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 .
Detailed Action
The Amendments and Remarks filed 1/15/26 in response to the Office Action of 7/15/25 are acknowledged and have been entered.
Claims 16-18 and 20-23 are pending.
Claim 16 has been amended by Applicant.
Claims 16-18 and 20-23 are currently under examination.
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
The following Office Action contains NEW GROUNDS of rejections Necessitated by Amendments.
Rejections Withdrawn
The rejection of claim 20 under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, is withdrawn.
The rejections under 35 U.S.C. 102(a)(1) are withdrawn.
The rejection of claims 16-18 under 35 U.S.C. 103 as being unpatentable over Wolf et al (Cancer Res, 2017, 77(4__Supp)(S2-06)) in view of Jiao et al (Clinical Cancer Research, 2017, 23(14): 3711-3720) is withdrawn.
The rejection of claim 20 under 35 U.S.C. 103 as being unpatentable over Wolf et al (Cancer Res, 2017, 77(4__Supp)(S2-06)) in view of Yau et al (Cancer Res, 2018, 78(4__Supp)(PD6-14)), Jiao et al (Clinical Cancer Research, 2017, 23(14): 3711-3720), Nanda et al (Journal of Clinical Oncology, 2016, 34(21): 2460-2467), and Lossos et al (WO 2018/081438 A1; 5/3/18) is withdrawn.
The rejection of claim 20 under 35 U.S.C. 103 as being unpatentable over Wolf et al (Cancer Res, 2017, 77(4__Supp)(S2-06)) in view of Yau et al (Cancer Res, 2018, 78(4__Supp)(PD6-14)), Jiao et al (Clinical Cancer Research, 2017, 23(14): 3711-3720), Nanda et al (Journal of Clinical Oncology, 2016, 34(21): 2460-2467), and Lossos et al (WO 2018/081438 A1; 5/3/18), Mavroudis et al (Annals of Oncology, 2016, 27: 1873-1878), and Lyseng-Williamson et al (Drugs, 2005, 65(17): 2513-2531) is withdrawn.
The rejection of claims 16-18 under 35 U.S.C. 103 as being unpatentable over Yau et al (Cancer Res, 2018, 78(4__Supp)(PD6-14)) in view of Wesseling et al (Virchows Arch, 2016, 469: 297-304) is withdrawn.
The rejection of claims 16 and 18 under 35 U.S.C. 103 as being unpatentable over Wolf et al (Cancer Res, 2017, 77(4__Supp)(S2-06)) in view of Wesseling et al (Virchows Arch, 2016, 469: 297-304) is withdrawn.
Rejections Maintained
Claim Rejections - 35 USC § 112
Claims 16-18 and 21-23 remain 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.
Claims 16-18 and 21-23 remain because claim 16 contains the trademark/trade name MammaPrint. Where a trademark or trade name is used in a claim as a limitation to identify or describe a particular material or product, the claim does not comply with the requirements of 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph. See Ex parte Simpson, 218 USPQ 1020 (Bd. App. 1982). The claim scope is uncertain since the trademark or trade name cannot be used properly to identify any particular material or product. A trademark or trade name is used to identify a source of goods, and not the goods themselves. Thus, a trademark or trade name does not identify or describe the goods associated with the trademark or trade name. In the present case, the trademark/trade name is used to identify/describe a MammaPrint assay and, accordingly, the identification/description is indefinite.
Response to Arguments
In the Reply of 1/15/26, Applicant argues the rejection should be withdrawn because a patent application underlying the MammaPrint assay was incorporated by reference into the instant application, the instant specification lists the 70 genes forming the basis of the MammaPrint 70 gene assay necessary for conducting the assay, and MammaPrint has a well-known meaning in the art and is not indefinite.
