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 .
DETAILED ACTION
This Office Action is a reply to Applicant’s Election (Response to Restriction Requirement) filed March 25, 2026.
Claims 1-32 are pending in the instant application.
Election/Restrictions
Applicant’s election (without traverse) of Group I (claims 1, 2 and 12-20) in the reply filed on March 25, 2026 is acknowledged.
Claims 3-11 and 21-32 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on March 25, 2026.
The requirement is still deemed proper and is therefore made FINAL.
Accordingly, claims 1, 2 and 12-20 have been examined on the merits as detailed below:
Information Disclosure Statement
Applicant’s information disclosure statement (IDS) filed March 13, 2025 is acknowledged. The submission is in compliance with the provisions of 37 CFR §1.97. Accordingly, the Examiner has considered the information disclosure statement, and a signed copy is enclosed herewith.
Applicant’s IDS filed January 17, 2024 is acknowledged. The submission is in compliance with the provisions of 37 CFR §1.97. Accordingly, the Examiner has considered the information disclosure statement, and a signed copy is enclosed herewith.
Applicant’s IDS filed September 1, 2023 is acknowledged. The submission is in compliance with the provisions of 37 CFR §1.97. Accordingly, the Examiner has considered the information disclosure statement, and a signed copy is enclosed herewith.
Drawings
The Drawings filed on September 1, 2023 are acknowledged. The Drawings are objected to because some Drawings reference the colors, "red" and "green". See Figures 11A and 13D, for example. In the instant application, color drawings have been filed without an accompanying petition. Corrected drawing sheets in compliance with 37 CFR 1.121(d) are required in reply to the Office action to avoid abandonment of the application. Any amended replacement drawing sheet should include all of the figures appearing on the immediate prior version of the sheet, even if only one figure is being amended. The figure or figure number of an amended drawing should not be labeled as “amended.” If a drawing figure is to be canceled, the appropriate figure must be removed from the replacement sheet, and where necessary, the remaining figures must be renumbered and appropriate changes made to the brief description of the several views of the drawings for consistency. Additional replacement sheets may be necessary to show the renumbering of the remaining figures. Each drawing sheet submitted after the filing date of an application must be labeled in the top margin as either “Replacement Sheet” or “New Sheet” pursuant to 37 CFR 1.121(d). If the changes are not accepted by the examiner, the applicant will be notified and informed of any required corrective action in the next Office action. The objection to the drawings will not be held in abeyance.
Color photographs and color drawings are not accepted unless a petition filed under 37 CFR 1.84(a)(2) is granted. Any such petition must be accompanied by the appropriate fee set forth in 37 CFR 1.17(h), three sets of color drawings or color photographs, as appropriate, and, unless already present, an amendment to include the following language as the first paragraph of the brief description of the drawings section of the specification:
Color photographs will be accepted if the conditions for accepting color drawings and black and white photographs have been satisfied. See 37CFR 1.84(b)(2). Note that the requirement for three sets of color drawings under 37 CFR 1.84(a)(2)(ii) is not applicable to color drawings submitted via EFS-Web. Therefore, only one set of such color drawings is necessary when filing via EFS-Web.
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 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.
Claim Rejections - 35 USC § 102
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.
Claims 1, 2, 12 and 13 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Spilman et al. (PLOS One, April 2010 | Volume 5 | Issue 4 | e9979, pages 1-8).
The claims are drawn to a method of inhibiting reactive astrocyte mediated neuronal and/or oligodendrocyte cell death in a subject, said method comprising: administering an inhibitor of Elongation of Very Long Chain Fatty Acids Protein 1 (ELOVL1) to a subject having or at risk of having a condition mediated by reactive astrocytes, wherein said ELOVL1 inhibitor is administered in an amount effective to inhibit reactive astrocyte mediate neuronal and/or oligodendrocyte cell death in the subject, wherein the ELOVL1 inhibitor comprises rapamycin, a derivative, or analog thereof.
Spilman et al. discloses that inhibition of mTOR by rapamycin abolishes cognitive deficits and reduces amyloid-b levels in a mouse model of Alzheimer’s Disease. See Abstract.
While Spilman et al. does not explicitly teach that administration of rapamycin to a subject having Alzheimer’s Disease inhibits reactive astrocyte mediated neuronal and/or oligodendrocyte cell death in the subject, Spilman et al. discloses the same method as claimed. Namely, administration of rapamycin to a subject having Alzheimer’s Disease. Any underlying mechanism of action would naturally flow and be inherent to administration of the rapamycin composition to the subject. See MPEP 2112 as it relates to inherency. Also, see In re Spada, 911 F.2d 705, 709, 15 USPQ2d 1655, 1658 (Fed. Cir. 1990) and In re Best, 562 F.2d 1252 (CCPA 1977).
The Examiner has provided sound basis in fact and technical reasoning that reasonably supports the determination that the allegedly inherent characteristic necessarily flows from what has been specifically disclosed within the prior art and has shifted the burden to Applicant to provide evidence to the contrary.
