DETAILED ACTION
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Claim(s) 1, 3-4, 9, 11-12, and 14-23 are pending.
Preliminary Amendments
Applicant’s preliminary amendment filed on 01/11/2024 is acknowledged. The claims was amended to (1) cancel claims 2, 5-8, 10, 13, and 24-37, and (2) amend claims 1, 3, 9, 11-12, and 14.
It is noted that the amendment to the claims filed on 08/11/2026 does not comply with the requirements of 37 CFR 1.121(c) because the status identifier of claim 3 should recite “previously presented”. However, in the interest of compact prosecution, the amendment to the claims has been entered.
Election/Restrictions
Applicant’s election without traverse of Group I in the reply filed on 08/11/2026 is acknowledged.
Claim(s) 17-23 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention of Group II, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 08/11/2026.
Claim(s) 1, 3-4, 9, 11-12, and 14-16 are under consideration.
Priority
Acknowledgement is made that this application is a 371 of PCT/US2022/073668 filed 07/13/2022 and claims priority based on provisional application filed as 63/222,336 on 07/15/2021.
This application makes reference to or appears to claim subject matter disclosed in Application No. 63/224,362, filed 07/21/2021. If applicant desires to claim the benefit of a prior-filed application under 35 U.S.C. 119(e), 120, 121, 365(c) or 386(c), the instant application must contain, or be amended to contain, a specific reference to the prior-filed application in compliance with 37 CFR 1.78. If the application was filed before September 16, 2012, the specific reference must be included in the first sentence(s) of the specification following the title or in an application data sheet (ADS) in compliance with pre-AIA 37 CFR 1.76; if the application was filed on or after September 16, 2012, the specific reference must be included in an ADS in compliance with 37 CFR 1.76. For benefit claims under 35 U.S.C. 120, 121, 365(c), or 386(c), the reference must include the relationship (i.e., continuation, divisional, or continuation-in-part) of the applications.
If the instant application is a utility or plant application filed under 35 U.S.C. 111(a), the specific reference must be submitted during the pendency of the application and within the later of four months from the actual filing date of the application or sixteen months from the filing date of the prior application. If the application is a national stage application under 35 U.S.C. 371, the specific reference must be submitted during the pendency of the application and within the later of four months from the date on which the national stage commenced under 35 U.S.C. 371(b) or (f), four months from the date of the initial submission under 35 U.S.C. 371 to enter the national stage, or sixteen months from the filing date of the prior application. See 37 CFR 1.78(a)(4) for benefit claims under 35 U.S.C. 119(e) and 37 CFR 1.78(d)(3) for benefit claims under 35 U.S.C. 120, 121, 365(c), or 386(c). This time period is not extendable and a failure to submit the reference required by 35 U.S.C. 119(e) and/or 120, where applicable, within this time period is considered a waiver of any benefit of such prior application(s) under 35 U.S.C. 119(e), 120, 121, 365(c), and 386(c). A benefit claim filed after the required time period may be accepted if it is accompanied by a grantable petition to accept an unintentionally delayed benefit claim under 35 U.S.C. 119(e) (see 37 CFR 1.78(c)) or under 35 U.S.C. 120, 121, 365(c), or 386(c) (see 37 CFR 1.78(e)). The petition must be accompanied by (1) the reference required by 35 U.S.C. 120 or 119(e) and by 37 CFR 1.78 to the prior application (unless previously submitted), (2) the applicable petition fee under 37 CFR 1.17(m)(1) or (2), and (3) a statement that the entire delay between the date the benefit claim was due under 37 CFR 1.78 and the date the claim was filed was unintentional. The presentation of a benefit claim may result in an additional fee under 37 CFR 1.17(w)(1) or (2) being required, if the earliest filing date for which benefit is claimed under 35 U.S.C. 120, 121, 365(c), or 386(c) and 1.78(d) in the application is more than six years before the actual filing date of the application. The Director may require additional information where there is a question whether the delay was unintentional. The petition should be addressed to: Mail Stop Petition, Commissioner for Patents, P.O. Box 1450, Alexandria, Virginia 22313-1450.
If the reference to the prior application was previously submitted within the time period set forth in 37 CFR 1.78 but was not included in the location in the application required by the rule (e.g., if the reference was submitted in an oath or declaration or the application transmittal letter), and the information concerning the benefit claim was recognized by the Office as shown by its inclusion on the first filing receipt, the petition under 37 CFR 1.78 and the petition fee under 37 CFR 1.17(m)(1) or (2) are not required. Applicant is still required to submit the reference in compliance with 37 CFR 1.78 by filing an ADS in compliance with 37 CFR 1.76 with the reference (or, if the application was filed before September 16, 2012, by filing either an amendment to the first sentence(s) of the specification or an ADS in compliance with pre-AIA 37 CFR 1.76). See MPEP § 211.02.
