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 .
Response to Arguments
Applicant’s arguments, see Page 1, filed 12/24/2025, with respect to the rejection(s) of claim(s) 1, 6-9, 14, 19, 23, 25, 30-31, 35-36, 38-39, 45, 49, 54-55 and 84 under Moores et al. (US 20200270351 A1) in view of Reddy (WO 2020005932) and Robichaux (WO 2019191279 A2) have been fully considered and are persuasive. Therefore, the rejection has been withdrawn. However, upon further consideration, a new ground(s) of rejection is made in view of Molina et al. (EP 3120851 A1), Reddy (WO 2020005932) and Kobayashi et al. EGFR Exon 18 Mutations in Lung Cancer: Molecular Predictors of Augmented Sensitivity to Afatinib or Neratinib as Compared with First- or Third-Generation TKIs, November 2015, Pages 5305-5313.
Applicant has additionally overcome the 112d rejection of claims 23, 30 and 38 by the redaction of EGFR TKI resistant mutation of V843.
The teachings of Reddy from the previous office action with the teachings of Molina and Kobayashi reads to the limitations of claim 1 of the administration of poziotinib to treat a cancer determined to have one or more epidermal growth factor receptor (EGFR) tyrosine inhibitor (TKI) resistant mutations, wherein the EGFR TKI resistant mutation resides on amino acids 688-728 of exon 18.
Applicant has canceled claim 83 and incorporated the limitation of claim 83 into claim 1. Claims 1, 6-9, 14, 19, 23, 25, 30-31, 35-36, 38-39, 45, 49, 54-55 and 84 are pending. Claims 1, 6-9, 14, 19, 23, 25, 30-31, 35-36, 38-39, 45, 49, 54-55 and 84 is now evaluated on its merits.
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.
Claims 1, 6-9, 14, 19, 23, 25, 30, 35-36, 38-39 and 54-55 are rejected under 35 U.S.C. 103 as being unpatentable over Molina et al. (EP 3120851 A1).
Regarding claims 1, 6-9, 14, 19, 23, 25, 30, 35-36, 38-39 and 54-55, Molina teaches a method for the treatment of solid cancers, in particularly non-small cell lung carcinoma (NSCLC) and small cell lung carcinoma (SCLC) (relevant to claims 54-55) (para. 0043-0044, 0053), comprising administration of
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in combination with a chemotherapeutic agent. The solid cancer as taught by Molina consist of an EGFR insertion, deletion and codon mutations on exons 18, 19, 20 and 21 of G719S, G719C, G719A, L858R and L861Q (relevant to claims 25, 30, 35-36, 38-39) (para. 0054). Of the chemotherapeutic agents Molina teaches a list of agents which consist of poziotinib (para. 0078). In a particular embodiment the SW48 cell line has an EGFR mutation of G719S in exon 18 (relevant to claims 1, 6-9) (para. 0105).
In terms of claims 14, 19 and 23, the limitations to exon 19-21 residues are merely further limiting the residues in the exon and not stating the mutation is the particular residue in the exon.
Although Molina does not teach an exact example of poziotinib in combination with
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in would have been obvious to someone of ordinary skill in the art at the time of filling to have administered the combination of
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and poziotinib to treat cancers that are EGFR TKI resistant of residue G719 in exon 18. One would be motivated to do so from the teachings of Molina of
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in combination with a chemotherapeutic drug selected from a list which includes poziotinib to treat cancers that have EGFR TKI resistant of residue G719 in exon 18. There is a reasonable expectation of treating cancers that are EGFR TKI resistant of residue G719 in exon 18 comprising administration of poziotinib from the teachings of Molina.
Claims 31, 45 and 49 are rejected under 35 U.S.C. 103 as being unpatentable over Molina et al. (EP 3120851 A1) in view of Reddy (WO 2020005932) which claims US benefit effective filling date 06/25/2018.
The teachings of Molina for the above 103 rejection of claims 1, 6-9, 14, 19, 23, 25, 30, 35-36, 38-39 and 54-55 are incorporated herein by reference.
