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 .
Claims 2, 3, 7-14, 17, 20-27 have been canceled. Claims 1, 4-6, 15, 16, 18, 19, 28-31 are pending.
When referencing the specification, please use page and paragraph number (and line number as necessary) of the original specification. Do not simply use paragraph numbers or refer to the US Patent Application Publication.
Applicant's arguments filed 3-18-26 have been fully considered but they are not persuasive.
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Election/Restrictions
Claim 7 (now canceled) was limited to PPT1, CLN2, CLN3, GALC or HEXA. Claim 8 (now canceled) was limited to palmitoyl-protein thioesterase-1 (PPT1), tripeptidyl peptidase 1 (TPP1), galactosylceramide (GLAC), battenin, or hexosaminidase A (HEXA). CLN2 in claim 7 is a synonym for tripeptidyl peptidase 1 (TPP1) in claim 8. Accordingly, Groups II and VI in the restriction sent 10-11-24 were determined to be equivalent and were combined into Group II. Group VII in the restriction sent 10-11-24 was renamed Group VI in the office action sent 2-25-25.
The Groups remain:
Group I, claims 1-8, 14-22, 27, 28, drawn to a method of treating disease using a vector encoding PPT1.
Group II, claims 1-8, 14-22, 27, 28, drawn to a method of treating disease using a vector encoding CLN2, aka TPP1.
Group III, claims 1-7, 14-22, 27, 28, drawn to a method of treating disease using a vector encoding CLN3.
Group IV, claims 1-8, 14-22, 27, 28, drawn to a method of treating disease using a vector encoding GALC (galactosylceramidase; pg 10, para 58).
Group V, claims 1-8, 14-22, 27, 28, drawn to a method of treating disease using a vector encoding HEXA.
Group VI, claims 1-6, 8, 14-22, 27, 28, drawn to a method of treating disease using a vector encoding battenin.
Applicants elected Group VI (now Group II), claims 1-8, 14-22, 27, 28, without traverse, in the reply filed on 12-11-24, drawn to a method of treating disease using a vector encoding TPP1 (aka CLN2).
Claims 1, 4-6, 15, 16, 18, 19, 28-31 remain under consideration as they relate to Group II, i.e. treating disease using a vector encoding CLN2, aka TPP1. They are not under consideration as they relate to a vector encoding CLN3, GALC, HEXA, or battenin as broadly encompassed by claim 1.
Specification
The title should be changed to more-closely reflect the claimed and examined subject matter to ---METHOD OF TREATING LATE-INFANTILE BATTEN DISEASE USING A VECTOR ENCODING TPP1---.
Claim interpretation
Claim 1 as amended has fixed the issue regarding the concept of a “gene encoding CLN2” not being interchangeable with “gene encoding TTP1”. Corti (Cell Reports Med., 2025, Vol. 6, #102244, pg 1-27) says ceroid lipofuscinosis neuronal 2 (CLN2) is the disease name and is caused by a mutant TPP1 gene which leads to absence or severe reduction in the TPP1 enzyme. (“CLN2 disease is caused by mutations in the tripeptidyl peptidase 1 (TPP1) gene, which leads to absence or severe reduction of the lysosomal protein TPP1” – pg 1, col. 1 of Corti). Claim 1 as amended is drawn to treating Batten disease by administering a nucleic acid sequence encoding TPP1.
Claim Objections
The active step a) in claim 1 should clearly set forth the nucleic acid sequence encoding TPP1 is administered to a mammal that has Batten disease. The preamble can delete reference to the human for clarity. Saying the cinnaminic acid, oleamide, or fibrate are in a “pharmaceutic agent” or are in “a therapeutically effective amount” is redundant because the claim requires administering the nucleic acid sequence encoding TPP1 and the cinnaminic acid, oleamide, or fibrate results in treating symptoms of Batten disease (“such that symptoms of late-infantile Batten disease are treated”). Claim 1 can be written more simply as ---A method of treating Batten disease, the method comprising: a) administering a nucleic acid sequence encoding TPP1 to a human that has Batten disease intranasally; and b) administering cinnaminic acid, oleamide, or fibrate to the human such that symptoms of Batten disease are treated--.
Claims 4 and 5 should refer to “the nucleic acid sequence”.
The active step a) in claim 29 should clearly set forth the nucleic acid sequence encoding TPP1 is administered to a mammal that has a mutant TPP1 gene but doesn’t display symptoms of Batten disease. The preamble can delete reference to the human for clarity. The claim never clearly sets forth that administering the nucleic acid sequence and the cinnaminic acid, oleamide, or fibrate prevents symptoms of Batten disease in the human. The term “subject” in the phrase “human subject” is redundant – delete “subject”. Claim 29 can be written more simply as ---A method of preventing Batten disease, the method comprising: a) administering a nucleic acid sequence encoding TPP1 to a human that has a mutant TPP1 gene but does not display symptoms of Batten disease intranasally; and b) administering cinnaminic acid, oleamide, or fibrate to the human such that symptoms of Batten disease are prevented--.
Claim Rejections - 35 USC § 112
Written Description
Claims 1, 4-6, 15, 16, 18, 19, 28-31 remain 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 claim(s) contains 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 rejection regarding a “gene encoding ceroid lipofuscinosis neuronal 2 (CLN), a lysosomal enzyme” as broadly encompassed by claim 1 or 29 other than administering a nucleic acid sequence encoding ceroid lipofuscinosis neuronal 2 (CLN) has been withdrawn in view of the amendment.
The rejection regarding the phrase “subject in need thereof” in claim 1 has been withdrawn in view of the amendment.
The specification lacks written description for preventing late-infantile Batten disease as required in claim 29. The specification and art do not teach administering a sequence encoding CLN2 to a mammal with a defective CLN2 gene “but is not yet displaying symptoms of late infantile Batten disease” as required in claim 29. Nor do they teach administering of the sequence would prevent symptoms of the disease from occurring. Applicants fail to correlate ameliorating symptoms of disease to preventing symptoms of disease. Accordingly, the specification lacks written description for claim 29 other than administering a nucleic acid sequence encoding TPP1 to a mammal that has late-infantile Batten disease such that symptoms of the disease are ameliorated.