It is of note that in the specification, Applicant lists 63/224,362 in the “Cross-Reference to Related Applications” statement, however, this is not consistent with what is listed on the Application Filing Receipt, i.e., 63/224,363 filed 07/21/2021 which does not have a common owner/inventor with the instant application. Thus the claim for the benefit of that application is not effective.
All claims are given the priority date of 07/15/2021.
Information Disclosure Statement
Receipt of the information disclosure statement(s) on 01/11/2024 and 08/03/2026 are acknowledged. The signed and initialed PTO-1449 form(s) has/have been mailed with this action.
Nucleotide and/or Amino Acid Sequence Disclosures
Summary of Requirements for Patent Applications Filed On Or After July 1, 2022, That Have Sequence Disclosures
37 CFR 1.831(a) requires that patent applications which contain disclosures of nucleotide and/or amino acid sequences that fall within the definitions of 37 CFR 1.831(b) must contain a “Sequence Listing XML”, as a separate part of the disclosure, which presents the nucleotide and/or amino acid sequences and associated information using the symbols and format in accordance with the requirements of 37 CFR 1.831-1.835. This “Sequence Listing XML” part of the disclosure may be submitted:
1. In accordance with 37 CFR 1.831(a) using the symbols and format requirements of 37 CFR 1.832 through 1.834 via the USPTO patent electronic filing system (see Section I.1 of the Legal Framework for Patent Electronic System (https://www.uspto.gov/PatentLegalFramework), hereinafter “Legal Framework”) in XML format, together with an incorporation by reference statement of the material in the XML file in a separate paragraph of the specification (an incorporation by reference paragraph) as required by 37 CFR 1.835(a)(2) or 1.835(b)(2) identifying:
a. the name of the XML file
b. the date of creation; and
c. the size of the XML file in bytes; or
2. In accordance with 37 CFR 1.831(a) using the symbols and format requirements of 37 CFR 1.832 through 1.834 on read-only optical disc(s) as permitted by 37 CFR 1.52(e)(1)(ii), labeled according to 37 CFR 1.52(e)(5), with an incorporation by reference statement of the material in the XML format according to 37 CFR 1.52(e)(8) and 37 CFR 1.835(a)(2) or 1.835(b)(2) in a separate paragraph of the specification identifying:
a. the name of the XML file;
b. the date of creation; and
c. the size of the XML file in bytes.
SPECIFIC DEFICIENCIES AND THE REQUIRED RESPONSE TO THIS NOTICE ARE AS FOLLOWS:
Specific deficiency - The incorporation by reference paragraph required by 37 CFR 1.834(c)(1), 1.835(a)(2), or 1.835(b)(2) is missing, defective or incomplete.
The size of the XML file must be in bytes (e.g., 62,554 bytes).
The file name is incorrect (correct name: VAND-0224-PCT.xml)
Required response - Applicant must:
• Provide a substitute specification in compliance with 37 CFR 1.52, 1.121(b)(3), and 1.125 inserting the required incorporation by reference paragraph, consisting of:
• A copy of the previously-submitted specification, with deletions shown with strikethrough or brackets and insertions shown with underlining (marked-up version);
• A copy of the amended specification without markings (clean version); and
• A statement that the substitute specification contains no new matter.
Specification
The disclosure is objected to because of the following informalities: On page 2, line 32, “DNA” should be “RNA.” Applicant defines ASO on page 2 lines 19-21, wherein “An "antisense oligonucleotide" or "ASO" refers to a synthetic, multi-nucleotide RNA compound that hybridizes to a target RNA sequence in a manner such that gene expression can be inhibited, including by inactivating an mRNA molecule.” It would be remedial to amend the specification to recite “RNA” instead of “DNA”.
Appropriate correction is required.
Claim Objections
Claim 14 is objected to because of the following informalities: the “o” in “SEQ ID No 4” is lowercase, however, it is upper case for every other SEQ ID and claim. It would be remedial to amend the claim to recite, “SEQ ID NO 4”. Appropriate correction is required.
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.
