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 .
Claims 1-33 are pending and examined on the merits.
Information Disclosure Statement
The reference on page 5 of the IDS submitted 9/15/2023 has been lined through because it is illegible.
Claim Rejections - 35 USC § 101
35 U.S.C. 101 reads as follows:
Whoever invents or discovers any new and useful process, machine, manufacture, or composition of matter, or any new and useful improvement thereof, may obtain a patent therefor, subject to the conditions and requirements of this title.
Claims 21, and 24 rejected under 35 U.S.C. 101 because the claimed invention is directed, in part, to an abstract idea without significantly more.
Claim 21 recites determining whether the tumor exhibits cMet overexpression defined by ≥ 25% of the neoplastic cells have 3+ membrane staining or cytoplasmic staining when measured by IHC, and “if” the tumor tissue exhibits c-Met overexpression administering to the subject (1)Osimertinib and (2) a pharmaceutical composition comprising an anti-Met antibody drug conjugate having the indicated structure and sequence for the anti-cMet antibody. The claim, in part, fails to recite an active method step for the subject whose tumor does not have ≥25% of the neoplastic cells having 3+ membrane and/or cytoplasmic staining. Thus, the claim in part is simply drawn toto the determination of the percentage of neoplastic cells having 3+ membrane and/or cytoplasmic staining. This judicial exception is not integrated into a practical application because for these subjects, because the measurement of c-Met expression is simply a data gathering step. The claim(s) does/do not include additional elements that are sufficient to amount to significantly more than the judicial exception because the subjects are excluded from receiving the inventive combination of Osimertinib and the anti-cMet conjugate.
.
Claim 24 recites determining either (i) c-Met overexpression defined by ≥25% of the neoplastic cells having 3+ membrane and/or cytoplasmic staining, or (ii) lack of c-Met expression defined by ≥25% of the neoplastic cells having 3+ membrane and/or cytoplasmic staining, wherein if the tumor tissue exhibits lack of c-Met overexpression the subject is excluded from treatment. The claim, in part, fails to recite an active method step for the subject whose tumor does not have c-Met overexpression defined by ≥25% of the neoplastic cells having 3+ membrane and/or cytoplasmic staining. Thus, the claim in part is simply drawn toto the determination of the percentage of neoplastic cells having 3+ membrane and/or cytoplasmic staining. This judicial exception is not integrated into a practical application because for these subjects, because the measurement of c-Met expression in the neoplastic cells is simply a data gathering step. The claim(s) does/do not include additional elements that are sufficient to amount to significantly more than the judicial exception because the subjects are excluded from receiving the inventive combination of Osimertinib and the anti-cMet conjugate.
Claim Rejections - 35 USC § 112
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 7, 8, 13, 17, 22 and 25 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.
(A)The term “preferably” in claims 13 and 22 renders the claims indefinite because it is unclear how this preference influences the scope of the claims.
(B)Claim 7 is vague ad indefinite in the recitation of “an objective response rate in the subject that is greater than 25%, greater than 30%, greater than 35%, greater than 40%,, greater than 45%, greater than 50%, greater than 55%, greater than 60%, greater than 65% or greater than 70% or more. Claims 13 and 22 are vague and indefinite in the recitation of response rate in the subject of greater than 25%, preferably greater than 35%. Claim 25 is vague and indefinite in the recitation of a response rate greater than 25%. It is unclear how a single subject can have a “response rate”. The terminology “response rate” refers to the number of patient within a group having a defined outcome after receiving the same treatment versus the total number of patients. It does not apply to a single subject. It is unclear what applicant intends to capture in claims 7, 13, 22 and 25.
(C) Claim 8 is vague and indefinite in the recitation of “a media duration of response” in reference to a single subject. A “median” is a term describing a middle value within a range of values. The median can be used to describe a range of response durations within a group of patients. The duration of response of a single patient being treated by the method of claim 1 will not have a median value. It is unclear what applicant intends to capture in claim 8.
