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 .
Claim Rejections - 35 USC § 103
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.
Claims 1-14 are rejected under 35 U.S.C. 103 as being unpatentable over GB 2531282 A to Guy et al. (“Guy”), and further in view of WO 2020176276 A1 to Millet et al. (“Millet”).
Guy teaches cannabidiol (CBD) for use in the treatment of epilepsy, wherein the epilepsy is treatment-resistant epilepsy (TRE), and wherein the epilepsy to be treated is characterized by atonic seizures. (Abstract). Guy teaches the main symptom of epilepsy is repeated seizures. ([0010]).
Guy teaches the CBD is preferably for use in combination with one or more concomitant anti-epileptic drugs (AED), in particular clobazam, levetiracetam, topiramate, stiripentol, phenobarbital, lacosamide, valproic acid, zonisamide, perampanel and fosphenytoin, wherein the dose of the anti-epileptic drug/s that is/are used in combination with CBD is reduced. (Abstract; ([0035]); claim 8).
Guy teaches that the CBD is present as a highly purified extract of cannabis which comprises at least 98% (w/w) CBD. Preferably the extract further comprises up to 1% CBDV (cannabidivarin) and less than 0.15% THC (tetrahydrocannabinol). (Abstract; claims 1-7). Guy teaches that the phytocannabinoids can be isolated from plants to produce a highly purified extract, or can be reproduced synthetically. ([0003]; [0042]).
Regarding the limitation of claim 4, wherein there is less than or equal to 2% (w/w) of other cannabinoids comprising the cannabinoids tetrahydrocannabinol (THC); cannabidiol-C1 (CBD-C1); cannabidivarin (CBDV); and cannabidiol-C4 (CBD-C4), and wherein the THC is present as a mixture of trans-THC and cis-THC. “Less than” can be interpreted as zero THC present in the mixture as trans-THC and cis-THC, thereby meeting the limitations of the instant claim.
Guy teaches that the dose of CBD is from 5 mg/kg/day to 25 mg/kg/day. (Abstract; ([0037]); claim 11).
Although Guy does not teach a dose of CBD of 50 mg/kg/day, it provides clear motivation for upward adjustment of the CBD dose with a reasonable expectation of success. Specifically, it discloses that a study in 1978 provided 200 mg/day of pure CBD to four adult patients, two of the four patients became seizure free, whereas in the remainder seizure frequency was unchanged. ([0025]). It also reports another study where 200 mg/day of pure CBD was ineffective in controlling seizures. ([0026]). All in all, this provides clear motivation to optimize the dose further to higher than 25 mg/kg/day and lower than 200 mg/kg/day.
Regarding doses, and the specific percentages of CBD and other cannabinoid present in the composition is considered, the determination of such is generally considered to be subject to mere optimization. Such optimization of doses and ranges will not support the patentability of subject matter encompassed by the prior art unless there is evidence indicating such concentration or temperature is critical. "When the general conditions of a claim are disclosed in the prior art, it is not inventive to discover the optimal or workable ranges by routine experimentation. In re Aller, 220 F.2d 454, 456, 105 USPQ 233, 235 (CCPA 1955); see also In re Peterson, 315 F. 3d at 1330, 65 USPQ 2d at 1382 "The normal desire of scientists or artisans to improve upon what is already generally known provides the motivation to determine where in a disclosed set of percentage ranges is the optimum combination of percentages." MPEP 2114.04.
Guy teaches generalized seizures involve the whole brain and can also be subdivided into types: Absence (petit mal) Seizures; Myoclonic Seizures; Clonic Seizures; Tonic Seizures; Tonic Clonic (grand mal) seizures; and Atonic Seizures [0012].
Guy does not teach that the patient population is associated with a GPHN mutation. However, based on the disclosure of Guy alone, of treating seizures broadly with CBD, it would have been obvious to a person of skill in the art before the effective filing date of the claimed invention to extend the teachings of Guy to seizures broadly, to seizures with specific mutations. “Obviousness does not require absolute predictability of success . . . all that is required is a reasonable expectation of success. In re O’Farrell, 853 F.2d 894, 903-4, 7 USPQ2d 1673, 1681 (Fed. Cir. 1988). Further motivation to do so is found in view of Millet.
