DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, 18271911, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Claims 6-11, 13-15, 26, 44-51 are pending.
Claims 9, 13-15, and 26, are withdrawn.
Claims 6-8, 10-11, and 44-51 are examined herein.
Priority
The filing receipt, mailed 3/14/2024, states that this application was filed 7/12/2023, and claims domestic priority benefit of as a 371 of PCT/US2022/012203, filed 01/12/2022 which claims benefit of 63/136,439, filed 01/12/2021.
Election/Restrictions
Applicant’s election of Group I, claims 6-11, in the reply filed on 2/9/2026 is acknowledged. Because applicant did not distinctly and specifically point out the supposed errors in the restriction requirement, the election has been treated as an election without traverse (MPEP § 818.01(a)).
Claims 13-15 and 26 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected Invention, there being no allowable generic or linking claim.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 2/9/2026.
Groups II and III are withdrawn by the examiner because the technical feature linking the claims are not considered special and does not represent a contribution over the prior art, especially as cited in the obviousness rejection below. Unity of invention will continue to be considered, particularly in respect to rejoinder, at the time of each forthcoming Office action. The subject matter of the claims of the different Groups of inventions are related but are not deemed to be commensurate in scope and are not linked by a technical feature that is special.
Applicant’s required election (at p. 6 of the election) of the species adrenergic receptor activator, the alpha-1 adrenergic receptor activator phenylephrine, a species as set forth in claims 46 and 61 that is an asparagine to aspartic acid substitution at amino acid 1768 of e.g., SEQ ID NO: 4, is acknowledged. Claim 9 is withdrawn as drawn to an unelected species of mechanical ventilation.
Claim Rejections - 35 USC § 103
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 (i.e., changing from AIA to pre-AIA ) 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.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
1. Claim(s) 6-8, 10-11, 44-46, 49-51 is/are rejected under 35 U.S.C. 103 as being unpatentable over Wagnon, 2014, Human Molecular Genetics, Volume 24, Issue 2, pages 506-515, Serdyuk, U.S. 20030004134, and Moran, WO2006021942.
Wagnon, 2014, Human Molecular Genetics, Volume 24, Issue 2, pages 506-515, (of record), throughout the publication and abstract, teaches a SCN8A missense mutation in a child with epileptic encephalopathy that included seizures, ataxia and sudden unexpected death in epilepsy (SUDEP). Wagon teaches the heterozygous missense mutation p.Asn1768Asp of the voltage-gated sodium channel gene SCN8A as present in a child suffering seizures, ataxia, and sudden unexpected death in epilepsy (SUDEP). Wagon discloses that Scn8a mutant mice exhibit seizures and SUDEP. Wagnon, at p. 511, para 4, teaches that lamotrigine was used to control epileptic seizures in a human proband patient with a SCN8A mutation.
Wagnon does not teach administering an alpha-1 adrenergic receptor activator in a method of treatment or prevention and does not teach SEQ ID NO: 4.
Serdyuk, 20030004134, throughout the publication and abstract, teaches the alpha-1 adrenergic receptor activator, phenylephrine, as potentiating anti-convulsive effects by intramuscular administration, (reading on injection), and at para 108-109 states:
[0108] Phenylephrine or midodrine at a threshold dose (0.012 mg/kg) in a composition with diazepam decrease its minimal effective dose causing a maximal anticonvulsive effect (elimination of clonico-tonic seizures caused by pentylenetetrazole at a. dose of 70 mg/kg in 80% of rats) 74 and 85 times, respectively. They also potentiate a mild (only in 20% of rats) anticonvulsive effect of diazepam in the maximal dose (10 mg/kg) with respect to clonic pentylenetetrazole seizures (ensures a complete protection against clonic seizures in 80% of rats).
[0109] Further increase of a dose of phenylephrine or midodrine up to 0.024 mg/kg, which also does not cause an independent effect, not only potentiates the effect of diazepam, but also decreases 5.5-6.3 times its minimal effective dose eliminating clonic seizures in 80% of rats.
Serdyuk at para [0108]-[0109].
