Notice of Pre-AIA or AIA Status
1. The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Election/Restrictions
2. Applicant’s election without traverse of Group I, claims 1-29, in the reply filed on 27 August 2025 is acknowledged.
Claim Rejections - 35 USC § 112
3. The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
4. Claims 11, 14, 16-17, 26 and 27-28 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 enablement requirement. The claims contains subject matter which was not described in the specification in such a way as to enable one skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention.
Claim 11 suggests that the entirety of the method of claim 1 is performed in a human patient. Claims 14, 16, 26 and 27 are similarly suggestive of the method of claim 1 occurring entirely in a human patient, a patient, a living cell, and preclinical animal models, respectively. The nature of the claimed method is such that this includes “purifying the compound and an RNA target cross-linked by the cross-linking module using affinity of the purification module,” “reverse transcribing the RNA with a primer to create cDNA from the purified RNA,” and “amplify the cDNA using a primer set suitable for RT-qPCR or high throughput sequencing (RNA-seq).” These steps, among others in the disclosed method of claim 1, are challenging, non-routine, and/or non-obvious to one of ordinary skill in the art regarding how they would be performed in living cells or in a patient. Therefore, practicing the entire method of claim 1 would be highly unpredictable, and the applicant provides no teaching or suggestion in their specification that would reduce that unpredictability or suggest how any of the described steps would occur “in” a live cell, human patient, or animal model. Applicant’s specification suggests embodiments wherein “various embodiments” of the method take place in a human patient (pg. 4 ¶ 1, pg. 12 ¶ 1 and surrounding paragraphs, for example) but neither they nor the closest prior art provide working examples of the entirety of method 1 being performed in some sort of living model system, and therefore the methods claimed cannot be practiced without undue experimentation.
Claim 17 is further rejected for being dependent on a previously rejected claim.
5. The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
6. Claims 4 and 6-16 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
A. Claim 4 recites “wherein the compound of claim 1 is of formula 2,” however the only mention of formula 2 in applicant’s specification seems to be in ¶ 5 on pg. 3. There is no structure provided for formula 2, therefore it is unclear what the limitations are for the compound in claim 4 and this claim is indefinite. For the purpose of prosecution this claim is being interpreted as though formula 2 is the same as compound 2 provided in applicant’s specification.
B. Claim 6 recites the limitation of “wherein the compound of claim 1 is Targaprimir-96 (compound 1).” However, the compound of claim 1 (¶ 2) specifically comprises an RNA cross-linking module and a purification module. Compound 1, shown on pg. 8 of applicant’s specification, comprises neither of these features. If the compound of claim 1 is compound 1, then there is improper antecedent basis for this limitation. For the purpose of examination, this claim is being interpreted as though the compound of claim 1 comprises Targaprimir-96.
C. Claim 7 suggests that the method of claim 1 is performed comprising “precisely targeting cellular inactivation of an oncogenic non-coding RNA precursor…” however the method of claim 1 is directed to screening an RNA sequence library in order to map the binding site of a compound. It is unclear how, when one is contacting an RNA sequence library in order to do a pull-down study, one is simultaneously precisely targeting a particular feature. The metes and bounds of claim 7, and how they relate to the screening method of claim 1, are unclear and therefore this claim is indefinite. For the purpose of prosecution this claim is being interpreted as though the method of claim 1 is used to determine the particular target and/or binding site of an RNA binding small molecule, and then that information is used in a separate assay to precisely target cellular inactivation of an oncogenic non-coding RNA.
D. Claims 10, 13, and 16 are unclear for reasons similar to those outlined for claim 7 above. Each of these three claims recite “The method of claim 1,…” followed by performing a specific effect or comprising a specific outcome in a cell type. It is unclear how these specific objectives are achieved within the method of claim 1, a generic method of mapping an RNA binding site of an RNA binding small molecule, and therefore the claim is indefinite. For the purpose of prosecution, these claims will each be interpreted as though a particular small molecule having a known binding site/RNA target (as determined by the method of claim 1) is then further used to perform the method steps of claims 10, 13 and 16.
E. Claims 8, 9, 11, 12, 14 and 15 are further rejected for being dependent on a previously rejected claim.
7. The following is a quotation of 35 U.S.C. 112(d):
(d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
The following is a quotation of pre-AIA 35 U.S.C. 112, fourth paragraph:
Subject to the following paragraph [i.e., the fifth paragraph of pre-AIA 35 U.S.C. 112], a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
8. Claim 18 is rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends.
Claim 18 is dependent on claim 15, however it simply provides the same limitations as claim 15 on which it depends (i.e., “wherein the compound is a covalent conjugate of Targaprimir-96 and chlorambucil”). Therefore claim 18 does not further limit claim 15.
