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 .
Status of the Claims
Claims 1-17 are pending in the instant application and subject to examination herein.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 04/06/2023 is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
Claim Interpretation
Applicant is permitted to be their own lexicographer provided that the claim and/or specification provides a definition for terms used in the claim; however, neither instant claim 1 nor the specification provides any specific definition of the term “ERK1/2 inhibitor”; therefore the Broadest Reasonable Interpretation of this term is applied by Examiner. The term “ERK1/2 inhibitor” is interpreted by the Examiner to refer to any composition that inhibits ERK1 and/or ERK2 protein kinase(s) in any of the following ways:
1. Inhibiting the expression of ERK1 and/or ERK2 kinase(s);
2. Inhibiting the activation of ERK1 and/or ERK2 kinase(s) (e.g., by phosphorylation);
3. Inhibiting the enzymatic process of ERK1 and/or ERK2 kinase(s).
Since ERK1/2 kinases are part of the RAS/MAPK cell signaling cascade (also known as the Ras-Raf-MEK-ERK pathway)1, an inhibitor that blocks or reduces the phosphorylation of ERK1/2 by interruption of this signaling cascade via direct (e.g., active site) inhibition of MEK kinase or another more upstream kinase in this signaling cascade, or blockade or reduction of protein expression of MEK kinase or a more upstream kinase in this signaling cascade are each considered to fall with the definition of “ERK1/2 inhibitor”.
Claim Rejections - 35 USC § 112(b)
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.
Claims 9-12 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.
Claim 9 is indefinite for reciting the intended-result terminology “wherein medial survival time increases by at least 3 months after treatment,” because one of ordinary skill in the art cannot reasonably determine metes and bounds of this limitation. Specifically, the manner of claiming this result does set forth how the method is further limited. It is not clear if this limitation is intended to limit, for example, the patient population, the dosage of the drug, or to even add a new limitation. The specification is silent on an explanation that would breathe any life into this term. See page 19 of the specification where the term “median survival time” is mentioned twice, however, there is no further elaboration on how this result is achieved other than the already established administration of the drug.
Claim 10 is indefinite for reciting the intended-result terminology “wherein said patient achieves an Hb improvement of ~2.0 g/dl or~ 1.5 g/dl after treatment,” because one of ordinary skill in the art cannot reasonably determine metes and bounds of this limitation. Specifically, the manner of claiming this result does set forth how the method is further limited. It is not clear if this limitation is intended to limit, for example, the patient population, the dosage of the drug, or to even add a new limitation. The specification is silent on an explanation that would breathe any life into this term. Review of the specification for instances of “Hb” and “Hemoglobin” finds the mention of a “≥2.0 g/dL or ≥1.5 g/dL” improvement of hemoglobin from baseline for patients with primary myelofibrosis, post-polycythemia vera myelofibrosis or post-essential thrombocythemia myelofibrosis (page 20, lines 13-16), but the improvement is provided only as “an embodiment of the invention” and no information is provided on how this embodiment structurally differs from the method of claim 1.
Claim 11 is indefinite for reciting the intended-result terminology “completely responds to the treatment”, because one of ordinary skill in the art cannot reasonably determine metes and bounds of this limitation. Specifically, the manner of claiming this result does set forth how the method is further limited. It is not clear if this limitation is intended to limit, for example, the patient population, the dosage of the drug, or to even add a new limitation. The specification is silent on an explanation that would breathe any life into this term. Review of the specification shows the established definition of a Complete Response to treatment for myelofibrosis as established by the International Working Group-Myeloproliferative Neoplasms Research and Treatment (IWG-MRT) and the European Leukemia Net (ELN) response criteria (Table E, bridging across pages 16-17), and the specification further details that “In one embodiment the present invention provides an ERK1/2 inhibitor, suitably Compound A, for use in the treatment of myelofibrosis, especially primary MF, wherein the patient achieves complete response to the treatment according to the criteria in Table,” (page 18, lines 32-34); however, the section provides no information on how this embodiment structurally differs from the method of claim 1.
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claims 1-3 and 8-11 and 13 are anticipated by Wood.
Claims 1-3, 8-11 and 13 are rejected under 35 U.S.C. 102(a)(1) and 102(a)(2) as being anticipated by Wood (WO 2015/051252 A1)2.
