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
1. Claims 1-20 are pending in the current application.
2. This application is a 371 of PCT/US2022/032774 06/09/2022; PCT/US2022/032774 has PRO 63/208,625 06/09/2021.
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.
3. Claim(s) 1-16, is/are rejected under 35 U.S.C. 102 (a)(1) as anticipated by Bauer WO 2018111707 A1 (cited on the IDS). According to page 4, lines 5-11, “Another aspect of the present invention provides a compound of Formula I or Ia, or a pharmaceutically acceptable salt thereof, for use in the treatment of a cancer expressing mutant IDH1 or mutant IDH2 which is glioma, glioblastoma, glioblastoma multiforme, astrocytomas, oligodendrogliomas, paraganglioma, fibrosarcoma, angioimmunoblastic T-cell lymphoma (AITL), myelodysplastic syndrome (MDS), B cell acute lymphoblastic leukemia (B-ALL), thyroid cancer, colorectal cancer, acute myeloid leukemia (AML), melanoma, prostate cancer, chondrosarcoma or cholangiocarcinoma.” These include specific cancers in claim 8 and 9. Most are solid tumors as per claim 7, i.e. glioma, glioblastoma, astrocytoma, oligodendroglioma, paraganglioma, fibrosarcoma, thyroid cancer, colorectal cancer, melanoma, prostate cancer, chondrosarcoma, and cholangiocarcinoma. Some are hematologic cancers (liquid tumors) of claim 11, e.g. AML, B-ALL, and AITL. AML appears in claims 12-14. According to page 4 lines 28-30 “The term "patient" means mammal and "mammal" includes, but is not limited to, a human.” Specific examples of the Formula I or Ia used in the cancer treatment method are disclosed on page 39 and the following Table 11. The first compound of claim 4 is disclosed on page 39:
PNG
media_image1.png
205
534
media_image1.png
Greyscale
The second compound in claim 4, which is the compound of claims 5-6, is Example 2 on page 40 Table 11:
PNG
media_image2.png
108
584
media_image2.png
Greyscale
The third compound in claim 4 is the compounds 11/121 on page 41-42:
PNG
media_image3.png
131
578
media_image3.png
Greyscale
PNG
media_image4.png
151
577
media_image4.png
Greyscale
Various pharmaceutical salts are described on page 6 lines 12 ff. and were exemplified including but not limited to the sulfate of compound 2 on page 46 as example 15, and the 4-hydroxybenzoate on page 46 as example 16.
According to page 59 lines 17 ff,
The following in vitro and in vivo studies demonstrate the mutant IDH1 and IDH2 protein inhibitory activity and efficacy of the tested compounds of Formula I or Ia against various specific cancer cell lines. These assays are generally recognized by those skilled in the art as indicative of human clinical therapeutic activity. Inhibition of mutant IDH1 or IDH2 neomorphic proteins in the disclosed studies is believed will be effective against further mutant IDH1 and IDH2 neomorphic proteins. Assays evidencing mutant IDH1 or IDH2 inhibitory activity and efficacy may be carried out substantially as follows or by similar assays affording similar data. The results of the following assays demonstrate that the compounds exemplified and tested are useful as IDH1 and IDH2 mutant inhibitors and may be useful in treating cancers expressing mutant IDH1 or IDH2.
Lines 30 ff. on page 60 states, “The results of this assay demonstrate that the exemplified and tested compounds inhibit mutant IDH1 activity against IDH1/R132H and IDH1/R132C and inhibit mutant IDH2 activity against IDH2/R140Q and IDH2/R172K”. Page 61 shows activity at the claimed mutants in the last two columns.
PNG
media_image5.png
221
594
media_image5.png
Greyscale
PNG
media_image6.png
99
550
media_image6.png
Greyscale
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.
4. Claim(s) 19-20 is/are rejected under 35 U.S.C. 103 as being unpatentable over Bauer WO 2018111707 A1 as applied to claims 1-16, above, and further in view of Petiti “Highly Sensitive Detection of IDH2 Mutations in Acute Myeloid Leukemia J. Clin. Med. 2020, 9, 271. With respect to claim 19, according to Bauer page 6, line 4 ff:
The compound of Formula I or Ia, or a pharmaceutically acceptable salt, may be administered either simultaneously with, or before, or after, one or more other therapeutic agents. The compound of Formula I or Ia, or a pharmaceutically acceptable salt, when administered with one or more other therapeutic agents, may be administered separately, by the same or different route of administration, or together in the same pharmaceutical composition as the other therapeutic agent(s). Where one or more additional therapeutic agents are administered, the administration of each therapeutic agent may be simultaneous, separate, or sequential.