The amendments to the claims and the arguments found in the Reply of 1/15/26 have been carefully considered, but are not deemed persuasive. The examiner disagrees with the argument that the rejection should be withdrawn because a patent application underlying the MammaPrint assay was incorporated by reference into the instant application, the instant specification lists the 70 genes forming the basis of the MammaPrint 70 gene assay necessary for conducting the assay, and MammaPrint has a well-known meaning in the art and is not indefinite. Recited “MammaPrint” is a trademark or trade name used to identify/describe a MammaPrint assay. Where a trademark or trade name is used in a claim as a limitation to identify or describe a particular material or product, the claim does not comply with the requirements of 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph. See Ex parte Simpson, 218 USPQ 1020 (Bd. App. 1982). The claim scope is uncertain since the trademark or trade name cannot be used properly to identify any particular material or product. A trademark or trade name is used to identify a source of goods, and not the goods themselves. Thus, a trademark or trade name does not identify or describe the goods associated with the trademark or trade name. In the present case, the trademark/trade name is used to identify/describe a MammaPrint assay and, accordingly, the identification/description is indefinite.
Claim Rejections - 35 USC § 103
Claim(s) 16-18 remain rejected under 35 U.S.C. 103 as being unpatentable over Wolf et al (Cancer Res, 2017, 77(4__Supp)(S2-06)) in view of Yau et al (Cancer Res, 2018, 78(4__Supp)(PD6-14)), Jiao et al (Clinical Cancer Research, 2017, 23(14): 3711-3720), Nanda et al (Journal of Clinical Oncology, 2016, 34(21): 2460-2467), and Lossos et al (WO 2018/081438 A1; 5/3/18).
Wolf et al teaches a therapeutic method of treating patients with HR+/HER2-, MammaPrint high risk 2 (MP2) breast cancer comprising administering the PAPR inhibitor veliparib in combination with carboplatin resulting in pCR in many of said patients (Abstract, in particular). The abstract of Woilf et al further teaches HR+/HER2- breast cancer patients identified as M2 and PARPi7-high (a signature relating to DNA damage repair deficiency) exhibited a 42% pCR rate to PAPR inhibitor veliparib in combination with carboplatin, as compared to the 13% pCR rate of unselected HR+/HER2- breast cancer patients.
Wolf et al does not specifically teach administering an immune checkpoint inhibitor. However, these deficiencies are made up in the teachings of Yau et al, Jiao et al, Nanda et al, and Lossos et al.
Yau et al teaches a method of treating a subject with HR+/HER2-, MP2 breast cancer comprising administering the anti-PD-1 immune checkpoint inhibitor pembrolizumab (Abstract, in particular). The abstract of Yau et al further teaches HR+/HER2- breast cancer patients identified as MP2 exhibited a 62% pCR rate to pembrolizumab, as compared to the 29% pCR rate of unselected HR+/HER2- breast cancer patients.
Jiao et al teaches inhibition of PARP in breast cancer cells upregulates PD-L1 (Abstract, in particular), the ligand of PD-1 that is therapeutically blocked from binding PD-1 by the anti-PD-1 immune checkpoint inhibitor pembrolizumab. Jao et al further teaches PARP inhibition inhibits anticancer immunity via upregulation of PD-L1, and blockade of PD-L1 with an immune checkpoint inhibitor resensitized PARP-inhibitor treated breast cancer cells to T-cell killing (Abstract and Figure 5, in particular). Jiao et al further teaches Olaparib and talazoparib as two different PARP inhibitors (left column on page 3714, in particular) that have both been shown to upregulate PD-L1 in breast cancer cells (Fig. 1A and left column on page 3714, in particular).
Nanda et al teaches the anti-PD-1 immune checkpoint inhibitor pembrolizumab is administered intravenously (Abstract, in particular).
Lossos et al teaches the PARP inhibitor Olaparib of Jiao et al can be administered intravenously ([0041], in particular), like the anti-PD-1 immune checkpoint inhibitor pembrolizumab.
One of ordinary skill in the art would have been motivated, with a reasonable expectation of success, to perform a combined method comprising the therapeutic method of Wolf et al wherein HR+/HER2- MP2 breast cancer patient are administered a PARP inhibitor in combination with an anti-PD-L1 immune checkpoint inhibitor (such as pembrolizumab) because the method of Wolf results in pCR in many patients and inhibits PARP in breast cancer cells, which according to Jiao et al is taught to mechanistically lead to upregulation of PD-L1 expression by breast cancer cells and said upregulated PD-L1 is a ligand of PD-1 that is therapeutically blocked from binding PD-1 by the anti-PD-1 immune checkpoint inhibitor pembrolizumab of Yau et al that has been shown to provide therapeutic benefit in vivo with HR+/HER2- MP2 breast cancer patients. This is an example of 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.
