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 .
Withdrawal of Rejections
The response and amendments filed on 03/10/2026 are acknowledged. Any previously applied minor objections and/or minor rejections (i.e., formal matters), not explicitly restated here for brevity, have been withdrawn necessitated by Applicant’s formality correction and/or amendments. For the purposes of clarity of the record, the reasons for the Examiner’s withdrawal, and/or maintaining, if applicable, of the substantive or essential claim rejections are detailed directly below and/or in the Examiner’s Response to Arguments section.
Briefly, the previous claim rejections under 35 U.S.C. 103 for obviousness have been withdrawn necessitated by Applicant’s amendments; however, new grounds of rejection are set forth below.
The following rejections and/or objections are either reiterated or newly applied. They constitute the complete set presently being applied to the instant application.
New Grounds of Rejection Necessitated by Amendments
Claim Rejections - 35 USC § 103, Obviousness
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 1-5, and 7 are rejected under 35 U.S.C. 103 as being unpatentable over Masuda (US 2013/0164383; Date of Publication: June 27, 2013 – previously cited) in view of Nakamura (Influenza A Virus-Induced Expression of GalNAc Transferase, GALNT3, via MicroRNAs is Required for Enhanced Viral Replication; 2015 – previously cited) and Sakai (Chondroitin Sulfate N-Acetylgalactosaminyltransferase-1 Plays a Critical Role in Chondroitin Sulfate Synthesis in Cartilage; 2006 – cited in the IDS filed on 12/30/2024 & previously cited).
Masuda’s general disclosure relates to promoting the synthesis of collagen and proteoglycan in chondrocytes, such as intervertebral disc cells, articular chondrocytes, and meniscal cells, through administration of an extract from inflamed tissue inoculated with vaccinia virus (see, e.g., Masuda, abstract). Moreover, Masuda discloses that “a preparation of an extract from inflamed skins of rabbits inoculated with vaccinia virus is commercially available as a pharmaceutical product” and that “the preparation is known to be effective against low back pain, cervicobrachial syndrome, symptomatic neuralgia, periarthritis scapulohumeralis, osteoarthritis, itchiness accompanied with skin diseases (eczema, dermatitis, urticaria), allergic rhinitis, sequelae of subacute myelo-optico-neuropathy such as coldness, paresthesia and pain, postherpetic neuralgia and the like” (see, e.g., Masuda, [0012]).
Regarding claim 1 pertaining to contacting the extract with intervertebral disc cells, Masuda teaches that the extract from inflamed tissue inoculated with vaccinia virus is contacted with intervertebral disc cells (see, e.g., Masuda, [0030], Example 3).
Regarding claims 1 and 2-4 pertaining to the expression of N-acetylgalactosaminyltransferase, the expression of N-acetylgalactosaminyltransferase following contact with an extract from inflamed tissues inoculated with vaccinia virus would be inherent. Masuda teaches the same method of contacting intervertebral disc cells with the same extract derived from inflamed tissues inoculated with vaccinia virus. Therefore, the prior art teaches administering the same composition (i.e., an extract from inflamed tissues inoculated with vaccinia virus) to the same cells (i.e., intervertebral disc cells), which would inherently lead to the same effect of promotion of expression of N-acetylgalactosaminyltransferase since the inherent properties exhibited by the extract would be present within the applied composition (see, e.g., MPEP 2112.02). Moreover, inherently, this would lead to increased N-acetylgalactosaminyltransferase 1, compared to N-acetylgalactosaminyltransferase 2.
Regarding claim 1 pertaining to disinfection and deproteinization, Masuda teaches that the extraction liquid is heated for deproteinization (see, e.g., Masuda, [0017]). Moreover, one of ordinary skill in the art would readily understand that heating the extract would also inherently result in disinfection because heat is used to kill pathogens (see, e.g., Art of Record, Dantherm Group). Furthermore, Masuda teaches “ the deproteinized solution is adjusted to an alkaline condition, heated, and then filtered or centrifuged” (see, e.g., Masuda, [0017]); therefore, heating the extract again after deproteinization would result in disinfection. Additionally, Masuda teaches that the extract is further heated at 90oC to 100oC for 15 minutes after deproteinization (see, e.g., Masuda, Example 1, [0028]); therefore, one of ordinary skill in the art would understand that this would result in disinfection by heating.
Regarding claim 5 pertaining to the inflamed tissues, Masuda teaches “a preparation of an extract from inflamed skins of rabbits inoculated with vaccinia virus is commercially available as a pharmaceutical product, and may be employed in the present invention” (see, e.g., Masuda, [0012]). Moreover, Masuda teaches that the preparation “is a medicinal agent containing non-proteinous active substances extracted and separated from the inflamed skin tissue of rabbits inoculated with vaccinia virus” (see, e.g., Masuda, [0012]).