Therefore, the subject matter of claims 1, 2, 12 and 13 is anticipated by Spilman et al.
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Claims 1, 2, 14 and 16 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Arcella et al. (Brain Research 1495 (2013) 37-51) and/or Heimberger et al. (Neuro Oncol. 2005 Jan;7(1):1-11).
The claims are as described above.
Arcella et al. discloses that when administered in vivo to brain xenografts in nude mice, rapamycin almost doubled the survival time of mice and inhibited by more than 95% of brain tumor volume. See Abstract, for example.
Heimberger et al. discloses that rapamycin treatment of established subcutaneous U-87 xenografts in vivo resulted in marked brain tumor regression. See page 1, right column; and Figure 5.
While neither Arcella et al. nor Heimberger et al. explicitly teach that administration of rapamycin to a subject having brain cancer or oligodendrogloima inhibits reactive astrocyte mediated neuronal and/or oligodendrocyte cell death in the subject, both Arcella et al. and Heimberger et al. teach the same method as claimed. Namely, administration of rapamycin to a subject having brain cancer or oligodendrogloima. Any underlying mechanism of action would naturally flow and be inherent to administration of the rapamycin composition to the subject. See MPEP 2112 as it relates to inherency. Also, see In re Spada, 911 F.2d 705, 709, 15 USPQ2d 1655, 1658 (Fed. Cir. 1990) and In re Best, 562 F.2d 1252 (CCPA 1977).
The Examiner has provided sound basis in fact and technical reasoning that reasonably supports the determination that the allegedly inherent characteristic necessarily flows from what has been specifically disclosed within the prior art and has shifted the burden to Applicant to provide evidence to the contrary.
Therefore, the subject matter of claims 1, 2, 14 and 16 is anticipated by Arcella et al. and/or Heimberger et al.
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Claims 1, 2 and 15 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Kwasnicki et al. (ANTICANCER RESEARCH 35: 689-696 (2015)).
The claims are as described above.
Kwasnicki et al. discloses the involvement of mTOR signaling pathways in regulating growth and dissemination of metastatic brain tumors via epithelial-mesenchymal transition (EMT). More specifically, Kwasnicki et al. disclose that the inhibition of mTOR signaling by rapamycin could provide therapeutic value in the management of patients with brain metastases. See Abstract, for example.
While Kwasnicki et al. does not explicitly teach that administration of rapamycin to a subject having a metastatic brain tumor inhibits reactive astrocyte mediated neuronal and/or oligodendrocyte cell death in the subject, Kwasnicki et al. discloses the same method as claimed. Namely, administration of rapamycin to a subject having a metastatic brain cancer. Any underlying mechanism of action would naturally flow and be inherent to administration of the rapamycin composition to the subject. See MPEP 2112 as it relates to inherency. Also, see In re Spada, 911 F.2d 705, 709, 15 USPQ2d 1655, 1658 (Fed. Cir. 1990) and In re Best, 562 F.2d 1252 (CCPA 1977).
The Examiner has provided sound basis in fact and technical reasoning that reasonably supports the determination that the allegedly inherent characteristic necessarily flows from what has been specifically disclosed within the prior art and has shifted the burden to Applicant to provide evidence to the contrary.
Therefore, the subject matter of claims 1, 2 and 15 is anticipated by Kwasnicki et al.
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Claims 1, 2 and 17 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Wang et al. (European Journal of Pharmacology 884 (2020) 173369, pages 1-9).
The claims are as described above.
Wang et al. discloses the topical administration of rapamycin promotes retinal ganglion cell survival and reduces intraocular pressure in a rat glaucoma model. See Abstract.
While Wang et al. does not explicitly teach that administration of rapamycin to a subject having glaucoma inhibits reactive astrocyte mediated neuronal and/or oligodendrocyte cell death in the subject, Wang et al. discloses the same method as claimed. Namely, administration of rapamycin to a subject having glaucoma. Any underlying mechanism of action would naturally flow and be inherent to administration of the rapamycin composition to the subject. See MPEP 2112 as it relates to inherency. Also, see In re Spada, 911 F.2d 705, 709, 15 USPQ2d 1655, 1658 (Fed. Cir. 1990) and In re Best, 562 F.2d 1252 (CCPA 1977).
The Examiner has provided sound basis in fact and technical reasoning that reasonably supports the determination that the allegedly inherent characteristic necessarily flows from what has been specifically disclosed within the prior art and has shifted the burden to Applicant to provide evidence to the contrary.
Therefore, the subject matter of claims 1, 2 and 17 is anticipated by Wang et al.
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Claims 1, 2 and 18 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Erlich et al. (Neurobiology of Disease 26 (2007) 86-93).
The claims are as described above.
Erlich et al. discloses that rapamycin is a neuroprotective treatment for traumatic brain injury. See Abstract.
