Prosecution Insights
Last updated: April 19, 2026
Application No. 17/625,440

TREATMENT OF GLYCOGEN STORAGE DISEASE (GSD)

Non-Final OA §103
Filed
Jan 07, 2022
Examiner
KOROTCHKINA, LIOUBOV G
Art Unit
1653
Tech Center
1600 — Biotechnology & Organic Chemistry
Assignee
UNIVERSITE D'EVRY VAL D'ESSONNE
OA Round
3 (Non-Final)
29%
Grant Probability
At Risk
3-4
OA Rounds
3y 7m
To Grant
88%
With Interview

Examiner Intelligence

Grants only 29% of cases
29%
Career Allow Rate
12 granted / 41 resolved
-30.7% vs TC avg
Strong +59% interview lift
Without
With
+59.0%
Interview Lift
resolved cases with interview
Typical timeline
3y 7m
Avg Prosecution
63 currently pending
Career history
104
Total Applications
across all art units

Statute-Specific Performance

§101
5.1%
-34.9% vs TC avg
§103
45.1%
+5.1% vs TC avg
§102
10.8%
-29.2% vs TC avg
§112
28.3%
-11.7% vs TC avg
Black line = Tech Center average estimate • Based on career data from 41 resolved cases

Office Action

§103
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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 07/21/2025 has been entered. Priority This application is a 371 of PCT/EP2020/069432 filed 07/09/2020. Applicant’s claim for the benefit of a prior-filed application under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, 365(c), or 386(c) is acknowledged. Acknowledgment is made of applicant’s claim for foreign priority under 35 U.S.C. 119 (a)-(d) based on EP 19305928.4 filed 07/09/2019. Receipt is acknowledged of certified copies of papers required by 37 CFR 1.55. Information Disclosure Statement The information disclosure statement (IDS) submitted on 09/25/2025 complies with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner. Status of the Claims Claims 2-4 and 6-8 are amended. Claims 2-10, 12, 13, 17-19 and 21-26 are pending (claims set filed 07/07/2025) and are examined on the merits herein. Withdrawal of Rejections The response and amendment filed on 07/07/2025 are acknowledged. All of the amendment and arguments have been thoroughly reviewed and considered. 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. Examiner’s Comment Amended claims 2-4 and 6-8 contain new limitation: “from the circulation”. Although “from the circulation” is not found in the specification, a new matter rejection is not made. MPEP 2163: “While there is no in haec verba requirement, newly added claims or claim limitations must be supported in the specification through express, implicit, or inherent disclosure.” Here the mechanism of circulation is an inherent mechanism and thus application of art will also take this into consideration. Claim Rejections - 35 USC § 103 The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action. Claims 2-10, 12, 13, 17-19 and 21-26 are rejected under 35 U.S.C. 103 as being unpatentable over Puzzo (Puzzo et al. Sci. Transl. Med., 2017, 9, eaam6375, 1-12) in view of Khanna (Khanna et al. PLOS One, 2012, 7, e40776, 1-12) and Lukas (Lukas et al. Molec. Therapy, 2015, 23, 456-464 on record in IDS). Regarding claims 2-4 and 6-8, Puzzo teaches treatment of glycogen storage disease or Pompe disease with secretable acid-α-glucosidase (GAA) expressed in liver. Puzzo describes using adeno-associated virus (AAV) vector optimized for hepatic expression to deliver the nucleic acid encoding GAA (Abstract). Puzzo discloses that treatment of knockout (Gaa-/-) mice with the AAV expressing GAA in liver rescued glycogen accumulation in central nervous system (Abstract). Puzzo describes that administration of AAV with hepatically expressed GGA results in uptake of GAA by spinal cord as detected by Western blot analysis of spinal cord lysates 10 months after AAV treatment (p. 4, right column, last paragraph and Figure 4B). Additionally, such treatment resulted in improvement of the survival of motor neurons and neuroinflammation and normalization of astrogliosis in spinal cord (p. 9, right column, 3rd paragraph). Puzzo mentions that even though GAA does not normally cross the blood-brain barrier (BBB), however the high circulating GAA may lead to a leakage across BBB or other mechanisms such as transport via exosomes may be involved (p. 9, right column 4th paragraph). Puzzo does not teach administration of pharmacological chaperons, i.e. DNJ and ABX, however indicates that combination of enzyme replacement therapy with chaperones leads to stabilization of recombinant GAA and results in greater therapeutic efficacy (p. 9, right column, 3rd paragraph). Khanna teaches that pharmacological chaperone AT2220 (DNJ, duvoglustat) increases recombinant human GGA (rhGGA) uptake and