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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 05/08/2026 has been entered.
Priority
This application is a 371 of PCT/KR2021/010001, filed on 07/30/2021, claiming priority to foreign application KR 10-2020-0095988, filed on 07/31/2020.
Claims Status
Claims 1-5, 7-8 are canceled. Claims 6 and 9-11 are pending and under examination.
Terminal Disclaimer
The terminal disclaimer filed on 04/08/2026 has been reviewed and is accepted. The terminal disclaimer has been recorded.
Action Summary
Claims 6 and 9-11 rejected under 35 U.S.C. 103 as being unpatentable over Sim et al (US2019/0047993 A1) in view of Piris-Villaespesa et al (Front Pharmacol. 2020 Apr 14; 11:443) Martelli et al (Int. J. Mol. Sci. June 1 2020, 21(11), 3987), and Crew et al (US2006/0063773 A1), are withdrawn in light of the claim amendment (deleting substitution of valine for glycine at amino acid position 560 of c Kit protein in claim 9 and the deletion of valine in claim 6).
Claims 6 and 9-11 rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 10 of U.S. Patent No. US10,442,796 B2 in view of Piris-Villaespesa et al (Front Pharmacol. 2020 Apr 14; 11:443), Martelli et al (Int. J. Mol. Sci. June 1 2020, 21(11), 3987), Crew et al (US2006/0063773 A1), are withdrawn in light of the claim amendment (deleting substitution of valine for glycine at amino acid position 560 of c Kit protein in claim 9 and the deletion of valine in claim 6).
Claims 6 and 9-11 rejected on the ground of nonstatutory double patenting as being unpatentable over claim 4 of U.S. Patent No. 18/006,582 in view of Piris-Villaespesa et al (Front Pharmacol. 2020 Apr 14; 11:443) and Martelli et al (Int. J. Mol. Sci. June 1 2020, 21(11), 3987), Crew et al (US2006/0063773 A1), are withdrawn in light of the terminal disclaimer filed on 04/08/2026, which has been approved.
Specification
The disclosure is objected to because the terminology “novel” appearing in paragraph [0007] is improper as it implies a conclusion regarding the patentability of the claimed invention. Applicant is required to amend the specification to delete such terminology or replace it with more neutral language such as “disclosed” described,” or “present.”
Appropriate correction is required.
New Rejection necessitated by claim amendment
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.
Claims 6 and 9-11 are rejected under 35 U.S.C. 103 as being unpatentable over Sim et al (US2019/0047993 A1) in view of Shivakrupa et al. (Cancer Research 63, 4412–4419, August 1, 2003) Jack Longley. et al (Proc. Natl. Acad. Sci. USA Vol. 96, pp. 1609±1614, February 1999), and Crew et al (US2006/0063773 A1).
Sim teaches a teach a method for the treatment, prevention, and alleviation of acute myeloid leukemia, the method comprising administering a pharmaceutical composition comprising as an active ingredient, a 2,3,5-substituted thiophene compound, preferably (S)-5-((3-fluorophenyl) ethynyl)-N-(piperidin-3-yl)-3-ureidothiophene-2-carboxamide
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. (See claims 1, 9, 10, and paragraph [0299].)
This compound corresponds to compound of Example 22. Moreover, Sim teaches the 2,3,5-substituted thiophene compound is excellent in ability to inhibit activity of Kit among other proteins. (See paragraph [0023].)
Sim does not teach systematic mastocytosis wherein the systematic mastocytosis is caused by substitution of histidine for aspartic acid at amino acid position 816 of c-kit protein and by substitution of aspartic acid for valine at amino acid position 559 of c-kit protein.
Shivakrupa teaches Kit, a type III receptor tyrosine kinase, binds to ligand SCF3 and initiates signals critical for the growth and development of mast cells, melanocytes, hematopoietic stem cells, and the interstitial cells of Cajal. Gain-of-function mutations in Kit are associated with a number of cancers in humans. Substitution of tyrosine/valine/ histidine for aspartic acid in codon 816 of the catalytic domain of the human gene (codon 814 of the murine gene) is found in patients with mastocytosis and mast cell leukemia, as well as some patients with acute myelogenous leukemia and germ cell tumors. (See first paragraph under Introduction Section of the left column of page 4412.) Moreover, Shivakrupa teaches because many patients with mastocytosis have mutations in codon 816, identification of signaling components activated by this mutant in mast cells could lead to identification of pharmaceuticals useful in the treatment of this disease. (See third paragraph of the right column of page 4412.)