Claim 1 is drawn to a method of treating myeloproliferative neoplasm (MPN) in a patient, comprising administering an ERK1/2 inhibitor to the patient.
Wood discloses methods and compositions for treating JAK2 inhibitor resistant cancers, comprising combination therapies wherein secondary and optionally tertiary agents are included along with JAK2 inhibitors, with the secondary/tertiary inhibitors being selected from AKT/PI3K inhibitors, ERK/MEK inhibitors and BCL-XL protein inhibitors (Abstract). Wood discloses that certain cancers are better treated with combined inhibition of JAK2 and Ras effector pathways can yield more robust and durable response than JAK inhibitor monotherapy (paragraph [0006]). The method includes the step of administering to the subject an effective amount of (a) an AKT and/or PI3K inhibitor; (b) an ERK/MEK inhibitor; (c) a BCL-XL protein inhibitor; or (d) any combination thereof whereby the cancer is successfully treated (paragraph [0007]). Wood specifically discloses treating myeloproliferative neoplasms, including polycythaemia vera (PCV), essential thrombocythaemia (ET), primary myelofibrosis (PMF), with the method (paragraph [0011]). Wood discloses a method of sensitizing a subject to a JAK2 inhibitor wherein the subject has developed resistance to a JAK2 inhibitor-based therapy and has an activated ATK and ERK pathway, including the step of administering to the subject a therapeutically effective amount of an AKT and/or PJ3K inhibitor and an ERK/MEK inhibitor in combination with the JAK2 inhibitor, whereby the subject is sensitized to the JAK2 inhibitor (paragraph [0039]). Similarly, Wood also discloses a method for “reversing resistance to JAK2 inhibitor therapy in a subject wherein the subject has an activated AKT and ERK/MEK pathway, comprising administering the combination of an AKT and/or PJ3K inhibitor and an ERK/MEK inhibitor in combination with the JAK2 inhibitor (paragraph [0045]). Wood also discloses that some of the methods disclosed therein can be particularly effective at treating subjects whose cancer has become ''drug resistant" or "multi-drug resistant." A cancer which initially responded to an anti-cancer drug, such as a JAK2 inhibitor, becomes resistant to that anticancer drug when the anti-cancer drug is no longer effective in treating the subject with the cancer (paragraph [0095]). As an example of reversing such JAK2 resistance, Wood discloses a study wherein a myeloproliferative neoplasm (MPN) cell line (HEL92.1.7) could be transduced with an ORF (open reading frame), “G12V” that activates Ras-driven resistance to JAK inhibition, and this resistance could then be overcome by combined treatment with INCB2018424 (ruxolitinib), a JAK inhibitor, MK-2206, an AKT inhibitor, and VX-11e, a known inhibitor of both ERK1 and ERK23 (paragraph [00129]). Wood’s Figure 2D shows how the combination of INCB2018424, MK-2206 (“AKTi”) and VX-11e (“ERKi”) was able to render the G12V-induced MPN cells to be as susceptible to JAK inhibition as the non-induced (control vector) MPN cells, while the G12V-induced MPN cells (“Ras G12V”) were resistant INCB2018424 alone or in combination with MK-2206 alone or with VX-11e alone:
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Thus, claim 1 is anticipated by the disclosure of Wood.
Claim 2 further limits claim 1 to particular myeloproliferative neoplasms to be treated, including myelofibrosis, and is met by the rejection above.
Claims 3 and 8 further limit claims 2 and 1, respectively, each to particular myeloproliferative neoplasm(s) including primary myelofibrosis, and each is met by the rejection above.
Thus, claims 2, 3 and 8 are anticipated by the disclosure of Wood.
Claims 9-11 require intended results of the method of treatment of claim 1, including improved median survival time, improvement hemoglobin level, and complete response to the treatment; however, these claims do not provide any further steps or modifications to the structure of the method of claim 1, and are therefore met by the rejection above.