While Erlich et al. does not explicitly teach that administration of rapamycin to a subject having a traumatic brain injury inhibits reactive astrocyte mediated neuronal and/or oligodendrocyte cell death in the subject, Wang et al. discloses the same method as claimed. Namely, administration of rapamycin to a subject having a traumatic brain injury. Any underlying mechanism of action would naturally flow and be inherent to administration of the rapamycin composition to the subject. See MPEP 2112 as it relates to inherency. Also, see In re Spada, 911 F.2d 705, 709, 15 USPQ2d 1655, 1658 (Fed. Cir. 1990) and In re Best, 562 F.2d 1252 (CCPA 1977).
The Examiner has provided sound basis in fact and technical reasoning that reasonably supports the determination that the allegedly inherent characteristic necessarily flows from what has been specifically disclosed within the prior art and has shifted the burden to Applicant to provide evidence to the contrary.
Therefore, the subject matter of claims 1, 2 and 18 is anticipated by Erlich et al.
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Claims 1, 2 and 19 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Reifsnyder et al. (AGING 2016, Vol. 8, No. 11, 3120-3130).
The claims are as described above.
Reifsnyder et al. discloses that rapamycin treatment benefits glucose metabolism in mouse models of type 2 diabetes. See Abstract, for example.
While Reifsnyder et al. does not explicitly teach that administration of rapamycin to a subject having type 2 diabetes inhibits reactive astrocyte mediated neuronal and/or oligodendrocyte cell death in the subject, Reifsnyder et al. discloses the same method as claimed. Namely, administration of rapamycin to a subject having type 2 diabetes. Any underlying mechanism of action would naturally flow and be inherent to administration of the rapamycin composition to the subject. See MPEP 2112 as it relates to inherency. Also, see In re Spada, 911 F.2d 705, 709, 15 USPQ2d 1655, 1658 (Fed. Cir. 1990) and In re Best, 562 F.2d 1252 (CCPA 1977).
The Examiner has provided sound basis in fact and technical reasoning that reasonably supports the determination that the allegedly inherent characteristic necessarily flows from what has been specifically disclosed within the prior art and has shifted the burden to Applicant to provide evidence to the contrary.
Therefore, the subject matter of claims 1, 2 and 19 is anticipated by Reifsnyder et al.
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Claims 1, 2 and 20 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Karim et al. (GLIA 58:1727-1738 (2010)).
The claims are as described above.
Karim et al. discloses rapamycin administration to a transgenic mouse model of the leukodystrophy, Pelizaeus-Merzbacher Disease. See Abstract.
While Karim et al. does not explicitly teach that administration of rapamycin to a subject having Pelizaeus-Merzbacher Disease inhibits reactive astrocyte mediated neuronal and/or oligodendrocyte cell death in the subject, Karim et al. discloses the same method as claimed. Namely, administration of rapamycin to a subject having Pelizaeus-Merzbacher Disease. Any underlying mechanism of action would naturally flow and be inherent to administration of the rapamycin composition to the subject. See MPEP 2112 as it relates to inherency. Also, see In re Spada, 911 F.2d 705, 709, 15 USPQ2d 1655, 1658 (Fed. Cir. 1990) and In re Best, 562 F.2d 1252 (CCPA 1977).
The Examiner has provided sound basis in fact and technical reasoning that reasonably supports the determination that the allegedly inherent characteristic necessarily flows from what has been specifically disclosed within the prior art and has shifted the burden to Applicant to provide evidence to the contrary.
Therefore, the subject matter of claims 1, 2 and 20 is anticipated by Karim et al.
Prior Art Made of Record but not Relied Upon
Inhibitors of elongation of Very Long Chain Fatty Acids Protein 1 (ELOVL1) are well-known in the art. Prior art made of record, but not relied upon is:
WO 2018/107056 – the reference teach and disclose organic compound inhibitors of ELOVL1.
Ohno et al. (PNAS ∣ October 26, 2010 ∣ Vol. 107 ∣ no. 43 ∣ 18439-18444) teach nucleic acid inhibitors of ELOVL1.
Siddiqui et al. (ACS Omega, 2023 Mar 8;8(11):9764-9774) disclose oleic erucic acids; Lorenzo’s oil; and other pyrimidine-ether-based and pyrazole amides as inhibitors of ELOVL1.
Guo et al. (Asian-Australas J Anim Sci. 2016 Jan 18;29(11):1646-1652) teach rapamycin inhibits expression of ELOVL1.
Conclusion
No claims are allowable at this time.
Any inquiry concerning this communication or earlier communications from the Examiner should be directed to Terra C. Gibbs whose telephone number is 571-272-0758. The Examiner can normally be reached from 8 am - 5 pm M-F.
If attempts to reach the Examiner by telephone are unsuccessful, the Examiner's supervisor, Ram Shukla can be reached on 571-272-0735. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/TERRA C GIBBS/Primary Examiner, Art Unit 1635
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