(D)The recitation of “subjects” in claim 17 lacks specific antecedent basis in claim 1, requiring a subject in the singular rather than the plural.
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 7-12, and 25 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the enablement requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to enable one skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention.
The factors considered when determining if the disclosure satisfies the enablement requirement and whether any necessary experimentation is undue include, but are not limited to: 1) nature of the invention, 2) state of the prior art, 3) relative skill of those in the art, 4) level of predictability in the art, 5) existence of working examples, 6) breadth of claims, 7) amount of direction or guidance by the inventor, and 8) quantity of experimentation needed to make or use the invention. In re wands, 858 F.2d 731, 737.8 USPQ2d 1400, 1404 (Fed. Cir. 1988).
Claim 7 requires that a human subject treated by the method of claim 1 achieves a certain objective response.
Claim 8 requires that the human subject treated by the method of claim 1 achieves a certain duration of response.
Claim 9 requires that the human subject treated by the method of claim 1 achieves a progression free survival of at least 5 months, at least 5.5 months, at least 6. Month or at least 7.5 months.
Claim 10 requires that the human subject treated by the method of claim 1 achieves an overall survival of at least 16 months or at least 19 months.
Claim 11 requires that the human subject treated by the method of claim 1 achieves a partial response.
Claim 12 requires that the human subject treated by the method of claim 1 achieves complete response.
Claim 25 requires that the human subject treated by the method of claim 24 achieves an objective response and a duration of response of at least 4 months.
In order to satisfy any of claims 7-12, it is necessary that a subject treated by the method of claim 1 has the required response to the treatment. The art teaches that covariates influencing a subjects response to treatment are typically attributed to heterogeneity in oncology populations include age, race, sex, patient performance status, tumor burden, clinical laboratory markers, renal function, renal impairment, liver function, hepatic impairment (Sheng et al, The Journal of Clinical Pharmacology, 2017, Vol. 57, pp. 526-542, see page S36, lines 17-23 under the heading “Exposure-Response Analysis”), metastatic sites at the time of treatment and immune cell score (page S36, second column, lines 15-18). Thus, factors intrinsic to the patient influence the response of the specific patient to anti-cancer therapy
The specification has taught to select a patient who progressed on Osimertinib, wherein the patient tumor has EGFR mutations and c-Met overexpression based on ≥25% of neoplastic cells being 3+ for treatment with Telisotuzumab vedotin combined with Osimertinib. The specification fails to teach a selection of a patient who will achieve a certain objective response, a certain duration of response, progression free survival of at least 5 months, at least 5.5 months, at least 6. Month or at least 7.5 months, overall survival of at least 16 months or at least 19 months, a partial response or a complete response or objective response and a duration of response of at least 4 months.
One of skill in the art would be subject to undue experimentation in order to find an appropriate subject to carry out the methods of claims 7-12 and/or 25,
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
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, 4-6, 14-18, 20, 21, 23, 24, 26, 27-31, 33 are rejected under 35 U.S.C. 103 as being unpatentable over the abstract of Camidge e et al (Annals of Oncology, (September 2020) Vol. 31, Supp. Supplement 4, pp. S894, reference of the IDS filed 9/15/2023) as evidenced by Copeland and Younes (Drugs of the Future, 2010, Vol. 35, page 797), and Fotin-Mleczek et al (WO2017/186928), in view of Chen et al (Molecules 2017, Vol. 22, 28 pages), the abstract of Camidge et al (Cancer Res , 2021, Vol. 81, No. 13 Supplement, abstract no. CT179) and Wang et al (Clinical Cancer Research, 2017, Vol. 23, pp. 992-1000, reference of the IDS submitted 9/15/20).
