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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 6/29/26 has been entered.
Claims 1, 4-6, and 13-19 are pending.
Claims 1, 4, 13, 15, 17, and 19 have been amended by Applicant.
Claims 1, 4-6, and 13-19 are currently under consideration.
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Rejections Withdrawn
The rejection of claims 1 and 14 under 35 U.S.C. 103 as being unpatentable over Ferber et al (eLIFE, 2017, 6(e25281): 1-34; 3/19/23 IDS) in view of Kreeger et al (US 2019/0241665 A1; 8/8/19; 3/19/23 IDS), the rejection of claims 13 and 15-17 under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ) second paragraph, and rejection of claims 1, 4-6, and 14 under 35 U.S.C. 103 as being unpatentable over Ferber et al (eLIFE, 2017, 6(e25281): 1-34; 3/19/23 IDS) in view of Kreeger et al (US 2019/0241665 A1; 8/8/19; 3/19/23 IDS) and Omuro et al (Neuro-Oncology, 2018, 20(5): 674-686) are withdrawn in view of amendments, arguments found in the 6/29/26 Reply, and the declaration submitted in the 6/29/26 Reply.
Rejections Maintained
Claim Rejections - 35 USC § 103
Claim(s) 18-19 remain rejected under 35 U.S.C. 103 as being unpatentable over Ferber et al (eLIFE, 2017, 6(e25281): 1-34; 3/19/23 IDS) in view of Kreeger et al (US 2019/0241665 A1; 8/8/19; 3/19/23 IDS) and Omuro et al (Neuro-Oncology, 2018, 20(5): 674-686).
Ferber et al teaches P-selectin is highly expressed in glioblastoma and P-selectin expression in glioblastoma correlates with patient survival (page 10 and Figure 3, in particular). Ferber et al further suggests targeting P-selectin in glioblastoma may have additional therapeutic benefit because high expression of P-selectin correlate with poor patient survival (page 21, in particular). Ferber et al further teaches a conjugate comprising paclitaxel (PTX) conjugated to a dendritic polyglycerol sulfate (dPGS) for treating glioblastoma (Abstract, in particular). Ferber et al further teaches dPGS is able to cross the blood-brain barrier (BBB), binds to P-selectin, inhibits P-selectin, and accumulate in intracranial tumors (Abstract and lines 2-3 on page 3, in particular). Ferber et al further teaches the anti-proliferative activity of PTX on glioblastoma cells is retained in the conjugate comprising PTX and dPGS (Figure 4, in particular) and that the conjugate is targeted to intracranial tumors (Figure 5, in particular).
Ferber et al does not specifically teach a composition comprising a pharmaceutically acceptable carrier and/or an antibody that binds to and inhibits P-selectin and an immunomodulatory agent. However, these deficiencies are made up in the teachings of Kreeger et al and Omuro et al.
Kreeger et al teaches inhibitors of P-selectin for therapeutic treatment include (unconjugated) antibodies that bind and inhibit P-selectin (crizanlizumab and inclacumab) and small molecule agents (rivipansel and tinzaparin) ([0039]-[0040], in particular). Kreeger et al further teaches inhibitors of P-selectin are administered in the form of pharmaceutical compositions comprising a pharmaceutically acceptable diluent ([0042]), which is a “pharmaceutically acceptable carrier” (as defined at paragraph spanning pages 39-40 of the instant specification, in particular).
Omuro et al teaches method of therapeutically treating glioblastoma administering the checkpoint inhibitor nivolumab optionally in combination with the checkpoint inhibitor ipilimumab (Abstract, in particular).
One of ordinary skill in the art would have been motivated, with a reasonable expectation of success, to perform a rendered obvious by Ferber et al comprising treating just any subject diagnosed with glioblastoma, such as a subject with an early stage glioblastoma or a subject with glioblastoma before or after resection, by administering a therapeutically effective amount of the conjugate comprising PTX and dPGS of Ferber et al to the subject because Ferber et al teaches the conjugate is to be used to treat glioblastoma, the anti-proliferative activity of PTX on glioblastoma cells is retained in the conjugate, and that the conjugate is targeted to intracranial tumors.