The specification lacks written description for a mammal 4 or 2 years of age or less as required in claims 30 and 31. Applicants point to paragraphs 6 and 62 for support; however, support cannot be found there or elsewhere in the specification. Pg 2, para 6, discusses late infantile neuronal ceroid lipofuscinosis. Pg 12, para 62, is just a heading that says “Pharmaceutical Compositions”. Accordingly, the claims lack written description.
Response to arguments
Applicants argue the amendment overcomes the rejections. Applicants’ argument is not persuasive for reasons set forth above.
Indefiniteness
Claims 29-31 remain and claim 28 is rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Withdrawn rejections
The rejection of claim 3 has been withdrawn because the claim has been canceled.
The rejection regarding the phrase “the gene encoding for a lysosomal enzyme” in claim 5 has been withdrawn in view of the amendment.
The rejection regarding the phrase “the therapeutically effective amount of the pharmaceutical agent is lower when the pharmaceutical agent is administered in combination with all-trans retinoic acid than when the pharmaceutical agent is delivered without all-trans retinoic acid” in claim 17 has been withdrawn because the claim has been canceled.
The rejection of claims 30 and 31 has been withdrawn in favor of a claim objection.
Pending rejections
Claim 29 remains indefinite because it requires “preventing” Batten disease in a human but the active steps never result in preventing symptoms of Batten disease. This makes the claim indefinite.
New rejection
Claim 28 is indefinite because “the human in need thereof” lacks antecedent basis. This makes the claim indefinite. Delete “in need thereof”.
Response to arguments
Applicants argue the amendment overcomes the rejections. Applicants’ argument is not persuasive for reasons set forth above.
Double Patenting
The objection of claim 29 under 37 CFR 1.75 as being a substantial duplicate of claim 1 has been withdrawn in view of the amendment.
Claim Rejections - 35 USC § 103
A) Claims 1, 4-6, 15, 16, 18, 19, 28-31 remain rejected under 35 U.S.C. 103 as being unpatentable over Anderson (20220184188; EFD=2-1-19) in view of Aronovich (“Lysosomal storage disease: Gene therapy on both sides of the blood–brain barrier”, Mol. Genetics & Metab., 2015, Vol. 114, pg 83-93), McIvor (RU2801511), Miller (20220090129), Pahan (WO 2018126000) or Pahan (WO 2014089449), and Best (Neurobiol. of Disease, 2017, Vol. 100, pg 62-74).
Anderson taught: “A method of treating a primate in need of tripeptidyl peptidase 1 (TPP1), comprising: (a) providing a recombinant adeno-associated virus (AAV) vector comprising a nucleic acid encoding TPP1; and (b) administering an amount of said recombinant AAV vector to the central nervous system (CNS) of said primate, wherein said TPP1 is expressed in said primate.” The primate is human (par a3, 4, 6, et al). Anderson taught using the method to decrease symptoms of CLN2 (pg 2, para 13-14), specifically late-infantile neuronal ceroid lipofuscinosis type 2 (CLN2) (para 2, 6, 143; claim 3) (and juvenile CLN2 - para 79) as required in claim 1. This is equivalent to administering a nucleic acid sequence encoding TTP1 to a human with late-infantile Batten disease as required in step a) of claim 1 and 27.
Anderson did not teach administering the AAV intranasally as required in step a) of claim 1. However, Aronovich taught intranasal administration of AAV as one of a number of options (including into the blood or the CSF) for delivering AAV across the blood brain barrier (pg 86, 3rd paragraph). McIvor taught intranasal administration of AAV9/IDUA to treat MPS I mice (Fig. 19). Miller taught intranasal AAV-CFTR (para 208-210). Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to administer AAV encoding TPP1 across the blood brain barrier to treat Batten disease as described by Anderson using nasal administration of AAV to treat lysosomal storage disease as described by Aronovich, McIvor, and Miller. Those of ordinary skill in the art at the time of filing would have been motivated to do so for ease of administration and to avoid surgery.
Anderson did not teach administering fibrate as required in claim 1, e.g. gemfibrozil or fenofibrate, as required in claim 15, or all-trans retinoic acid as required in claim 16. However, Anderson taught using AAV along with other agents (praa 82, 87, 88, 90, 94, 98, 107, 109, 110, 118, 120-122). And Pahan ‘000 taught daily oral administration of gemfibrozil for treating CLN2 deficiency in mice (para 12, 53, 58; Fig. 1; Example 4), and Pahan ‘449 taught daily oral administration of gemfibrozil, fenofibrate, or “all-trans” retinoic acid for treating CLN2 deficiency in mice (para 9-17; Fig. 7, 14-16). Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to administer a viral vector encoding TPP1 across the blood brain barrier to treat Batten disease as described by Anderson in combination with gemfibrozil as described by Pahan ‘000 or gemfibrozil, fenofibrate, or “all-trans” retinoic acid as described by Pahan ‘449. Those of ordinary skill in the art at the time of filing would have been motivated to do for increasing levels of TPP1. Further motivation either way is provided by Best who taught combining a viral vector encoding a protein deficient in cells with a defective gene that causes Batten disease along with fibrate drugs, gemfibrozil and fenofibrate to correct the gene deficiency.
In the reverse, Pahan ‘000 taught daily oral administration of gemfibrozil for treating CLN2 deficiency in mice (para 12, 53, 58; Fig. 1; Example 4), and Pahan ‘449 taught daily oral administration of gemfibrozil, fenofibrate, or “all-trans” retinoic acid for treating CLN2 deficiency in subject (para 9-17; Fig. 7, 14-16). Pahan ‘000 and Pahan ‘449 did not teach administering a TPP1 gene to the subject. However, Anderson taught administering a viral vector encoding TPP1 to a subject with a CLN2 deficiency for reasons set forth above. Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to administer gemfibrozil as described by Pahan ‘000 or “all-trans” retinoic acid as described by Pahan ‘449 in combination with a viral vector encoding TPP1 as described by Anderson. Those of ordinary skill in the art at the time of filing would have been motivated to do so to increase TPP1 levels. Further motivation either way is provided by Best who taught combining a viral vector encoding a protein deficient in cells with a defective gene that causes Batten disease along with fibrate drugs, gemfibrozil and fenofibrate to correct the gene deficiency.
