DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 12-17-25 has been entered.
Claims 5, 6, 8-12, 17, 19, 20, 24-32 have been canceled. Claims 1-4, 7, 13-16, 18, 21-23 remain pending and under consideration.
Applicant's arguments filed 12-17-25 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.
Claim Rejections - 35 USC § 112
Written Description
Claims 1-4, 7, 13-16, 18, 21-23 are 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.
Withdrawn rejections
The rejection regarding administering the rAAV of claim 18 to a cell in a mammal that has Usher syndrome such that symptoms of Usher syndrome are ameliorated as required in claim 24 has been withdrawn because claim 24 has been canceled.
The rejection regarding administering the rAAV of claim 18 to any eye cell in vivo as broadly encompassed by claim 26 has been withdrawn because claim 26 has been canceled.
The rejection of claim 28 has been withdrawn because it has been canceled.
The rejection of claim 31 has been withdrawn because it has been canceled.
New rejections
The specification lacks written description for a “transgene encoding a USH2A minigene encoded by a nucleotide sequence consisting of the nucleic acid sequence [ ] of SEQ ID NO”: 3,4,5,6,7,8,9,10,11,12,13, or 14 as required in claim 1 other than an isolated nucleic acid sequence encoding USH2A consisting of the nucleotide sequence of SEQ ID NO: 3,4,5,6,7,8,9,10,11,12,13, or 14. While an isolated nucleic acid sequence may encode USH2A and consist of the nucleotide sequence of SEQ ID NO: 3,4,5,6,7,8,9,10,11,12,13, or 14, the specification does not contemplate making/using a “transgene” encoding a “USH2A minigene” encoded by “a nucleotide sequence consisting” SEQ ID NO: 3-14 as required in claim 1. It is also unclear whether the “transgene”, the “minigene”, or the “nucleic acid sequence” within the “minigene” consists of SEQ ID NO: 3,4,5,6,7,8,9,10,11,12,13, or 14 (see 112/2nd). Accordingly, the concept lacks written description other than an isolated nucleic acid sequence encoding USH2A consisting of the nucleotide sequence of SEQ ID NO: 3,4,5,6,7,8,9,10,11,12,13, or 14.
The specification lacks written description for a nucleic acid encoding “MiniUSH2A” consisting of the amino acid sequence of SEQ ID NO: 15,16,17,18,19,20,21,22,23,24,25, or 26 as required in claim 7 other than a nucleic acid sequence encoding USH2A. The specification does not teach when an USH2A protein is a “MiniUSH2A” protein. The specification does not correlate regular USH2A protein to a MiniUSH2A protein. It is unclear whether “MiniUSH2A” is just a truncated USH2A or if it is a different protein all together. Accordingly, the concept lacks written description other than a nucleic acid sequence encoding USH2A.
The specification does not correlate delivering the rAAV to cells of mammals with Usher syndrome to administering the rAAV to a cell from any plant, invertebrate, insect, fish, amphibian, reptile, bird or mammal in vivo or vitro with or without Usher syndrome as broadly encompassed by claim 23. The specification does not teach delivering the vector to a plant, invertebrate, insect, fish, amphibian, reptile, or bird cell. The specification does not teach administering the vector any healthy mammal cell as broadly encompassed by claim 23. The specification does not teach treating any cell of a subject with any disease as broadly encompassed by claim 23 other than Usher syndrome. The claim encompasses administering rAAV comprising a nucleic acid sequence consisting of any one of SEQ ID NO: 3-14 to a subject that has Usher Syndrome. However, SEQ ID NO: 3-14 are fragments of USH2A. The specification and the art at the time of filing do not provide adequate guidance that AAV8 comprising a nucleic acid sequence consisting of any one of SEQ ID NO: 3-14 is adequate to treat symptoms of Usher disease because they are fragments of USH2A and do not have adequate domains capable or restoring USH2A function in patients that lack USH2A function. See Fig. 1.