Further, one of ordinary skill in the art would have been motivated, with a reasonable expectation of success, to perform a combined method comprising the method rendered obvious by Ferber et al wherein dPGS of the conjugate (that targets P-selectin and happens to inhibit P-selectin) is substituted with an antibody that binds and inhibits P-selectin (such as crizanlizumab or inclacumab that both target P-selectin and happen to inhibit P-selectin) as the targeting agent of the conjugate in a pharmaceutical composition of Kreeger et al and a therapeutically effective amount of the composition is intracranially administered to the subject with glioblastoma because both dPGS of the conjugate and the antibodies of Kreeger et al function by targeting P-selectin. This is an example of a simple substitution of one known element (P-selectin targeting antibodies of Kreeger et al) in place of (P-selectin targeting reagent of dPGS of Ferber et al) of the administered conjugate of Ferber et al to obtain predictable results (targeting PTX to glioblastoma).
Further, one ordinary skill in the art would have been motivated, with a reasonable expectation of success, to treat just any subject with glioblastoma by performing the combined methods of Ferber et al and Kreeger et al wherein checkpoint inhibitor(s) of Omuro et al are administered to the subject with glioblastoma within the composition of the combined method because both the composition of the combined method of Ferber et al and Kreeger et al (by targeting PTX to glioblastoma cells) and the checkpoint inhibitors of Omuro (checkpoint inhibition) provide therapeutic benefit to subjects with glioblastoma. This is an example of both (1) combining prior art elements according to known methods to yield predictable results and (2) some teaching, suggestion, or motivation in the prior art that would have led one of ordinary skill to combine prior art reference teachings to arrive at the claimed invention. See MPEP 2143. Therefore, the invention as a whole would have been prima facie obvious to one of ordinary skill in the art, absent unexpected results.
Response to Arguments
In the Reply of 6/29/26, Applicant argues a lack of motivation with an expectation of success to therapeutically treat glioblastoma by methods comprising inhibiting P-selectin with anti-P-selectin antibodies. Applicant further argues the claims are non-obvious because the specification discloses a combination of a P-selectin inhibitor (SELPi) with an immune modulator comprising a dendritic-cell targeting PLA/PLGA-mannose nano particle entrapping a glioblastoma GL261 neoantigen peptide demonstrated an unexpected synergistic effect on tumor volume reduction and survival.
The amendments to the claims and the arguments found in the Reply of 6/29/26 have been carefully considered, but are not deemed persuasive. In regards to the argument that there is a lack of motivation with an expectation of success to therapeutically treat glioblastoma by methods comprising inhibiting P-selectin with anti-P-selectin antibodies, the combined method is not based on motivation to inhibit P-selectin with anti-P-selectin antibodies. Rather, the combined method is based on motivation to target PTX to glioblastoma cells using anti-P-selectin antibodies that happen to also inhibit P-selectin. This is an example of a simple substitution of one known element (P-selectin targeting antibodies of Kreeger et al) in place of (P-selectin targeting reagent of dPGS of Ferber et al) of the administered conjugate of Ferber et al to obtain predictable results (targeting PTX to glioblastoma).
In regards to the indication the claims are non-obvious because the specification discloses a combination of a P-selectin inhibitor (SELPi) with an immune modulator comprising a dendritic-cell targeting PLA/PLGA-mannose nano particle entrapping a glioblastoma GL261 neoantigen peptide demonstrated an unexpected synergistic effect on tumor volume reduction and survival, the examiner disagrees. MPEP 716.02(d) states "objective evidence of nonobviousness must be commensurate in scope with the claims which the evidence is offered to support." The evidence involves a combination of a P-selectin inhibitor (SELPi) with an immune modulator comprising a dendritic-cell targeting PLA/PLGA-mannose nano particle entrapping a glioblastoma GL261 neoantigen peptide and the claims do not require SELPi in combination with a dendritic-cell targeting PLA/PLGA-mannose nano particle entrapping a glioblastoma GL261 neoantigen peptide.
New Rejections
Claim Rejections - 35 USC § 112
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.