Claim 20 is drawn to the use of enasidenib for the treatment before the compounds of Bauer. Bauer does not mention enasidenib. According to Petiti page 2 lines 3-5, “The Food and Drug Administration has recently approved Enasidenib, a specific molecular inhibitor for patients with AML with mutated IDH2”. Combining two things known for the same purpose, treating cancer, is obvious. See In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980) (MPEP § 2144.06). This is especially true in oncology where drugs are constantly combined.
5. Claim(s) 17-18 is/are rejected under 35 U.S.C. 103 as being unpatentable over Bauer WO 2018111707 A1 as applied to claims 1-16, above, and further in view of Intlekofer “Acquired resistance to IDH inhibition through trans or cis dimer-interface mutations.” Nature (London, United Kingdom), 2018, 559(7712), 125-129 (cited on the IDS). Claims 17-18 are drawn to treating patients with mutations additional mutations in the IDH2 enzymes, including Q316E and I319M. Intlekofer explains that these mutations arise in patients treated with the approved drug enasidenib. “We investigated two patients with IDH2-mutant AML who developed acquired resistance to enasidenib, hypothesizing that we could identify molecular mechanisms of resistance to small-molecule IDH inhibition.” Page 126 col 1 last paragraph explains how such mutations arise:
We hypothesized that clinical resistance to enasidenib in the setting of a progressive increase in 2HG levels might be due to acquisition of a new somatic mutation that mediates drug resistance. In both cases, we identified new mutations in the IDH2 gene at the time of acquired resistance, missense mutations that resulted in a substitution of glutamine 316 with glutamate (Q316E) in the first patient and substitution of isoleucine 319 with methionine (I319M) in the second patient (Fig. 1d, h). Droplet digital PCR (ddPCR) (Extended Data Table 1) demonstrated the secondary IDH2 mutations were not detectable before treatment with enasidenib. Thus, the secondary IDH2 mutations were either acquired during the course of treatment or originated in a rare subclone that was below the limit of detection of the ddPCR assay.
The identification of second-site mutations in IDH2 in the setting of acquired resistance to enasidenib therapy raised the possibility of a resistance mechanism similar to those previously reported for tyrosine kinases such as BCR-ABL and EGFR13–16. The Q316E and I319M mutations are encoded in exon 7 of the IDH2 gene, whereas the neomorphic R140Q mutation is encoded upstream in exon 4 (Fig. 2a). To determine the allelic conformation of the different IDH2 mutations, we performed long-range PCR amplification of genomic DNA spanning exons 4–7 of IDH2 followed by subcloning and sequence analysis of individual clones (Fig. 2a–c).
“The expression of either of these mutant disease alleles alone did not induce the production of 2HG; however, the expression of the Q316E or I319M mutation together with the R140Q mutation in trans allowed 2HG production that was resistant to inhibition by enasidenib.” (abstract). Since the patients are resistant to enasidenib, it would be obvious to treat them with the additional compounds of Bauer inhibiting these mutant enzymes generated by enasidenib therapy.
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 claims at issue 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); and 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 a nonstatutory double patenting ground provided the reference application or patent either is shown to be commonly owned with this application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The USPTO internet Web site contains terminal disclaimer forms which may be used. Please visit http://www.uspto.gov/forms/. The filing date of the application will determine what form 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 http://www.uspto.gov/patents/process/file/efs/guidance/eTD-info-I.jsp.