Further, of ordinary skill in the art would have been motivated, with a reasonable expectation of success, to perform said combined method wherein Olaparib is substituted in place of veliparib of Wolf et al and the Olaparib is intravenously administered in the same pharmaceutical composition with the anti-PD-1 immune checkpoint inhibitor pembrolizumab of Yau et al because veliparib of Wolf et al provides therapeutic benefit to subjects with breast cancer by inhibiting PARP, Jiao et al teaches Olaparib as a PARP inhibitor and illustrates therapeutically treating breast cancer by administering Olaparib to a subject with breast cancer, and cited references teach both the PARP inhibitor Olaparib and the anti-PD-1 immune checkpoint inhibitor pembrolizumab can be administered intravenously. This is an example of 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 and a simple substitution of one known element for another to obtain predictable results.
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 1/15/26, Applicant cites [0065], Example 1, and Figure 3 of the specification and indicates the claims are non-obvious because HER2- MP2 breast cancer patients having MP2 are surprisingly likely to have pathological complete response (pCR) upon treatment with the claimed combination therapy. Applicant further indicates this rejection is based on hindsight reconstruction, combining disparate references to piece together the claimed invention. Applicant further argues the cited references fail to teach or suggest the claimed methods with a reasonable expectation of success. Applicant further argues Jiao is mechanistic and pre-clinical and does not disclose (1) treatment of MP2 breast cancer patients, (2) clinical efficacy in humans, (3) combination therapy in any HER2-negative MP2 patient populations, or (4) any teaching that a PARP inhibitor – ICI combination would be effective in the claimed patient population. Applicant further argues that identification of a biological mechanism of Jiao (PD-L1 upregulation upon PARP inhibition) does not inherently motivate a specific therapeutic solution (anti-PD-1 therapy) without impermissible hindsight reconstruction and Jiao does not teach or suggest that PD-L1 upregulation upon PARP inhibition should be clinically addressed by administering the PD-1 inhibitor pembrolizumab or that such intervention would be effective in MP2 breast cancer patients. Applicant further argues Yau teaching clinical benefit of the ICI pembrolizumab monotherapy in HR+/HER2- MP2 breast cancer patients that is independent of PARP inhibition or PD-L1 upregulations undermines, rather than supports, any motivation to add a PARP inhibitor, particularly in view of Jiao’s disclosure that PARP inhibition may suppress anticancer immunity. Applicant further argues Nanda teaches pembrolizumab administration in triple-negative breast cancer patients (not MP2 patients) and does not disclose PARP inhibitor with pembrolizumab in MP2 patients. Applicant further argues there is no teaching or motivation to combined a PARP inhibitor with pembrolizumab in MP2 patients. Applicant further argues Lossos is directed to formulations and not routes of administration and not to therapeutic combinations in breast cancer populations. Applicant further argues Lossos is silent as to disease context and does not teach combination with pemrolizumab. Regarding teachings of Lossos, Applicant further states merely showing that two drugs could be formulated for intravenous administration does not provide motivation to combine them in the claimed patient population and that formulations or route-of-administration disclosures cannot supply a motivation to combine therapeutically unrelated agents nor can they cure the absence of a teaching that agents should be co-administered to treat a specific disease or patient subgroup. Applicant further indicates substituting Olaparib in place of Veliparib is not a “simple substitution” or a matter of routine optimization because the PARP inhibitors are not interchangeable due to Veliparib having markedly different PARP-trapping potency, toxicity, and pharmacokinetic profile than Olaparib. Applicant argues clinical responses and tolerability vary substantially between Veliparib and Olaparib. Applicant further argues ICI combinations are unpredictable and that immune-related adverse events, overlapping toxicities, and unexpected synergy (or lack thereof) cannot be predicted from in vitro assays. Applicant further states MP2 genomic signature is not related to BRCA mutation or HRD status. Applicant further argues a skilled artisan would not have reasonably expected success in combining PARP inhibition with immune checkpoint blockade in MP2 patients given the known risks of overlapping hematologic and immune-related toxicities, the absence of any clinical data supporting such a combination in breast cancer at the relevant time, and the lack of any predictive biomarker linking MP2 status to responsiveness to PARP-ICI combinations. Applicant further argues cited references do not provide a reasonable expectation that a PARP inhibitor (e.g., Olaparib) and pembrolizumab, administered together, would be safe or effective in HER2-negative, MP2 breast cancer patients.