Injection can be repeated 1-7, 7-12, 12-24, 24-48 days (para 113) or at 30 and 90 days (para 138) which is “every 7-30 days” as required in claim 4.
Anderson taught AAV which is a viral vector as required in claim 5.
Anderson taught AAV (claim 1) as required in claim 6.
Claims 15-16 are taught by Pahan, Pahan, and Best (see above).
Claim 18 has been included because Pahan taught administering the fibrate or all-trans retinoic acid orally (see above).
Pahan taught administering fibrate or all-trans retinoic acid once daily (see above) as required in claim 19. And Anderson taught administration of the 2nd agent can be repeated 1-7, 7-12, 12-24, 24-48 days (para 113) or at 30 and 90 days (para 138) which is “once daily” as required in claim 19.
The concept of the “lifespan of the human [increasing] by about 100 days” as required in claim 28 inherently MUST occur because Anderson taught administering two reagents that are described as being part of the invention and because the two reagents taught by Anderson are within the metes and bounds of the claim.
Claim 29 has been included because Anderson taught preventing disease (para 13, 99, 107, 115, 123; claim 25).
Claims 30 and 31 have been included because it was well-known the patients with late-infantile Batten disease are under 4 or 2 years old (pg 2, para 6 of Anderson).
Response to arguments
Applicant points to case law (pg 7) which is not persuasive because the fact patterns in those cases are not the same as the fact patterns in this case.
Applicant reiterates claim 1 and say the combined references do not make the claim obvious (pg 8 of the response). Applicants’ argument is not persuasive because the statement fails to teach one limitation missing from the combined references.
Applicants appear to go on to argue the rejections collectively by discussing primary references Maxfield and Szabolcs (pg 8-10) and secondary references Aronovich, McIvor, Miller (pg 10-15). This is unacceptable because the issues for each rejection and different. Pg 8-15 do not discuss the specific issues at hand using Anderson and the other references in this rejection. Please argue each rejection separately. Arguments may be copied and pasted or referenced, but the arguments should not be combined.
Applicants do not substantially address the combined teachings of Anderson, Aronovich, McIvor, Miller Pahan (WO 2018126000), Pahan (WO 2014089449), and Best.
Applicants’ discussion of Addelman and targeting the hippocampus on pg 9 is irrelevant because Anderson taught treating Batten disease for reasons cited above.
Applicants’ discussion of Aronovich, McIvor and Miller on pg 10 is noted but does not rise to the level of an argument. Aronovich taught intranasal administration of AAV as valid option for delivering AAV across the blood brain barrier (pg 86, 3rd paragraph); McIvor taught intranasal administration of AAV9/IDUA to treat MPS I mice (Fig. 19); and Miller taught intranasal AAV-CFTR (para 208-210). It would have been obvious to those of ordinary skill in the art at the time of filing to administer AAV encoding TPP1 across the blood brain barrier to treat Batten disease as described by Maxfield using nasal administration of AAV to treat lysosomal storage disease as described by Aronovich, McIvor, and Miller. Those of ordinary skill in the art at the time of filing would have been motivated to do so for ease of administration and to avoid surgery.
Applicants discuss the paper by McIvor and the paper published by Belur in 2017 about the McIvor document. Belur says intranasal delivery “was limited to the olfactory bulb” and allowed diffusion “into deeper areas of the brain” (pg 10, last partial paragraph of the response filed 3-18-26). The statement by Belur cited by applicants is proof that McIvor enabled intranasal delivery of AAV across the blood brain barrier because it allowed diffusion into the brain.
Applicants go on to discuss a reference by Chukwu (2025) on pg 11 of the response which shows intranasal delivery of gene therapies resulted in negligible distribution in the brain. Applicants’ argument is not persuasive. The claims encompass any amount of expression anywhere. If the brain MUST be targeted, and the claims encompass any amount of expression in the brain, then any negligible distribution of gene expression in the brain is adequate to meet the limitations of claim 1.
Applicants argue Miller does not teach treating Batten disease (pg 11, last full paragraph). Applicants’ argument is not persuasive because Miller is not relied upon in this rejection.
The paragraph bridging pg 11-12 and the first full paragraph on pg 12 repeat arguments and are not persuasive for reasons set forth above.
Applicants’ discussion of Pahan, Pahan and Best on pg 12-13 is noted but is merely a summary of the teachings in those references; the discussion does not rise to the level of an argument.
B) Claims 1, 4-6, 15, 16, 18, 19, 28-31 remain rejected under 35 U.S.C. 103 as being unpatentable over Davidson (RU 2805606) in view of Aronovich (“Lysosomal storage disease: Gene therapy on both sides of the blood–brain barrier”, Mol. Genetics & Metab., 2015, Vol. 114, pg 83-93), McIvor (RU2801511), Miller (20220090129), Pahan (WO 2018126000) or Pahan (WO 2014089449), and Best (Neurobiol. of Disease, 2017, Vol. 100, pg 62-74).
Davidson taught “TPP1 levels (pmol TPP1 per mg protein) in the CSF of non-human primates following unilateral injection of the AAV2.CAGhTPP1 vector into the cerebral ventricle. Data represent TPP1 levels over time. Day 0 represents endogenous TPP1 levels before injection. N=3 animals (para 27 of translation; Fig. 6).
Davidson taught “Intraventricular administration of the AAV vector. The animals were completely anesthetized. The injection site was shaved, mice were placed in a Kopf stereotactic unit, and they continued to receive 2% isoflurane/oxygen via the nasal circuit. Before the incision, an analgesic (meloxicam, 1-10 mg/kg) was administered subcutaneously. Ophthalmic ointment was applied topically to prevent drying of the eyes during surgery. A 10 or 25 .Math.l Hamilton syringe with a 0.4" 33GA Hamilton needle was prepared by sucking and expelling a sample of the test drug 20 times; this sample of the test drug was discarded. The syringe was loaded with a fresh sample of the test drug, and then injected into the injector (Stoelting Company) . The incision site was cleaned. The injection site was calculated from bregma (+0.3 mm anterior, -1.0 mm lateral), then a burr hole was made in the skull. Then the needle with a sample of the test drug was lowered to a depth of -2.0 mm from the surface of the head brain, a sample of the test drug was injected at a rate of 200 nl/min, and the needle was left in place for 5 minutes before being removed. The incision was closed using non-absorbable sutures. To reduce pain and discomfort after surgery, a local analgesic (Bupivicaine HCl, 0 ,5%)” (para 138).