Jack Longley Jr. teaches human mastocytosis is characterized by increased mast cells. It usually occurs as a sporadic disease including systemic involvement that is often transient and limited in children and persistent or progressive in adults. The c-KIT protooncogene encodes KIT, a tyrosine kinase that is the receptor for mast cell growth factor. Because mutated KIT can transform cells, we examined c-KIT in skin lesions of 22 patients with sporadic mastocytosis and 3 patients with familial mastocytosis. All patients with adult sporadic mastocytosis had somatic c-KIT mutations in codon 816 causing substitution of valine for aspartate and spontaneous activation of mast cell growth factor receptor. (See Abstract and Table 1.) Moreover, Jack Longley Jr. teaches most known c-KIT mutations cause loss of function of KIT, resulting in piebaldism in humans and the W spotted phenotype in the mouse. However, c-KIT mutations in codon 816 causing substitution of aspartate or tyrosine for valine, and a codon 559 mutation causing substitution of valine for glycine, have been found in neoplastic mast cell lines and have been reported to cause constitutive phosphorylation and activation of KIT. (See last paragraph of the right column of page 1609.)
Crew teaches a compound represented by the formula (I)
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having cKIT activity for treating tumors or cancers such as mastocytosis/mast cell leukemia among others. (See Abstract, claim 1, and paragraph [0079].)
It would have been prima facie obvious to one of ordinary skill in the art at the time the invention was filed to administer the Kit inhibitory compound taught by Sim for treating mastocytosis and mast cell leukemia caused by activating c-KIT mutations, including substitution of histidine for aspartic acid at amino acid position 816 of c-KITt protein and by substitution of aspartic acid for valine at amino acid position 559 of c-kIT protein. Sime teaches the same compound recited in the instant claims and teaches that the compound is excellent in its ability to inhibit KIT activity. Shivakrupa and Jack Longley Jr. teach that mastocytosis and mast cell leukemia are associated with activating c-KIT, including codon 816 and 559 mutations and that such mutations result in constitutive activation of KIT signaling. Mast cell leukemia is a systemic mastocytosis. Crew is relied upon not for the claimed compound, but for the further teaching that cKIT activity is therapeutically relevant to mastocytosis/mast cell leukemia and that c KIT inhibitors are useful for treating such diseases.
Therefore, one of ordinary skill in the art would have been motivated to use Sim’s KIT inhibitor in a patient having mastocytosis and mast cell leukemia (systemic mastocytosis) caused by activating c-KIT mutations because the cited art identifies aberrant KIT activation as a cause or driver of mastocytosis/mast cell leukemia and teaches treatment of such diseases through inhibition of cKIT activity. The motivation is not based on bodily incorporation of Crew’s compound into Sim, but on the combined teachings that: (1) Sim provides the same claimed active compound and teaches KIT inhibition; (2) Shivakrupa and Jack Longley Jr. identity the claimed c-KIT mutations as activating mutations associated with mastocytosis/mast cell leukemia; and (3) Crew confirms that cKIT inhibition is a recognized therapeutic approach for mastocytosis/mast cell leukemia.
One of ordinary skill in the art would have had a reasonably expectation of success because the claimed disease is characterized by aberrant KIT activation, and Sim’s compound is expressly taught to inhibit cKIT activity. Thus, using Sim’s KIT inhibitor to treat a KIT-driven mastocytosis/mast cell leukemia would have been predictable use of a known KIT inhibitor for its established purpose, namely inhibiting KIT signaling in a disease in which KIT activation is implicated. The fact that Crew discloses different cKIT inhibitors does not detract from the rejection because Crew is cited to show the known therapeutic relevance of cKIT inhibition in mastocytosis/mast cell leukemia, not to supply the claimed compound.
