/793,371, 18/037,299, and 18/037,300. The provisional rejections cannot be held in abeyance and have been maintained. The rejection of application ‘371 has been modified to account for the amendments in that application. The rejection of application ‘300 is withdrawn because the copending application has been abandoned.
Maintained double patenting rejections
Claims 1 and 6-14 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-20 of U.S. Patent No. 11,400,142 B2 in view of Goldenberg (Pharmacy and Therapeutics, 2012, vol. 37(3), pages 175-184).
Although the claims at issue are not identical, they are not patentably distinct from each other for the following reasons.
Regarding claim 1, claims 1 and 5 of ‘142 are directed to methods of repairing diabetic nerve injury comprising administering an effective amount of plasminogen. Although the claims of ‘142 do not teach that the method is for treating multiple sclerosis, claim 18 of ‘142 teaches that the nerve injury is neuroinflammation or nerve tissue injury.
Goldenberg reviews multiple sclerosis and teaches that multiple sclerosis is a chronic autoimmune, inflammatory neurological disease and goals of multiple sclerosis therapies include providing symptomatic relief, which is aimed at maintaining function and improving quality of life (p. 175, left col., par. 1 and p. 176, left col., par. 4-5).
Since the claims of ‘142 teach that plasminogen is suitable for the treatment of nerve tissue injury and neuroinflammation and Goldenberg teaches that multiple sclerosis is a chronic neuroinflammatory disease, it would have been obvious to have modified the method of ‘142 such that it was instead directed to treating multiple sclerosis. There would have been a reasonable expectation of success because the etiology of multiple sclerosis (neuroinflammation) is the mechanism of treatment of the methods of ‘142. This obviousness is based upon the “Some Teaching, Suggestion, or Motivation in the Prior Art That Would Have Led One of Ordinary Skill To Modify the Prior Art Reference or To Combine Prior Art Reference Teachings To Arrive at the Claimed Invention” rationale set forth in KSR Int'l Co. v. Teleflex Inc., 550 U.S. 398, 415-421, 82 USPQ2d 1385, 1395-97 (2007). See MPEP 2143(I)(G).
Regarding claims 6-8, the claims of ‘142 encompass administration of plasminogen having at least 80% sequence identity with SEQ ID NO: 2 (claims 4 and 16-17). As discussed above in the rejection under 35 U.S.C. § 103 (applied to the pre-grant publication of this patent), applicant’s SEQ ID NO: 2 is 100% identical to the prior art SEQ ID NO: 2.
Regarding claim 9, although the claims of ‘142 do not directly teach a “conservative substitution”, a person having ordinary skill in the art would be prompted to experiment with various “variants” of SEQ ID NO: 2 and would have arrived at a plasminogen having a conservative substitution with a reasonable expectation of success.
Regarding claim 10, SEQ ID NO: 2 is the natural human plasminogen (see the sequence listing for SEQ ID NO: 2 in col. 37-38 of the ‘142 patent).
Regarding claims 11-13, claims 1 and 5 of ‘142 teach that the method further comprises additional therapy such as physical therapy or drugs including neurotrophic drugs, anti-infective drugs (e.g., antibiotics or antivirals).
Regarding claim 14, claim 2 of ‘142 teaches intravenous administration.
Maintained but Modified Provisional Rejections
Claims 1 and 6-14 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 12-15, and 18-26 of copending Application No. 17/793,371 in view of Shaw et al. (Journal of Neuroscience, 2017, vol. 37(14), pages 3776-3788; cited in IDS filed on 07/27/2023) and Goldenberg (Pharmacy and Therapeutics, 2012, vol. 37(3), pages 175-184).
Although the claims at issue are not identical, they are not patentably distinct for the following reasons.
Regarding claim 1, claim 1 of ‘371 is directed to a method for treating nerve injury comprising administering to a subject a therapeutically effective amount of plasminogen.
Copending claim 1 differs because it is not directed to a method of treating multiple sclerosis.
Nevertheless, Shaw teaches that multiple sclerosis is a chronic demyelinating disease of the central nervous system characterized by autoreactive CD4+ T cells causing microglial- and macrophage-mediated destruction and phagocytosis of the myelin sheath (p. 3776, left col., par. 1 through right col., par. 2). Additionally, fibrin is “the premier” proteolytic target of plasmin, has been documented in demyelinating plaques of MS patients, and fibrin matrices appear to drive microglial and macrophage migration, leading to demyelination and loss of motor function (p. 3784, left col., par. 3 through right col., par. 1).
Accordingly, because the copending application is directed to a method for treating nerve injury, such as by promoting the repair of damaged nerve (claim 18) or regeneration of the myelin sheath (claim 19), it would have been obvious to have modified the method of treating nerve injury such that the method is instead for treating multiple sclerosis because (i) it was known that myelin sheath damage is the causative factor for multiple sclerosis and (ii) it was known that the fibrinolytic pathway could alleviate demyelination.