Accordingly, the specification lacks written description for claim 23 other than administering an rAAV vector encoding USH2A to cells of a mammal that has Usher Syndrome such that symptoms of Usher Syndrome are ameliorated.
Enablement
Claims 1-4, 7, 13-16, 18, 21-23 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for administering an AAV vector encoding USH2A to the eye of a mammal that has Usher Syndrome such that symptoms of Usher Syndrome are ameliorated, does not reasonably provide enablement for the claims as broadly written. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make/use the invention commensurate in scope with these claims.
Withdrawn rejections
The rejection regarding administering the rAAV of claim 18 to a cell in a mammal that has Usher syndrome such that symptoms of Usher syndrome are ameliorated as required in claim 24 has been withdrawn because claim 24 has been canceled.
The rejection regarding administering the rAAV of claim 18 to any eye cell in vivo as broadly encompassed by claim 26 has been withdrawn because claim 26 has been canceled.
The rejection of claim 28 has been withdrawn because it has been canceled.
The rejection of claim 31 has been withdrawn because it has been canceled.
New rejection
The specification does not enable making/using a “transgene encoding a USH2A minigene encoded by a nucleotide sequence consisting of the nucleic acid sequence [ ] of SEQ ID NO”: 3,4,5,6,7,8,9,10,11,12,13, or 14 as required in claim 1 other than an isolated nucleic acid sequence encoding USH2A consisting of the nucleotide sequence of SEQ ID NO: 3,4,5,6,7,8,9,10,11,12,13, or 14. While an isolated nucleic acid sequence may encode USH2A and consist of the nucleotide sequence of SEQ ID NO: 3,4,5,6,7,8,9,10,11,12,13, or 14, the specification does not contemplate making/using a “transgene” encoding a “USH2A minigene” encoded by “a nucleotide sequence consisting” SEQ ID NO: 3-14 as required in claim 1. It is also unclear whether the “transgene”, the “minigene”, or the “nucleic acid sequence” within the “minigene” consists of SEQ ID NO: 3,4,5,6,7,8,9,10,11,12,13, or 14 (see 112/2nd). Given the lack of guidance in the specification taken with the art at the time of filing, it would have required those of skill undue experimentation to determine how to make/use anything other than an isolated nucleic acid sequence encoding USH2A consisting of the nucleotide sequence of SEQ ID NO: 3,4,5,6,7,8,9,10,11,12,13, or 14.
The specification does not enable making/using a nucleic acid encoding “MiniUSH2A” consisting of the amino acid sequence of SEQ ID NO: 15,16,17,18,19,20,21,22,23,24,25, or 26 as required in claim 7 other than a nucleic acid sequence encoding USH2A. The specification does not teach when an USH2A protein is a “MiniUSH2A” protein. The specification does not correlate regular USH2A protein to a MiniUSH2A protein. It is unclear whether “MiniUSH2A” is just a truncated USH2A or if it is a different protein all together. Given the lack of guidance in the specification taken with the art at the time of filing, it would have required those of skill undue experimentation to determine how to make/use anything other than a nucleic acid sequence encoding USH2A.
The specification does not enable delivering the rAAV to any cell as broadly encompassed by claim 23 other than cells of a mammal that has Usher syndrome. The specification does not correlate cells of a mammal that has Usher syndrome to healthy mammalian cells. The specification does not correlate mammalian cells to a cell from any plant, invertebrate, insect, fish, amphibian, reptile, or bird in vivo or vitro with or without Usher syndrome as broadly encompassed by claim 23. The specification does not teach delivering the vector to a plant, invertebrate, insect, fish, amphibian, reptile, or bird cell. The specification does not teach administering the vector any healthy mammal cell as broadly encompassed by claim 23. The specification does not teach treating any cell of a subject with any disease as broadly encompassed by claim 23 other than Usher syndrome. The claim encompasses administering rAAV comprising a nucleic acid sequence consisting of any one of SEQ ID NO: 3-14 to a subject that has Usher Syndrome. However, SEQ ID NO: 3-14 are fragments of USH2A. The specification and the art at the time of filing do not provide adequate guidance that AAV8 comprising a nucleic acid sequence consisting of any one of SEQ ID NO: 3-14 is adequate to treat symptoms of Usher disease because they are fragments of USH2A and do not have adequate domains capable or restoring USH2A function in patients that lack USH2A function. See Fig. 1 above. Given the lack of guidance in the specification taken with the art at the time of filing, it would have required those of skill undue experimentation to determine how to perform the method of claim 23 other than administering an rAAV vector encoding USH2A to cells of a mammal that has Usher Syndrome such that symptoms of Usher Syndrome are ameliorated.