Millet claims a method of improving seizure control in a patient experiencing uncontrolled seizures persisting 10 mins or more, comprising administering fenfluramine or a pharmaceutically acceptable salt, base, acid or amine thereof (claim 1), wherein at least one co-therapeutic agent is administered, and wherein said agent is selected from the group consisting of CBD, lamotrigine, progabide.
Millet specifically discloses that known mutations of various seizure types occur in a number of genes, to specifically include GPHN. ([0064]). Millet discloses that it can be desirable to test the patients for a genetic mutation prior to administration of some of the therapeutic agents, especially in cases where use of specific agent is contraindicated either because the agent is ineffective or because it would have undesired or serious side effects. Thus, it is in some cases desirable to test patients prior to treatment with fenfluramine. ([0056]).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have employed compositions containing CBD for the treatment of epilepsy as taught by Guy and employed said treatments on patient populations with a GPHN mutation, as taught by Millet. The motivation, provided by Millet, teaches GPHN mutation as a genetic marker indicative of association of seizure. Thus, the skilled artisan would have found it obvious to treat seizures with CBD comprising compositions to patients possessing a GPHN mutation since this patient population is known to be associated with seizures, and since Millet specifically disclose an explicit need to first assess the genetic mutation for any known contraindication or knowledge of lack of efficacy. In the instant case, since no such contraindications are known in the art, nor is there a known lack of efficacy, it would have been obvious to a person of skill in the art, based on a known therapeutic effect of CBD against seizures, as disclosed in Guy, and a known association of seizures with a GPHN mutation, as disclosed in Millet, to treat seizures associated with a GPHN mutation comprising administering a CBD preparation with a reasonable expectation of success.
Thus, based on the foregoing reasons, the instant claims are deemed unpatentable over the cited references.
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 § 2146 et seq. 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 filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual 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/apply/applying-online/eterminal-disclaimer.
Claims 1-14 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over the co-pending claims of the following recited below patent applications (reference applications), and further in view of WO 2020176276 A1 to Millet et al. (“Millet”).
The claims of the instant application are directed to a method of treating seizures associated with a GPHN mutation comprising administering a CBD preparation.
claims 1-14 of copending Application No. 18/006,133
The claims of the co-pending application are directed to a method of treating seizures associated with a SPATA5 mutation comprising administering a CBD preparation.
Claims 1-14 of copending Application No. 18/006,125
The claims of the co-pending application are directed to a method of treating seizures associated with encephalocele comprising administering a CBD preparation.
Claims 1-13 of copending Application No. 18/006,121
The claims of the co-pending application are directed to a method of treating seizures associated with a PCDH19 mutation comprising administering a CBD preparation and not more than 0.15% THC.
Of note, not more than 0.15% THC is inclusive of no THC. Further, the instant dependent claims also recite THC.
claims 1-14 of copending Application No. 18/005,961
The claims of the co-pending application are directed to a method of treating seizures associated with a ZDHHC9 mutation comprising administering a CBD preparation.
claims 1-14 of copending Application No. 18/005,960
The claims of the co-pending application are directed to a method of treating seizures associated with congenital disorder of glycosylation 1P comprising administering a CBD preparation.
claims 1-14 of copending Application No. 18/005,959
The claims of the co-pending application are directed to a method of treating seizures associated with a CLCN4 mutation comprising administering a CBD preparation.
Claims 1-14 of copending Application No. 18/005,868
The claims of the co-pending application are directed to a method of treating seizures associated with a CHRNA4 mutation comprising administering a CBD preparation.
claims 1-14 of copending Application No. 18/005,853
The claims of the co-pending application are directed to a method of treating seizures associated with a DEPDC5 mutation comprising administering a CBD preparation.
claims 1-14 of copending Application No. 18/005,852
The claims of the co-pending application are directed to a method of treating seizures associated with potassium channel (KCN) mutation, wherein the KCN gene mutation is one of KCNA1 and KCNQ2 comprising administering a CBD preparation.
claims 1-13 of copending Application No. 18/005,848
The claims of the co-pending application are directed to a method of treating seizures associated with a SYNGAP1 mutation comprising administering a CBD preparation and not more than 0.15% THC.