Serdyuk at para [0112]-[0114], teaches intragastric administration, reading on an injectable, of a combination diazepam and phenylephrine to decrease clonico-tonic seizure and to intensify anticonvulsive effect of the combination.
Moran, WO2006021942, describes an amino acid sequence of human SCN8A, at reference SEQ ID NO: 33, with 100% identity to instant SEQ ID NO: 4. Moran, teaches reference SEQ ID NO: 18, P.9, 10, para 7, p. 11, para 3, teaches SCN8A is a sodium channel protein, and mouse mutants of SCNA leads to “neurological disorders.”
It would have been prima facie obvious before the filing date of the instant application for one of ordinary skill in the art to have combined administering an alpha-1 adrenergic receptor activator in a method of treatment or prevention a death associated with a seizure in a subject. and to have a gain of function missense mutation p.Asn1768Asp of the voltage-gated sodium channel gene in a SCN8A polypeptide of instant SEQ ID NO: 4.
One of ordinary skill in the art would have motivated to have combined administering an alpha-1 adrenergic receptor activator, as taught by Serdyuk, in a method of treatment or prevention a death associated with a seizure in a subject, as taught by Wagnon, because Serdyuk teaches that administration of the alpha-1 adrenergic receptor activator, phenylephrine, supports anti-convulsive treatment associated with seizure.
One of ordinary skill in the art would have treated seizure associated have a gain of function missense mutation p.Asn1768Asp of a voltage-gated sodium channel gene in a SCN8A polypeptide, as taught by Wagnon, of instant SEQ ID NO: 4, as taught by Moran, because mutation in the teaches SCN8A, sodium channel protein, as taught by Moran, SCNA leads to “neurological disorders” in mice with mutation in instant SEQ ID NO: 4.
2. Claim(s) 47, 48 is/are rejected under 35 U.S.C. 103 as being unpatentable over Wagnon, 2014, Human Molecular Genetics, Volume 24, Issue 2, pages 506-515, Serdyuk, U.S. 20030004134, and Moran, WO2006021942, as applied to claims 6-8, 10-11, 44-46, 49-51, above, and further in view of Johnston, 1995, Ann Neurol, Vol 37, pages 531 to 537, (of record, Notice of References Cited, PTO-892, mailed 12/10/2025).
The teachings of Wagnon, 2014, Human Molecular Genetics, Volume 24, Issue 2, pages 506-515, Serdyuk, U.S. 20030004134, and Moran, WO2006021942, are relied upon, as above.
Wagnon, 2014, Human Molecular Genetics, Volume 24, Issue 2, pages 506-515, Serdyuk, U.S. 20030004134, and Moran, WO2006021942, do not teach combined stimulating breathing of a subject via mechanical ventilation until restoration of unassisted breathing.
Johnston, 1995, Ann Neurol, Vol 37, pages 531 to 537, throughout the publication and abstract teaches an etiological association between epileptic sudden death and central hypoventilation and pulmonary edema. Johnston, at p. 532, para 1, teaches use of mechanical ventilation to deliver halothane in oxygen to anesthetize sheep. Johnston, at p. 536, para 6, state: “We conclude that epileptic sudden death is caused by hypoventilation, which is probably centrally induced.” Johnston, at p. 536, para 7, contemplate “family training in cardiopulmonary resuscitation” in order to avoid epileptic sudden death.
It would have been prima facie obvious before the filing date of the instant application for one of ordinary skill in the art to have combined stimulating breathing of a subject via mechanical ventilation until restoration of unassisted breathing in combination with alpha-1 adrenergic receptor activation, as taught by Wagnon.
One of ordinary skill in the art would have motivated to have combined stimulating breathing of a subject via mechanical ventilation until restoration of unassisted breathing in combination with alpha-1 adrenergic receptor activation, as taught by Wagnon, would have been desirable because Johnston teaches mechanical ventilation to deliver oxygen and Johnston teaches that epileptic sudden death is caused by hypoventilation.
Conclusion
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MARK L. SHIBUYA
Primary Patent Examiner
Art Unit 1631
/MARK L SHIBUYA/Primary Patent Examiner, Art Unit 1631
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