Claim 13 further limits claim 1 to wherein the patient is receiving or has received prior therapy with ruxolitinib. Wood discloses that clinical trial have been carried out to evaluate the efficacy of ruxolitinib (INCB018424) in patient suffering from MPNs, and that such trials show that, while ruxolitinib transiently shows efficacy in reducing spleen size and alleviating some symptoms (in about 50% of patient), ruxolitinib-resistance is a real problem facing the drug moving forward in the clinic (paragraph [0004]). In this light, Wood further discloses that the need being addressed in the invention disclosed therein is the need to develop effective therapies for the treatment of cancers having developed resistance to JAK2 inhibitors (paragraph [0005]) and, as discussed above, discloses the method of reversing JAK2 inhibition resistance with the combination administration of a JAK2 inhibitor with a AKT or PI3K inhibitor and an MEK/ERK inhibitor and a JAK2 inhibitor (paragraph [0045]) and the example of doing so with an MPN cell line induced with Ras-driven JAK2 resistance (paragraph [00129] and Figure 2D).
Thus, claim 13 is anticipated by the disclosure of Wood.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 1-11 and 13-14 are unpatentable over Wood in view of Harrison and National Cancer Institute.
Claims 1-11 and 13-14 are rejected under 35 U.S.C. 103 as being unpatentable over Wood (WO 2015/051252 A1)4 in view of Harrison (Harrison, et al.; Leukemia, v30, pp.1701-1707; 2016) and National Cancer Institute (National Cancer Institute, Common Terminology Criteria for Adverse Events, version 5.0, U.S. Department of Health and Human Services; 2017).
The limitations of claims 1-3, 8-11 and 13 and the disclosure of Wood are discussed in the rejection above and hereby incorporated into the instant rejection.
Claim 4 further limits claim 3 to wherein the patient has thrombocytopenia associated myelofibrosis.
Claim 5 further limits claim 3 to wherein the patient has neutropenia associated with myelofibrosis.
Claim 6 further limits claim 3 to wherein the patient has a peripheral blood platelet count of less than or equal to 50,000/mL before treatment.
Claim 7 further limits claim 3 to wherein the patient has a peripheral blood platelet count of less than or equal to 75,000/mL before treatment.
Claim 14 further limits claim 13 to wherein prior therapy with ruxolitinib is administration twice daily at dose of 5 mg, 10 mg, 15 mg, 20 mg or 25 mg.
While Wood discloses a method of combination treatment of myeloproliferative neoplasms (MPNs), including primary myelofibrosis, with an AKT or PI3K inhibitor, MEK/ERK inhibitor, and a JAK2 inhibitor, and provides an example using the known JAK1/2 inhibitor ruxolitinib in an exemplary study of overcoming JAK2 resistance in MPN cells, as discussed in the rejection above, Wood does not disclose that patients to be treated for JAK2 resistance may have thrombocytopenia, including platelet counts below the thresholds of 75,000/mL and/or 50,000/mL, or may have neutropenia. However, a person of ordinary skill in the art would have a reasonable expectation of treating a patient suffering from primary myelofibrosis with JAK2 resistance using the method of Wood, while the patient also has one or more of the immunodeficient conditions required in claims 4-7, because it was known in the art that patients treated with ruxolitinib can develop grade 3 or grade 4 neutropenia and/or thrombocytopenia, per the teaching of Harrison, and that grade 3 thrombocytopenia corresponds to a platelet count of below 50,000 counts/mL, per the teaching of CTCAE.
Harrison teaches an analysis of the results of “COMFORT-II”, a clinical trial studying ruxolitinib for the treatment of myelofibrosis, compared with treatment by ‘best available therapy’ (BAT). Harrison teaches that in the COMFORT-II study, patients began dosing at 15 mg bid (i.e., twice daily) or 20 mg bid (page 1702). Harrison teaches that patients treated with ruxolitinib achieved ≥35% reduction in spleen volume compared to no patients on BAT achieving the same (Abstract). Harrison further teaches that patients treated with ruxolitinib experienced significant anemia and immune-deficiency adverse events in the initial weeks of the study, including 18.8% of patients experiencing grade 3/4 thrombocytopenia and 8.9% of patients experiencing grade 3/4 neutropenia (page 1704). Thrombocytopenia and neutropenia are well-known terms in the art that refers to low platelet count and low neutrophil count, respectively.5 While Harrison does not elaborate on the definitions of the grading of neutropenia and thrombocytopenia, this information was known in the art per the teaching of National Cancer Institute.