Of note, not more than 0.15% THC is inclusive of no THC. Further, the instant dependent claims also recite THC.
claims 1-14 of copending Application No. 18/005,847
The claims of the co-pending application are directed to a method of treating seizures associated with a PURA mutation comprising administering a CBD preparation.
claims 1-14 of copending Application No. 18/005,845
The claims of the co-pending application are directed to a method of treating seizures associated with GR1N2B and CACNA1H mutations comprising administering a CBD preparation.
Claims 1-24 of copending Application No. 18/005,843
The claims of the co-pending application are directed to a method of treating seizures associated with a chromosomal mutation, comprising administering a CBD preparation, wherein the gross chromosomal mutation is one of 11q11.2 microdeletion; 1p36 deletion; 22Q11 duplication; 9p21.1 deletion with autistic spectrum disorder, monosomy 16p13.3 and trisomy 2p25.3; chromosome 3q duplication; or trisomy 13.
claims 1-14 of copending Application No. 18/005,841
The claims of the co-pending application are directed to a method of treating seizures associated with a BRAF mutation comprising administering a CBD preparation.
Although the claims at issue are not identical, they are not patentably distinct from each other because they disclose overlapping subject matter of a method of treating seizures associated with [x] mutation (or a specific disorder associated with a mutation) comprising administering a CBD preparation.
The difference is the specific mutation (or a specific disorder associated with a mutation). However, this difference is rendered obvious further in view of Millet.
Millet claims a method of improving seizure control in a patient experiencing uncontrolled seizures persisting 10 mins or more, comprising administering fenfluramine or a pharmaceutically acceptable salt, base, acid or amine thereof (claim 1), wherein at least one co-therapeutic agent is administered, and wherein said agent is selected from the group consisting of CBD, lamotrigine, progabide.
Millet specifically discloses that known mutations of various seizure types occur in a number of genes, to specifically include GPHN. ([0064]). Millet discloses that it can be desirable to test the patients for a genetic mutation prior to administration of some of the therapeutic agents, especially in cases where use of specific agent is contraindicated either because the agent is ineffective or because it would have undesired or serious side effects. Thus, it is in some cases desirable to test patients prior to treatment with fenfluramine. ([0056]).
Millet discloses a very long list of specific mutations associated with seizures, to specifically include the ones claimed by Applicant in the co-pending applications. The list below also very specifically discloses that the list of mutations are linked to some specific named disorders.
[0056] In some cases, it can be desirable to test the patients for a genetic mutation prior to administration of some of the therapeutic agents, especially in cases where use of specific agent is contraindicated either because the agent is ineffective or because it would have undesired or serious side effects. Thus, it is in some cases desirable to test patients prior to treatment with fenfluramine. In the case of patients having Dravet syndrome, testing can be carried out for mutations in the SCN1A (such as partial or total deletion mutations, truncating mutations and/or missense mutations e.g. in the voltage or pore regions S4 to S6), SCN1 B (such as the region encoding the sodium channel bΐ subunit), SCN2A, SCN3A, SCN9A, GABRG2 (such as the region encoding the g2 subunit), GABRD (such as the region encoding the s subunit) and I or PCDH19 genes have been linked to Dravet syndrome.
[0057] In some instances, the mutations occur in genes that are linked diseases and conditions characterized by various seizure types including, for example, generalized seizures, myoclonic seizures, absence seizures, and febrile seizures. Mutations may occur in one or more of the following genes: ALDH7A1, CACNA1A, CACNA1H, CACNB4, CASR, CHD2, CHRNA2, CHRNA4, CHRNB2, CLCN2, CNTN2, CSTB, DEPDC5, EFHC1, EPM2A, GABRA1, GABRB3, GABRD, GABRG2, GOSR2, GPR98, GRIN 1 , GRIN 2 A, GRIN2B, KCNMA1, KCNQ2, KCNQ3, KCTD7, MBD5, ME2, NHLRC1, PCDH19, PRICKLEl, PRICKLE2, PRRT2, SCARB2, SCN1A, SCN1B, SCN2A, SCN4A, SCN9A, SLC2A1, TBC1D24.
[0058] In some instances, the mutations occur in genes that are linked to age-related epileptic encephalopathies including, for example, early infantile epileptic encephalopathy. Mutations may occur in one or more of the following genes: ALDH7A1, ARHGEF9, ARX, CDKL5, CNTNAP2, FH, FOXG1, GABRG2, GRIN 2 A, GRIN2B, KCNT1, MAGI2, MAPK10, MECP2, NRXN1, PCDH19, PFCB1, PNKP, PNPO, PRRT2, RNASEH2A, RNASEH2B, RNASEH2C, SAMHD1, SCN1A, SCN1B, SCN2A, SCN8A, SCN9A, SFC25A22, SFC2A1, SFC9A6, SPTAN1, STXBP1, TCF4, TREX1, UBE3A, ZEB2.