Claim Rejections - 35 USC § 102
Claims 1, 13, 22 remain rejected under 35 U.S.C. 102a1 as being anticipated by NM_007123 as supported by Baux (Human Mutation, 2007, Vol. 28, No. 8, pg 781-789) and Roux (J. Mod. Genet. 2006, Vol. 43, pg 763-768).
NM_007123 is a 6372 bp mRNA sequence first described in 1993, in Baux in 2007 (pg 782, col. 1, “PCR Amplification of the USH2A gene and sequencing”) (see description of NM_007123.6 of record). Nucleotides 440-3439 of NM_007123 are 100% identical to the nucleic acid sequence of SEQ ID NO: 3. See alignment provided previously.
NM_007123 is the “transgene” encoding a USH2A “minigene”. Nucleotides 440-3439 are the “nucleotide sequence consisting of the nucleic acid sequence of SEQ ID NO: 3” as required in claim 1. Claim 1 is not limited to an isolated nucleic acid sequence encoding USH2A consisting of SEQ ID NO: 3.
Claims 13 has been included because Baux implicitly taught a vector comprising the nucleic acid sequence of NM_007123 for sequencing using the method described by Roux (pg 782, col. 1, “PCR Amplification of the USH2A gene and sequencing” which cited Roux). Roux amplified DNA fragments of 189 “amplicons” which are vectors as required in claim and are equivalent to the vector of claim 13.
Claim 22 has been included because the sequencing inherently MUST occur in a pharmaceutically acceptable excipient as indicated by successful sequence. Baux inherently MUST have used a pharmaceutically acceptable excipient capable of maintaining the structure of the nucleic acid sequence.
Response to arguments
Applicants argue the amendment in claim 1 overcomes the rejection. Applicants’ argument is not persuasive. NM_007123 is the “transgene” encoding a USH2A “minigene”. Nucleotides 440-3439 are the “nucleotide sequence consisting of the nucleic acid sequence of SEQ ID NO: 3” as required in claim 1. Claim 1 is not limited to an isolated nucleic acid sequence encoding USH2A consisting of SEQ ID NO: 3.
Even if claim 1 were limited to an isolated nucleic acid molecule comprising a nucleotide sequence encoding USH2A consisting of the nucleic acid sequence of SEQ ID NO: 3, NM_007123 would be the isolated nucleic acid sequence, and nucleotides 440-3439 would be the “nucleotide sequence encoding USH2A consisting of SEQ ID NO: 3”.
Applicants point to NM_206933.1 which is not the basis of the rejection.
Claim Rejections - 35 USC § 103
Pending rejection
Claims 1-4, 7, 13-16, 18, 21-24, 26, 28, 31, 33 remain rejected under 35 U.S.C. 103 as being unpatentable over Hildinger (20070042462) in view of NM_007123 and Baux (Human Mutation, 2007, Vol. 28, No. 8, pg 781-789).
Hildinger taught an adeno-associated viral (AAV) vector encoding Usherin-2A (USH2A) (para 7, 71, 75, 214).
Hildinger did not teach the vector comprised the nucleic acid sequence of SEQ ID NO: 3 as required in claim 1.
