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 .
1. Claims 2-28 are pending and under examination.
2. The rejection of claims 11 and 12 under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112 is withdrawn in response to applicant’s arguments.
Claim Rejections - 35 USC § 103
3. 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 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.
4. Claims 2, 3, and 8-28 are rejected under 35 U.S.C. 103 as being unpatentable over Kelly et al. (Mol. Ther., 2007, 15: 211-219), in view of Rio et al. (DNA Repair and Human Health, 2011, Chapter 12, p. 349-372). Kelly and Rio are of record in the parent application 16/331,455.
Kelly et al. teach a method for treating Fanconi anemia A (FA-A) in human subjects, the method comprising administering G-CSF to the human subjects, obtaining a blood or bone marrow sample from the G-CSF-treated human subjects, isolating a population of cells enriched for CD34+ from the blood or marrow sample, transducing the cells with MSCV-FANCA (a retroviral-based vector encoding human FANCA), and administering the transduced cells to the human subjects (claims 24 and 25) (see p. 212, column 2; paragraph bridging p. 212 and 213; p. 214; p. 215, Fig. 3; p. 217, column 2; p. 218, column 1). Kelly et al. teach that the human subjects were non-conditioned (claims 3 and 26) (see p. 216, column 2, last paragraph); this is also acknowledged by Rio et al. disclosing that the human subjects in Kelly et al. were non-conditioned (see paragraph bridging p. 356 and 357; see the cited reference 96 in the reference listing).
Kelly et al. teach a retroviral vector and not the lentiviral vector (LV) comprising PGK-FANCA-WPRE expression cassette (claims 2, 12, 16-18, and 22). However, using an LV comprising a PGK-FANCA-WPRE expression cassette is rendered obvious by the prior art. For example, Kelly et al. teach that using the retroviral vector results in prolonged but transient increase in Hb levels and platelet counts; transient increase could be due to insufficient ex vivo expansion, defective engraftment, and lack of sufficient cell number for infusion; Kelly et al. teach the need for: improving the conditions for cell collection by using a combination of G-CSF and AMD3100 (i.e., plerixafor); improving the conditions for genetic modification (using an LV); and improving engraftment (see p. 214, column 2, last paragraph; p. 216, column 2, first full paragraph; paragraph bridging p. 216 and 217; p. 217, column 1, first full paragraph). Rio et al. teach that rapid transduction with the optimized PGK-FANCA-WPRE* LV (comprising an expression cassette containing in 5’ to 3’ order the human PGK promoter, a human FANCA-encoding sequence, and WPRE*, a modified WPRE) markedly improves transduction efficiency and the engraftment of FA-A hematopoietic stem/progenitor cells; the optimized PGK-FANCA-WPRE LV has improved safety properties compared to retroviral vectors and facilitates stable transgene expression in vivo as opposed to transgene inactivation when retroviral vectors are used (see p. 356, third and fourth full paragraphs; paragraph bridging p. 356 and 357; p. 358-359; p. 360, Fig. 2). Based on these teachings, one of skill in the art would have found obvious to modify the method of Kelly et al. by using rapid transduction with the optimized PGK-FANCA-WPRE LV (claim 2), with the reasonable expectation that doing so would result in a safer therapy with CD34+ cells exhibiting stable expression of human FANCA and improved engraftment providing stable increase in Hb levels and platelet counts. By doing so, one of skill in the art would have obtained and used a CD34+ cell comprising the PGK-FANCA-WPRE* expression cassette and a pharmaceutical composition comprising the cell (claims 10-21 and 23).
With respect to the combination of G-SCF or Filgrastin and Plerixafor recited in claim 24, Kelly et al. suggest using CD34+ cells mobilized from bone marrow with a combination of G-CSF and AMD3100 (plerixafor) for enhanced mobilization and genetic modification (see p. 216, column 2, first full paragraph). One of skill in the art would have found obvious to modify the method of Kelly et al. and Rio et al. by obtaining the CD34+ cells-enriched cell population from G-CSF/AMD3100-treated human subjects, with the reasonable expectation that doing so would mobilize CD34+ cells in numbers sufficient for ex vivo therapy.
With respect to claims 27 and 28, Kelly et al. teach infusing 4x105 or 3x105 cells/kg; they also teach the need to use higher cell number and that successful engraftment require the infusion of up to 10x106 cells/kg (see p. 214, column 2, second paragraph; paragraph bridging p. 216 and 217). One of skill in the art would have found obvious to use routine experimentation and vary the cell numbers within the range 3x105-10x106 cells/kg with the reasonable expectation that doing so would identify the number of cells leading to optimal therapy. Routine optimization is not considered inventive and no evidence has been presented that the selection the claimed sequences was other than routine or that the results should be considered unexpected in any way as compared to the closest prior art (see MPEP 2144.05 II).