Additionally, Crew’s compounds are noted to possess a structurally similar heteroaryl kinase-inhibitor scaffold and are likewise disclosed as possessing cKIT inhibitory activity useful for treating mastocytosis/mast cell leukemia. Thus, Crew further evidences that compounds having kinase-inhibitory scaffolds and cKIT inhibitory activity were recognized in the art as useful for treating c-KTI-driven mastocytosis disorders including mast cell leukemia, a systemic mastocytosis.
Applicant’s arguments
Applicant argues that the combination of Sim, Piris-Villaespesa, Martelli, and Crew fails to teach or suggest that the compound of Example 22 of Sim possesses inhibitory activity against mastocytosis associated with the specific KIT mutations recited in amended claims 6 and 9. Applicant contends that Sim merely discloses the compound for AML and does not teach treatment of mastocytosis or activity against any specific c-KIT mutation. Applicant further argues that the additional references merely identify mutation associated with systemic mastocytosis, but do not teach that any particular compound would be effective against such mutations.
Applicant additionally argues that Crew neither discusses the claimed compound nor the claimed mutations and merely lists mastocytosis among a broad range of cancers. Applicant further asserts that the Examiner failed to demonstrate that the genus disclosed in Crew encompasses the claimed compound. Accordingly, Applicant concludes that the rejection relies upon impermissible hindsight reconstruction and that there would have been no reasonable expectation of success in using the compound of Example 22 of Sim for treating mastocytosis associated with the claimed c-KIT mutations.
Response to Arguments
Applicant’s arguments have been fully considered but are not persuasive.
As an initial matter, the presently applied rejection relies upon Shivakrupa et al. and Jack Longley Jr. et al. in place of Piris-Villaespesa and Martelli. Nevertheless, Applicant’s arguments directed to the prior references have been considered to the extent relevant to the presently applied rejection.
In response to applicant's arguments against the references individually, one cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986). In the present case, the rejection does not rely upon Crew to disclose the claimed compound. Rather, Sim expressly teaches the same compound recited in the instant claims, namely the compound of Example 22, and further teaches inhibitory activity against KIT. Therefore, Applicant’s argument that Crew fails to disclose the claimed compound or encompass the claimed compound within its genus is not persuasive because Crew is not relied upon for teaching the claimed compound.
Additionally, the rejection does not require that Sim expressly disclose expressly disclose treatment of mastocytosis associated with each specifically recited c-KIT mutation. Obviousness does not require an express teaching in a single reference of the precise claimed therapeutic application. Rather, the proper inquiry is whether the combined teachings of the references would have suggested the claimed invention to one of ordinary skill in the art with a reasonable expectation of success. Here, Shivakrupa teaches that activating KIT mutations, including substitution of tyrosine/valine/histidine for aspartic acid at codon 816, are associated with mastocytosis and mast cell leukemia. Shivakrupa also teaches that identification of signaling components activated by mutant KIT could lead to identification of pharmaceuticals useful for treating mastocytosis. Jack Longley Jr. further teaches that c-KIT mutations at codon 816 and codon 559 cause constitutive phosphorylation and activation of KIT mastocytosis and mast cell leukemia. Thus, the cited references establish that aberrant KIT activation caused by the claimed mutations is implicated in mastocytosis pathology. Crew further teaches that inhibition of cKIT activity is a recognized therapeutic approach for treating mastocytosis and mast cell leukemia. Crew additionally teaches structurally related heteroaryl kinase inhibitors possessing cKIT inhibitory activity useful for treating mastocytosis/mast cell leukemia. Crew is relied upon to demonstrate the known therapeutic relevance of cKIT inhibition in mastocytosis and mast cell leukemia, not to disclose the claimed compounds.
Because Sim expressly teaches the claimed compound and teaches the compound possesses excellent KIT inhibitory activity, one of ordinary skill in the art would have reasonably expected that administering Sim’s KIT inhibitor to patients suffering from KIT-driven mastocytosis, including mastocytosis associated with the claimed mutations, would provide therapeutic benefit. The rejection is therefore, based on the combined teachings of: 1) Sim provides the same claimed active compound and teaches KIT inhibition; (2) Shivakrupa and Jack Longley Jr. identity the claimed c-KIT mutations as activating mutations associated with mastocytosis/mast cell leukemia; and (3) Crew confirms that cKIT inhibition is a recognized therapeutic approach for mastocytosis/mast cell leukemia.