Claims 1, 4-6, and 13-17are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for methods of treating glioblastoma by administering therapeutic agents/compositions that comprise or consist of polynucleotides that bind a polynucleotide encoding P-selectin and inhibit expression of P-selectin, does not reasonably provide enablement for methods of treating glioblastoma by administering agents/compositions that comprise or consist of polynucleotides that merely bind a polynucleotide encoding P-selectin. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to perform the invention commensurate in scope with these claims.
Factors to be considered in determining whether undue experimentation is required are summarized in Ex parte Forman, 230 USPQ 546 (BPAI 1986). They include the nature of the invention, the state of the prior art, the relative skill of those in the art, the amount of direction or guidance disclosed in the specification, the presence or absence of working examples, the predictability or unpredictability of the art, the breadth of the claims, and the quantity of experimentation which would be required in order to practice the invention as claimed.
The instant claims are drawn to methods of treating glioblastoma by administering agents/compositions that comprise or consist of polynucleotides that bind a polynucleotide encoding P-selectin. This broadly encompasses polynucleotides that do not bind functional regulatory or coding regions of P-selectin polynucleotides that are not capable of interfering with transcription, mRNA processing, or translation.
This invention is in a class of invention which the CAFC has characterized as "the unpredictable arts such as chemistry and biology". Mycogen Plant Sci., Inc. v. Monsanto Co., 243 F.3d 1316, 1330 (Fed. Cir. 2001).
The specification discloses inhibition of P-selectin treats glioblastoma (see entire document). One obvious mechanism to inhibit P-selectin would be to use antisense constructs to interfere with P-selectin expression. However, polynucleotides that bind P-selectin polynucleotides that that do not bind functional regulatory or coding regions of P-selectin polynucleotides that are not capable of interfering with transcription, mRNA processing, or translation of P-selectin would not predictably treat glioblastoma.
One cannot extrapolate the teachings of the specification to the scope of the claims because the claims are broadly drawn to methods of treating glioblastoma by administering agents/compositions that comprise or consist of polynucleotides that bind a polynucleotide encoding P-selectin – including those polynucleotides that do not inhibit P-selectin expression, and Applicant has not enabled said method because it has not been shown that just any polynucleotide that binds a polynucleotide encoding P-selectin predictably provides therapeutic benefit when administered to a subject with glioblastoma. Further, undue experimentation would be required to determine which, if any, polynucleotide that binds P-selectin that does not inhibit expression of P-selectin provides therapeutic benefit to subjects with glioblastoma in order to perform the method as broadly claimed.
In view of the teachings above and the lack of guidance, workable examples and or exemplification in the specification, it would require undue experimentation by one of skill in the art to determine with any predictability, that the method would function as claimed.
Claim Rejections - 35 USC § 103
Claim(s) 1 and 13-17 is rejected under 35 U.S.C. 103 as being unpatentable over Ferber et al (eLIFE, 2017, 6(e25281): 1-34; 3/19/23 IDS) in view of Kreeger et al (US 2019/0241665 A1; 8/8/19; 3/19/23 IDS) and Wyatt et al (Mol Pharm, 2020, 17(2): 717-721).
Ferber et al teaches P-selectin is highly expressed in glioblastoma and P-selectin expression in glioblastoma correlates with patient survival (page 10 and Figure 3, in particular). Ferber et al further suggests targeting P-selectin in glioblastoma may have additional therapeutic benefit because high expression of P-selectin correlate with poor patient survival (page 21, in particular). Ferber et al further teaches a conjugate comprising paclitaxel (PTX) conjugated to a dendritic polyglycerol sulfate (dPGS) for treating glioblastoma (Abstract, in particular). Ferber et al further teaches dPGS is able to cross the blood-brain barrier (BBB), binds to P-selectin, inhibits P-selectin, and accumulate in intracranial tumors (Abstract and lines 2-3 on page 3, in particular). Ferber et al further teaches the anti-proliferative activity of PTX on glioblastoma cells is retained in the conjugate comprising PTX and dPGS (Figure 4, in particular) and that the conjugate is targeted to intracranial tumors (Figure 5, in particular).
Ferber et al does not specifically teach a composition comprising a nanoparticle and/or targeting moiety attached to an anti-P-selectin antibody wherein the targeting moiety increases delivery across the blood brain barrier. However, these deficiencies are made up in the teachings of Kreeger et al and Wyatt et al.