The cited prior art teaches WPRE* and not a WPRE at least 90% identical to SEQ ID NO: 23 (claims 2 and 10). However, as per MPEP § 716.02, [a]ny differences between the claimed invention and the prior art may be expected to result in some differences in properties. The issue is whether the properties differ to such an extent that the difference is really unexpected. In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986). In this case, there is no evidence of record indicating that using a WPRE having a sequence at least 90% identical to SEQ ID NO: 23 leads to unexpected result compared to the WPRE*. The specification discloses that SEQ ID NO: 23 is the sequence of a chimeric WPRE consisting of the WPRE* and an extra 88 nucleotide long fragment (see [0181]). The addition of the 88 nucleotide long fragment to WPRE* may be patentable if it produces a new and unexpected result over WPRE*. In this case, there is no evidence of record that the 88 nucleotide long fragment imparts unexpected properties as compared to WPRE*. The presence of an extra 88-long segment is not significant if it does not provide a novel feature over the prior art and cannot be the basis for finding the claims non-obvious.
Kelly et al. and Rio et al. do not specifically teach that the human PKG promoter is set forth by SEQ ID NO: 7 (claims 8 and 9), nor do they specifically teach that the PGK-FANCA-WPRE cassette corresponds to nucleotides 3541-9178 of SEQ ID NO: 24 (claims 11 and 12). However, as per MPEP § 716.02, [a]ny differences between the claimed invention and the prior art may be expected to result in some differences in properties. The issue is whether the properties differ to such an extent that the difference is really unexpected. In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986). In this case, there is no evidence of record indicating that specifically using the human PGK promoter set forth by SEQ ID NO: 7 or the cassette corresponding to the nucleotides 3541-9178 of SEQ ID NO: 24 leads to unexpected result compared to the human PGK promoter and the PGK-FANCA-WPRE cassette taught by the prior art.
With respect to claim 13, the specification discloses that WPRE* is an enhancer (see [0271]).
With respect to claims 14 and 15, Rio et al. teach that PGK-FANCA-WPRE* LV comprises a PPT and a packaging signal ([Symbol font/0x79]) (see Fig. 2).
Thus, the claimed invention was prima facie obvious at the time of its effective
filing date.
5. Claims 2-28 are rejected under 35 U.S.C. 103 as being unpatentable over Kelly et al. taken with Rio et al., in further view of Joenje et al. (U.S. Patent No. 5,952,190).
The teachings of Kelly et al. and Rio et al. are applied as above for claims 2, 3, 8-28. Kelly et al. and Rio et al. do not specifically teach that the sequence encoding the human FANCA has at least 95% identity to SEQ ID NO: 8 or that the human FANCA polypeptide has at least 90% identity to SEQ ID NO: 25 (claims 4-7). However, the human FANCA cDNA set forth by SEQ ID NO: 8 (encoding the polypeptide set forth by SEQ ID NO: 25) was known and used in the prior art, for example by Joenje et al. (see Fig. 2A and 3; column 5, lines 58-67; SEQ ID NOs: 1 and 2 in the Sequence listing; see the attached Sequence Alignments). Using the human FANCA cDNA set forth by SEQ ID NO: 8 would have been obvious to one of skill in the art to achieve the predictable result of treating Fanconi anemia A (FA-A) in human subjects.
Thus, the claimed invention was prima facie obvious at the time of its effective
filing date.
6. Claims 2, 3, and 8-28 are rejected under 35 U.S.C. 103 as being unpatentable over Kelly et al., in view of all Muller et al. (Mol Ther., 2008, 16: 1154-1160), Rio et al., and Tolar et al. (Human Gene Therapy, 2012, 23: 141-144). Muller and Tolar are of record in the parent application 16/331,455.