Davidson taught: “CSF collection . Animals were placed in an isoflurane induction chamber and exposed to a 2.5% isoflurane/oxygen mixture until complete anesthesia and absence of leg response. The injection site was shaved, mice were placed in a RWD Life Science stereotactic unit (Shenzhen, China), and continued to receive 2% isoflurane/oxygen through the nasal circuit. The membrane over the cisterna magna was opened by making an incision along the neck, and the skin and muscles of the neck were separated. A glass capillary was inserted into a large tank and CSF was collected by capillary force for 20 minutes” (para 140).
Davidson taught treating Batten disease (claim 45) which is equivalent to late-infantile Batten disease as required in claim 1.
Davidson did not teach administering the AAV intranasally as required in step a) of claim 1. However, Aronovich taught intranasal administration of AAV as one of a number of options (including into the blood or the CSF) for delivering AAV across the blood brain barrier (pg 86, 3rd paragraph). McIvor taught intranasal administration of AAV9/IDUA to treat MPS I mice (Fig. 19). Miller taught intranasal AAV-CFTR (para 208-210). Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to administer AAV encoding TPP1 across the blood brain barrier to treat Batten disease as described by Davidson using nasal administration of AAV to treat lysosomal storage disease as described by Aronovich, McIvor, and Miller. Those of ordinary skill in the art at the time of filing would have been motivated to do so for ease of administration and to avoid surgery.
Davidson did not teach administering fibrate as required in step b) of claim 1, e.g. gemfibrozil or fenofibrate, as required in claim 15, or all-trans retinoic acid as required in claim 16. However, Pahan ‘000 taught daily oral administration of gemfibrozil for treating CLN2 deficiency in mice (para 12, 53, 58; Fig. 1; Example 4), and Pahan ‘449 taught daily oral administration of gemfibrozil, fenofibrate, or “all-trans” retinoic acid for treating CLN2 deficiency in mice (para 9-17; Fig. 7, 14-16). Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to administer a viral vector encoding TPP1 across the blood brain barrier to treat Batten disease as described by Davidson in combination with gemfibrozil as described by Pahan ‘000 or gemfibrozil, fenofibrate, or “all-trans” retinoic acid as described by Pahan ‘449. Those of ordinary skill in the art at the time of filing would have been motivated to do for increasing levels of TPP1. Further motivation either way is provided by Best who taught combining a viral vector encoding a protein deficient in cells with a defective gene that causes Batten disease along with fibrate drugs, gemfibrozil and fenofibrate to correct the gene deficiency.
In the reverse, Pahan ‘000 taught daily oral administration of gemfibrozil for treating CLN2 deficiency in mice (para 12, 53, 58; Fig. 1; Example 4), and Pahan ‘449 taught daily oral administration of gemfibrozil, fenofibrate, or “all-trans” retinoic acid for treating CLN2 deficiency in subject (para 9-17; Fig. 7, 14-16). Pahan ‘000 and Pahan ‘449 did not teach administering a TPP1 gene to the subject. However, Davidson taught administering a viral vector encoding TPP1 to a subject with a CLN2 deficiency for reasons set forth above. Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to administer gemfibrozil as described by Pahan ‘000 or “all-trans” retinoic acid as described by Pahan ‘449 in combination with a viral vector encoding TPP1 as described by Davidson. Those of ordinary skill in the art at the time of filing would have been motivated to do so to increase TPP1 levels. Further motivation either way is provided by Best who taught combining a viral vector encoding a protein deficient in cells with a defective gene that causes Batten disease along with fibrate drugs, gemfibrozil and fenofibrate to correct the gene deficiency.
Davidson taught AAV which is a viral vector as required in claim 5.
Davidson taught AAV as required in claim 6.
Claims 15-16 are taught by Pahan, Pahan, and Best (see above).
Claim 18 has been included because Pahan taught administering the fibrate or all-trans retinoic acid orally (see above).
Pahan taught administering fibrate or all-trans retinoic acid once daily (see above) as required in claim 19.
The concept of the “lifespan of the human [increasing] by about 100 days” as required in claim 28 inherently MUST occur because Davidson taught administering two reagents that are described as being part of the invention and because the two reagents taught by Davidson are within the metes and bounds of the claim.
Claim 29 has been included because Davidson taught preventing disease (para 28, 94, 95, 121, 139).
Claims 30 and 31 have been included because it was well-known the patients with late-infantile Batten disease are under 4 or 2 years old.
Response to arguments
Applicants do not substantially address the combined teachings of Davidson, Aronovich, McIvor, Miller Pahan (WO 2018126000), Pahan (WO 2014089449), and Best.
Applicants’ other arguments are not persuasive for reasons set forth above.
C) Claims 1, 4-6, 15, 16, 18, 19, 28-31 remain rejected under 35 U.S.C. 103 as being unpatentable over Katz (“AAV gene transfer delays disease onset in a TPP1-deficient canine model of the late infantile form of Batten disease”, Science Translational Medicine, 2015, Vol. 7, No. 313, pg 1-10) in view of Aronovich (“Lysosomal storage disease: Gene therapy on both sides of the blood–brain barrier”, Mol. Genetics & Metab., 2015, Vol. 114, pg 83-93), McIvor (RU2801511), and Miller (20220090129) in view of Aronovich (“Lysosomal storage disease: Gene therapy on both sides of the blood–brain barrier”, Mol. Genetics & Metab., 2015, Vol. 114, pg 83-93), McIvor (RU2801511), Miller (20220090129), Pahan (WO 2018126000) or Pahan (WO 2014089449), and Best (Neurobiol. of Disease, 2017, Vol. 100, pg 62-74).