Molina fails to teach poziotinib administered at a dose of 8mg, 12mg or 16mg and wherein the subjects may be determined to not have an EGFR mutation at residue C797.
Reddy teaches a method for treating non-small cell lung , breast , stomach, colon , pancreatic , prostate , myeloma, head and neck , ovarian , esophageal and metastatic cell carcinoma cancers (claim 18) by administration of poziotinib at an amount of .01 to 50 mg (relevant to claim 45) (para. 0052) in combination with another anti-cancer therapy (relevant to claim 49) (abstract) to subject who has already been treated with an EGFR TKI (para. 0006) and has EGFR TKI resistant mutations of exon 18, 19, 20 and 21 (para. 0038). Reddy additionally teaches the subjects may be determined to not have an EGFR mutation at residue C797 (relevant to claim 31) (para. 0038) and in some embodiments one or more EGFR exon 20 mutations comprise one or more point mutations, insertions, and/or deletions of 3-18 nucleotides between amino acids 763- 778 (para 0038).
Therefore, it would have been obvious to someone of ordinary skill in the art at the time of filling to have administered poziotinib in an amount of 8mg, 12mg or 16 mg in combination with another anti-cancer therapy to treat a cancer in a subject who was determined to have a EGFR TKI resistant mutation of G719 in exon 18 and determined to not have an EGFR mutation at residue C797. One would have been motivated to do so from the teachings of Molina and Reddy on the treatment of cancers in which the subject has a EGFR TKI resistant mutation of exon 18 by administration of an effective amount of poziotinib. One would be motivated to administer the same mg range amount of poziotinib, addition of an anti-cancer therapy and wherein the subject does not have a C797 mutation as taught by Reddy to the composition of Molina as both teachings are for treatments for the same cancers with subjects determined to have one or more EGFR TKI resistant mutation of exon 18. There is a reasonable expectation of treating a cancer that’s has EGFR TKI resistant mutation of G719 in exon 18 and wherein the patient does not have a C797 mutation, comprising administration of poziotinib at the claimed range from the teachings of Molina and Reddy.
Claim 84 is rejected under 35 U.S.C. 103 as being unpatentable over Molina et al. (EP 3120851 A1) in view of Kobayashi et al. EGFR Exon 18 Mutations in Lung Cancer: Molecular Predictors of Augmented Sensitivity to Afatinib or Neratinib as Compared with First- or Third-Generation TKIs, November 2015, Pages 5305-5313.
The teachings of Molina for the above 103 rejection of claims 1, 6-9, 14, 19, 23, 25, 30, 35-36, 38-39 and 54-55 are incorporated herein by reference.
Molina fails to teach the composition to treat cancer wherein the cancer comprises EGFR TKI resistant mutation of E709, S720 or G724 in exon 18.
Kobayashi teaches 3% to 4% of all EGFR mutations are exon 18 mutations, which includes G719X, E709X, and exon 18deletion. Of the exon 18 mutations, codon 709 and 719 accounted for 84% (551/654) of all mutations, in which E709 and G719A being the most common (abstract, Pg. 5307 last para.).
Therefore it would have been obvious for someone of ordinary skill in the art at the time of filling to have administered the composition taught by Molina to treat a cancer that is resistant to EGFR TKI of E709 in exon 18. One would be motivated to do so from the teachings of Kobayashi of G719 and E709 being the most common exon 18 mutations and the teachings of Molina of cancers having resistance to EGFR TKI of exon 18 mutations, in particular G719. There is a reasonable expectation of treating a cancer that is resistant to EGFR TKI of E709 in exon 18 from the teachings of Molina and Kobayashi.
Conclusion
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MIKHAIL O'DONNEL. ROBINSON
Examiner
Art Unit 1627
/MIKHAIL O'DONNEL ROBINSON/Examiner, Art Unit 1627
/SARAH PIHONAK/Primary Examiner, Art Unit 1627