The amendments to the claims and the arguments found in the Reply of 1/15/26 have been carefully considered, but are not deemed persuasive. In regards to the citation of [0065], Example 1, and Figure 3 of the specification, indication the claims are non-obvious because HER2- MP2 breast cancer patients having MP2 are surprisingly likely to have pathological complete response (pCR) upon treatment with the claimed combination therapy, the argument there is no teaching or motivation to combined a PARP inhibitor with pembrolizumab in MP2 patients, and a skilled artisan would not have reasonably expected success in combining PARP inhibition with immune checkpoint blockade in MP2 patients given the known risks of overlapping hematologic and immune-related toxicities, the absence of any clinical data supporting such a combination in breast cancer at the relevant time, and the lack of any predictive biomarker linking MP2 status to responsiveness to PARP-ICI combinations, and that cited references do not provide a reasonable expectation that a PARP inhibitor (e.g., Olaparib) and pembrolizumab, administered together, would be safe or effective in HER2-negative, MP2 breast cancer patients, the examiner disagrees. The combined method predictably provides therapeutic benefit for the reasons stated above. Again, one of ordinary skill in the art would have been motivated, with a reasonable expectation of success, to perform a combined method comprising the therapeutic method of Wolf et al wherein HR+/HER2- MP2 breast cancer patients are administered a PARP inhibitor (resulting in pCR in many patients) in combination with the anti-PD-L1 immune checkpoint inhibitor (such as pembrolizumab) because the method of Wolf results in pCR in many patients and inhibits PARP in breast cancer cells, which according to Jiao et al is taught to mechanistically lead to upregulation of PD-L1 expression by breast cancer cells and said upregulated PD-L1 is a ligand of PD-1 that is therapeutically blocked from binding PD-1 by the anti-PD-1 immune checkpoint inhibitor pembrolizumab of Yau et al that has been shown to provide therapeutic benefit in vivo with HR+/HER2- MP2 breast cancer patients. Further, the instant specification does not provide unexpected results of the combined method. Rather, the instant specification provides a statistical approach (Bayesian modeling) rather than an actual demonstration of unexpected beneficial results of the combined method.
In response to applicant's argument that the examiner's conclusion of obviousness is based upon improper hindsight reasoning, it must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon hindsight reasoning. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made, and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin, 443 F.2d 1392, 170 USPQ 209 (CCPA 1971).
In regards to the argument cited references fail to teach or suggest the claimed methods with a reasonable expectation of success, the examiner disagrees. Again, one of ordinary skill in the art would have been motivated, with a reasonable expectation of success, to perform a combined method comprising the therapeutic method of Wolf et al wherein HR+/HER2- MP2 breast cancer patient are administered a PARP inhibitor in combination with the anti-PD-L1 immune checkpoint inhibitor (such as pembrolizumab) because the method of Wolf results in pCR in many patients and inhibits PARP in breast cancer cells, which according to Jiao et al is taught to mechanistically lead to upregulation of PD-L1 expression by breast cancer cells and said upregulated PD-L1 is a ligand of PD-1 that is therapeutically blocked from binding PD-1 by the anti-PD-1 immune checkpoint inhibitor pembrolizumab of Yau et al that has been shown to provide therapeutic benefit in vivo with HR+/HER2- MP2 breast cancer patients. This is an example of 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.