6. Claims 1-16 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-8 of U.S. Patent No. 11,001,596. Although the claims at issue are not identical, they are not patentably distinct from each other because the compounds in claim 1 are the same as those in the method claim 1 and the compounds in claims 2, 5, 8 are in claims 3-6. The method of the instant claims is disclosed in the specification of the ‘596 patent as discussed in the rejection over Bauer.2 Such a disclosure in the specification makes the method obvious over the compound claims; see Sun Pharmaceutical Industries v. Eli Lilly and Co., 611 F.3d 1381, 1389 (2010). As per MPEP 804 II. (B) (2) (a): “In AbbVie Inc. v. Kennedy Institute of Rheumatology Trust, 764 F.3d 1366, 112 USPQ2d 1001 (Fed. Cir. 2014), the court explained that it is also proper to look at the disclosed utility in the reference disclosure to determine the overall question of obviousness in a nonstatutory double patenting context. See Pfizer, Inc. v. Teva Pharm. USA, Inc., 518 F.3d 1353, 86 USPQ2d 1001 (Fed. Cir. 2008); Geneva Pharmaceuticals Inc. v. GlaxoSmithKline PLC, 349 F3d 1373, 1385-86, 68 USPQ2d 1865, 1875 (Fed. Cir. 2003).” In Geneva Pharmaceuticals Inc. v. GlaxoSmithKline PLC, 349 F.3d 1373, 1385-86, 68 USPQ2d 1865, 1875 (Fed. Cir. 2003), the earlier patent claimed a compound and the written description disclosed the utility of that compound. The later patent claimed nothing more than the earlier patent’s disclosed utility as a method of using the compound. Thus, the court found that the claims of the later patent and the claims of the earlier patent were not patentably distinct. The instant application is not related to the application and as such the safe harbor provision of 35 U.S.C 121 does not apply to this relationship.
7. Claims 1-16 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-3 of U.S. Patent No. 11,649,247. Although the claims at issue are not identical, they are not patentably distinct from each other because the compounds in claim 1 are the same as those in the method claim 1 and the compounds in claim 2 are the first two compounds in claim 4. The method of the instant claims is disclosed in the specification of the ‘247 patent as discussed in the rejection over Bauer.3 Such a disclosure in the specification makes the method obvious over the compound claims; see Sun Pharmaceutical Industries v. Eli Lilly and Co., 611 F.3d 1381, 1389 (2010). As per MPEP 804 II. (B) (2) (a): “In AbbVie Inc. v. Kennedy Institute of Rheumatology Trust, 764 F.3d 1366, 112 USPQ2d 1001 (Fed. Cir. 2014), the court explained that it is also proper to look at the disclosed utility in the reference disclosure to determine the overall question of obviousness in a nonstatutory double patenting context. See Pfizer, Inc. v. Teva Pharm. USA, Inc., 518 F.3d 1353, 86 USPQ2d 1001 (Fed. Cir. 2008); Geneva Pharmaceuticals Inc. v. GlaxoSmithKline PLC, 349 F3d 1373, 1385-86, 68 USPQ2d 1865, 1875 (Fed. Cir. 2003).” In Geneva Pharmaceuticals Inc. v. GlaxoSmithKline PLC, 349 F.3d 1373, 1385-86, 68 USPQ2d 1865, 1875 (Fed. Cir. 2003), the earlier patent claimed a compound and the written description disclosed the utility of that compound. The later patent claimed nothing more than the earlier patent’s disclosed utility as a method of using the compound. Thus, the court found that the claims of the later patent and the claims of the earlier patent were not patentably distinct. The instant application is not related to the application and as such the safe harbor provision of 35 U.S.C 121 does not apply to this relationship.
8. Claims 1-16 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6 of U.S. Patent No. 11,629,156. Although the claims at issue are not identical, they are not patentably distinct from each other because the method of treating the cancers is the subject of patent claim 1, which are said to be mutant IDH2 cancers. Claims 4 and 5 are drawn to the compounds of claim 4-6 in the method. As to what constitutes a mutant, col. 59 and 60 list the claimed mutants at lines 24-ff and show in Table 14 that they are active at the claimed mutants in the last 2 columns. It is appropriate to consult the specification to determine the meaning of the claimed mutants.
9. Claims 19-20 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-8 of U.S. Patent No. 11,001,596 as applied to claims 1-16 above and further in view of Petiti “Highly Sensitive Detection of IDH2 Mutations in Acute Myeloid Leukemia J. Clin. Med. 2020, 9, 271. Claim 20 is drawn to the used of enasidenib for the treatment before the compounds of ‘596. The ‘596 does not mention enasidenib. According to Petiti page 2 lines 3-5, “The Food and Drug Administration has recently approved Enasidenib, a specific molecular inhibitor for patients with AML with mutated IDH2”. Combining two things known for the same purpose, treating cancer, is obvious. See In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980) (MPEP § 2144.06). This is especially true in oncology where drugs are constantly combined.