Kelly et al. teach a method for treating Fanconi anemia A (FA-A) in human subjects, the method comprising administering G-CSF to the human subjects, obtaining a blood or bone marrow sample from the G-CSF-treated human subjects, isolating a population of cells enriched for CD34+ from the blood or marrow sample, transducing the cells with MSCV-FANCA (a retroviral-based vector encoding human FANCA), and administering the transduced cells to the human subjects (claims 24 and 25) (see p. 212, column 2; paragraph bridging p. 212 and 213; p. 214; p. 215, Fig. 3; p. 217, column 2; p. 218, column 1). Kelly et al. teach that the human subjects were non-conditioned (claims 3 and 26) (see p. 216, column 2, last paragraph); this is also acknowledged by Rio et al. disclosing that the human subjects in Kelly et al. were non-conditioned (see paragraph bridging p. 356 and 357; see the cited reference 96 in the reference listing).
Kelly et al. teach a retroviral vector and not the lentiviral vector (LV) comprising PGK-FANCA-WPRE expression cassette (claims 2, 16-18, and 22). However, using an LV comprising a PGK-FANCA-WPRE expression cassette is rendered obvious by the prior art. For example, Kelly et al. teach that using the retroviral vector results in prolonged but transient increase in Hb levels and platelet counts; transient increase could be due to insufficient ex vivo expansion, defective engraftment, and lack of sufficient cell number for infusion; Kelly et al. teach the need for: improving the conditions for cell collection by using a combination of G-CSF and AMD3100 (plerixafor); improving the conditions for genetic modification (using an LV); and improving engraftment (see p. 214, column 2, last paragraph; p. 216, column 2, first full paragraph; paragraph bridging p. 216 and 217; p. 217, column 1, first full paragraph). Muller et al. teach that rapid transduction of FA HSCs with a FANCA-encoding lentiviral vector leads to stable and significantly enhanced engraftment and to long-term repopulating HSCs as compared to conventional transduction; Muller et al. suggest using rapid lentiviral transduction for gene therapy in FA (see Abstract; paragraph bridging p 1155 and 1156; p. 1156, paragraph bridging columns 1 and 2). Rio et al. teach that rapid transduction with PGK-FANCA-WPRE* LV (comprising an expression cassette containing in 5’ to 3’ order the human PGK promoter, a human FANCA-encoding sequence, and WPRE*, a modified WPRE) markedly improves transduction efficiency and the engraftment of FA-A hematopoietic stem/progenitor cells; the optimized PGK-FANCA-WPRE* LV has improved safety properties compared to retroviral vectors and facilitates stable transgene expression in vivo as opposed to transgene inactivation when retroviral vectors are used. Rio et al. teach that short transduction would improve the engrafting of genetically corrected cells in FA patients, as was already shown in FA-A mouse models (see p. 356, third and fourth full paragraphs; paragraph bridging p. 356 and 357; p. 358-359; p. 360, Fig. 2). Tolar et al. teach that the clinical observation in mosaic FA patient that the self-corrected FA HSCs can expand and restore the hematopoietic compartment and the preclinical studies such as the one of Muller et al. established a platform for the state-of-the-art clinical trials; Tolar et al. teach that clinical trials using mobilization with G-CSF/plerixafor and rapid transduction with PGK-FANCA-WPRE* LV have been approved to start enrolling patients (see p. 142, paragraph bridging columns 1 and 2; p. 142, column 2, fourth paragraph; paragraph bridging p. 142 and 143; p. 143, paragraph bridging columns 1 and 2). Based on these teachings, one of skill in the art would have found obvious to modify the method of Kelly et al. by using a rapid transduction with the optimized PGK-FANCA-WPRE LV with the reasonable expectation that doing so would result in a safer therapy with CD34+ cells exhibiting stable expression of human FANCA and improved engraftment to reverse the bone marrow failure (BMF) and provide a stable increase in Hb levels.
With respect to the combination of G-SCF or Filgrastin and Plerixafor recited in claim 24, Kelly et al. suggest using CD34+ cells mobilized from bone marrow with a combination of G-CSF and AMD3100 (plerixafor) for enhanced mobilization and genetic modification (see p. 216, column 2, first full paragraph) and Tolar et al. teach clinical trials using mobilization with G-CSF and plerixafor. One of skill in the art would have found obvious to obtain the CD34+ cells-enriched cell population from G-CSF/AMD3100-treated human subjects, with the reasonable expectation that doing so would mobilize CD34+ cells in numbers sufficient for ex vivo therapy.
With respect to claims 27 and 28, Kelly et al. teach infusing 4x105 or 3x105 cells/kg; they also teach the need to use higher cell number and that successful engraftment require the infusion of up to 10x106 cells/kg (see p. 214, column 2, second paragraph; paragraph bridging p. 216 and 217). One of skill in the art would have found obvious to use routine experimentation and vary the cell numbers within the range 3x105-10x106 cells/kg with the reasonable expectation that doing so would identify the number of cells leading to optimal therapy. Routine optimization is not considered inventive and no evidence has been presented that the selection the claimed sequences was other than routine or that the results should be considered unexpected in any way as compared to the closest prior art (see MPEP 2144.05 II).