The examiner agrees with the argument Jiao is mechanistic. The examiner maintains inhibition of PARP in breast cancer cells is taught by Jiao et al to mechanistically lead to upregulation of PD-L1 expression by breast cancer cells and said upregulated PD-L1 is a ligand of PD-1 that is therapeutically blocked from binding PD-1 by the anti-PD-1 immune checkpoint inhibitor pembrolizumab of Yau et al that has been shown to provide therapeutic benefit in vivo with HR+/HER2- MP2 breast cancer patients.
In regards to the arguments that Jiao does not disclose (1) treatment of MP2 breast cancer patients, (2) clinical efficacy in humans, (3) combination therapy in any HER2-negative MP2 patient populations, or (4) any teaching that a PARP inhibitor – ICI combination would be effective in the claimed patient population, one cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986).
In regard to the arguments that identification of a biological mechanism of Jiao (PD-L1 upregulation upon PARP inhibition) does not inherently motivate a specific therapeutic solution (anti-PD-1 therapy) without impermissible hindsight reconstruction and Jiao does not teach or suggest that PD-L1 upregulation upon PARP inhibition should be clinically addressed by administering the PD-1 inhibitor pembrolizumab or that such intervention would be effective in MP2 breast cancer patients, the rejection is not solely based on Jiao teaching PD-L1 upregulation upon PARP inhibition. Rather, the rejection is based on a combination of cited references. Again, it must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon hindsight reasoning. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made, and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin, 443 F.2d 1392, 170 USPQ 209 (CCPA 1971).
In regards to the argument that Yau teaching clinical benefit of the ICI pembrolizumab monotherapy in HR+/HER2- MP2 breast cancer patients that is independent of PARP inhibition or PD-L1 upregulations undermines, rather than supports, any motivation to add a PARP inhibitor, particularly in view of Jiao’s disclosure that PARP inhibition may suppress anticancer immunity, the examiner disagrees. Yau teaching clinical benefit of the ICI pembrolizumab monotherapy in HR+/HER2- MP2 breast cancer patients that is independent of PARP inhibition or PD-L1 upregulations undermines in no way teaches-away or disparages adding PARP inhibitor. In regards to Jiao’s disclosure that PARP inhibition may suppress anticancer immunity, Jiao et al teaches blockade of PD-L1 (as found in the combined method) “can restore the attenuated antitumor immunity ad potentiate PARPi in tumor suppression” (see Translational Relevance box on page 3712, in particular) – which provides a motivation to combine a PD-L1 inhibitor with a PARP inhibitor for tumor suppression.
The examiner agrees with the argument that Nanda teaches pembrolizumab administration in triple-negative breast cancer patients (not MP2 patients) and does not disclose PARP inhibitor with pembrolizumab in MP2 patients. However, it must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon hindsight reasoning. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made, and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin, 443 F.2d 1392, 170 USPQ 209 (CCPA 1971).
In regard to the arguments that Lossos is directed to formulations and not routes of administration and not to therapeutic combinations in breast cancer populations and Lossos is silent as to disease context and does not teach combination with pemrolizumab, 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). Lossos et al is cited as teaching the PARP inhibitor Olaparib of Jiao et al can be administered intravenously ([0041], in particular), like the anti-PD-1 immune checkpoint inhibitor pembrolizumab.
In regards to the argument that merely showing that two drugs could be formulated for intravenous administration does not provide motivation to combine them in the claimed patient population, the examiner agrees.
In regards to the argument that formulations or route-of-administration disclosures cannot supply a motivation to combine therapeutically unrelated agents nor can they cure the absence of a teaching that agents should be co-administered to treat a specific disease or patient subgroup, the examiner hears applicant’s hypothetically broad argument. However, the rejection is not based on co-administering multiple reagents to treat a disease because of a disclosed route of administration. It is further noted no pending claim recites a route of administration.
In regards to the argument that substituting Olaparib in place of Veliparib is not a “simple substitution” or a matter of routine optimization because the PARP inhibitors are not interchangeable due to Veliparib having markedly different PARP-trapping potency, toxicity, and pharmacokinetic profile than Olaparib, the examiner disagrees. Substituting one PARP inhibitor for another PARP inhibitor, when they both have been shown to upregulate PD-L1 in breast cancer cells (Fig. 1A and left column on page 3714 of Jiao et al, in particular), is a simple substitution of one PARP inhibitor for another PARP inhibitor. Applicant is reminded that obviousness is based on “reasonable expectation of success” and not “absolute” predictability. See MPEP 2143.02. It is further noted, no claim requires administering Veliparib or Olaparib.