Regarding claim 7 pertaining to the preparation, Masuda teaches that the preparation can be formed for intramuscular and intravenous injection, and as a tablet (see, e.g., Masuda, [0012]).
However, Masuda does not teach: measuring the expression of an N-acetylgalactosaminyltransferase (claim 1); or wherein the N-acetylgalactosaminyltransferase is at least one selected from the group consisting of N-acetylgalactosaminyltransferase-1 and N-acetylgalactosaminyltransferase 2 (claim 1) .
Nakamura’s general disclosure pertains to “the molecular mechanism underlying rapid mucin production during influenza A virus (IAV) infection but also the contribution of O-linked glycosylation to the replication and propagation of IAV in lung cells” (see, e.g., Nakamura, abstract). Moreover, Nakamura discloses that IAV induces the expression of N-acetylgalactosaminyltransferase (see, e.g., Nakamura, Introduction, pg. 1789).
Regarding claim 1 pertaining to measuring expression of N-acetylgalactosaminyltransferase, Nakamura teaches measuring the expression of N-acetylgalactosaminyltransferase following IAV infection (see, e.g., Nakamura, Introduction, pg. 1789).
Sakai’s general disclosure relates to demonstrating that chondroitin sulfate N-acetylgalactosaminyltransferase 1 plays a critical role in chondroitin sulfate biosynthesis in cartilage (see, e.g., Sakai, abstract). Moreover, Sakai discloses that chondroitin sulfate N-acetylgalactosaminyltransferase 1 exhibits the highest level of expression in developing cartilage (see, e.g., Sakai, abstract). Furthermore, Sakai identified that chondroitin sulfate N-acetylgalactosaminyltransferase 1 is critical for cartilage CS biosynthesis and overexpression of the enzyme leads to elevated levels of CS biosynthesis (see, e.g., Sakai, Introduction, pg. 4153).
Regarding claim 1 pertaining to N-acetylgalactosaminyltransferase being either N-acetylgalactosaminyltransferase 1 or N-acetylgalactosaminyltransferase 2, Sakai teaches that N-acetylgalactosaminyltransferase 1 is critical for cartilage CS biosynthesis and has the highest level of expression in developing cartilage (see, e.g., Sakai, abstract & Introduction, pg. 4153). Moreover, Sakai teaches that upon measuring N-acetylgalactosaminyltransferase 1 and N-acetylgalactosaminyltransferase 2 in developing mouse cartilage, chondroitin sulfate N-acetylgalactosaminyltransferase 1 is expressed at the highest level, while chondroitin sulfate N-acetylgalactosaminyltransferase 2 is expressed at very low levels (see, e.g., Sakai, Figure 2 & Results, pg. 4155).
It would have been first obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to measure expression of N-acetylgalactosaminyltransferase, as taught by Nakamura, in intervertebral disk cells following contact with an extract derived from inflamed tissues inoculated with vaccinia virus, as taught by Masuda. One would have been motivated to do so because Nakamura teaches that viral infection, specifically with IAV, induces expression of N-acetylgalactosaminyltransferase (see, e.g., Nakamura, Introduction, pg. 1789). Moreover, Masuda teaches contacting intervertebral disk cells with an extract derived from inflamed tissues inoculated with vaccinia virus (see, e.g., Masuda, [0030], Example 3), which would inherently lead to increased expression of N-acetylgalactosaminyltransferase. Therefore, based on the teachings of Masuda and Nakamura, it would have been obvious to measure N-acetylgalactosaminyltransferase following vaccinia virus infection since Masuda teaches that viral infection induces expression of N-acetylgalactosaminyltransferase. One would have expected success because Seki and Nakamura both teach infection by viruses, wherein these viruses increase expression of N-acetylgalactosaminyltransferase.