Claim(s) 1, 3-4, 9, 11-12, and 14-16 are rejected under 35 U.S.C. 103 as being unpatentable over Verstovsek et al (Safety and Efficacy of INCB018424, a JAK1 and JAK2 Inhibitor, in Myelofibrosis, NEJM, vol 363, issue 12, pages 1117-1127, published September 16th, 2010) in view of Jedidi et al (Selective reduction of JAK2V617F-dependent cell growth by siRNA/shRNA and its reversal by cytokines, blood, vol 114, issue 9, pages 1842-1851, published August 27th, 2009) and further in view of Alderstein et al (supra).
Of note: The instant specification defines ASO as the following: “An "antisense oligonucleotide" or "ASO" refers to a synthetic, multi-nucleotide RNA compound that hybridizes to a target RNA sequence in a manner such that gene expression can be inhibited, including by inactivating an mRNA molecule.”, (see page 2, lines 19-21).
Verstovsek et al teaches, “The discovery of JAK2 V617F, a somatic gain-of-function mutation in the Janus kinase 2 (JAK2) in classic Philadelphia chromosome (Ph)–negative myeloproliferative neoplasms, which include essential thrombocythemia, polycythemia vera, and primary myelofibrosis, generated interest in the development of JAK2-targeted therapies for these diseases.6,7 The JAK2 V617F mutation is present in approximately 50% of patients with myelofibrosis. Some clinical signs of the disease, such as anemia and splenomegaly, and the risk of transformation to acute myeloid leukemia (AML) have been related to JAK2 V617F mutational status or the JAK2 V617F allele burden.”, (p. 1118, col 1, para 2).
Verstovsek et al teaches, “About half of patients with myelofibrosis carry a gain-of-function mutation in the Janus kinase 2 gene (JAK2 V617F) that contributes to the pathophysiology of the disease. INCB018424 is a potent and selective Janus kinase 1 (JAK1) and JAK2 inhibitor.”, (background).
Regarding claim(s) 1, 3-4, 9, and 11, Verstovsek et al teaches, “Patients 18 years of age or older with primary myelofibrosis, post−essential thrombocythemia myelofibrosis, or post−polycythemia vera myelofibrosis (according to World Health Organization criteria revised in 2001)13 were eligible for enrollment . . .”, (p. 1118, col 1, para 3). Further, “The starting dose of INCB018424 was 25 mg twice daily followed by escalation to 50 mg twice daily.”, (p. 1119, col 2, para 1).
Despite teaching treating patients diagnosed with MDS or PV via administering a JAK2 inhibitor, Vertosvsek et al does not teach antisense oligonucleotides targeting JAK2, specifically SEQ ID NO: 2 or 3, with SEQ ID NO: 4 or 5.
Jedidi et al teaches, “Ongoing clinical trials of Janus kinase 2 (JAK2) inhibitors in myeloproliferative disorder patients use small molecules targeting both wild-type and mutated JAK2. To selectively target malignant cells, we developed JAK2V617F-specific small interfering RNAs or short hairpin RNAs.”, (abstract).
“Breakpoint cluster region (BCR)/Abelson (ABL)–negative classical myeloproliferative disorders (MPD) include essential thrombocythemia (ET), polycythemia vera (PV), and primary myelofibrosis (PMF).”, (p. 1842, col 1, para 1). In these disorders, we5 and others6-8 have identified a unique and recurrent acquired mutation of the Janus kinase 2 (JAK2) protein corresponding to a valine-to-phenylalanine substitution (JAK2V617F) in the pseudokinase domain. The JAK2V617F mutation is present in a majority of PV patients and in approximately half of the patients suffering from PMF or ET.”, (p. 1842, col 1, para 2).
“Preclinical and clinical studies using several orally available small molecule inhibitors have recently been reported.13 These inhibitors are more or less specific for JAK2 among other kinases, but to date none is specific for the JAK2V617F mutation. Although the lack of specificity of the JAK2 inhibitors provides the advantage of extending their use to JAK2V617F-negative MPD and other pathologies involving the JAK2/signal transducer and activator of transcription (STAT) pathway, the fundamental role of JAK2 in hematopoiesis has raised concerns on the long-term efficacy and safety of these drugs. The location of the JAK2V617F mutation outside of the kinase domain presents a genuine challenge for the development of small molecule inhibitors targeting JAK2V617F. In contrast, mutation-specific inhibition of single point-mutated protein using transfected syn thetic small interfering RNA (siRNA) duplexes or virally transduced short hairpin RNAs (shRNAs) has been reported with several genes, including p53R248W,14 TauV337M,15 or BRAFV599E.16 These RNAs selectively match to the endogenous target mRNA, leading to its degradation and the inhibition of the related protein expression in mammalian cells. A single-base mismatch between the siRNA and its target is believed to prevent mRNA degradation, thus allowing this type of inhibition to be highly specific to the targeted gene. Using this strategy, we succeeded in developing siRNAs and shRNAs selectively suppressing JAK2V617F without affecting normal JAK2WT protein production.”, (p. 1842, col 2, para 1-2)
Regarding claim(s) 1 and 3, Jedidi et al teaches in Figure 1A the target sequence of JAK2 and the siRNA targeting JAK2 mRNA (see image below). Specifically, Jedidi et al teaches, “These RNAs abrogated JAK2V617F dependent autonomous growth of cell lines and primary cells from MPD patients.”, (p. 1842, col 2, para 2).