Katz injected AAV encoding TPP1 into a canine model of TPP1 deficiency intraventricularly (pg 2, col. 2; Fig. S1, S4; Table S1) along with mofetil and cyclosporine daily (pg 3, 1st partial paragraph). Katz taught treating canines with an inactivated TPP1 gene which is a model of late-infantile Batten disease (Title; abstract; pg 9, “Study design”) as required in claim 1.
Katz did not teach administering the AAV intranasally as newly required in claim 1. However, Aronovich taught intranasal administration of AAV as one of a number of options (including into the blood or the CSF) for delivering AAV across the blood brain barrier (pg 86, 3rd paragraph). McIvor taught intranasal administration of AAV9/IDUA to treat MPS I mice (Fig. 19). Miller taught intranasal AAV-CFTR (para 208-210). Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to administer AAV encoding TPP1 across the blood brain barrier to treat Batten disease as described by Katz using nasal administration of AAV to treat lysosomal storage disease as described by Aronovich, McIvor, and Miller. Those of ordinary skill in the art at the time of filing would have been motivated to do so for ease of administration and to avoid surgery.
Katz did not teach administering fibrate as required in claim 1, e.g. gemfibrozil or fenofibrate, as required in claims 14 and 15, or all-trans retinoic acid as required in claim 16. However, Pahan ‘000 taught daily oral administration of gemfibrozil for treating CLN2 deficiency in mice (para 12, 53, 58; Fig. 1; Example 4), and Pahan ‘449 taught daily oral administration of gemfibrozil, fenofibrate, or “all-trans” retinoic acid for treating CLN2 deficiency in mice (para 9-17; Fig. 7, 14-16). Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to administer a viral vector encoding TPP1 across the blood brain barrier to treat Batten disease as described by Katz in combination with gemfibrozil as described by Pahan ‘000 or gemfibrozil, fenofibrate, or “all-trans” retinoic acid as described by Pahan ‘449. Those of ordinary skill in the art at the time of filing would have been motivated to do for increasing levels of TPP1. Further motivation either way is provided by Best who taught combining a viral vector encoding a protein deficient in cells with a defective gene that causes Batten disease along with fibrate drugs, gemfibrozil and fenofibrate to correct the gene deficiency.
In the reverse, Pahan ‘000 taught daily oral administration of gemfibrozil for treating CLN2 deficiency in mice (para 12, 53, 58; Fig. 1; Example 4), and Pahan ‘449 taught daily oral administration of gemfibrozil, fenofibrate, or “all-trans” retinoic acid for treating CLN2 deficiency in subject (para 9-17; Fig. 7, 14-16). Pahan ‘000 and Pahan ‘449 did not teach administering a TPP1 gene to the subject. However, Katz taught administering a viral vector encoding TPP1 to a subject with a CLN2 deficiency for reasons set forth above. Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to administer gemfibrozil as described by Pahan ‘000 or “all-trans” retinoic acid as described by Pahan ‘449 in combination with a viral vector encoding TPP1 as described by Katz. Those of ordinary skill in the art at the time of filing would have been motivated to do so to increase TPP1 levels. Further motivation either way is provided by Best who taught combining a viral vector encoding a protein deficient in cells with a defective gene that causes Batten disease along with fibrate drugs, gemfibrozil and fenofibrate to correct the gene deficiency.
Katz taught AAV which is a viral vector as required in claim 5.
Katz taught AAV as required in claim 6.
Claims 15-16 are taught by Pahan, Pahan, and Best (see above).
Claim 18 has been included because Pahan taught administering the fibrate or all-trans retinoic acid orally (see above).
Pahan taught administering fibrate or all-trans retinoic acid once daily (see above) as required in claim 19.
The concept of the “lifespan of the human [increasing] by about 100 days” as required in claim 28 inherently MUST occur because Katz taught administering two reagents that are described as being part of the invention and because the two reagents taught by Katz are within the metes and bounds of the claim.
Claim 29 has been included because Katz taught preventing Batten disease.
Claims 30 and 31 have been included because it was well-known the patients with late-infantile Batten disease are under 4 or 2 years old.
Response to arguments
Applicants do not substantially address the combined teachings of Katz, Aronovich, McIvor, Miller, Pahan (WO 2018126000), Pahan (WO 2014089449), and Best.
Applicants’ other arguments are not persuasive for reasons set forth above.
D) Claims 1, 4-6, 15, 16, 18, 19, 28-31 remain rejected under 35 U.S.C. 103 as being unpatentable over Maxfield (20110166074) in view of Pahan (WO 2018126000) or Pahan (WO 2014089449), and Best (Neurobiol. of Disease, 2017, Vol. 100, pg 62-74).
Maxfield taught administering AAV encoding CLN2 intracranially (para 162, 174, 175, 190, 191) or intranasally (para 101) to treat Alzheimer’s disease along with a second reagent (claim 7). The second compound can be immunosuppressive reagents daily for thirty days (para 159). Maxfield taught treating Batten disease (para 30, 85, 118, 123) and supplementing a deficiency in a CLN2/PPT1 gene (para 94, 117, 153) which is equivalent to treating late-infantile Batten disease as required in claim 1. Maxfield taught administering AAV intranasally (para 101) as required in claim 1.
Maxfield did not teach administering fibrate as required in claim 1, e.g. gemfibrozil or fenofibrate, as required in claims 14 and 15, or all-trans retinoic acid as required in claim 16. However, Pahan ‘000 taught daily oral administration of gemfibrozil for treating CLN2 deficiency in mice (para 12, 53, 58; Fig. 1; Example 4), and Pahan ‘449 taught daily oral administration of gemfibrozil, fenofibrate, or “all-trans” retinoic acid for treating CLN2 deficiency in mice (para 9-17; Fig. 7, 14-16). Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to administer a viral vector encoding TPP1 across the blood brain barrier to treat Batten disease as described by Maxfield in combination with gemfibrozil as described by Pahan ‘000 or gemfibrozil, fenofibrate, or “all-trans” retinoic acid as described by Pahan ‘449. Those of ordinary skill in the art at the time of filing would have been motivated to do for increasing levels of TPP1. Further motivation either way is provided by Best who taught combining a viral vector encoding a protein deficient in cells with a defective gene that causes Batten disease along with fibrate drugs, gemfibrozil and fenofibrate to correct the gene deficiency.