However, NM_007123 was first described in 1993, in Baux in 2007 (pg 782, col. 1, “PCR Amplification of the USH2A gene and sequencing”), et al. (see attached description of NM_007123.6) which is 100% identical to the nucleic acid sequence of SEQ ID NO: 3. See alignment above.
Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to make a vector encoding USH2A as described Hildinger using NM_007123 first described in 1993, in Baux in 2007, et al. Those of ordinary skill in the art at the time of filing would have been motivated to replace the USH2A coding sequence of Hildinger with the transcript variant of NM_007123 to express the variant in vitro to investigate the role of the variant in disease.
NM_007123 is the isolated nucleic acid sequence encoding USH2A. The sequence that matches SEQ ID NO: 3 is the “minigene having the nucleic acid sequence of SEQ ID NO: 3” that “is no more than 3609 nucleotides” as required in claim 1.
Claim 2 has been included because Hildinger taught expressing USH2A in a vector under the control of a promoter (para 148), e.g. a tissue-specific or inducible promoters (para 151), e.g. muscle-specific, liver-specific, photoreceptor-specific (para 152).
Hildinger taught expressing USH2A in a vector under the control of a CMV promoter (para 148) which is a “constitutive promoter” as required in claim 3, a tissue-specific or inducible promoter (para 151) as set forth in claim 3, specifically a muscle-specific, liver-specific, photoreceptor-specific (para 152) which is a “tissue-specific” promoter as encompassed by claim 3, or a Dex-inducible promoter (para 154) as encompassed by “inducible promoter” in claim 3.
Hildinger taught the vector was AAV encoding USH2A flanked by ITRs (end of para 148) as required in claim 4.
NM_007123 encodes the amino acid sequence of SEQ ID NO: 15 as required in claim 7.
Hildinger taught expressing USH2A in a vector (para 148) as required in claim 13.
Hildinger taught the vector was AAV (end of para 148) which is a viral vector as required in claim 14.
Hildinger taught the vector was AAV (end of para 148) as required in claim 15.
Hildinger taught expressing the protein in a cell (para 106, 148, 151, 154, 187, 189, 198, 275; claims 17-24) as required in claim 16.
Hildinger taught expressing the protein using AAV with a capsid (para 20, 22, 38, 65, 66, 86, 90, 94, 95, 98, 118, 119, 123, 132, 134, 140, 142, 143, 170, 171, 178, et al.) as required in claim 18.
Hildinger taught expressing the protein in the eye (para 40, 220, 269) and using AAV8 (para 134, 142, 170, 185, 251, 252, 253) which is equivalent to formulation for delivery to the eye as required in claim 21.
Hildinger taught formulating the vector in a pharmaceutically acceptable excipient (para 204, 205, 233, 267, 272, 281, 300) as required in claim 22.
Hildinger taught expressing the protein in the eye (para 40, 220, 269) and using AAV8 (para 134, 142, 170, 185, 251, 252, 253) which is equivalent to administration to a cell as required in claim 23.
Hildinger taught expressing the protein in the eye (para 40, 220, 269) and using AAV8 (para 134, 142, 170, 185, 251, 252, 253) which is equivalent to administration to a cell in a subject as required in claim 24.
Hildinger taught expressing the protein in the eye (para 40, 220, 269) and using AAV8 (para 134, 142, 170, 185, 251, 252, 253) which is equivalent to administration to an eye cell in a subject as required in claim 26.
Hildinger taught the gene therapy is used to treat Usher disease (para 75) as required in claim 28.
Hildinger taught the gene therapy is administered by subretinal injection ((para 205, 220-225, 264, 269, 274, 289, 296) which is “to the eye of a subject” as required in claim 31.
Hildinger taught expression is under the control of a rhodopsin kinase promoter for “photoreceptor-directed promoters” (para which is “to the eye of a subject” as required in claim 33.
Response to arguments
Applicants argue the limitation of “the USH2A minigene is no more than 3609 nucleotides” in claim 1 overcomes the rejection. Applicants’ argument is not persuasive. NM_007123 is the isolated nucleic acid sequence encoding USH2A. The sequence that matches SEQ ID NO: 3 is the “USH2A minigene having the nucleic acid sequence of SEQ ID NO: 3” that “is no more than 3609 nucleotides” as required in claim 1.
