DETAILED ACTION
Claims 21-31 are currently under examination. An action on the merits follows. The present application is being examined under the pre-AIA first to invent provisions.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 12/14/23 is in compliance with the provisions of 37 CFR 1.97 and 1.98. Accordingly, the information disclosure statement has been considered by the examiner, and an initialed and signed copy of the 1449 is attached to this action.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103(a) which forms the basis for all obviousness rejections set forth in this Office action:
(a) A patent may not be obtained though the invention is not identically disclosed or described as set forth in section 102 of this title, if the differences between the subject matter sought to be patented and the prior art are such that the subject matter as a whole would have been obvious at the time the invention was made to a person having ordinary skill in the art to which said subject matter pertains. Patentability shall not be negatived by the manner in which the invention was made.
This application currently names joint inventors. In considering patentability of the claims under pre-AIA 35 U.S.C. 103(a), the examiner presumes that the subject matter of the various claims was commonly owned at the time any inventions covered therein were made absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and invention dates of each claim that was not commonly owned at the time a later invention was made in order for the examiner to consider the applicability of pre-AIA 35 U.S.C. 103(c) and potential pre-AIA 35 U.S.C. 102(e), (f) or (g) prior art under pre-AIA 35 U.S.C. 103(a).
Claims 21-31 are rejected under 35 U.S.C. 103(a) as being unpatentable over WO 2008/150477 (December 11, 2008), with an effective filing date of May 31, 2007, hereafter referred to as Huizing et al., in view of Noguchi et al. (2004) J. Biol. Chem., Vol. 279(12), 11402-11407.
Huizing et al. teaches that an underlying genetic defect in HIBM patients is related to mutations in the GNE gene which results in decreased production of sialic acid and hyposialylation of proteins (Huizing et al., pages 11-16). Huizing et al. teaches that HIBM is associated with myopathy and muscular atrophy and is further associated with kidney dysfunction (Huizing et al., pages 11-16). Huizing et al. teaches methods of treating HIBM, particularly in subjects with an M712T mutation commonly found in GNE gene of Iranian-Jewish HIBM patients, by increasing the amount of sialic acid, most specifically by administering N-acetyl-D-mannosamine (ManNAc)- a key compound in the sialic acid biosynthetic pathway, to produce sialic acid in vivo (Huizing et al., pages 9-11, 32-34, and 47). Huizing et al. further teaches to administer the ManNAc orally (Huizing et al., pages 17-18). As an example, Huizing et al. teaches the production of a mouse model of HIBM in which the endogenous GNE gene has a homozygous M712T mutation, testing the resulting mouse for the homozygous mutation, and treating the symptoms of myopathy present in the mouse model by orally administering ManNAc (Huizing et al., pages 24-25, and 28). Huizing et al. further teaches the oral administration of ManNAc to human patients with HIBM, where as part of the procedure, the patients DNA is tested for GNE gene mutations (Huizing et al., pages 34-35).
While Huizing et al. teaches to treat HIBM by increasing sialic acid in a patient, Huizing et al. does not specifically teach to administer sialic acid to treat HIBM. However, at the time of filing, Noguchi et al. teaches that both HIBM and DMRV are autosomal recessive disorders of muscle weakness caused by mutations in the GNE gene resulting in decreased sialic acid production and impaired sialylation (Noguchi et al., pages 11402-11403). Noguchi et al. teaches a number of these mutations in the GNE gene identified in human patients with DMRV/HIBM (Noguchi et al., Table 1, page 11403). Noguchi et al. further teaches that exposing cells from DMRV patients to ManNAc or NeuAc, a member of the sialic acid family, increased sialic acid concentrations in the cells to normal levels (Noguchi et al., page 11406). Noguchi et al. concludes that these results strongly suggest that pharmacological therapy may be effective against DMRV/HIBM (Noguchi et al., page 11406). Noguchi et al. further teaches that treatment with NeuAc resulted in more rapid and potent effects on the restoration of sialylation than treatment with ManNAc (Noguchi et al., page 11406).