In the reverse, Pahan ‘000 taught daily oral administration of gemfibrozil for treating CLN2 deficiency in mice (para 12, 53, 58; Fig. 1; Example 4), and Pahan ‘449 taught daily oral administration of gemfibrozil, fenofibrate, or “all-trans” retinoic acid for treating CLN2 deficiency in subject (para 9-17; Fig. 7, 14-16). Pahan ‘000 and Pahan ‘449 did not teach administering a TPP1 gene to the subject. However, Maxfield taught administering a viral vector encoding TPP1 to a subject with a CLN2 deficiency for reasons set forth above. Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to administer gemfibrozil as described by Pahan ‘000 or “all-trans” retinoic acid as described by Pahan ‘449 in combination with a viral vector encoding TPP1 as described by Maxfield. Those of ordinary skill in the art at the time of filing would have been motivated to do so to increase TPP1 levels. Further motivation either way is provided by Best who taught combining a viral vector encoding a protein deficient in cells with a defective gene that causes Batten disease along with fibrate drugs, gemfibrozil and fenofibrate to correct the gene deficiency.
Maxfield did not teach treating late-infantile Batten disease as required in claim 1; however, doing so was obvious in view of Pahan who taught treating late-infantile Batten disease (abstract). Those of ordinary skill in the art at the time of filing would have been motivated to do so to save infants from disease.
The second compound can be administered daily for thirty days (para 159) which is equivalent to claim 4.
AAV-CLN2 is a viral vector as required in claim 5.
Maxfield taught AAV as required in claim 6.
Claims 15-16 are taught by Pahan, Pahan, and Best (see above).
Claim 18 has been included because Pahan taught administering the fibrate or all-trans retinoic acid orally (see above).
Pahan taught administering fibrate or all-trans retinoic acid once daily (see above) as required in claim 19.
The concept of the “lifespan of the human [increasing] by about 100 days” as required in claim 28 inherently MUST occur because Maxfield taught administering two reagents that are described as being part of the invention and because the two reagents taught by Maxfield are within the metes and bounds of the claim.
Claim 29 has been included because it is indefinite and because claim 29 is a substantial duplicate of claim 1.
Claims 30 and 31 have been included because it was well-known the patients with late-infantile Batten disease are under 4 or 2 years old.
Response to arguments
Applicants discussion on pg 9 says Maxwell is limited to treating Alzheimer’s disease. Applicants’ argument is not persuasive. Maxfield taught treating Batten disease (para 30, 85, 118, 123) and supplementing a deficiency in a CLN2/PPT1 gene (para 94, 117, 153) which is equivalent to treating late-infantile Batten disease as required in claim 1. Applicants argue Maxwell is limited to intracranial administration. Applicants’ argument is not persuasive because Maxwell taught intranasal administration.
Applicants’ discussion of Aronovich, McIvor, Miller are irrelevant because they are not part of this rejection.
Applicants’ other arguments regarding Pahan, Pahan, and Best are not persuasive for reasons set forth above.
E) Claims 1, 4-6, 15, 16, 18, 19, 28-31 remain rejected under 35 U.S.C. 103 as being unpatentable over Goss (WO 2017218519) in view of Aronovich (“Lysosomal storage disease: Gene therapy on both sides of the blood–brain barrier”, Mol. Genetics & Metab., 2015, Vol. 114, pg 83-93), McIvor (RU2801511), Miller (20220090129), Pahan (WO 2018126000) or Pahan (WO 2014089449), and Best (Neurobiol. of Disease, 2017, Vol. 100, pg 62-74).
Goss taught administering a lentiviral vector encoding TPP1 to treat late-infantile or juvenile Batten disease (claims 33, 34) via intravascular, intravenous, intraarterial, intraosseously, intraventricular, intracerebral, intracranial, intraspinal, intrathecal, and intramedullary administration (pg 51). The therapy may be combined any of a number of other therapies, “e.g. cytokines, growth factors, hormones, small molecules, pro-drugs, drugs, antibodies, or other various pharmaceutically-active agents.” “There is virtually no limit to other components that may also be included in the compositions, provided that the additional agents do not adversely affect the ability of the composition to deliver the intended therapy” (pg 46, 1st full paragraph).
Goss did not teach administering the AAV intranasally as newly required in claim 1. However, Aronovich taught intranasal administration of AAV as one of a number of options (including into the blood or the CSF) for delivering AAV across the blood brain barrier (pg 86, 3rd paragraph). McIvor taught intranasal administration of AAV9/IDUA to treat MPS I mice (Fig. 19). Miller taught intranasal AAV-CFTR (para 208-210). Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to administer AAV encoding TPP1 across the blood brain barrier to treat Batten disease as described by Goss using nasal administration of AAV to treat lysosomal storage disease as described by Aronovich, McIvor, and Miller. Those of ordinary skill in the art at the time of filing would have been motivated to do so for ease of administration and to avoid surgery.
Goss did not teach administering fibrate as required in claim 1, e.g. gemfibrozil or fenofibrate, as required in claims 14 and 15, or all-trans retinoic acid as required in claim 16. However, Pahan ‘000 taught daily oral administration of gemfibrozil for treating CLN2 deficiency in mice (para 12, 53, 58; Fig. 1; Example 4), and Pahan ‘449 taught daily oral administration of gemfibrozil, fenofibrate, or “all-trans” retinoic acid for treating CLN2 deficiency in mice (para 9-17; Fig. 7, 14-16). Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to administer a viral vector encoding TPP1 across the blood brain barrier to treat Batten disease as described by Goss in combination with gemfibrozil as described by Pahan ‘000 or gemfibrozil, fenofibrate, or “all-trans” retinoic acid as described by Pahan ‘449. Those of ordinary skill in the art at the time of filing would have been motivated to do for increasing levels of TPP1. Further motivation either way is provided by Best who taught combining a viral vector encoding a protein deficient in cells with a defective gene that causes Batten disease along with fibrate drugs, gemfibrozil and fenofibrate to correct the gene deficiency.