Applicant may cancel the claim(s), amend the claim(s) to place the claim(s) in proper dependent form, rewrite the claim(s) in independent form, or present a sufficient showing that the dependent claim(s) complies with the statutory requirements.
Claim Rejections - 35 USC § 103
9. 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.
10. Claims 1, 19, 21-23 and 25 are rejected under 35 U.S.C. 103 as being unpatentable over Petter et al (United States Patent Application No. US20200115372, effectively filed 31 July 2018) in view of Yu et al (Estimating RNA structure chemical probing reactivities from reverse transcriptase stops and mutations, BioRxiv, 292532).
Regarding claim 1, Petter teaches a method for determining RNA transcripts that bind compounds and are thus druggable, screening drug candidates and methods of determining drug binding sites on a target RNA (i.e., a method of mapping an RNA binding site of an RNA-binding small molecule; [0003]). Petter teaches that RNAs in cells are screened, and that all RNAs in the cells are isolated and sequenced ([0328]-[0330], [0363], [0367]). In these embodiments, the cellular transcriptome represents the claimed “RNA sequence library.” Petter teaches contacting the RNA with a compound comprising an RNA binding small molecule, a reactive warhead (i.e., an RNA cross-linking module []), and biotin ([0347]). Petter teaches that the RNA that has reacted is isolated by passing the total RNA over a streptavidin column (i.e., using affinity of the purification module and a complementary immobilized reagent; [0347]). Petter teaches that the RNA is reverse transcribed with a primer to create cDNA of the RNA linked to the small molecule ([0694]-[0695] and [0347]). Petter teaches that the cDNAs are analyzed by sequencing (i.e., RNA-seq) and that only riboses proximal to the ligand binding pocket are acylated (i.e., reacted with the warhead; [0349]).
Petter teaches that acylated sites on the RNA targets are read through by reverse transcriptase and observed as mutations in the sequencing results ([0349] and [0341]), but does not teach that these adducts introduce reverse transcriptase sequence stops.
However, Yu teaches that when performing different chemical probing experiments on RNA, different reaction conditions (e.g., different reverse transcriptase enzymes) show distinct biases for detecting adducts as either RT-stops or RT-mutations (abstract).
It would have been obvious to one having ordinary skill in the art to have modified the mutation-based analysis taught by Petter with the transcription stop analysis taught by Yu to arrive at the instantly claimed invention with a reasonable expectation of success. The ordinary artisan would have been motivated to make this substitution because Yu specifically teaches that approaches that only incorporate either RT-stops or RT-mutations miss information about adduct distribution (pg. 3 ¶ 3). In addition, one having ordinary skill in the art would have recognized that the known techniques in the cited references could have been combined with predictable results because the known techniques of the cited references predictably result in the detection of RNA adducts by sequencing.
Regarding claim 19, Petter teaches the transcriptome-wide target identification of RNA-small molecule binder interactions ([0367]).
Regarding claims 21 and 22, Petter teaches that the cells in which the RNA mapping occurs are bacterial or mammalian cells ([0345]).
Regarding claim 23, Petter teaches the transcriptome-wide target identification of RNA-small molecule binder interactions (“the transcriptome” is inherently natural RNA; [0367]) and the exposure of the small molecule binder to synthetic RNA ([0661]).
Regarding claim 25, Petter teaches that the activity of a compound (i.e., assays of their disclosure are utilized in vitro ([0271]).
11. Claims 2-10, 12-13, 15-18 are rejected under 35 U.S.C. 103 as being unpatentable over Petter et al (United States Patent Application No. US20200115372, effectively filed 31 July 2018) in view of Yu et al (Estimating RNA structure chemical probing reactivities from reverse transcriptase stops and mutations, BioRxiv, 292532) as applied to claim 1 above, and further in view of Velagapudi et al (Design of a small molecule against an oncogenic noncoding RNA, PNAS, 113, 21, 5898-5903, published 24 May 2016).
Regarding claims 2 and 9, Petter teaches a number of RNA warheads (i.e., RNA cross-linking modules; see pg. 52 for example) however Petter does not specifically teach that these cross-linking modules comprise a chlorambucil group.