10. Claims 19-20 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6 of U.S. Patent No. 11,629,156 as applied to claims 1-16 above and further in view of Petiti “Highly Sensitive Detection of IDH2 Mutations in Acute Myeloid Leukemia J. Clin. Med. 2020, 9, 271. Claim 20 is drawn to the used of enasidenib for the treatment before the compounds of ‘156. The ‘156 does not mention enasidenib. According to Petiti page 2 lines 3-5, “The Food and Drug Administration has recently approved Enasidenib, a specific molecular inhibitor for patients with AML with mutated IDH2”. Combining two things known for the same purpose, treating cancer, is obvious. See In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980) (MPEP § 2144.06). This is especially true in oncology where drugs are constantly combined.
11. Claims 19-20 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-3 of U.S. Patent No. 11,649,247 as applied to claims 1-16 above and further in view of Petiti “Highly Sensitive Detection of IDH2 Mutations in Acute Myeloid Leukemia J. Clin. Med. 2020, 9, 271. Claim 20 is drawn to the used of enasidenib for the treatment before the compounds of ‘247. The ‘247 does not mention enasidenib. According to Petiti page 2 lines 3-5, “The Food and Drug Administration has recently approved Enasidenib, a specific molecular inhibitor for patients with AML with mutated IDH2”. Combining two things known for the same purpose, treating cancer, is obvious. See In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980) (MPEP § 2144.06). This is especially true in oncology where drugs are constantly combined.
12. Claim(s) 17-18 i are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-3 of U.S. Patent No. 11,649,247 as applied to claims 1-16 above and further in view of Intlekofer “Acquired resistance to IDH inhibition through trans or cis dimer-interface mutations.” Nature (London, United Kingdom), 2018, 559(7712), 125-129. Claims 17-18 are drawn to treating patients with additional mutations in the IDH2 enzymes, including Q316E and I319M. Intlekofer explains that these mutations arise in patients treated with the approved drug enasidenib. “We investigated two patients with IDH2-mutant AML who developed acquired resistance to enasidenib, hypothesizing that we could identify molecular mechanisms of resistance to small-molecule IDH inhibition.” Page 126 col 1 last paragraph explains how such mutations arise as discussed above. Since the patients are resistant to enasidenib, it would be obvious to treat them with the additional compounds of the ‘247 patent.
13. Claim(s) 17-18 i are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-8 of U.S. Patent No. 11,001,596 as applied to claims 1-16 above and further in view of Intlekofer “Acquired resistance to IDH inhibition through trans or cis dimer-interface mutations.” Nature (London, United Kingdom), 2018, 559(7712), 125-129. Claims 17-18 are drawn to treating patients with additional mutations in the IDH2 enzymes, including Q316E and I319M. Intlekofer explains that these mutations arise in patients treated with the approved drug enasidenib. “We investigated two patients with IDH2-mutant AML who developed acquired resistance to enasidenib, hypothesizing that we could identify molecular mechanisms of resistance to small-molecule IDH inhibition.” Page 126 col 1 last paragraph explains how such mutations arise as discussed above. Since the patients are resistant to enasidenib, it would be obvious to treat them with the additional compounds of the ‘596 patent.
14. Claim(s) 17-18 i are rejected on the ground of nonstatutory double patenting as being unpatentable over 1-6 of U.S. Patent No. 11,629,156 as applied to claims 1-16 above and further in view of Intlekofer “Acquired resistance to IDH inhibition through trans or cis dimer-interface mutations.” Nature (London, United Kingdom), 2018, 559(7712), 125-129. Claims 17-18 are drawn to treating patients with additional mutations in the IDH2 enzymes, including Q316E and I319M. Intlekofer explains that these mutations arise in patients treated with the approved drug enasidenib. “We investigated two patients with IDH2-mutant AML who developed acquired resistance to enasidenib, hypothesizing that we could identify molecular mechanisms of resistance to small-molecule IDH inhibition.” Page 126 col 1 last paragraph explains how such mutations arise as discussed above. Since the patients are resistant to enasidenib, it would be obvious to treat them with the additional compounds of the ‘156 patent.