In the reverse, Pahan ‘000 taught daily oral administration of gemfibrozil for treating CLN2 deficiency in mice (para 12, 53, 58; Fig. 1; Example 4), and Pahan ‘449 taught daily oral administration of gemfibrozil, fenofibrate, or “all-trans” retinoic acid for treating CLN2 deficiency in subject (para 9-17; Fig. 7, 14-16). Pahan ‘000 and Pahan ‘449 did not teach administering a TPP1 gene to the subject. However, Goss taught administering a viral vector encoding TPP1 to a subject with a CLN2 deficiency for reasons set forth above. Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to administer gemfibrozil as described by Pahan ‘000 or “all-trans” retinoic acid as described by Pahan ‘449 in combination with a viral vector encoding TPP1 as described by Goss. Those of ordinary skill in the art at the time of filing would have been motivated to do so to increase TPP1 levels. Further motivation either way is provided by Best who taught combining a viral vector encoding a protein deficient in cells with a defective gene that causes Batten disease along with fibrate drugs, gemfibrozil and fenofibrate to correct the gene deficiency.
The lentiviral vector encoding TPP1 is a viral vector encoding a lysosomal enzyme as required in claim 5.
Claims 15-16 are taught by Pahan, Pahan, and Best (see above).
Claim 18 has been included because Pahan taught administering the fibrate or all-trans retinoic acid orally (see above).
Pahan taught administering fibrate or all-trans retinoic acid once daily (see above) as required in claim 19.
The concept of the “lifespan of the human ]increasing] by about 100 days” as required in claim 28 inherently MUST occur because Goss taught administering two reagents that are described as being part of the invention and because the two reagents taught by Goss are within the metes and bounds of the claim.
Claim 29 has been included because Goss taught preventing disease (first sentence of detailed description; first paragraph under “H. Gene Therapy Methods”).
Claims 30 and 31 have been included because it was well-known the patients with late-infantile Batten disease are under 4 or 2 years old.
Response to arguments
Applicants do not substantially address the combined teachings of Goss, Aronovich, McIvor, Miller, Pahan (WO 2018126000), Pahan (WO 2014089449), and Best.
Applicants’ other arguments are not persuasive for reasons set forth above.
F) Claims 1, 4-6, 15, 16, 18, 19, 28-31 remain rejected under 35 U.S.C. 103 as being unpatentable over Szabolcs (WO 2018136710) in view of in view of Pahan (WO 2018126000) or Pahan (WO 2014089449), and Best (Neurobiol. of Disease, 2017, Vol. 100, pg 62-74).
Szabolcs taught administering an AAV vector encoding a protein to treat lysosomal storage disease (Examples), specifically CLN2 to treat Batten disease (pg 35) via subcutaneous, intramuscular, intradermal, intraperitoneal, intrathecal, intraosseous, and intravenous), transdermal, intranasal, and inhalation routes (pg 5, “Administration”). The therapy may be combined with HSCs, G-CSF, or immunosuppressive therapy (pg 30-31). Szabolcs taught administering the vector intranasally (pg 5) as required in claim 1.
Szabolcs did not teach administering fibrate as required in claim 1, e.g. gemfibrozil or fenofibrate, as required in claims 14 and 15, or all-trans retinoic acid as required in claim 16. However, Pahan ‘000 taught daily oral administration of gemfibrozil for treating CLN2 deficiency in mice (para 12, 53, 58; Fig. 1; Example 4), and Pahan ‘449 taught daily oral administration of gemfibrozil, fenofibrate, or “all-trans” retinoic acid for treating CLN2 deficiency in mice (para 9-17; Fig. 7, 14-16). Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to administer a viral vector encoding TPP1 across the blood brain barrier to treat Batten disease as described by Szabolcs in combination with gemfibrozil as described by Pahan ‘000 or gemfibrozil, fenofibrate, or “all-trans” retinoic acid as described by Pahan ‘449. Those of ordinary skill in the art at the time of filing would have been motivated to do for increasing levels of TPP1. Further motivation either way is provided by Best who taught combining a viral vector encoding a protein deficient in cells with a defective gene that causes Batten disease along with fibrate drugs, gemfibrozil and fenofibrate to correct the gene deficiency.
In the reverse, Pahan ‘000 taught daily oral administration of gemfibrozil for treating CLN2 deficiency in mice (para 12, 53, 58; Fig. 1; Example 4), and Pahan ‘449 taught daily oral administration of gemfibrozil, fenofibrate, or “all-trans” retinoic acid for treating CLN2 deficiency in subject (para 9-17; Fig. 7, 14-16). Pahan ‘000 and Pahan ‘449 did not teach administering a TPP1 gene to the subject. However, Szabolcs taught administering a viral vector encoding TPP1 to a subject with a CLN2 deficiency for reasons set forth above. Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to administer gemfibrozil as described by Pahan ‘000 or “all-trans” retinoic acid as described by Pahan ‘449 in combination with a viral vector encoding TPP1 as described by Szabolcs. Those of ordinary skill in the art at the time of filing would have been motivated to do so to increase TPP1 levels. Further motivation either way is provided by Best who taught combining a viral vector encoding a protein deficient in cells with a defective gene that causes Batten disease along with fibrate drugs, gemfibrozil and fenofibrate to correct the gene deficiency.
Szabolcs did not teach treating late-infantile Batten disease as required in claim 1; however, doing so was obvious in view of Pahan who taught treating late-infantile Batten disease (abstract). Those of ordinary skill in the art at the time of filing would have been motivated to do so to save infants from disease.
The AAV vector encoding TPP1 is a viral vector encoding a lysosomal enzyme as required in claim 5.
Claims 15-16 are taught by Pahan, Pahan, and Best (see above).
Claim 18 has been included because Pahan taught administering the fibrate or all-trans retinoic acid orally (see above).
Pahan taught administering fibrate or all-trans retinoic acid once daily (see above) as required in claim 19.
The concept of the “lifespan of the subject in need thereof increase[ing] by about 100 days” as required in claim 28 inherently MUST occur because Szabolcs taught administering two reagents that are described as being part of the invention and because the two reagents taught by Szabolcs are within the metes and bounds of the claim.
Claim 29 has been included because Szabolcs taught preventing disease.
Claims 30 and 31 have been included because it was well-known the patients with late-infantile Batten disease are under 4 or 2 years old.