The abstract of Camidge (2020) et al teaches the administration of the ADC, telisotuzumab vedotin, in combination with Osimertinib in patient with advanced metastatic NSCLC, said patients having progressed while being treated with Osimertinib, wherein the patients tumor exhibited Osimertinib -sensitive EGFR mutations and c-met overexpression define by central IHC in tumor tissue taken after progression on Osimertinib, which meets the same limitation in claims 18 and 31 because after progression on Osimertinib is prior to the administration of the ADC. Copeland and Younes provide evidence that conjugates comprising maleimidocaproyl-Val-Cit-p-aminobenzyloxycarbonyl-MMAE are termed vedotin (Title):
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which meets the limitations of the structure in claims 1, 21, 24, and 27.
Chen et al teach that conventional attachment of a linker-payload is through the cysteine or lysine residues of the antibody (Figure 1, page 2/28). One of skill in the art would understand that the sulfur of the vedotin structure above, is from a cysteine residue of the antibody, thus meeting the requirement for a thioether linkage from an antibody cysteine in claims 1, 21, 24, and 27.
Wang et al provide evidence that ABBV-399 (otherwise known as telisotuzumab vedotin, or ABT-399) has an average drug to antibody ratio of 3.1 (page 994, lines 1-3 under the heading “Binding properties of ABBV-399 for cMet”).
Thus, the telisotuzumab vedotin of the abstract of Camidge (2020) et al meets the limitations of claims 14, 15, 23, 26 with respect to the DAR. The telisotuzumab vedotin of the abstract of Camidge (2020) et al also meets the limitation of n being 2 or 4 in claims 1, 21, 24, 27 in order to accommodate the DAR of 3.1.
Fotin-Mleczek and Hoerr provide evidence that the heavy and light chains of Telisotuzumab vedotin are SEQ ID NO: 1078 and 1079 respectively (page 297) which is identical to the instant SEQ ID NO:5 and SEQ ID NO:10.
ID BEN78246 standard; protein; 445 AA.
XX
AC BEN78246;
XX
DT 11-JAN-2018 (first entry)
XX
DE Cancer treatment Telisotuzumab_vedotin_heavy chain, SEQ 1078.
XX
KW antimicrobial-gen.; autoimmune disease; cancer; cardiovascular disease;
KW cardiovascular-gen.; cytostatic; gene therapy; genetic-disease-gen.;
KW heavy chain; immunosuppressive; infectious disease; monoclonal antibody;
KW monogenic disorder; prophylactic to disease; therapeutic;
KW vaccine, general; viral infection; virucide.
XX
OS Unidentified.
XX
CC PN WO2017186928-A1.
XX
CC PD 02-NOV-2017.
XX
CC PF 28-APR-2017; 2017WO-EP060226.
XX
PR 29-APR-2016; 2016WO-EP059711.
XX
CC PA (CURE-) CUREVAC AG.
XX
CC PI Fotin-Mleczek M, Hoerr I;
XX
DR WPI; 2017-74479H/76.
XX
CC PT New RNA comprises coding sequence, useful for treating or preventing
CC PT cancer (e.g. breast cancer), cardiovascular diseases, neurological
CC PT diseases, infectious diseases, autoimmune diseases, virus diseases or
CC PT monogenetic diseases.
XX
CC PS Claim 24; SEQ ID NO 1078; 780pp; English.
XX
SQ Sequence 445 AA;
ALIGNMENT:
Query Match 100.0%; Score 2380; Length 445;
Best Local Similarity 100.0%;
Matches 445; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 QVQLVQSGAEVKKPGASVKVSCKASGYIFTAYTMHWVRQAPGQGLEWMGWIKPNNGLANY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 QVQLVQSGAEVKKPGASVKVSCKASGYIFTAYTMHWVRQAPGQGLEWMGWIKPNNGLANY 60
Qy 61 AQKFQGRVTMTRDTSISTAYMELSRLRSDDTAVYYCARSEITTEFDYWGQGTLVTVSSAS 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 AQKFQGRVTMTRDTSISTAYMELSRLRSDDTAVYYCARSEITTEFDYWGQGTLVTVSSAS 120
Qy 121 TKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGL 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 121 TKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGL 180
Qy 181 YSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDCHCPPCPAPELLGGPSVF 240
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 181 YSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDCHCPPCPAPELLGGPSVF 240
Qy 241 LFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYR 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 241 LFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYR 300
Qy 301 VVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKN 360
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 301 VVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKN 360
Qy 361 QVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGN 420
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 361 QVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGN 420
Qy 421 VFSCSVMHEALHNHYTQKSLSLSPG 445
|||||||||||||||||||||||||
Db 421 VFSCSVMHEALHNHYTQKSLSLSPG 445
ID BEN78247 standard; protein; 218 AA.