The cited prior art teaches WPRE* and not a WPRE at least 90% identical to SEQ ID NO: 23 (claims 2 and 10). However, as per MPEP § 716.02, [a]ny differences between the claimed invention and the prior art may be expected to result in some differences in properties. The issue is whether the properties differ to such an extent that the difference is really unexpected. In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986). In this case, there is no evidence of record indicating that using a WPRE having a sequence at least 90% identical to SEQ ID NO: 23 leads to unexpected result compared to the WPRE*. The specification discloses that SEQ ID NO: 23 is the sequence of a chimeric WPRE consisting of the WPRE* and an extra 88 nucleotide long fragment (see [0181]). The addition of the 88 nucleotide long fragment to WPRE* may be patentable if it produces a new and unexpected result over WPRE*. In this case, there is no evidence of record that the 88 nucleotide long fragment imparts unexpected properties as compared to WPRE*. The presence of an extra 88-long segment is not significant if it does not provide a novel feature over the prior art and cannot be the basis for finding the claims non-obvious.
Kelly et al. and Rio et al. do not specifically teach that the human PKG promoter is set forth by SEQ ID NO: 7 (claims 8 and 9), nor do they specifically teach that the PGK-FANCA-WPRE cassette corresponds to nucleotides 3541-9178 of SEQ ID NO: 24 (claims 11 and 12). However, as per MPEP § 716.02, [a]ny differences between the claimed invention and the prior art may be expected to result in some differences in properties. The issue is whether the properties differ to such an extent that the difference is really unexpected. In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986). In this case, there is no evidence of record indicating that specifically using the human PGK promoter set forth by SEQ ID NO: 7 or the cassette corresponding to the nucleotides 3541-9178 of SEQ ID NO: 24 leads to unexpected result compared to the human PGK promoter and the PGK-FANCA-WPRE cassette taught by the prior art.
With respect to claim 13, the specification discloses that WPRE* is an enhancer (see [0271]).
With respect to claims 14 and 15, Rio et al. teach that PGK-FANCA-WPRE LV comprises a PPT and a packaging signal ([Symbol font/0x79]) (see Fig. 2).
Thus, the claimed invention was prima facie obvious at the time of its effective
filing date.
7. Claims 2-28 are rejected under 35 U.S.C. 103 as being unpatentable over Kelly et al. taken with all Muller et al., Rio et al. and Tolar et al. , in further view of Joenje et al.
The teachings of Kelly et al., Muller et al., Rio et al., and Tolar et al. are applied as above for claims 2, 3, and 8-28. Kelly et al., Muller et al., Rio et al., and Tolar et al. do not specifically teach that the sequence encoding the human FANCA has at least 95% identity to SEQ ID NO: 8 or that the human FANCA polypeptide has at least 95% identity to SEQ ID NO: 25 (claims 4-7). However, the human FANCA cDNA set forth by SEQ ID NO: 8 (encoding the polypeptide set forth by SEQ ID NO: 25) was known and used in the prior art, for example by Joenje et al. (see Fig. 2A and 3; column 5, lines 58-67; SEQ ID NOs: 1 and 2 in the Sequence listing; see the attached Sequence Alignments). Using the human FANCA cDNA set forth by SEQ ID NO: 8 would have been obvious to one of skill in the art to achieve the predictable result of treating Fanconi anemia A (FA-A) in human subjects.
Thus, the claimed invention was prima facie obvious at the time of its effective
filing date.
Response to Arguments
8. The arguments addressing the references individually are not found persuasive because none of the reference hast to teach every claim limitation.
The applicant argues that the cited prior art does not teach or suggest a chimeric WPRE having a sequence at least 90% identical to SEQ ID NO: 23.
This is not found persuasive for the reasons set forth in the rejection.
The applicant argues that none of the cited references provides a motivation to restore wild-type WPRE sequence. The applicant argues that the examiner’s conclusion of adding back the 88 terminal nucleotides is based on hindsight reasoning. The applicant argue that the chimeric WPRE set forth by SEQ ID NO: 23 is a non-obvious selection from countless possible variants.
These arguments are not material to the rejection because the rejection is not based on modifying WPRE* by adding the 88 terminal nucleotides, nor is the rejection based on choosing from countless possible variants.