Response to arguments
Applicants discussion of Szabolcs bridging pg 9-10 of the response filed 3-18-26 says Szabolcs is limited to treating Krabbe disease and merely lists intranasal delivery as an option. Applicants’ argument is not persuasive. Szabolcs taught treating lysosomal storage disease including late infantile Batten disease using AAV encoding TPP1 which is equivalent to treating late-infantile Batten disease as required in claim 1. Applicants somehow argue that Szabolcs’s disclosure of intranasal delivery in a list is inadequate. Applicants’ argument is not persuasive because Szabolcs taught intranasal administration.
Applicants’ discussion of Aronovich, McIvor, Miller are irrelevant because they are not part of this rejection.
Applicants’ other arguments regarding Pahan, Pahan, and Best are not persuasive for reasons set forth above.
G) Claims 1, 4-6, 15, 16, 18, 19, 28-31 remain rejected under 35 U.S.C. 103 as being unpatentable over Macauley (J. Neurosci., 2014, Vol. 34, No. 39, pg 13077-13082) in view of Aronovich (“Lysosomal storage disease: Gene therapy on both sides of the blood–brain barrier”, Mol. Genetics & Metab., 2015, Vol. 114, pg 83-93), McIvor (RU2801511), Miller (20220090129), Pahan (WO 2018126000) or Pahan (WO 2014089449), and Best (Neurobiol. of Disease, 2017, Vol. 100, pg 62-74).
Macauley taught administering an AAV vector encoding TPP1 intracranially and MW151 intravenously to treat a model of infantile neuronal ceroid lipofuscinosis (abstract; pg 13078, “intracranial injections”, “MW151 injections”, “Treatment groups”). Macauley taught treating late-infantile or juvenile Batten disease (pg 13081, col. 2, last 10 lines) as required in claim 1.
Macauley did not teach administering the AAV intranasally as newly required in claim 1. However, Aronovich taught intranasal administration of AAV as one of a number of options (including into the blood or the CSF) for delivering AAV across the blood brain barrier (pg 86, 3rd paragraph). McIvor taught intranasal administration of AAV9/IDUA to treat MPS I mice (Fig. 19). Miller taught intranasal AAV-CFTR (para 208-210). Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to administer AAV encoding TPP1 across the blood brain barrier to treat Batten disease as described by Macauley using nasal administration of AAV to treat lysosomal storage disease as described by Aronovich, McIvor, and Miller. Those of ordinary skill in the art at the time of filing would have been motivated to do so for ease of administration and to avoid surgery.
Macauley did not teach administering fibrate as required in claim 1, e.g. gemfibrozil or fenofibrate, as required in claims 14 and 15, or all-trans retinoic acid as required in claim 16. However, Pahan ‘000 taught daily oral administration of gemfibrozil for treating CLN2 deficiency in mice (para 12, 53, 58; Fig. 1; Example 4), and Pahan ‘449 taught daily oral administration of gemfibrozil, fenofibrate, or “all-trans” retinoic acid for treating CLN2 deficiency in mice (para 9-17; Fig. 7, 14-16). Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to administer a viral vector encoding TPP1 across the blood brain barrier to treat Batten disease as described by Macauley in combination with gemfibrozil as described by Pahan ‘000 or gemfibrozil, fenofibrate, or “all-trans” retinoic acid as described by Pahan ‘449. Those of ordinary skill in the art at the time of filing would have been motivated to do for increasing levels of TPP1. Further motivation either way is provided by Best who taught combining a viral vector encoding a protein deficient in cells with a defective gene that causes Batten disease along with fibrate drugs, gemfibrozil and fenofibrate to correct the gene deficiency.
In the reverse, Pahan ‘000 taught daily oral administration of gemfibrozil for treating CLN2 deficiency in mice (para 12, 53, 58; Fig. 1; Example 4), and Pahan ‘449 taught daily oral administration of gemfibrozil, fenofibrate, or “all-trans” retinoic acid for treating CLN2 deficiency in subject (para 9-17; Fig. 7, 14-16). Pahan ‘000 and Pahan ‘449 did not teach administering a TPP1 gene to the subject. However, Macauley taught administering a viral vector encoding TPP1 to a subject with a CLN2 deficiency for reasons set forth above. Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to administer gemfibrozil as described by Pahan ‘000 or “all-trans” retinoic acid as described by Pahan ‘449 in combination with a viral vector encoding TPP1 as described by Macauley. Those of ordinary skill in the art at the time of filing would have been motivated to do so to increase TPP1 levels. Further motivation either way is provided by Best who taught combining a viral vector encoding a protein deficient in cells with a defective gene that causes Batten disease along with fibrate drugs, gemfibrozil and fenofibrate to correct the gene deficiency.
The AAV vector encoding TPP1 is a viral vector encoding a lysosomal enzyme as required in claim 5.
Claims 15-16 are taught by Pahan, Pahan, and Best (see above).
Claim 18 has been included because Pahan taught administering the fibrate or all-trans retinoic acid orally (see above).
Pahan taught administering fibrate or all-trans retinoic acid once daily (see above) as required in claim 19.
The concept of the 1st composition increasing the “lifespan of the subject in need thereof by about 100 days” as required in claim 27 inherently MUST occur because Macauley taught administering two reagents that are described as being part of the invention and because the two reagents taught by Macauley are within the metes and bounds of the claim.
The concept of the “lifespan of the subject in need thereof increase[ing] by about 100 days” as required in claim 28 inherently MUST occur because Macauley taught administering two reagents that are described as being part of the invention and because the two reagents taught by Macauley are within the metes and bounds of the claim.
Claim 29 has been included because Macauley taught administering treatment before onset of neurodegeneration (Discussion).
Claims 30 and 31 have been included because it was well-known the patients with late-infantile Batten disease are under 4 or 2 years old.
Response to arguments
Applicants do not substantially address the combined teachings of Goss, Aronovich, McIvor, Miller, Pahan (WO 2018126000), Pahan (WO 2014089449), and Best.
Applicants’ other arguments are not persuasive for reasons set forth above.
Conclusion
No claim is 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.
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Michael C. Wilson
/MICHAEL C WILSON/
Primary Examiner, Art Unit 1638
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