However, Velagapudi teaches the RNA binding small molecule Targaprimir-96-CA-Biotin, which comprises a chlorambucil group (FIG 6A, grey box).
It would have been obvious to one having ordinary skill in the art to have substituted the RNA binding compound taught by Petter for Targaprimir-96 as taught by Velagapudi to arrive at the instantly claimed invention with a reasonable expectation of success. The ordinary artisan would have been motivated to make this substitution because Velagapudi specifically teaches that “selective” drugs modulate disease targeting biomolecules, and it would be obvious to the ordinary artisan to change the drug in order to target a different biomolecule (pg. 5898 column 2 “significance” box). In addition, one having ordinary skill in the art would have recognized that the known techniques in the cited references could have been combined with predictable results because the known techniques in the cited references predictably result in the development of small molecule RNA binders comprising a purification module and a cross-linking module.
Regarding claim 3, Velagapudi teaches that the purification module comprises a biotin group (FIG 6A, blue box).
Regarding claims 4-6, Velagapudi teaches that the RNA binding compound is compound 4 (FIG 6A). The compound taught by Velagapudi comprises Targaprimir-96, which itself comprises an N-methyl-piperazinyl-bis-benzimidazole group.
Regarding claims 7 and 8, the method of claim 1 is discussed fully above and incorporated here. Briefly, Petter and Yu teach a method wherein a compound comprising an RNA binding module, a cross-linking module, and a purification module is used to bind RNAs present in the transcriptome of cells, pull the bound RNAs down, reverse transcribe and sequence the pulled-down RNAs in order to determine the binding site of the RNA binding module.
Neither Petter nor Yu teach the limitation of precisely targeting cellular inactivation of an oncogenic non-coding RNA precursor via cross-linking, comprising contacting a cell expressing the non-coding RNA precursor and an effective amount of the compound of the claim 1.
Velagapudi teaches a compound comprising an RNA binding module, a cross-linking module, and a purification module (Targaprimir-96-CA-Biotin, compound 4, FIG 6A) and teaches contacting MDA-MB-231 cells (i.e., cells expressing the non-coding RNA precursor) with compound 4 (i.e., the compound of claim 1; pg. 5900 column 2 ¶ 4) and that this compound selectively inhibited biogenesis of the miR-96 hairpin precursor (i.e., precisely targeting cellular inactivation of an oncogenic non-coding RNA precursor via crosslinking). Velagapudi teaches that Targaprimir-96 inhibits the drosha processing of pri-miR-96 (FIG 2). It is noted here that while Velagapudi teaches a variety of effects resulting from the administration of compound 3 rather than compound 4 (i.e., Targaprimir-96 without the cross-linking and purification modules vs. with the cross-linking and purification modules, respectively), compound 4 retains the specific RNA binding domains of compound 3 and is shown to compete with compound 3 for binding pri-miR-96 (pg. 5900 column 2 ¶ 5). Therefore without additional limitations to the claims, compound 4 inherently has the properties disclosed by Velagapudi for compound 3.
It would have been obvious to one having ordinary skill in the art to have substituted the generic RNA binding compound taught by Petter with compound 4 taught by Velagapudi to arrive at the instantly claimed invention with a reasonable expectation of success. The ordinary artisan would have been motivated to make this substitution in order to precisely target the RNA structure bound by the compound of claim 1 as determined by the method of claim 1. In addition, on having ordinary skill in the art would have recognized that the known techniques in the cited references could have been combined with predictable results because the known techniques in the cited references predictably result in assays related to the binding of structured RNAs by small molecules.
Regarding claim 9, Velagapudi teaches a compound that is a cross-linking conjugate of Targaprimir-96 and chlorambucil (Compound 4).
Regarding claim 10, Velagapudi teaches that contacting MDA-MB-231 cells (i.e., breast cancer cells) with Targaprimir-96 boosted the expression of FOXO1 ~2-fold (pg. 5900 column 1 ¶ 4). If the expression of FOXO1 was boosted then this is inherently an effective amount of the compound without further limitation to the claim. It is again noted here that while Velagapudi teaches a variety of effects resulting from the administration of compound 3 rather than compound 4 (i.e., Targaprimir-96 without the cross-linking a purification modules vs. with the cross-linking and purification modules, respectively), compound 4 retains the specific RNA binding domains of compound 3 and is shown to compete with compound 3 for binding pri-miR-96 (pg. 5900 column 2 ¶ 5). Therefore without additional limitations to the claims, compound 4 inherently has the properties disclosed by Velagapudi for compound 3.