New rejection
B) Claims 1, 13, 22 are rejected under 35 U.S.C. 103 as being unpatentable over NM_007123 in view of Luzzio (20210292316), Chung (210190337987) and supported by Baux (Human Mutation, 2007, Vol. 28, No. 8, pg 781-789) and Roux (J. Mod. Genet. 2006, Vol. 43, pg 763-768).
NM_007123 is a 6372 bp mRNA sequence first described in 1993, in Baux in 2007 (pg 782, col. 1, “PCR Amplification of the USH2A gene and sequencing”) (see description of NM_007123.6 of record). Nucleotides 440-3439 of NM_007123 are 100% identical to the nucleic acid sequence of SEQ ID NO: 3. See alignment provided previously.
NM_007123 did not teach an isolated nucleic acid sequence encoding USH2A consisting of the nucleotide sequence of SEQ ID NO: 3 as possibly encompassed by claim 1.
However, truncating coding sequences was well-within the purview of the skilled artisan at the time of filing (Luzzio - para 80; claims 140-143; Chung - para 18). Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to isolate mRNA encoding USH2A as described by NM_007123 and truncate it as was well-known in the art. Those of ordinary skill in the art at the time of filing would have been motivated to do so to determine where functional domains lie within the protein and the coding sequence.
Claims 13 has been included because Baux implicitly taught a vector comprising the nucleic acid sequence of NM_007123 for sequencing using the method described by Roux (pg 782, col. 1, “PCR Amplification of the USH2A gene and sequencing” which cited Roux). Roux amplified DNA fragments of 189 “amplicons” which are vectors as required in claim and are equivalent to the vector of claim 13.
Claim 22 has been included because the sequencing inherently MUST occur in a pharmaceutically acceptable excipient as indicated by successful sequence. Baux inherently MUST have used a pharmaceutically acceptable excipient capable of maintaining the structure of the nucleic acid sequence.
Thus, Applicants' claimed invention as a whole is prima facie obvious in the absence of evidence to the contrary.
Pending rejection
C) Claims 1-4, 7, 13-16, 18, 21-24, 26, 28, 31, 33 are rejected under 35 U.S.C. 103 as being unpatentable over Hildinger (20070042462) in view of NM_007123, Luzzio (20210292316), Chung (210190337987) and Baux (Human Mutation, 2007, Vol. 28, No. 8, pg 781-789).
Hildinger taught an adeno-associated viral (AAV) vector encoding Usherin-2A (USH2A) (para 7, 71, 75, 214).
Hildinger did not teach the vector comprised a nucleic acid sequence encoding USH2A consisting of the nucleotide sequence of SEQ ID NO: 3 as possibly encompassed by claim 1.
However, NM_007123 was first described in 1993, in Baux in 2007 (pg 782, col. 1, “PCR Amplification of the USH2A gene and sequencing”), et al. (see attached description of NM_007123.6) which is 100% identical to the nucleic acid sequence of SEQ ID NO: 3. See alignment above. While NM_007123 was not an isolated nucleic acid sequence encoding USH2A consisting of the nucleotide sequence of SEQ ID NO: 3 as possibly encompassed by claim 1 is was well-within the purview of the skilled artisan at the time of filing (Luzzio - para 80; claims 140-143; Chung - para 18). Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to isolate mRNA encoding USH2A as described by NM_007123 and truncate it as was well-known in the art. Those of ordinary skill in the art at the time of filing would have been motivated to do so to determine where functional domains lie within the protein and the coding sequence.
Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to make a vector encoding USH2A as described Hildinger using NM_007123 first described in 1993, in Baux in 2007, et al. Those of ordinary skill in the art at the time of filing would have been motivated to replace the USH2A coding sequence of Hildinger with the nucleic acid sequence consisting of SEQ ID NO: 3 to investigate the role of the variant in disease.