[0059] In some instances, the mutations occur in genes that are linked to malformation disorders including, for example, neuronal migration disorders, severe microcephaly, pontocerebellar hypoplasia, Joubert syndrome and related disorders, holoprosencephaly, and disorders of the RAS/MAPK pathway. Mutations may occur in one or more of the following genes: AHI1, ARFGEF2, ARF13B, ARX, ASPM, ATR, BRAF,C12orf57, CASK, CBF, CC2D2A, CDK5RAP2, CDON, CENPJ, CEP 152, CEP290, COL18A1, COL4A1, CPT2, DCX, EMX2, EOMES, FGF8, FGFR3, FKRP, FKTN, FLNA, GLI2, GLI3, GPR56, HRAS, INPP5E, KAT6B, KRAS, LAMA2, LARGE, MAP2K1, MAP2K2, MCPH1, MED17, NF1, NPHP1, NR AS, OFD1, PAFAH1B1, PAX6, PCNT, PEX7, PNKP, POMGNT1, POMT1, POMT2, PQBP1, PTCH1, PTPN11, RAB3GAP1, RAF1, RARS2, RELN, RPGRIP1L, SHH, SHOC2, SIX3, SLC25A19, SNAP29, SOS1, SPRED1, SRD5A3, SRPX2, STIL, TGIF1, TMEM216, TMEM67, TSEN2, TSEN34, TSEN54, TUBA1A, TUBA8, TUBB2B, VDAC1, WDR62,VRK1, ZIC2.
[0060] In some instances, the mutations occur in genes that are linked to epilepsy in X- linked intellectual disability. Mutations may occur in one or more of the following genes: ARHGEF9, ARX, ATP6AP2, ATP7A, ATRX, CASK, CDKL5, CUL4B, DCX, FGD1, GPC3, GRIA3, HSD17B10, IQSEC2, KDM5C, MAGT1, MECP2, OFD1, OPHN1, PAK3, PCDH19, PHF6, PLP1, PQBP1, RAB39B, SLC16A2, SLC9A6, SMC1A, SMS, SRPX2, SYN1, SYP.
[0061] In some instances, the mutations occur in genes that are linked to storage diseases and conditions characterized by organelle dysfunction including, for example, neuronal ceroid lipofuscinosis, lysosomal storage disorders, congenital disorders of glycosylation, disorders of peroxisome biogenesis, and leukodystrophies. Mutations may occur in one or more of the following genes: AGA, ALG1, ALG12, ALG2, ALG3, ALG6, ALG8, ALG9, ALG11, ALG13, ARSA, ARSB, ASPA, B4GALT1, CLN3, CLN5, CLN6, CLN8, COG1, COG4, COG5, COG6, COG7, COG8, CTSA, CTSD, DDOST, DOLK, DPAGT1, DPMI, DPM3, EIF2B1, EIF2B2, EIF2B3, EIF2B4, EIF2B5, FUCA1, GALC, GALNS, GFAP, GLB 1, GNE, GNPTAB, GNPTG, GNS, GUSB, HEXA, HEXB, HGSNAT, HYAL1, IDS, IDUA, MCOLN1, MFSD8, MGAT2, MLC1, MOGS, MPDU1, MPI, NAGLU, NEU1, NOTCH3, NPC1, NPC2, PEX1, PEX12, PEX14, PEX2, PEX26, PEX3, PEX5, PEX6, PEX7, PEX10, PEX13, PEX16, PEX19, PGM1, PLP1, PMM2, PPT1, PSAP, RFT1, RNASEH2A, RNASEH2B, RNASEH2C, SAMHD1, SDHA, SGSH, SLC17A5, SLC35A1, SLC35A2, SLC35C1, SMPD1, SUMF1, TMEM165, TPP1, TREX1.