XX
AC BEN78247;
XX
DT 11-JAN-2018 (first entry)
XX
DE Cancer treatment Telisotuzumab_vedotin_light chain, SEQ 1079.
XX
KW antimicrobial-gen.; autoimmune disease; cancer; cardiovascular disease;
KW cardiovascular-gen.; cytostatic; gene therapy; genetic-disease-gen.;
KW immunosuppressive; infectious disease; light chain; monoclonal antibody;
KW monogenic disorder; prophylactic to disease; therapeutic;
KW vaccine, general; viral infection; virucide.
XX
OS Unidentified.
XX
CC PN WO2017186928-A1.
XX
CC PD 02-NOV-2017.
XX
CC PF 28-APR-2017; 2017WO-EP060226.
XX
PR 29-APR-2016; 2016WO-EP059711.
XX
CC PA (CURE-) CUREVAC AG.
XX
CC PI Fotin-Mleczek M, Hoerr I;
XX
DR WPI; 2017-74479H/76.
XX
CC PT New RNA comprises coding sequence, useful for treating or preventing
CC PT cancer (e.g. breast cancer), cardiovascular diseases, neurological
CC PT diseases, infectious diseases, autoimmune diseases, virus diseases or
CC PT monogenetic diseases.
XX
CC PS Claim 24; SEQ ID NO 1079; 780pp; English.
XX
CC The present invention relates to a novel RNA encoding an antibody or a
CC variant, useful for treating or preventing disorder in a subject. The
CC invention further relates to: (1) a combination of at least two distinct
CC RNAs preferably for use in medicine; (2) a composition comprising the RNA
CC and a pharmaceutical carrier; (3) a vaccine comprising the RNA, the
CC pharmaceutical carrier or the composition; (4) a kit; and (5) a method
CC for treating or preventing a disorder which involves administering an
CC amount of the RNA, the composition, the vaccine or the kit to the
CC subject. The disorder includes cancer, cardiovascular disease, infectious
CC disease, autoimmune disease, virus disease or monogenetic disease. The
CC present sequence represents an antibody sequence, which is encoded by the
CC RNA used in treating or preventing the above-mentioned disorders in a
CC subject.
XX
SQ Sequence 218 AA;
ALIGNMENT:
Query Match 100.0%; Score 1127; Length 218;
Best Local Similarity 100.0%;
Matches 218; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 DIVMTQSPDSLAVSLGERATINCKSSESVDSYANSFLHWYQQKPGQPPKLLIYRASTRES 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DIVMTQSPDSLAVSLGERATINCKSSESVDSYANSFLHWYQQKPGQPPKLLIYRASTRES 60
Qy 61 GVPDRFSGSGSGTDFTLTISSLQAEDVAVYYCQQSKEDPLTFGGGTKVEIKRTVAAPSVF 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 GVPDRFSGSGSGTDFTLTISSLQAEDVAVYYCQQSKEDPLTFGGGTKVEIKRTVAAPSVF 120
Qy 121 IFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLS 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 121 IFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLS 180
Qy 181 STLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC 218
||||||||||||||||||||||||||||||||||||||
Db 181 STLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC 218
which meets the limitations of SEQ ID NO:5 and 10 in claims 1, 21, 24, and 27.
Thus, one of skill in the art would understand that the instant claims are drawn to Telisotuzumab vedotin.