Regarding claim 12, Velagapudi teaches that the compound is a covalent conjugate of Targaprimir-96 and chlorambucil (FIG 6A).
Regarding claim 13, the method of claim 1 is discussed fully above and incorporated here. Neither Petter nor Yu specifically teach that the RNA sequence library is present in triple negative breast cancer (TNBC) cells, nor do they teach that an effective amount of the compound of claim 1 triggers apoptosis in TNBC cells.
Velagapudi teaches that 50 nM (i.e., an effective amount) of compound 3 triggers apoptosis in TNBC cells, and Velagapudi additionally teaches contacting TNBC cells with 50 nM of compound 4 (i.e., the compound of claim 1). It is again noted here that while Velagapudi teaches a variety of effects resulting from the administration of compound 3 rather than compound 4 (i.e., Targaprimir-96 without the cross-linking a purification modules vs. with the cross-linking and purification modules, respectively), compound 4 retains the specific RNA binding domains of compound 3 and is shown to compete with compound 3 for binding pri-miR-96 (pg. 5900 column 2 ¶ 5). Therefore without additional limitations to the claims, compound 4 inherently has the properties disclosed by Velagapudi for compound 3 and would inherently trigger apoptosis in TNBC cells.
It would have been obvious to one having ordinary skill in the art to have substituted the generic RNA sequence library taught by Petter with the TNBC cells taught by Velagapudi to arrive at the instantly claimed invention with a reasonable expectation of success. The ordinary artisan would have been motivated to make this substitution because, as discussed fully above and incorporated here, Petter specifically teaches that these compounds are used to pull down RNAs from within cells and further teaches the use of these compounds for the treatment of disorders such as cancer ([0276]). In addition, on having ordinary skill in the art would have recognized that the known techniques of the cited references could have been combined with predictable results because the known techniques in the cited references predictably result in the design and testing of RNA binding small molecules.
Regarding claims 15 and 18, Velagapudi teaches that the compound is a covalent conjugate of Targaprimir-96 and Chlorambucil.
12. Claims 20 and 24 are rejected under 35 U.S.C. 103 as being unpatentable over Petter et al (United States Patent Application No. US20200115372, effectively filed 31 July 2018) in view of Yu et al (Estimating RNA structure chemical probing reactivities from reverse transcriptase stops and mutations, BioRxiv, 292532) as applied to claim 19 above, and further in view of Hermann (Small molecules targeting viral RNA, WIREs RNA, 7, 726-743, published 16 June 2016).
Regarding claims 20 and 24, Petter and Yu teach the method of claim 19 as discussed fully above and incorporated here. Briefly, Petter and Yu teach that the RNA sequence library comprises a transcriptome, but neither Petter nor Yu teach that the transcriptome is viral or that the RNA sequence library comprises the genome of an RNA virus.
However, Hermann teaches a number of small molecule RNA binders that are used in cell-based assays to screen for small molecule activity in virally infected cells (i.e., the transcriptome is viral and the RNA sequence library comprises the genome of an RNA virus; pg. 736 column 2 ¶ 3).
It would have been obvious to one having ordinary skill in the art to have applied the method taught by Petter and Yu to virally-infected cells as taught by Hermann to arrive at the instantly claimed invention with a reasonable expectation of success. The ordinary artisan would have been motivated to make this modification because Petter specifically discusses the benefits of performing RNA binding and covalent capture screening in cells due to the specificity of RNA folding and the presence of post-translation RNA modifications that occur in the cell ([0321]). In addition, one having ordinary skill in the art would have recognized that the known techniques in the cited references could have been combined with predictable results because the known techniques in the cited references predictably result in the identification of therapeutic small molecule RNA binders.
13. Claim 29 is rejected under 35 U.S.C. 103 as being unpatentable over Petter et al (United States Patent Application No. US20200115372, effectively filed 31 July 2018) in view of Yu et al (Estimating RNA structure chemical probing reactivities from reverse transcriptase stops and mutations, BioRxiv, 292532) as applied to claim 19 above, and further in view of Velagapudi et al (Defining RNA-Small Molecule Affinity Landscapes Enables Design of a Small Molecule Inhibitor of an Oncogenic Noncoding RNA, ACS Central Science, 3, 205-216, published 6 March 2017), hereafter referred to as Velagapudi2.