NM_007123 is the isolated nucleic acid sequence encoding USH2A. The sequence that matches SEQ ID NO: 3 is the “minigene [ ] consisting of the nucleic acid sequence of SEQ ID NO: 3” as required in claim 1.
Claim 2 has been included because Hildinger taught expressing USH2A in a vector under the control of a promoter (para 148), e.g. a tissue-specific or inducible promoters (para 151), e.g. muscle-specific, liver-specific, photoreceptor-specific (para 152).
Hildinger taught expressing USH2A in a vector under the control of a CMV promoter (para 148) which is a “constitutive promoter” as required in claim 3, a tissue-specific or inducible promoter (para 151) as set forth in claim 3, specifically a muscle-specific, liver-specific, photoreceptor-specific (para 152) which is a “tissue-specific” promoter as encompassed by claim 3, or a Dex-inducible promoter (para 154) as encompassed by “inducible promoter” in claim 3.
Hildinger taught the vector was AAV encoding USH2A flanked by ITRs (end of para 148) as required in claim 4.
NM_007123 encodes the amino acid sequence of SEQ ID NO: 15 as required in claim 7.
Hildinger taught expressing USH2A in a vector (para 148) as required in claim 13.
Hildinger taught the vector was AAV (end of para 148) which is a viral vector as required in claim 14.
Hildinger taught the vector was AAV (end of para 148) as required in claim 15.
Hildinger taught expressing the protein in a cell (para 106, 148, 151, 154, 187, 189, 198, 275; claims 17-24) as required in claim 16.
Hildinger taught expressing the protein using AAV with a capsid (para 20, 22, 38, 65, 66, 86, 90, 94, 95, 98, 118, 119, 123, 132, 134, 140, 142, 143, 170, 171, 178, et al.) as required in claim 18.
Hildinger taught expressing the protein in the eye (para 40, 220, 269) and using AAV8 (para 134, 142, 170, 185, 251, 252, 253) which is equivalent to formulation for delivery to the eye as required in claim 21.
Hildinger taught formulating the vector in a pharmaceutically acceptable excipient (para 204, 205, 233, 267, 272, 281, 300) as required in claim 22.
Hildinger taught expressing the protein in the eye (para 40, 220, 269) and using AAV8 (para 134, 142, 170, 185, 251, 252, 253) which is equivalent to administration to a cell as required in claim 23.
Hildinger taught expressing the protein in the eye (para 40, 220, 269) and using AAV8 (para 134, 142, 170, 185, 251, 252, 253) which is equivalent to administration to a cell in a subject as required in claim 24.
Hildinger taught expressing the protein in the eye (para 40, 220, 269) and using AAV8 (para 134, 142, 170, 185, 251, 252, 253) which is equivalent to administration to an eye cell in a subject as required in claim 26.
Hildinger taught the gene therapy is used to treat Usher disease (para 75) as required in claim 28.
Hildinger taught the gene therapy is administered by subretinal injection ((para 205, 220-225, 264, 269, 274, 289, 296) which is “to the eye of a subject” as required in claim 31.
Hildinger taught expression is under the control of a rhodopsin kinase promoter for “photoreceptor-directed promoters” (para which is “to the eye of a subject” as required in claim 33.
Thus, Applicants' claimed invention as a whole is prima facie obvious in the absence of evidence to the contrary.
Conclusion
The prior art made of record and not relied upon is considered pertinent to applicant's disclosure:
NM_206933.4 (1993) and AY481573.1 (2003) are 100% identical to SEQ ID NO: 3 and were available at the time of filing (see alignments attached).
No claim is allowed.
Inquiry concerning this communication or earlier communications from the examiner should be directed to Michael C. Wilson who can normally be reached at the office on Monday through Friday from 9:30 am to 6:00 pm at 571-272-0738.
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Michael C. Wilson
/MICHAEL C WILSON/
Primary Examiner, Art Unit 1638