National Cancer Institute provides the “Common Terminology Criteria for Adverse Events” as a descriptive terminology which can be utilized for Adverse Event (AE) reporting. A grading (severity) scale is provided for each AE term, with higher grades corresponding to more severe conditions. For thrombocytopenia, specific definitions for grades are provided that define grade 3 for “Platelet count decreased” as having a platelet count of below 50,000 counts/dL and above 25,000 counts/dL (page 82). Thus, the grade 3/4 thrombocytopenia experienced by patients in the COMFORT-II trial taught by Harrison would have correspond to platelet counts below 50,000 counts/dL.
Applicant’s invention is unpatentable over the disclosure of Wood in view of the teachings of Harrison and National Cancer Institute, because a person of ordinary skill in the art would have a reasonable expectation of success in treating patients suffering myelofibrosis who have developed JAK2 resistance from prior ruxolitinib treatment, including at dosing of 15 mg bid or 20 mg bid, and also have neutropenia and/or grade 3/4 thrombocytopenia, corresponding to platelet count below 50,000 counts/dL, with a combination administration of an AKT or PI3K inhibitor, a MEK/ERK inhibitor and a JAK2 inhibitor, because it was known in the art that such a combination treatment can overcome JAK2 resistant cancers including myelofibrosis in patients treated with ruxolitinib who have developed JAK2-resistance, per the teaching of Wood, and it was known in the art that ruxolitinib treatment at dosing of 15 mg bid or 20 mg bid induces neutropenia and/or grade 3/4 thrombocytopenia in patients, per the teaching of Harrison, and that grade 3 thrombocytopenia corresponds to a platelet count of below 50,000 counts/dL, per the teaching of National Cancer Institute.
Thus, the invention was prima facie obvious at the time of filing.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 1-17 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-12 and 18-22 of copending Application No. 18/248,124 (hereafter referred to as “Brkic”). Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of Brkic anticipate the instant claims, as shown in the table below:
Claim Number(s) of Instant Application
Instant Application
Related Application Number 18/248,124 (“Brkic”)
1
A method of treating myeloproliferative neoplasm (MPN) in a patient, comprising administering an ERK1/2 inhibitor for use in the treatment of a myeloproliferative neoplasm (MPN) in a to the patient.
Brkic Claim 1:
A method of treating myeloproliferative neoplasm (MPN) in a patient, comprising administering an ERK1/2 inhibitor in combination with at least one further active agent to the patient, wherein the at least one further active agent is a JAK1/JAK2 inhibitor, a JAK2/FLT3 inhibitor, a JAK2v617F inhibitor, a JAK2 inhibitor, JAK1 inhibitor or a JAK2/Src inhibitor.
2
The method of claim 1 wherein the myeloproliferative neoplasm is selected from myelofibrosis (MF), essential thrombocythemia (ET), polycythemia vera (PV) and combinations thereof.
Brkic Claim 2:
The method of claim 1 wherein the myeloproliferative neoplasm is selected from myelofibrosis (MF), essential thrombocythemia (ET), polycythemia vera (PV) and combinations thereof
3
The method of claim 2, wherein the myelofibrosis comprises is primary myelofibrosis (PMF), post-essential thrombocythemia myelofibrosis (PET-MF) or post-polycythemia vera myelofibrosis
(PPV-MF).
Brkic Claim 3:
The method of claim 2, wherein the myelofibrosis comprises is primary myelofibrosis (PMF), post-essential thrombocythemia myelofibrosis (PET-MF) or post-polycythemia vera myelofibrosis (PPV-MF).
4
The method of claim 3, wherein said patient has thrombocytopenia associated with myelofibrosis
Brkic Claim 4:
The method of claim 3, wherein said patient has thrombocytopenia associated with myelofibrosis
5
The method of claim 3, wherein said patient has neutropenia associated with myelofibrosis.
Brkic Claim 5:
The method of claim 3, wherein said patient has neutropenia associated with myelofibrosis.
6
The method of claim 3, wherein said patient has a peripheral blood platelet count of less than or equal to 50,000/μL before treatment.
Brkic Claim 6:
The method of claim 3, wherein said patient has a peripheral blood platelet count of less than or equal to 50,000/μL before treatment.