Kreeger et al teaches inhibitors of P-selectin for therapeutic treatment include (unconjugated) antibodies that bind and inhibit P-selectin (crizanlizumab and inclacumab) and small molecule agents (rivipansel and tinzaparin) ([0039]-[0040], in particular). Kreeger et al further teaches inhibitors of P-selectin are administered in the form of pharmaceutical compositions comprising a pharmaceutically acceptable diluent ([0042]), which is a “pharmaceutically acceptable carrier” (as defined at paragraph spanning pages 39-40 of the instant specification, in particular).
Wyatt et al teaches attaching a mucic acid-based, targeted nanoparticle to an antibody and drug to enhance the ability of the antibody and drug to cross the blood-brain barrier and (Abstract, in particular).
One of ordinary skill in the art would have been motivated, with a reasonable expectation of success, to perform a rendered obvious by Ferber et al comprising treating just any subject diagnosed with glioblastoma, such as a subject with an early stage glioblastoma or a subject with glioblastoma before or after resection, by administering a therapeutically effective amount of the conjugate comprising PTX and dPGS of Ferber et al to the subject because Ferber et al teaches the conjugate is to be used to treat glioblastoma, the anti-proliferative activity of PTX on glioblastoma cells is retained in the conjugate, and that the conjugate is targeted to intracranial tumors.
Further, one of ordinary skill in the art would have been motivated, with a reasonable expectation of success, to perform a combined method comprising the method rendered obvious by Ferber et al wherein dPGS of the conjugate (that targets P-selectin and happens to inhibit P-selectin) is substituted with an antibody that binds and inhibits P-selectin (such as crizanlizumab or inclacumab that both target P-selectin and happen to inhibit P-selectin) as the targeting agent of the conjugate (to form an ADC) in a pharmaceutical composition of Kreeger et al and a therapeutically effective amount of the composition is intracranially administered to the subject with glioblastoma because both dPGS of the conjugate and the antibodies of Kreeger et al function by targeting P-selectin. This is an example of a simple substitution of one known element (P-selectin targeting antibodies of Kreeger et al) in place of (P-selectin targeting reagent of dPGS of Ferber et al) of the administered conjugate of Ferber et al to obtain predictable results (targeting PTX to glioblastoma).
Further, one ordinary skill in the art would have been motivated, with a reasonable expectation of success, to treat just any subject with glioblastoma by performing the combined methods of Ferber et al and Kreeger et al wherein the targeting moiety of Wyatt et al is attached to the ADC of the combined method and administered to a subject with a glioblastoma because an ADC is an antibody conjugated to a drug and the targeting moiety of Wyatt et al has demonstrated the ability to permit antibodies and drugs to cross the blood-brain barrier where the ADCs can therapeutically contact glioblastomas.
Further, it is the examiner’s position that an ADC of the combined method is “pharmaceutical composition comprising a single therapeutic agent consisting of…an inhibitory antibody…that binds to and inhibits P-selectin” because the ADC comprises a single therapeutic agent consisting of an inhibitory antibody that binds to and inhibits P-selectin.
This is an example of both (1) combining prior art elements according to known methods to yield predictable results and (2) some teaching, suggestion, or motivation in the prior art that would have led one of ordinary skill to combine prior art reference teachings to arrive at the claimed invention. See MPEP 2143. Therefore, the invention as a whole would have been prima facie obvious to one of ordinary skill in the art, absent unexpected results.
Claim Rejections - 35 USC § 103
Claim(s) 1, 13, 14, and 17 is rejected under 35 U.S.C. 103 as being unpatentable over Ferber et al (eLIFE, 2017, 6(e25281): 1-34; 3/19/23 IDS) in view of Kreeger et al (US 2019/0241665 A1; 8/8/19; 3/19/23 IDS) and Demeule et al (Cancer Res, 2015, 75(15_Supp): 2465).