glycogen reduction in mouse model of Pompe disease (Abstract). Khanna describes that “oral pre-administration of AT2220 to rats led to a greater than two-fold increase in the circulating half-life of intravenous rhGAA. Importantly, co-administration of AT2220 and rhGAA to GAA knock-out (KO) mice resulted in significantly greater rhGAA levels in plasma, and greater uptake and glycogen reduction in heart and skeletal muscles, compared to administration of rhGAA alone. “ (Abstract). Khanna mentions that AT2220 has been shown to bind GAA, increase its stability, lysosomal trafficking and activity and that may explain the increase in the half-life of rhGAA in circulation and uptake of rhGAA by tissues (p. 10, left column, 1st and 2nd paragraphs). Lukas teaches combination of chaperones that stabilize activity of enzymes of lysosomal storage disorders, i.e. α-galactosidase (for Fabry disease) and α-glucosidase (for Pompe disease). Lucas describes that co-administration of two pharmacological chaperones, DNJ with ABX, led to higher stabilization of α-galactosidase during thermal denaturation than with DNJ alone and that: “ABX alone does not preserve enzyme activity but when used with DGJ has a synergistic positive effect” (p. 458, right column, p. 459, left column, 1st paragraph). Lucas discloses significant increase in the activity of GAA mutants upon administration of DNJ in combination with ABX (p. 459, left column, 2nd paragraph). Lukas mentions that pharmacological chaperones correct misfolding, stabilize protein structure, prevent proteasomal degradation and facilitate transport to lysosome (p. 457, left column, 3rd paragraph). Lukas suggests that combination of chaperones can improve current treatment strategies for Fabry and Pompe diseases (Abstract). It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to combine teachings of Puzzo and Khanna and co-administer DNJ with GAA treatment taught by Puzzo. One would have been motivated to make this combination since Khanna showed co-administration of rhGAA and DNJ to result in prolonged half-life of GAA in circulation and increase in uptake of GAA by heart and skeletal muscle and Puzzo mentioned that higher level of GAA in circulation may be necessary for its uptake by spinal cord. A skilled artisan would have reasonably expected success in this combination since both Puzzo and Khanna developed methods for treatment of Pompe disease with GAA deficiency by enzyme replacement therapy. It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to co-administer ABX with DNJ as described by Lukas for treatment of GSD and CNS disfunction during GSD and to increase the GAA uptake in the spinal cord based on Puzzo and Khanna teachings. One would have been motivated to do that since Lukas showed stabilization of α-galactosidase and enhancement of GAA activity by combination of DNJ and ABX compared to DNJ alone. A skilled artisan would have reasonably expected success in this combination since Puzzo, Khanna and Lukas teach treatment of GSD disease with GAA deficiency. The recitations “increasing the uptake of a therapeutic acid-alpha glucosidase (GAA) polypeptide in the spinal cord from the circulation” in claims 3 and 7 are interpreted as recitation of intended use. The intended use is given weight to the extent that it imparts a structural limitation and the prior art needs to be capable of performing the intended use. See MPEP 2111.02, section II. In instant case, the prior art renders the instantly claimed method steps obvious, Puzzo teaches uptake of therapeutic GAA in the spinal cord, Khanna showed increase in GAA uptake in heart and muscle in the presence of chaperone DNJ and Lukas showed benefits of combination of ABX and DNJ chaperones. Therefore, the method described in prior art is capable of achieving the same goal, i.e. to increase the uptake of a therapeutic acid-alpha glucosidase (GAA) polypeptide in the spinal cord from the circulation. The recitations in the wherein clause of claims 2, 4, 6 and 8: “wherein the pharmacological chaperones increase the uptake of the therapeutic GAA polypeptide in the spinal cord from the circulation” are interpreted as recitation of intended use. MPEP 2111.04 states: “whereby clause in a method claim is not given weight when it simply expresses the intended result of a process step positively recited.’" Id. (quoting Minton v. Nat’l Ass’n of Securities Dealers, Inc., 336 F.3d 1373, 1381, 67 USPQ2d 1614, 1620 (Fed. Cir. 2003))”. In instant case, the prior art renders the instantly claimed method steps obvious, Puzzo indicates the necessity of higher amount of