15. Claims 1-16 provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-15 of copending Application No. 17/911,746 in view of Bauer. Although the claims at issue are not identical, they are not patentably distinct from each other because the copending claims are drawn to treating IDH1 mutant cancers, while the instant claims are drawn to cancers with certain IDH2 mutations with the same compounds. Bauer explains that the compounds treat cancers with both types of mutants, “Another aspect of the present invention provides a compound of Formula I or Ia, or a pharmaceutically acceptable salt thereof, for use in the treatment of a cancer expressing mutant IDH1 or mutant IDH2…” Bauer discloses treating the specific claimed mutants. Lines 30 ff. on page 60 state, “The results of this assay demonstrate that the exemplified and tested compounds inhibit mutant IDHI activity against IDH1/R132H and IDH1/R132C and inhibit mutant IDH2 activity against IDH2/R140Q and IDH2/R172K”. The compounds treat the same tumors, which could harbor all these mutations at the same time. The artisan or ordinary skill would give the compounds to any patient having AML with any of these mutations.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
16. Claims 17-20 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-15 of copending Application No. 17/911,746 in view of Bauer as applied to claims 1-16 above and further in view of Intlekofer and Petiti “Highly Sensitive Detection of IDH2 Mutations in Acute Myeloid Leukemia J. Clin. Med. 2020, 9, 271. Claims 17-18 are drawn to treating patients with additional mutations in the IDH2 enzymes, including Q316E and I319M. Intlekofer explains that these mutations arise in patients treated with the approved drug enasidenib. “We investigated two patients with IDH2-mutant AML who developed acquired resistance to enasidenib, hypothesizing that we could identify molecular mechanisms of resistance to small-molecule IDH inhibition.” Page 126 col 1 last paragraph explains how such mutations arise as discussed above. Since the patients are resistant to enasidenib, it would be obvious to treat them with the additional compounds. Petiti on page 126 explains, “For these reasons, it is mandatory to monitor IDH2 mutations to better characterize AML patients.” As such one would look to characterize the mutants in each patient. Claims 19-20 are drawn to using another IDH@ inhibitor. Claim 20 is drawn to the used of enasidenib for the treatment before the compounds of ‘247. The ‘247 does not mention enasidenib. According to Petiti page 2 lines 3-5, “The Food and Drug Administration has recently approved Enasidenib, a specific molecular inhibitor for patients with AML with mutated IDH2”. Combining two things known for the same purpose, treating the same cancer, is obvious. See In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980) (MPEP § 2144.06). This is especially true in oncology where drugs are constantly combined.
Conclusion
17. Any inquiry concerning this communication or earlier communications from the examiner should be directed to DAVID K O'DELL whose telephone number is (571)272-9071. The examiner can normally be reached on Monday - Friday 9:30 - 7:00 PM.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Clinton Brooks can be reached on 571-270-7682. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of an application may be obtained from Patent Center. Status information for published applications may be obtained from Patent Center. Status information for unpublished applications is available through Patent Center for authorized users only. Should you have questions about access to Patent Center, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free).
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) Form at https://www.uspto.gov/patents/uspto-automated- interview-request-air-form.
/DAVID K O'DELL/Primary Examiner, Art Unit 1621
1 The name in claim 4 lacks a stereochemical descriptor for a carbon, and therefore includes both epimers, compounds 11/12.
2 Bauer is the WIPO Publication of the 371 national stage entry 16/349,873 which is the application from which the ‘596 issued. The citations in the 102 rejection over correspond to Bauer as follows, (page 4, lines 5-11: col. 2 lines 52 -63; page 4 lines 28-30: col. 3 lines 42-43; Page 39-42 Table 11: col. 42-46; page 6 lines 12 ff.: col. 4 lines 13-21; page 46: col 59-60; Page 60 Table 14: col. 61.)
3 Bauer is the WIPO Publication of the 371 national stage entry 16/349,873 which is the parent application of the 17/202,515 application from which the ‘247 issued. The citations in the 102 rejection over correspond to Bauer as follows, (page 4, lines 5-11: col. 2 lines 52 -63; page 4 lines 28-30: col. 3 lines 42-43; Page 39-42 Table 11: col. 42-46; page 6 lines 12 ff.: col. 4 lines 13-21; page 46: col 59-60; Page 60 Table 14: col. 61.)
Prosecution Insights