Ferber et al teaches P-selectin is highly expressed in glioblastoma and P-selectin expression in glioblastoma correlates with patient survival (page 10 and Figure 3, in particular). Ferber et al further suggests targeting P-selectin in glioblastoma may have additional therapeutic benefit because high expression of P-selectin correlate with poor patient survival (page 21, in particular). Ferber et al further teaches a conjugate comprising paclitaxel (PTX) conjugated to a dendritic polyglycerol sulfate (dPGS) for treating glioblastoma (Abstract, in particular). Ferber et al further teaches dPGS is able to cross the blood-brain barrier (BBB), binds to P-selectin, inhibits P-selectin, and accumulate in intracranial tumors (Abstract and lines 2-3 on page 3, in particular). Ferber et al further teaches the anti-proliferative activity of PTX on glioblastoma cells is retained in the conjugate comprising PTX and dPGS (Figure 4, in particular) and that the conjugate is targeted to intracranial tumors (Figure 5, in particular).
Ferber et al does not specifically teach a composition comprising a targeting moiety attached to an anti-P-selectin antibody wherein the targeting moiety increases delivery across the blood brain barrier. However, these deficiencies are made up in the teachings of Kreeger et al and Demeule et al.
Kreeger et al teaches inhibitors of P-selectin for therapeutic treatment include (unconjugated) antibodies that bind and inhibit P-selectin (crizanlizumab and inclacumab) and small molecule agents (rivipansel and tinzaparin) ([0039]-[0040], in particular). Kreeger et al further teaches inhibitors of P-selectin are administered in the form of pharmaceutical compositions comprising a pharmaceutically acceptable diluent ([0042]), which is a “pharmaceutically acceptable carrier” (as defined at paragraph spanning pages 39-40 of the instant specification, in particular).
Demeule et al teaches attaching a targeting moiety to an antibody-drug conjugate (ADC) to enhance the ability of the ADC to cross the blood-brain barrier and give rise to a high rate of entry of ADC into the brain to treat a brain tumor (Abstract, in particular).
One of ordinary skill in the art would have been motivated, with a reasonable expectation of success, to perform a rendered obvious by Ferber et al comprising treating just any subject diagnosed with glioblastoma, such as a subject with an early stage glioblastoma or a subject with glioblastoma before or after resection, by administering a therapeutically effective amount of the conjugate comprising PTX and dPGS of Ferber et al to the subject because Ferber et al teaches the conjugate is to be used to treat glioblastoma, the anti-proliferative activity of PTX on glioblastoma cells is retained in the conjugate, and that the conjugate is targeted to intracranial tumors.
Further, one of ordinary skill in the art would have been motivated, with a reasonable expectation of success, to perform a combined method comprising the method rendered obvious by Ferber et al wherein dPGS of the conjugate (that targets P-selectin and happens to inhibit P-selectin) is substituted with an antibody that binds and inhibits P-selectin (such as crizanlizumab or inclacumab that both target P-selectin and happen to inhibit P-selectin) as the targeting agent of the conjugate (to form an ADC) in a pharmaceutical composition of Kreeger et al and a therapeutically effective amount of the composition is intracranially administered to the subject with glioblastoma because both dPGS of the conjugate and the antibodies of Kreeger et al function by targeting P-selectin. This is an example of a simple substitution of one known element (P-selectin targeting antibodies of Kreeger et al) in place of (P-selectin targeting reagent of dPGS of Ferber et al) of the administered conjugate of Ferber et al to obtain predictable results (targeting PTX to glioblastoma).
Further, one ordinary skill in the art would have been motivated, with a reasonable expectation of success, to treat just any subject with glioblastoma by performing the combined methods of Ferber et al and Kreeger et al wherein the targeting moiety of Demeule et al is attached to the ADC of the combined method and administered to a subject with a glioblastoma wherein the ADC predictably exhibits a high rate of entry into the brain because the targeting moiety of Demeule et al permits ADCs to cross the blood-brain barrier and has demonstrated a high rate of entry into the brain where the ADCs can therapeutically contact glioblastomas.
Further, it is the examiner’s position that an ADC of the combined method is “pharmaceutical composition comprising a single therapeutic agent consisting of…an inhibitory antibody…that binds to and inhibits P-selectin” because the ADC comprises a single therapeutic agent consisting of an inhibitory antibody that binds to and inhibits P-selectin.