In regards to the argument that clinical responses and tolerability vary substantially between Veliparib and Olaparib, the examiner acknowledges Veliparib and Olaparib are not identical. However, both Veliparib and Olaparib have been shown to inhibit PARP, treat cancer, and upregulate PD-L1 (see Jiao et al, in particular). It is further noted, no claim requires administering Veliparib or Olaparib.
In regards to the argument that ICI combinations are unpredictable and that immune-related adverse events, overlapping toxicities, and unexpected synergy (or lack thereof) cannot be predicted from in vitro assays. The rejection is not solely based on in vitro assays. Further, applicant is reminded that obviousness is based on “reasonable expectation of success” and not “absolute” predictability. See MPEP 2143.02.
In regards to the statement MP2 genomic signature is not related to BRCA mutation or HRD status, this rejection is not based on a particular relationship (or lack thereof) between M2P genomic signature and BRCA mutation or HRD status.
Claim Rejections - 35 USC § 103
Claim(s) 16-18 and 21-23 remain rejected under 35 U.S.C. 103 as being unpatentable over Wolf et al (Cancer Res, 2017, 77(4__Supp)(S2-06)) in view of Yau et al (Cancer Res, 2018, 78(4__Supp)(PD6-14)), Jiao et al (Clinical Cancer Research, 2017, 23(14): 3711-3720), Nanda et al (Journal of Clinical Oncology, 2016, 34(21): 2460-2467), and Lossos et al (WO 2018/081438 A1; 5/3/18), as applied to claims 16-18 above, further in view of Mavroudis et al (Annals of Oncology, 2016, 27: 1873-1878), and Lyseng-Williamson et al (Drugs, 2005, 65(17): 2513-2531).
Teachings of Wolf et al, Yau et al, Jiao et al, Nanda et al, and Lossos et al are discussed above.
Wolf et al, Yau et al, Jiao et al, Nanda et al, and Lossos et al do not specifically teach administering a taxane or pharmaceutical compositions comprising a taxane. Further, Wolf et al, Yau et al, Jiao et al, Nanda et al, and Lossos et al do not differentiate hormone receptor positive (HR+) breast cancers as being ER+ and/or PR+. However, these deficiencies are made up in the teachings of Mavroudis et al and Lyseng-Williamson et al.
Mavroudis et al teaches therapeutically treating HR+/HER2- breast cancer patients, including those that are ER+ and/or PR+, comprising administering the patients docetaxel (Abstract, in particular).
Lyseng-Williamson et al teaches docetaxel is administered intravenously (left column on page 2515, 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 Wolf et al, Yau et al, Jiao et al, Nanda et al, and Lossos et al wherein the HR+/HER2- patients include patients that are ER+ and the docetaxel of Mavroudis et al is included in the intravenously administered pharmaceutical composition because the combined method treats HR+/HER2- patients, HR+ patients are all PR+ and/or ER+, and Mavroudis et al teaches therapeutically treating HR+/HER2- breast cancer patients, including those that are ER+ and/or PR+, comprising administering the patients docetaxel. Further, like the PARP inhibitor and the anti-PD-1 immune checkpoint inhibitor pembrolizumab of the combined method, Lyseng-Williamson et al teaches docetaxel is administered intravenously. This is an example of 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. 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 1/15/26, Applicant repeats arguments addressed above.
New Rejections Necessitated by Amendments
Claim Rejections - 35 USC § 112
Claim 20 is 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.
Claim 20 is rejected for reciting “The method of claim 19, wherein….” Claim 19 has been cancelled by Applicant. Therefore, the metes-and-bounds of claim 20 are unclear because it unclear which method claim 20 is further limiting.
Conclusion
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). 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.
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/SEAN E AEDER/Primary Examiner, Art Unit 1642