Regarding claims 6-8, claims 12-14 of ‘371 limit the plasminogen to one having at least 75% similarity to the natural plasminogen sequence (SEQ ID NO: 2) or the active fragment (SEQ ID NO: 14).
Regarding claim 9, claim 13 of ‘371 teaches that the variant is a conservative substitution variant.
Regarding claim 10, claim 15 of ‘371 teaches that the plasminogen is natural or synthetic human plasminogen.
Regarding claims 11-13, as discussed above, it would have been obvious to have arrived at a method of treating multiple sclerosis. The copending claims do not teach that the compound is administered in combination with one or more other therapeutic method or medicaments.
Goldenberg reviews the therapeutic regimens typically employed in the treatment of multiple sclerosis and teaches that there are eight FDA-approved therapeutic agents to reduce disease activity and progression in patients with MS (p. 176, left col., par. 5). Among these are beta interferons, glatiramer acetate, mitoxantrone, natalizumab, and fingolimod (p. 176, Table 1). Goldenberg teaches that laquinimod, teriflunomide, BG-12, daclizumab, alemtuzumab, rituximab, and ocrelizumab may be potential medications for multiple sclerosis (p. 179, Table 2) and teaches the off-label use of azathioprine, methotrexate, and cyclophosphamide, mycophenolate mofetil, and cladribine (p. 179, left col., par. 1 through right col., par. 2). Finally, Goldenberg teaches that “a combination of drugs, and physical, speech, and occupational therapies” may relieve symptoms and promote a satisfactory quality of life (p. 183, left col., par. 1).
Since ‘372 in view of Shaw makes obvious the use of the components recited in claim 1 to treat multiple sclerosis, it would have been obvious to have further modified the method such that it further involves the administration of one or more other therapeutic methods or medicaments (claim 11) such as physical therapy (claim 12) or an immunosuppressant (claim 13) such as azathioprine or methotrexate (p. 178, right col., par. 9 through p. 179, left col., par. 1). There would have been a reasonable expectation of success because Goldenberg teaches therapies as combinable and the modification would have been expected to more effectively treat the symptoms of multiple sclerosis.
Regarding claim 14, although the copending claims do not teach any particular route of administration, it would have been obvious to have experimented with various administration routes to arrive at the most efficacious routes, such as those recited in the instant claim. There would have been a reasonable expectation of success because this claim is not particularly limited and encompasses dozens of potential routes of administration.
This is a provisional nonstatutory double patenting rejection.
Claims 1 and 6-14 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-18 of copending Application No. 18/037,299.
Although the claims at issue are not identical, they are not patentably distinct for the following reasons.
Regarding claim 1, claim 1 of ‘299 is directed to a method for promoting the formation of mature BDNF and/or increasing BDNF levels comprising administering to a subject a therapeutically effective amount of a plasminogen pathway activator. Claim 15 of ‘299 limits the activator to plasminogen.
Although copending claim 1 is not directed to a method of treating multiple sclerosis, claim 6 of ‘299 defines the method as being used in subjected having neuronal injuries from multiple sclerosis and instant claim 4 recites the increase in the level of BDNF. Moreover, claim 7 of ‘299 is for “preventing or treating a BDNF-associated disease or condition”, which can be multiple sclerosis (see claim 8). Accordingly, these claims encompass overlapping subject matter.
Regarding claims 6-8, claims 16-17 of ‘299 limit the plasminogen to one having at least 80% similarity to the natural plasminogen sequence (SEQ ID NO: 2) or the active fragment (SEQ ID NO: 14).
Regarding claim 9, claim 18 of ‘299 teaches that the plasminogen can be a “variant” of plasminogen. Paragraphs [0052]-[0053] of the specification of ‘299 defines “variant” as including proteins obtained by substitution of 1-100 conservative amino acids.
Regarding claim 10, as discussed above, SEQ ID NO: 2 is the natural synthetic human plasminogen.
Regarding claims 11-13, claim 10 of ‘299 teaches the use of one or more other drugs or therapies.
Regarding claim 14, claim 11 of ‘299 teaches intravenous, intramuscular, intrathecal, nasal, aerosol, nasal drop, or eye drop administration routes.
This is a provisional nonstatutory double patenting rejection.
Conclusion
No claim is allowed.
All claims are identical to or patentably indistinct from, or have unity of invention with claims in the application prior to the entry of the submission under 37 CFR 1.114 (that is, restriction (including a lack of unity of invention) would not be proper) and all claims could have been finally rejected on the grounds and art of record in the next Office action if they had been entered in the application prior to entry under 37 CFR 1.114. Accordingly, THIS ACTION IS MADE FINAL even though it is a first action after the filing of a request for continued examination and the submission under 37 CFR 1.114. See MPEP § 706.07(b). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
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/GRANT C CURRENS/Examiner, Art Unit 1651