Thus, the telisotuzumab vedotin of the abstract of Camidge (2020) et al meets the structural requirement of the claims, in addition to the combination with Osimertinib and the requirement for patients with NSLC with (i) disease which progressed while on Osimertinib, (ii) tumor tissue which overexpresses c-Met, and (iii) and patients with Osimertinib-sensitive EGFR mutations. The abstract of Godman et al teaches the intravenous administration every two weeks of Teliso-V (telisotuzumab vedotin) at 1.6 mg/kg, escalated to 1.9 mg/kg, combined with daily oral Osimertinib at 80 mg which meets the limitations of claims 16 and 17 , and the dosage limitation in claim 23. The abstract of Camidge (2020) et al teaches that the combination with Osimertinib is “Arm E” of the phase 1/1b trial NCT02099058.
The abstract of Camidge (2020) et al do not teach that the NSCLC is non-squamous NSCLC. The abstract of Camidge (2020) et al teaches that the combination with Osimertinib is Arm E of the clinical trial NCT 02099058. The abstract of Camidge (2020) et al do not teach that high expression of c-Met is ≥25% of neoplastic cells having ≥1+ membrane or cytoplasmic staining by IHC.
The abstract of Camidge et al teaches monotherapy with telisotuzumab vedotin wherein membrane staining of 25% +3 was considered positive for non-squamous NSLCL with mutant EGFR (Table) . The abstract teaches that enrollment into the squamous cohort was stopped, but that enrollment into the non-squamous cohort with EGFR mutation was continued.
It would have been prima facie obvious at the time prior to the effective filing date to treat subjects with non-squamous NSLC by the method of the abstract of Camidge (2020) et al wherein said patients were determined to have high expression of c-Met at ≥25% of neoplastic cells having 3+ staining, meeting the limitation of ≥25% of neoplastic cells from the tumor tissue have a ≥1+ membrane staining in claims 1, and 27; a ≥2+ membrane staining in claims 4 and 28; and a 3+ membrane staining in claims 5, 21, 24, and 29. One of skill in the art would have been motivated to do so by the abstract of Camidge (2020) that teaches membrane staining of 25% +3 was considered positive for non-squamous NSLCL and the further teachings of the abstract on the continuing treatment of patients with non-squamous NSLCL but the discontinuation of treatment of patients with squamous NSCLC.
Regarding claims 6 and 30, it would have been prima facie obvious to include subjects having ≥50% of neoplastic cells from tumor tissue having 3+ staining because the abstract of Camidge et al teaches that subjects with ≥50% 3+ staining in EGFR mutant included confirmed responses (Table).
Regarding claims 20 and 33, Wang et al teach that the IHC to determine c-Met expression was done using CONFIRM anti-c-Met(SP-44) rabbit monoclonal primary antibody on the Ventana Benchmark Autostainer according to the manufacture’s protocol (page 994, under “IHC”). The instant specification defines the Teliso-V staining protocol as
the “c-Met Teliso-V staining protocol.” Briefly, a c-Met IHC staining assay for c-Met overexpression was developed using the Ventana c-Met CONFIRM (SP44) kit (Catalog Number 790-4430) which uses the UltraView detection system, and is contemplated for use in the selection of patients for treatment with Teliso-V. In this assay, tissue samples are stained with the Ventana anti-c-Met antibody and then scored by determining the percentages of neoplastic cells of the tumor tissue that stain at certain intensity levels from weak/low to strong/high (i.e., 0, 1+, 2+, to 3+). This assay produces staining of the c-Met protein both in the cytoplasm and in the cell membrane, of which the membranous staining and/or cytoplasmic staining is used in IHC score determination.
Thus, the method of Wang et al is the same as the instant method claimed.