It would have been secondly obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to measure chondroitin sulfate N-acetylgalactosaminyltransferase 1, as taught by Sakai, in intervertebral disk cells following contact with an extract derived from inflamed tissues inoculated with vaccinia virus, as taught by Masuda. One would have been motivated to do so because Sakai teaches that N-acetylgalactosaminyltransferase 1 is critical for cartilage CS biosynthesis and has the highest level of expression in developing cartilage (see, e.g., Sakai, abstract & Introduction, pg. 4153). Moreover, Sakai teaches that in developing mouse cartilage, chondroitin sulfate N-acetylgalactosaminyltransferase 1 is expressed at the highest level, while chondroitin sulfate N-acetylgalactosaminyltransferase 2 is expressed at very low levels (see, e.g., Sakai, Figure 2 & Results, pg. 4155). Moreover, Masuda teaches that since neurotropin (i.e., NTP; “a nonprotein extract from the inflamed skin of rabbits following inoculation with vaccinia virus as an active ingredient” (see, e.g., Masuda, [0002])) promotes the synthesis of collagen and proteoglycan in chondrocytes such as intervertebral disc cells, “it is indicated that NTP has a regenerating activity on a chondrocyte extracellular matrix of various cartilages (see, e.g., Masuda, [0041]). Furthermore, Moreover, Masuda teaches contacting intervertebral disk cells with an extract derived from inflamed tissues inoculated with vaccinia virus (see, e.g., Masuda, [0030], Example 3), which would inherently lead to increased expression of N-acetylgalactosaminyltransferase. Therefore, based on the teachings of Masuda and Sakai, it would have been obvious to measure expression of chondroitin sulfate N-acetylgalactosaminyltransferase 1 because this enzyme is highly expressed in developing cartilage and cartilage is present in intervertebral disc cells. One would have expected success because Masuda and Sakai both teach regeneration of extracellular matrix components, especially cartilage.
Examiner’s Response to Arguments
Applicant’s response and amendments filed on 08/15/2025 have been considered, but they are not sufficient to overcome the prior arts of record.
Regarding Applicant’s arguments pertaining to amended independent claim 1 not being taught by Masuda nor Nakamura (remarks, pages 5-6), as discussed above, the previous 35 U.S.C. 103 rejection for obviousness in view of Masuda and Nakamura was withdrawn, however new grounds of rejection have been set forth above. Although Masuda and Nakamura were relied upon in the above presented rejection, they were not relied upon to teach that the N-acetylgalactosaminyltransferase is at least one selected from the group consisting of N-acetylgalactosaminyltransferase-1 and N-acetylgalactosaminyltransferase 2. Therefore, Applicant’s arguments pertaining to amended claim 1 are moot.
Regarding Applicant’s arguments pertaining to the teachings of Nakamura (remarks, pages 5-6), these arguments are not persuasive because Nakamura was merely recited to teach the limitation that N-acetylgalactosaminyltransferase was measured in the samples (see, e.g., Nakamura, Introduction, pg. 1789). However, the newly taught reference of Sakai also teaches measuring N-acetylgalactosaminyltransferase, and more specifically N-acetylgalactosaminyltransferase 1 and N-acetylgalactosaminyltransferase 2, in cartilage and specifically teaches that in developing mouse cartilage, chondroitin sulfate N-acetylgalactosaminyltransferase 1 is expressed at the highest level, while chondroitin sulfate N-acetylgalactosaminyltransferase 2 is expressed at very low levels (see, e.g., Sakai, Figure 2 & Results, pg. 4155). One of ordinary skill in the art would have been motivated to apply the teachings of Nakamura and Sakai to measure N-acetylgalactosaminyltransferase 1 and N-acetylgalactosaminyltransferase 2 in intervertebral disc cells treated with neurotropin because Masuda teaches that neurotropin promotes the synthesis of collagen and proteoglycan in chondrocytes such as intervertebral disc cells and “it is indicated that NTP has a regenerating activity on a chondrocyte extracellular matrix of various cartilages (see, e.g., Masuda, [0041]). Furthermore, Masuda teaches contacting intervertebral disk cells with an extract derived from inflamed tissues inoculated with vaccinia virus (see, e.g., Masuda, [0030], Example 3), which would inherently lead to increased expression of N-acetylgalactosaminyltransferase. Therefore, Nakamura and Sakai both teach measuring N-acetylgalactosaminyltransferase isotypes, and Sakai was cited as motivation for specifically measuring N-acetylgalactosaminyltransferase 1 vs. N-acetylgalactosaminyltransferase 2 during cartilage biosynthesis.
Art of Record
Dantherm Group. Harnessing heat for effective disinfection. 13 Feb 2025. https://www.danthermgroup.com/uk/insights/harnessing-heat-for-effective-disinfection
Conclusion
Claims 1-5 and 7 are rejected.
No claims are allowed.
THIS ACTION IS MADE FINAL. 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.
Correspondence Information
Any inquiry concerning this communication or earlier communications from the examiner should be directed to NATALIE IANNUZO whose telephone number is (703)756-5559. The examiner can normally be reached Mon - Fri: 8:30-6:00 EST.
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/NATALIE IANNUZO/Examiner, Art Unit 1653
/SHARMILA G LANDAU/Supervisory Patent Examiner, Art Unit 1653
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