In response to applicant's argument that the examiner's conclusion of obviousness is based upon improper hindsight reasoning, it must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon hindsight reasoning. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made, and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin, 443 F.2d 1392, 170 USPQ 209 (CCPA 1971). In the present case, the rejection is based upon explicit teachings of the prior art identifying the relationship between KIT activation and mastocytosis/mast cell leukemia, together with the known therapeutic use of KIT inhibitors for treating KIT-driven disorders. The claimed invention merely represents the predictable use of a known KIT inhibitor for treatment of a known KIT-driven disease associated with activating KIT mutations.
New Rejection necessitated by claim amendment
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 6 and 9-11 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 10 of U.S. Patent No. US10,442,796 B2 in view Shivakrupa et al. (Cancer Research 63, 4412–4419, August 1, 2003) Jack Longley. et al (Proc. Natl. Acad. Sci. USA Vol. 96, pp. 1609±1614, February 1999), and Crew et al (US2006/0063773 A1).
The U.S. patent claims teach a method for the treatment, prevention, and alleviation of acute myeloid leukemia, the method comprising administering a pharmaceutical composition comprising as an active ingredient, a 2,3,5-substituted thiophene compound, preferably (S)-5-((3-fluorophenyl) ethynyl)-N-(piperidin-3-yl)-3-ureidothiophene-2-carboxamide
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as the active ingredient. (See claims 1 and 10)
Although, the U.S. patent claims do not teach the compound is excellent in ability to inhibit activity of Kit among other proteins, the specification of the U.S. patent claims disclose the compound is excellent in ability to inhibit activity of Kit. (See paragraph [0023].)
The U.S. patent claims do not systematic mastocytosis wherein the systematic mastocytosis is caused by substitution of histidine for aspartic acid at amino acid position 816 of c-kit protein and by substitution of aspartic acid for valine at amino acid position 559 of c-kit protein.
Shivakrupa teaches Kit, a type III receptor tyrosine kinase, binds to ligand SCF3 and initiates signals critical for the growth and development of mast cells, melanocytes, hematopoietic stem cells, and the interstitial cells of Cajal. Gain-of-function mutations in Kit are associated with a number of cancers in humans. Substitution of tyrosine/valine/ histidine for aspartic acid in codon 816 of the catalytic domain of the human gene (codon 814 of the murine gene) is found in patients with mastocytosis and mast cell leukemia, as well as some patients with acute myelogenous leukemia and germ cell tumors. (See first paragraph under Introduction Section of the left column of page 4412.) Moreover, Shivakrupa teaches because many patients with mastocytosis have mutations in codon 816, identification of signaling components activated by this mutant in mast cells could lead to identification of pharmaceuticals useful in the treatment of this disease. (See third paragraph of the right column of page 4412.)
Jack Longley Jr. teaches human mastocytosis is characterized by increased mast cells. It usually occurs as a sporadic disease including systemic involvement that is often transient and limited in children and persistent or progressive in adults. The c-KIT protooncogene encodes KIT, a tyrosine kinase that is the receptor for mast cell growth factor. Because mutated KIT can transform cells, we examined c-KIT in skin lesions of 22 patients with sporadic mastocytosis and 3 patients with familial mastocytosis. All patients with adult sporadic mastocytosis had somatic c-KIT mutations in codon 816 causing substitution of valine for aspartate and spontaneous activation of mast cell growth factor receptor. (See Abstract and Table 1.) Moreover, Jack Longley Jr. teaches most known c-KIT mutations cause loss of function of KIT, resulting in piebaldism in humans and the W spotted phenotype in the mouse. However, c-KIT mutations in codon 816 causing substitution of aspartate or tyrosine for valine, and a codon 559 mutation causing substitution of valine for glycine, have been found in neoplastic mast cell lines and have been reported to cause constitutive phosphorylation and activation of KIT. (See last paragraph of the right column of page 1609.)