[0062] In some instances, the mutations occur in genes that are linked to syndromic disorders with epilepsy including, for example, juvenile myoclonic epilepsy, childhood absence epilepsy, benign rolandic epilepsy, Lennox-Gastaut syndrome, Dravet syndrome, Ohtahara syndrome, West syndrome, etc. Mutations may occur in one or more of the following genes: ATP2A2, ATP6V0A2, BCKDK, CACNA1A, CACNB4, CCDC88C, DYRK1A, HERC2, KCNA1, KCNJ10, KIAA1279, KMT2D, LBR, LGI1, MAPK10, MECP2, MEF2C, NDE1, NIPBL, PANK2, PIGV, PLA2G6, RAI1, RBFOX1, SCN8A, SERPINI1, SETBP1, SLC1A3, SLC4A10, SMC3, SYNGAP1, TBX1, TSC1, TSC2, TUSC3, UBE3A, VPS13A, VPS13B.
[0063] In some instances, the mutations occur in genes that are linked to the occurrence of migraines. Mutations may occur in one or more of the following genes: ATP1 A2, CACNA1 A, NOTCH3, POLG, SCN1A, SLC2A1.
[0064] In some instances, the mutations occur in genes that are linked to Hyperekplexia. Mutations may occur in the following genes: ARHGEF9, GLRA1, GLRB, GPHN, SLC6A5.
[0065] In some instances, the mutations occur in genes that are linked to inborn errors of metabolism including, for example, disorders of carbohydrate metabolism, amino acid metabolism disorders, urea cycle disorders, disorders of organic acid metabolism, disorders of fatty acid oxidation and mitochondrial metabolism, disorders of porphyrin metabolism, disorders of purine or pyridine metabolism, disorders of steroid metabolism, disorders of mitochondrial function, disorders of peroxisomal function, and lysosomal storage disorders. Mutations may occur in one or more of the following genes: ABAT, ABCC8, ACOX1, ACY1, ADCK3, ADSL, ALDH4A1, ALDH5A1, ALDH7A1, AMT, ARG1, ATIC, ATP5A1, ATP7A, ATPAF2, BCS1L, BTD, C120RF65, CABC1, COQ2, COQ9, COX10, COX15, DDC, DHCR7, DLD, DPYD, ETFA, ETFB, ETFDH, FOLR1, GAMT, GATM, GCDH, GCSH, GLDC, GLUD1, GLUL,HPD, HSD17B10, HSD17B4, KCNJ11, L2HGDH, LRPPRC, MGME1, MMACHC, MOCS1, MOCS2, MTHFR, MTR, MTRR, NDUFA1, NDUFA2, NDUFAF6, NDUFS1, NDUFS3, NDUFS4, NDUFS7, NDUFS8, NDUFV1, PC, PDHA1, PDHX, PDSS1, PDSS2, PGK1, PHGDH, POFG, PRODH, PSAT1, QDPR, RARS2, SC02, SDHA, SFC19A3, SFC25A15, SFC46A1, SFC6A8, SUCFA2, SUOX, SURF1, TACOl,TMEM70, VDAC1.
Millet further discloses treating subtypes of epilepsy, which are classified as encephalopathies. ([0019]). To one of skill in the art this would indicate inclusive of encephalocele. Millet further specifically discloses with which disorders the mutations further correlate.
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have employed compositions containing CBD for the treatment of epilepsy as taught by Millet, and applied them the treatment of various seizures of various known mutations, as taught by Millet. The motivation, provided by Millet, teaches the specific mutations as known genetic markers indicative of association of seizure. Thus, the skilled artisan would have found it obvious to treat seizures with CBD comprising compositions to patients possessing a GPHN mutation since this patient population is known to be associated with seizures, as in the instant application, and to have applied the claimed method to further known mutations associated with seizures in the same method of treatment, as in the co-pending applications. Motivation to do so is since Millet specifically disclose an explicit need to first assess the genetic mutation for any known contraindication or knowledge of lack of efficacy. In the instant case, since no such contraindications are known in the art, nor is there a known lack of efficacy, it would have been obvious to a person of skill in the art, based on a known therapeutic effect of CBD against seizures, and a known association of seizures with the various mutation, as disclosed in Millet, to treat seizures associated with these various mutation comprising administering a CBD preparation with a reasonable expectation of success.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to SVETLANA M IVANOVA whose telephone number is (571)270-3277. The examiner can normally be reached 8:30-5:00.
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/SVETLANA M IVANOVA/ Primary Examiner, Art Unit 1627