This is an example of both (1) combining prior art elements according to known methods to yield predictable results and (2) some teaching, suggestion, or motivation in the prior art that would have led one of ordinary skill to combine prior art reference teachings to arrive at the claimed invention. See MPEP 2143. Therefore, the invention as a whole would have been prima facie obvious to one of ordinary skill in the art, absent unexpected results.
Claim Rejections - 35 USC § 103
Claim(s) 1, 4-6, and 13-17 is/are rejected under 35 U.S.C. 103 as being unpatentable over Ferber et al (eLIFE, 2017, 6(e25281): 1-34; 3/19/23 IDS) in view of Kreeger et al (US 2019/0241665 A1; 8/8/19; 3/19/23 IDS) and Wyatt et al (Mol Pharm, 2020, 17(2): 717-721) as applied to claims 1 and 13-17 above, and further in view of Omuro et al (Neuro-Oncology, 2018, 20(5): 674-686).
Teachings of Ferber et al, Kreeger et al, and Wyatt et al.
Ferber et al, Kreeger et al, and Wyatt et al do not specifically teach a method further comprising administering an immunomodulatory agent. However, these deficiencies are made up in the teachings of Omuro et al.
Omuro et al teaches method of therapeutically treating glioblastoma administering the checkpoint inhibitor nivolumab optionally in combination with the checkpoint inhibitor ipilimumab (Abstract, in particular).
One of ordinary skill in the art would have been motivated, with a reasonable expectation of success, to perform the combined method of Ferber et al, Kreeger et al, and Wyatt et al wherein the subject with glioblastoma is further administered checkpoint inhibitor(s) of Omuro et al because Omuro et al teaches method of therapeutically treating glioblastoma administering the checkpoint inhibitor nivolumab optionally in combination with the checkpoint inhibitor ipilimumab (Abstract, in particular). This is an example of both (1) combining prior art elements according to known methods to yield predictable results and (2) some teaching, suggestion, or motivation in the prior art that would have led one of ordinary skill to combine prior art reference teachings to arrive at the claimed invention. See MPEP 2143. Therefore, the invention as a whole would have been prima facie obvious to one of ordinary skill in the art, absent unexpected results.
Claim Rejections - 35 USC § 103
Claim(s) 1, 4-6, 13, 14, and 17 is/are rejected under 35 U.S.C. 103 as being unpatentable over Ferber et al (eLIFE, 2017, 6(e25281): 1-34; 3/19/23 IDS) in view of Kreeger et al (US 2019/0241665 A1; 8/8/19; 3/19/23 IDS) and Demeule et al (Cancer Res, 2015, 75(15_Supp): 2465) as applied to claims 1, 13, 14, and 17 above, and further in view of Omuro et al (Neuro-Oncology, 2018, 20(5): 674-686).
Teachings of Ferber et al, Kreeger et al, and Demeule et al.
Ferber et al, Kreeger et al, and Demeule et al do not specifically teach a method further comprising administering an immunomodulatory agent. However, these deficiencies are made up in the teachings of Omuro et al.
Omuro et al teaches method of therapeutically treating glioblastoma administering the checkpoint inhibitor nivolumab optionally in combination with the checkpoint inhibitor ipilimumab (Abstract, in particular).
One of ordinary skill in the art would have been motivated, with a reasonable expectation of success, to perform the combined method of Ferber et al, Kreeger et al, and Demeule et al wherein the subject with glioblastoma is further administered checkpoint inhibitor(s) of Omuro et al because Omuro et al teaches method of therapeutically treating glioblastoma administering the checkpoint inhibitor nivolumab optionally in combination with the checkpoint inhibitor ipilimumab (Abstract, in particular). This is an example of both (1) combining prior art elements according to known methods to yield predictable results and (2) some teaching, suggestion, or motivation in the prior art that would have led one of ordinary skill to combine prior art reference teachings to arrive at the claimed invention. See MPEP 2143. Therefore, the invention as a whole would have been prima facie obvious to one of ordinary skill in the art, absent unexpected results.
Conclusion
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/SEAN E AEDER/ Primary Examiner, Art Unit 1642
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