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Regarding claim 4, Jedidi et al teaches inhibition of expression of JAK2
in Figure 1B (see above). More specifically, Jedidi et al teaches inhibition of JAK2 in PV patient cells in figure 6.
Regarding claim(s) 9 and 11, Jedidi et al teaches “The silencing of the JAK2V617F gene in HEL cells treated with the Jak2-, mt1-, and mt4- siRNAs caused a decrease in phospho-STAT5 and phospho-ERK1/2 without affecting their total protein levels (Figure1B).”, (p. 1845, col 1, para 2).
Despite Verstovsek et al teaching the use of a small molecule JAK2 inhibitor in patients in a clinical trial with MDS and PV, and Jedidi et al teaching antisense (siRNA/shRNA) targeting the V617F mutation, Verstovsek et al et al and Jedidi et al does not explicitly teach SEQ ID NOs: 2-5.
Adlerstein et al teaches oligonucleotides targeting around the V617F JAK2 mutation.
Regarding claim(s) 1, 3-4, 9, and 11, Alderstein et al teaches, “The scope of the invention further comprises an isolated oligonucleotide primer selected from the group consisting of SEQ ID NO:3, SEQ ID NO:4, SEQ ID NO:5, SEQ ID NO:6 and SEQ ID NO:8, as well as a Peptide Nucleic Acid (PNA) of 6-24 bases in length, comprising a base sequence which is capable of hybridizing to a region of the JAK 2 genomic DNA (SEQ ID NO:2) including position 93526 of SEQ ID NO:2 or to a region of the JAK 2 cDNA (SEQ ID NO:1) including position 2343 of SEQ ID NO:1. . .”, (col 7, lines 42-55).
Wherein SEQ ID NO: 5 of Alderstein et al is 100% similar to both SEQ ID NOs:
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4 and 5, which target SEQ ID NOs: 2 or 3 (see below).
Regarding claim(s) 12 and 14, Alderstein et al discloses antisense nucleotide SEQ ID NO: 5, which comprises instant SEQ ID NOs: 4 and 5, and target SEQ ID NOs: 2 and 3 (see col 7, lines 42-55 and sequence alignment above).
Regarding claim 15-16, Alderstein et al teaches compositions of the antisense sequences in sterile water (col 26, line 50 and table 3).
Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to substitute the small molecule inhibitor of Verstovsek et al with the antisense taught by Jedidi et al to yield the predictable results of using antisense to selectively target the JAK2 mutant gene, to yield the predictable results of treating a patient with MDS or PV with antisense targeting the JAK2 mutant gene. Both the structures and functions of small molecule inhibitors of JAK2 and antisense targeting JAK2 were known in the art before the effective filing date of the claimed invention. Vertovsek et al teaches targeting JAK2 with a small molecule because JAK2 V617F gain of function mutation is present in approximately 50% of patients of myelofibrosis (e.g., thrombocythemia, polycythemia vera, and primary myelofibrosis). Jedidi et al teaches clinical trials of Janus kinase 2 (JAK2) inhibitors in myeloproliferative disorder patients use small molecules target both wild-type and mutated JAK2 and that the lack of specificity and the fundamental role of JAK2 in hematopoiesis has raised concerns on the long-term efficacy and safety of these drugs. Further, Jedidi et al teaches that to selectively target malignant cells, they developed JAK2V617F-specific small interfering RNAs that do not affect normal JAK2-WT protein production. One of skill could look to the teachings of Vertovsek et al and Jedidi et al, and substitute the small molecule for the antisense, and arrive at treating a patient with MDS or PV with antisense targeting the JAK2 mutant gene.