It would have been prima facie obvious to use said protocol to determine if ≥25% neoplastic cells stained at 0, 1, 2 or 3 intensity. One of skill in the art would have been motivated to use the assay of Wang et al because it reports both percent positivity and intensity which is necessary to determine c-Met high expression
Claims 1, 4-6, 14-18, 20, 21, 23, 24, 26, 27-31, 33 are rejected under 35 U.S.C. 103 as being unpatentable over the abstract of Camidge (2020) et al, Copeland and Younes, Fotin-Mleczek et al, Wang et al, Chen et al and the abstract of Camidge et al (2021) as applied to claims 1, 4-6, 14-18, 20, 21, 23, 24, 26, 27-31, 33 above, and further in view of Strickler et al (journal of Clinical Oncology, 2018, Vol, 36, pp. 3298-3306, reference of the IDS filed 9/15/2023).
Claims 19 and 32 require that the subject has received prior systemic therapy in the locally advanced or metastatic setting in the methods of claims 1 and 27, respectively
The combined teachings of the abstract of Camidge (2020) et al, Copeland and Younes, Fotin-Mleczek et al, Wang et al, Chen et al and the abstract of Camidge et al render obvious instant claims 1, 4-6, 14-18, 20, 21, 23, 24, 26, 27-31, 33 for the reason set forth above. None of the abstract of Camidge (2020) et al, Copeland and Younes, Fotin-Mleczek et al, Wang et al, Chen et al nor the abstract of Camidge et al tech that the subject has received prior systemic therapy in the locally advanced or metastatic setting.
The abstract of Camidge (2020) et al teaches that the combination with Osimertinib is “Arm E” of the phase 1/1b trial NCT02099058.
Strickler et al teach that all patients in the NCT 02099058 trial were refractory to standard therapies and had received a median of three prior therapies for metastatic disease (page 3302, second column, lines 8-11) which renders obvious the limitations of claims 19 and 32 because the abstract of Camidge (2020) et al teach the addition of Osimertinib was Arm E within the NCT 02099058 trial. Thus, if all patients within the NCT 02099058 trial received a median of three prior therapies for metastatic disease, then all patients being treated with Osimertinib and telisotuzumab vedotin in Arm E had received a median of three prior therapies for metastatic disease
Claims 1-6, 14-18, 20, 21, 23, 24, 26, 27-31, 33 are rejected under 35 U.S.C. 103 as being unpatentable over the abstract of Camidge (2020) et al, Copeland and Younes, Fotin-Mleczek et al, Wang et al, Chen et al and the abstract of Camidge et al as applied to claims 1, 4-6, 14-18, 20, 21, 23, 24, 26, 27-31, 33 above, and further in view of Schmid et al (Lung Cancer, 2020, Vol. 147, pp. 123-129).
Claim 2 requires that the mutated EGFR gene comprises an exon 19 deletion, or an exon 21 L858R mutation. Claim 3 requires that the mutated EGFR gene comprises a T790M mutation.
The abstract of Camidge (2020) et al teaches that the patients had a documented Osimertinib-sensitive EGFR mutation. None of abstract of Camidge (2020) et al, Copeland and Younes, Fotin-Mleczek et al, Wang et al, Chen et al nor the abstract of Camidge et al tech that the subject has an exon 19 deletion, or an exon 21 L858R mutation, and a T790M mutation.
Schmid et al teach that Osimertinib is selective for the EGFR mutation T790M Osimertinib resistance mutation (page 124, second column, lines 2-3 of the bottom paragraph). Schmid et al teach an exon 21 L858R mutation (page 124, lines 10-14 under the heading “Mechanisms of resistance”).
It would have been prima facie obvious a the time prior to the effective filing date that patients with the T790M and L858R mutations were included in the method of claim 1. One of skill in the art would have been motivated to do so because the abstract of Camidge (2020) teaches that the patients must have documented evidence of Osimertinib-sensitive EGFR mutations, and Schmid et al teach T790M and L858R as Osimertinib-sensitive EGFR mutations.
All claims are rejected.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to KAREN A CANELLA whose telephone number is (571)272-0828. The examiner can normally be reached M-F 10-6:30.
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KAREN A. CANELLA
Examiner
Art Unit 1643
/Karen A. Canella/Primary Examiner, Art Unit 1643