Crew teaches a compound represented by the formula (I)
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having cKIT activity for treating tumors or cancers such as mastocytosis/mast cell leukemia among others. (See Abstract, claim 1, and paragraph [0079].)
It would have been prima facie obvious to one of ordinary skill in the art at the time the invention was filed to administer the Kit inhibitory compound taught by Sim for treating mastocytosis and mast cell leukemia caused by activating c-KIT mutations, including substitution of histidine for aspartic acid at amino acid position 816 of c-KITt protein and by substitution of aspartic acid for valine at amino acid position 559 of c-kIT protein. Sime teaches the same compound recited in the instant claims and teaches that the compound is excellent in its ability to inhibit KIT activity. Shivakrupa and Jack Longley Jr. teach that mastocytosis and mast cell leukemia are associated with activating c-KIT, including codon 816 and 559 mutations and that such mutations result in constitutive activation of KIT signaling. Mast cell leukemia is a systemic mastocytosis. Crew is relied upon not for the claimed compound, but for the further teaching that cKIT activity is therapeutically relevant to mastocytosis/mast cell leukemia and that c KIT inhibitors are useful for treating such diseases.
Therefore, one of ordinary skill in the art would have been motivated to use U.S. patent claims’ KIT inhibitor in a patient having mastocytosis and mast cell leukemia (systemic mastocytosis) caused by activating c-KIT mutations because the cited art identifies aberrant KIT activation as a cause or driver of mastocytosis/mast cell leukemia and teaches treatment of such diseases through inhibition of cKIT activity. The motivation is not based on bodily incorporation of Crew’s compound into Sim, but on the combined teachings that: (1) Sim provides the same claimed active compound and teaches KIT inhibition; (2) Shivakrupa and Jack Longley Jr. identity the claimed c-KIT mutations as activating mutations associated with mastocytosis/mast cell leukemia; and (3) Crew confirms that cKIT inhibition is a recognized therapeutic approach for mastocytosis/mast cell leukemia.
One of ordinary skill in the art would have had a reasonably expectation of success because the claimed disease is characterized by aberrant KIT activation, and the U.S. patent claims’ compound is expressly taught to inhibit cKIT activity. Thus, using the U.S. patent claims’ KIT inhibitor to treat a KIT-driven mastocytosis/mast cell leukemia would have been predictable use of a known KIT inhibitor for its established purpose, namely inhibiting KIT signaling in a disease in which KIT activation is implicated. The fact that Crew discloses different cKIT inhibitors does not detract from the rejection because Crew is cited to show the known therapeutic relevance of cKIT inhibition in mastocytosis/mast cell leukemia, not to supply the claimed compound.
Additionally, Crew’s compounds are noted to possess a structurally similar heteroaryl kinase-inhibitor scaffold and are likewise disclosed as possessing cKIT inhibitory activity useful for treating mastocytosis/mast cell leukemia. Thus, Crew further evidences that compounds having kinase-inhibitory scaffolds and cKIT inhibitory activity were recognized in the art as useful for treating c-KTI-driven mastocytosis disorders including mast cell leukemia, a systemic mastocytosis
Applicant’s arguments regarding the nonstatutory obviousness-type double patenting rejection have been fully considered but are not persuasive for substantially the same reasons discussed above with respect to the rejection under 35 U.S.C. 103.
As explained above, Sim teaches the same compound recited in the instant claims and further teaches KIT inhibitory activity. Shivakrupa and Jack Longley Jr and Crew collectively teach that activating c-KT mutations are associated with mastocytosis/mast cell leukemia and that inhibition of cKIT activity is a recognized therapeutic strategy for such disorders. Therefore, one would expect the compound taught by Sim to successfully treat mastocytosis associated with the recited cKIT mutations claimed wither a reasonable expectation of success.
Conclusion
Claims 6 and 9-11 are not allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to JEAN P CORNET whose telephone number is (571)270-7669. The examiner can normally be reached Monday-Thursday from 7.00am-5.30pm.
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/JEAN P CORNET/ Primary Examiner, Art Unit 1628
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