Moreover, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to substitute the one of the antisense sequence found in Figure 1A above of the combined teachings of Vertovsek et al and Jedidi et al, with the antisense sequence of SEQ ID NO:5 of Alderstein et al. Both structures and functions of these sequences were known in the art before the effective filing date of the claimed invention. All three references teach JAK2 V617F mutations. One of skill in the art could look to the teachings of Vertovsek et al, Jedidi et al, and Alderstein et al and arrive at the claimed invention with a high likelihood of success.
Accordingly, claim(s) 1, 3-4, 9, 11-12, and 14-16 are rejected as being unpatentable over Vertovsek et al and Jedidi et al in view of Alderstein et al.
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.
Claim(s) 1, 3, 9, 11, 12, and 14-16 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claim(s) 5-6, 9, and 12-13 of copending Application No. 19/478,624 in view of Alderstein et al (supra).
Of note: The instant specification defines ASO as the following: “An "antisense oligonucleotide" or "ASO" refers to a synthetic, multi-nucleotide RNA compound that hybridizes to a target RNA sequence in a manner such that gene expression can be inhibited, including by inactivating an mRNA molecule.”, (see page 2, lines 19-21).
Claim 5 of 624 recites, “The method of “treating a patient diagnosed with a myeloproliferative disorder (MPD) which comprises: administering to said patient an amount of an ASO-T-JAK2 compound effective to treat such disorder.”, wherein the MPD is selected from a group consisting of: polycythemia vera (PV) and myelodysplastic syndrome (MDS).”
Claim 6 of 624 recites, “A method of inhibiting expression of the JAK2 gene in an individual which comprises: administering to the individual an amount of an ASO-T-JAK2 compound effective to inhibit JAK2 expression in the individual.”
Claim 9 of 624 recites, “An antisense oligonucleotide (ASO) targeted to a nucleic acid molecule encoding JAK2.”
Claim 12 of 624 recites, “A pharmaceutical composition which comprises:the ASO of claim 9; and a pharmaceutically acceptable diluent, carrier, adjuvant, or combination thereof.”
Claim 13 of 624 recites, “The pharmaceutical composition of claim 12 which further comprises a sterile parenteral dosage form.”
Claims 5, 6, and 9 of 624 do not require the ASO-T-JAK2 compound to target SEQ ID NO: 2 or 3.
Alderstein et al teaches targeting JAK2. More specifically, Alderstein et al teaches, “Alderstein et al teaches, “The scope of the invention further comprises an isolated oligonucleotide primer selected from the group consisting of SEQ ID NO:3, SEQ ID NO:4, SEQ ID NO:5, SEQ ID NO:6 and SEQ ID NO:8, as well as a Peptide Nucleic Acid (PNA) of 6-24 bases in length, comprising a base sequence which is capable of hybridizing to a region of the JAK 2 genomic DNA (SEQ ID NO:2) including position 93526 of SEQ ID NO:2 or to a region of the JAK 2 cDNA (SEQ ID NO:1) including position 2343 of SEQ ID NO:1. . .”, (col 7, lines 42-55).
Wherein SEQ ID NO: 5 of Alderstein et al is 100% similar to both SEQ ID NOs:
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4 and 5, which target SEQ ID NOs: 2 or 3 (see below).
Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to combine the teaches of claim(s) 5, 6, and 9 of 624, i.e., a ASO-T-JAK2 compound, with the teachings of Alderstein et al, i.e., an isolated oligonucleotide of SEQ ID NO: 5 targeting JAK2, to yield the predictable results of a JAK2 compound targeted to instant SEQ ID NOs: 2 or 3. One would be motivated to do so because 624 requires a JAK2 antisense oligonucleotides and Alderstein et al teaches targeting the V617F mutation of the JAK2 gene and specifically teaches SEQ ID NO: 5 as a JAK2 antisense oligonucleotide hybridizing and targeting the JAK2 gene. One of skill in the art could look to the requirements of claims 5, 6, and 9 of 624 and the teachings of Alderstein et al, and arrive at the claimed invention with a high likelihood of success.
Claim(s) 1, 3, 9, 11, 12, and 14-16 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over copending Application No. 19/478,624 in view of Alderstein et al (supra).
This is a provisional nonstatutory double patenting rejection.
Conclusion
No claims allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to LEXUS M TATGE whose telephone number is (571)272-0061. The examiner can normally be reached Monday-Friday: 8:30am to 5:30pm.
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/L.M.T./Examiner, Art Unit 1637
/Jennifer Dunston/Supervisory Patent Examiner, Art Unit 1637
Prosecution Insights