7
The method of claim 3, wherein said patient has a peripheral blood platelet count of less than or equal to 75,000/μL before treatment.
Brkic Claim 7:
The method of claim 3, wherein said patient has a peripheral blood platelet count of less than or equal to 75,000/μL before treatment.
8
The method of claim 1, wherein the myeloproliferative neoplasm (MPN) is primary myelofibrosis (PMF).
Brkic Claim 8:
The method of claim 1 claim 1 or 2, wherein the myeloproliferative neoplasm (MPN) is primary myelofibrosis (PMF).
9
The method of claim 1 wherein median survival time increases by at least 3 months after treatment.
Brkic Claim 9:
The method of claim 1 wherein median survival time increases by at least 3 months after treatment.
10
The method of claim 1 wherein said patient achieves an Hb improvement of ~2.0 g/dl or~ 1.5 g/dl after treatment.
Brkic Claim 10:
The method of claim 1 wherein said patient achieves an Hb improvement of ~2.0 g/dl or~ 1.5 g/dl after treatment.
11
The method of claim 1 wherein said patient completely responds to the treatment.
Brkic Claim 11:
The method of claim 1 any one of the claims 1 to 8 wherein said patient completely responds to the treatment.
12
The method of claim 1 wherein said myeloproliferative neoplasm (MPN) is newly diagnosed MF.
Brkic Claim 12:
The method claim 1 wherein the myeloproliferative neoplasm (MPN) is newly diagnosed MF.
13
The method of claim 1 wherein the patient is receiving or has received prior therapy with ruxolitinib.
Brkic Claim 18:
The method of claim 1 any one of the claims 1 to 17, wherein the patient is receiving or has received prior therapy with ruxolitinib.
14
The method of claim 13 wherein the prior therapy with ruxolitinib is administration at 5 mg twice daily, 10 mg twice daily, 15 mg twice daily, 20 mg twice daily or 25 mg twice daily.
Brkic Claim 19:
The method of claim 18 wherein the prior therapy with ruxolitinib is administration at 5 mg twice daily, 10 mg twice daily, 15 mg twice daily, 20 mg twice daily or 25 mg twice daily.
15
The method of claim 1 wherein said ERK1/2 inhibitor is [rineterkib] (Compound A), or pharmaceutical acceptable salt thereof.
Brkic Claim 20:
The method of claim 1 wherein said ERK1/2 inhibitor is [rineterkib] (Compound A), or pharmaceutical acceptable salt thereof.
16
The method of claim 15 wherein Compound A is administered at a total daily dose of 100-300 mg, or 200-300 mg
Brkic Claim 21:
The method of claim 1 wherein Compound A is administered at a total daily dose of 100-300 mg, or 200-300 mg.
17
The method of claim 16 wherein Compound A is administered at a total daily dose of 100 mg or 200 mg, preferably administered once a day.
Brkic Claim 22:
The method of claim 1 wherein Compound A is administered at a total daily dose of 100 mg or 200 mg, preferably administered once a day.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Conclusion
Any inquiry concerning this communication or earlier communications from the examiner should be directed to W. JUSTIN YOUNGBLOOD whose telephone number is (703)756-5979. The examiner can normally be reached on Monday-Thursday from 8am to 5pm. The examiner can also be reached on alternate Fridays.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Jeffrey S. Lundgren, can be reached at telephone number (571) 272-5541. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/W.J.Y./Examiner, Art Unit 1629
/JEFFREY S LUNDGREN/Supervisory Patent Examiner, Art Unit 1629
1 See, for example, Roberts, P.J. and Der, C.J.; Oncogene, v26, pp.3291-3310; 2007.
2 Cited in Applicant’s Information Disclosure Statement dated 04/06/2023.
3 Wood describes VX-11e as an ERK inhibitor; for further evidence of ERK1/2 inhibition by VX-11e, see Shin (Shin, et al.; Chemical Science, v9, pp.2387-2634; 2018).
4 Cited in Applicant’s Information Disclosure Statement dated 04/06/2023.
5 See for example, Wikipedia: For thrombocytopenia, https://en.wikipedia.org/wiki/Thrombocytopenia; for neutropenia, https://en.wikipedia.org/wiki/Neutropenia.