It is also noted that the claimed SEQ ID NO: 23 is not the sequence of the wild type WPRE, as it comprises the mutated WPRE* and the extra 88 nucleotide long fragment.
The argument of unpredictability of RNA regulatory elements is not found persuasive because the rejection is based on a single and efficient element (WPRE*).
The argument that the examiner improperly inverts the burden under § 103 is not found persuasive because the examiner established a prima facie case of obviousness. The applicant provided no evidence that the obviousness determination necessarily requires a motivation to modify the WPRE* adding the extra 88 nucleotide fragment. As per MPEP § 716.02, [a]ny differences between the claimed invention and the prior art may be expected to result in some differences in properties. The issue is whether the properties differ to such an extent that the difference is really unexpected. In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986).
The burden is on the applicant to establish that the claimed chimeric WPRE provides unexpected results over the WPRE* taught by the prior art. However, there is no evidence of unexpected results of record.
The specification provides no comparative data between the claimed chimeric WPRE and the WPRE* taught by the prior art. The applicant refers to Example 4 in the specification. Example 4 provides no comparative data. The applicant also refers to [0314]-[0316] in the specification. As there are no [0314]-[0316] in the specification, the examiner assumes that the intent was to refer to Example 9, [0304]-[0306]. Example 9 and Fig. 24-26 and 35 provide no comparative data. Thus, the data in the specification does not evidence unexpected results over the prior art.
With respect to the lentiviral copy number in patient’s blood compared to Kelly, Rio’s teaches that: (1) LVs are the most efficient clinical vectors for stably transducing HSPCs with the short transduction protocol; (2) PGK-FANCA-WPRE* LV markedly improves transduction efficiency and the engraftment of the transduced FA-A HSPCs; (3) the transduced patient’s FA-AHSPCs are expected to develop a proliferative advantage over the uncorrected cell upon transplantation in the patient (see p. 356, fourth full paragraph; p. 358, first two full paragraphs; p. 359). Thus, enhanced lentiviral copy numbers as compared to Kelly were reasonably expected from the teachings in the prior art.
The argument that the results in the specification could not have been predicted from the teachings in the prior art is not found persuasive. That administering genetically-corrected FA-A cells of the prior art to non-conditioned patients would lead to long-term engraftment and FANCA transgene expression, and thus, durable therapeutic effect was reasonably expected from the teaching in the prior art. Because there is no comparison with WPRE*, the data in the specification does not provide for more than was expected from the teachings in the prior art.
The applicant refers to Roncero Declaration filed in the parent application 16/331,455, which was not provided. Affidavits or declarations, such as those submitted under 37 CFR 1.130, 1.131 and 1.132, filed during the prosecution of the prior application do not automatically become a part of this application. Where it is desired to rely on an earlier-filed affidavit or declaration, the applicant should make the remarks of record in this application and include a copy of the original affidavit or declaration filed in the prior application.
Regardless, the Roncero Declaration has been considered in the parent application and not found persuasive.
The argument of failed clinical trials is not found persuasive because it addresses Kelly individually.
Kelly teaches prolonged but transient therapy in human patients. Kelly also teaches the conditions needed to improve therapy: enhancing cell mobilization (G-CSF and plerixafor); using LV instead of retroviral vector; and improving engraftment. Rio provides the reasonable expectation that using PGK-FANCA-WPRE* LV would result in stable FANCA expression and improved engraftment leading to a stable increase in Hb levels and platelet counts. Along these lines, Tolar teaches the existence of approved clinical trials using mobilization with G-CSF/plerixafor and rapid transduction with PGK-FANCA-WPRE* LV.
For these reasons, the following arguments are not found persuasive: (1) Rio, Muller, Tolar, and Joenje do not predict success in human patients; and (2) the expression cassette was not validated in human clinical trials.
The argument that Tolar confirms uncertainty is not found persuasive because it is just an argument not supported by any evidence. Tolar does not have to confirm clinical success. An obviousness-type rejection only requires a reasonable expectation of success, which is provided by the combined teachings of the cited prior art.
With respect to the argument that the FA mouse model taught by Muller does not recapitulate the human disease, it is noted that the primary reference already teaches therapy in human patients.
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).
Conclusion
9. THIS ACTION IS MADE FINAL. Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to ILEANA POPA whose telephone number is (571)272-5546. The examiner can normally be reached 8:00 am to 4:30 pm.
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/ILEANA POPA/Primary Examiner, Art Unit 1633
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