Regarding claim 29, the method of claim 1 is discussed fully above and incorporated here. Neither Petter nor Yu teach a set of RNA sequences and a set of candidate RNA-binding small molecules assayed in a 2-dimensional parallel array.
However, Velagapudi2 teaches a small molecule microarray wherein a set of RNA sequences and a set of candidate RNA-binding small molecules are assayed in a 2 dimensional parallel array (abstract, FIG 1, and pg. 205 column 2 ¶ 1).
It would have been obvious to one having ordinary skill in the art to have simply substituted the screening method taught by Petter and Yu with the 2 dimensional screening method taught by Velagapudi2 to arrive at the instantly claimed invention with a reasonable expectation of success. The ordinary artisan would have been motivated to make this substitution in order to simultaneously screen an RNA sequence library and a small molecule library in order to increase the throughput of the screening assay. In addition, one having ordinary skill in the art would have recognized that the known techniques in the cited references could have been combined with predictable results because the known techniques in the cited references predictably result in the identification of small molecules that bind structured RNAs.
Double Patenting
14. 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.
15. Claims 1, 3-8 and 19-29 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-22 of copending Application No. 17622005. Although the claims at issue are not identical, they are not patentably distinct from each other because both sets of claims are drawn to identifying the binding sites of a small molecule to an RNA target.
Claims 1 and 7 of the copending application teach a method which as steps that include all of the limitations of instant claim 1.
The limitations of instant claims 3-8 and 19-29 are given in claims 4 and 10-22 of the copending application.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 2, 9-10, 12-13, 15 and 18 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-22 of copending Application No. 17622005 in view of Velagapudi et al (Design of a small molecule against an oncogenic noncoding RNA, PNAS, 113, 21, 5898-5903, published 24 May 2016).
Copending application 17622005 does not teach the limitations of claim 2, 9-10, 12-13, 15 or 18. However, Velagapudi teaches these limitations as discussed fully above and incorporated here.
It would have been obvious to modify the claims of the copending application to include the limitations taught by Velagapudi to arrive at the instantly claimed invention with a reasonable expectation of success. The ordinary artisan would have been motivated to make these changes because Velagapudi teaches a number of additional assays and methods that are used to further characterize small molecule RNA binders such as those characterized by the method of claim 1. In addition, it would have been obvious to one of ordinary skill in the art that the known techniques in the cited references could have been combined with predictable results because the known techniques in the cited references predictably result in the characterization of small molecule RNA binders.
This is a provisional nonstatutory double patenting rejection.
16. Claims 1, 3, 7 and 19-29 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-22 of copending Application No. 17622032. Although the claims at issue are not identical, they are not patentably distinct from each other because both sets of claims are drawn to identifying the binding sites of a small molecule to an RNA target.
Claim 1 of the copending application teach a method which as steps that include all of the limitations of instant claim 1.
The limitations of instant claims 3, 7 and 19-29 are given in claims 1, 3 and 8-14 of the copending application.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 2, 4-6, 8-10, 12-13, 15 and 18 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-22 of copending Application No. 17622032 in view of Velagapudi et al (Design of a small molecule against an oncogenic noncoding RNA, PNAS, 113, 21, 5898-5903, published 24 May 2016).
Copending application 17622005 does not teach the limitations of claim 2, 9-10, 12-13, 15 or 18. However, Velagapudi teaches these limitations as discussed fully above and incorporated here.
It would have been obvious to modify the claims of the copending application to include the limitations taught by Velagapudi to arrive at the instantly claimed invention with a reasonable expectation of success. The ordinary artisan would have been motivated to make these changes because Velagapudi teaches a number of additional assays and methods that are used to further characterize small molecule RNA binders such as those characterized by the method of claim 1. In addition, it would have been obvious to one of ordinary skill in the art that the known techniques in the cited references could have been combined with predictable results because the known techniques in the cited references predictably result in the characterization of small molecule RNA binders.
This is a provisional nonstatutory double patenting rejection.
Conclusion
17. No claims are allowed.
18. Any inquiry concerning this communication or earlier communications from the examiner should be directed to BRIAN ELLIS YOUNG whose telephone number is (703)756-5397. The examiner can normally be reached M-F 0730 - 1700.
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/BRIAN ELLIS YOUNG/Examiner, Art Unit 1684
/JULIET C SWITZER/Primary Examiner, Art Unit 1682