circulating GAA to achieve uptake by spinal cord and Khanna demonstrates that co-administration of GAA and chaperone, DNJ, increases the half-life of GAA and hence increases the circulating amount and that will facilitate the uptake of GAA in the spinal cord. Therefore, the method described in prior art is capable of achieving increase in the uptake of a therapeutic GAA polypeptide in the spinal cord from the circulation in the presence of pharmacological chaperones. Thus, Puzzo, Khanna and Lukas teachings render claims 2-4 and 6-8 obvious. Regarding claims 9 and 17, Puzzo teaches nucleic acids encoding GAA and viral vectors comprising nucleic acids encoding GAA for transgene delivery (Abstract) and hence Puzzo teaching in combination with Khanna and Lukas teachings renders claims 9 and 17 obvious. Regarding claims 5, 10 and 19, Puzzo teaches administration of the viral vector with nucleic acid encoding GAA (Abstract). Khanna teaches administration of duvoglustat (Abstract) as described above. Lukas teaches administration of ABX in the form of Ambroxol hydrochloride (p.462. right column, last paragraph). Thus, Puzzo, Khanna and Lukas teachings render claims 5, 10 and 19 obvious. Regarding claim 12, Puzzo teaches treatment of Pompe disease which is GSDII disease (Abstract). Thus, Puzzo, Khanna and Lukas teachings render claim 12 obvious. Regarding claims 13 and 18, Khanna teaches co-administration of rhGAA and DNJ chaperone (Abstract). It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention that chaperones can be co-administered with the nucleic acid molecule encoding GAA similar to co-administration of DNJ and rhGAA described by Khanna. One would have been motivated to do that since Khanna showed increase in the half-life of GAA in circulation and increase in uptake of GAA by tissues with co-administration of rhGAA and DNJ. Alternatively, one would be motivated to optimize the administration regimen to achieve the highest level of GAA in circulation and tissues. A skilled artisan would have reasonably expected success in that because Puzzo, Khanna and Lukas teach treatment of GSD disease and optimization of administration regimen is within the skill of artisan in the field. Thus, Khanna teaching in combination with Puzzo and Lukas teachings render claims 13 and 18 obvious. Regarding claims 21-26, Puzzo teaches that adeno-associated virus vectors encode the GAA constructs under the control of a hepatocyte-specific promoter, hAAT (p. 3, right column, 2nd paragraph). Thus, Puzzo, Khanna and Lukas teachings render claims 21-26 obvious. Response to Arguments Applicant's arguments filed 07/07/2025 have been fully considered but they are not persuasive. Applicant’s arguments with respect 35 U.S.C. 103 rejection have been considered but are moot because the new ground of rejection does not rely on any reference applied in the prior rejection of record for any teaching or matter specifically challenged in the argument. Current 35 U.S.C. 103 rejection is based on combination of prior art of Puzzo, Khanna and Lucas as described above. Conclusion No claims are allowed. Any inquiry concerning this communication or earlier communications from the examiner should be directed to LIOUBOV G KOROTCHKINA whose telephone number is (571)270-0911. The examiner can normally be reached Monday-Friday: 8:00-5:30. Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice. If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Sharmila G Landau can be reached at (571)272-0614. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300. Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000. /L.G.K./Examiner, Art Unit 1653 /SHARMILA G LANDAU/Supervisory Patent Examiner, Art Unit 1653
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Prosecution Timeline

Jan 07, 2022
Application Filed
Sep 19, 2024
Non-Final Rejection — §103
Feb 20, 2025
Response Filed
May 18, 2025
Final Rejection — §103
Jul 07, 2025
Response after Non-Final Action
Jul 21, 2025
Request for Continued Examination
Jul 22, 2025
Response after Non-Final Action
Nov 18, 2025
Non-Final Rejection — §103
Mar 30, 2026
Examiner Interview Summary

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Study what changed to get past this examiner. Based on 5 most recent grants.

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Prosecution Projections

3-4
Expected OA Rounds
29%
Grant Probability
88%
With Interview (+59.0%)
3y 7m
Median Time to Grant
High
PTA Risk
Based on 41 resolved cases by this examiner. Grant probability derived from career allow rate.

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