Therefore, in view of the teachings of Noguchi et al. that NeuAc treatment increases sialic acid levels in cells from patients with mutations in the GNE gene, and that NeuAc resulted in more rapid and potent effects on the restoration of sialylation than treatment with ManNAc, it would have been prima facie obvious to the skilled artisan at the time of filing to increase the levels of sialic acid and treat HIBM according to Huizing et al. by orally administering NeuAc instead of ManNAc to a patient with HIBM with a reasonable expectation of success in treating and/or preventing myopathy, including increasing muscle strength and limb movement. Furthermore, based on the teachings of both Huizing et al and Noguchi et al. to identify patients with GNE mutations associated with HIBM/DMRV, including the M712T mutation, prior to treatment, it would have been prima facie obvious to the skilled artisan at the time of filing to first identify a mutation in the GNE of the patient to be treated prior to the oral administration of sialic acid with a reasonable expectation of success.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP §§ 706.02(l)(1) - 706.02(l)(3) for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/process/file/efs/guidance/eTD-info-I.jsp.
Claims 21-31 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-4 of U.S. Patent No. 9,018,174, hereafter referred to as the ‘174 patent, in view of 2008/150477 (December 11, 2008), with an effective filing date of May 31, 2007, hereafter referred to as Huizing et al.. Although the claims at issue are not identical, they are not patentably distinct from each other for the following reasons.
Claims 1-4 of the ‘174 patent recite method of orally administering free sialic acid to a treat HIBM or hyposialylation in a subject or skeletal muscle in a subject (claims 1 and 3), and further where the subject exhibits myopathic symptoms (claims 2 and 4).
The ‘174 patent claims differ in scope from the instant claims by not specifically reciting that the subject with HIBM has a mutation in the GNE gene, specifically an M712T mutation, or further recite that the methods include identification of a mutation in the GNE gene prior to treatment.
Huizing et al. supplements the ‘174 patent claims by teaching that an underlying genetic defect in HIBM patients is related to mutations in the GNE gene which results in decreased production of sialic acid and hyposialylation of proteins (Huizing et al., pages 11-16). Huizing et al. teaches that HIBM is associated with myopathy and muscular atrophy (Huizing et al., pages 11-16). Huizing et al. teaches methods of treating HIBM, particularly in subjects with an M712T mutation commonly found in GNE gene of Iranian-Jewish HIBM patients, by increasing the amount of sialic acid (Huizing et al., pages 9-11, 32-34, and 47). Huizing et al. further teaches the oral administration of a compound to increase sialic acid to human patients with HIBM, where as part of the procedure, the patients DNA is tested for GNE gene mutations prior to treatment (Huizing et al., pages 34-35).
Therefore, in view of the known association of mutations in GNE with HIBM as taught by Huizing et al., and the further teachings of Huizing et al. to identify mutations in the GNE prior to treatment with a compound to increase sialic acid in patients with HIBM, it would have been prima facie obvious to the skilled artisan at the time of filing to further include in the methods of claims 1-4 of the ‘172 patent a step of identifying a mutation in GNE in a subject, and specifically the mutation M712T, prior to oral administration of free sialic acid to the subject in order to treat myopathy with a reasonable expectation of success.
No claims are allowed.
Any inquiry concerning this communication from the examiner should be directed to Anne Marie S. Wehbé, Ph.D., whose telephone number is (571) 272-0737. If the examiner is not available, the examiner’s supervisor, Maria Leavitt, can be reached at (571) 272-1085. For all official communications, the technology center fax number is (571) 273-8300. Please note that all official communications and responses sent by fax must be directed to the technology center fax number. For informal, non-official communications only, the examiner’s direct fax number is (571) 273-0737. For any inquiry of a general nature, please call (571) 272-0547.
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Dr. A.M.S. Wehbé
/ANNE MARIE S WEHBE/Primary Examiner, Art Unit 1634