Ex Parte Gevas et al

Patent Trial and Appeal BoardJul 26, 2016

13012433 (P.T.A.B. Jul. 26, 2016)

UNITED STA TES p A TENT AND TRADEMARK OFFICE APPLICATION NO. FILING DATE 13/012,433 01124/2011 25297 7590 07/28/2016 Jenkins, Wilson, Taylor & Hunt, P.A. 3100 Tower Blvd. Suite 1200, University Tower Durham, NC 27707 FIRST NAMED INVENTOR Philip C. Gevas UNITED STATES DEPARTMENT OF COMMERCE United States Patent and Trademark Office Address: COMMISSIONER FOR PATENTS P.O. Box 1450 Alexandria, Virginia 22313-1450 www .uspto.gov ATTORNEY DOCKET NO. CONFIRMATION NO. 1734/10/11/3 CON 6775 EXAMINER SANG, HONG ART UNIT PAPER NUMBER 1643 NOTIFICATION DATE DELIVERY MODE 07/28/2016 ELECTRONIC Please find below and/or attached an Office communication concerning this application or proceeding. The time period for reply, if any, is set in the attached communication. Notice of the Office communication was sent electronically on above-indicated "Notification Date" to the following e-mail address( es): usptomail@jwth.com mmcjunkin@jwth.com PTOL-90A (Rev. 04/07) UNITED STATES PATENT AND TRADEMARK OFFICE BEFORE THE PATENT TRIAL AND APPEAL BOARD Ex parte PHILIP C. GEV AS, DOV MICHAELI, and STEPHEN GRIMES Appeal2014-004349 Application 13/012,433 1 Technology Center 1600 Before ULRIKE W. JENKS, JOHN G. NEW, and ELIZABETH A. LA VIER, Administrative Patent Judges. LA VIER, Administrative Patent Judge. DECISION ON APPEAL This is an appeal pursuant to 35 U.S.C. Â§ 134(a) of the Examiner's rejections of claims 1-5, 8-14, and 16-19. We have jurisdiction under 35 U.S.C. Â§ 6(b). For the reasons set forth below, we AFFIRM. 1 Appellants state the real party in interest is Cancer Advances, Inc. Br. 2. Appeal2014-004349 Application I3/0I2,433 The Specification describes treatment of lung and other cancers by immunizing a patient against gastrin or a gastrin receptor. See Spec. 6. Claim I is illustrative: A method for the treatment of a cancerous condition of the lung or esophagus, comprising: identifying a patient with a cancerous condition of the lung or esophagus; and administering to the patient an immunogen that induces antibodies in the patient against gastrin I 7 (GI 7), wherein: the antibodies inhibit the binding of GI 7 to its receptor on cancerous cells; the cancerous condition is gastrin-induced or dependent; and the cancerous condition of the lung is a primary non- small cell cancerous condition. Br. 33 (Claims Appendix). Claims 2, 3, I3, and I4 are also independent, and also recite methods for treating non-small cell lung cancer involving GI 7, whether by administering anti-GI 7 antibodies (claims 2 and I3) or an immunogen that elicits anti-GI 7 antibodies (claim 3), or either/both (claim I4). See Br. 33- 36 (Claims Appendix). Claims 3 and I3 specify that the cancer is gastrin- induced or gastrin-dependent. See id. Claim I 4 further recites administering docetaxel concomitantly or sequentially with the anti-gastrin immunotherapy. See id. Treatment with one or more of several chemotherapy agents is also recited in dependent claim 8. Certain dependent claims specify the amino acid sequences for the GI 7 immunogen (e.g., claims 9 and I 0) or the epitopes to which the anti-GI 7 antibodies bind 2 Appeal2014-004349 Application 13/012,433 (e.g., claim 13). Some dependent claims also identify spacer sequences and/or carriers for the immunogen (e.g., claims 10 and 11). REJECTIONS ON APPEAL 1. Claims 1-5, 8-14, and 16-19 are rejected under 35 U.S.C. Â§ 103(a) as unpatentable over Gevas '628,2 Gevas '970, 3 Zhou,4 and Belani. 5 Final Action 3-6. 2. Claims 1-5, 8-14, and 16-19 are rejected for non-statutory, obviousness-type double patenting over claims 7 and 8 of Gevas '970, in view of Gevas '628, Zhou, and Belani. Final Action 6-7. DISCUSSION A. Obviousness The Examiner relies on Gevas '628 to teach gastrin dependence of several tumor types, as well as treating such tumors by actively or passively immunizing a patient with anti-G 17 immunogen, and by treating the patient with one or more chemotherapy agents, such as 5-fluorouracil and leucovorin. Ans. 4 (citing Gevas '628 1-2, 6; claims 1--4, 8). Gevas '628 further teaches particular anti-G 17 immunogen sequences, conjugates, and a spacer. See id. at 5 (citing Gevas '628 8:3-14, 10:10-15; claims). Similarly, the Examiner also relies on Gevas '970 as teaching administering anti-G 17 antibodies to inhibit G 17 from binding to receptors on tumors, and 2 Gevas et al., WO 99/59628, published Nov. 25, 1999. 3 Gevas et al., US Patent No. 5,785,970, issued July 28, 1998. 4 Zhou et al., Pre- and Postoperative Sequential Study on the Serum Gastrin Level in Patients With Lung Cancer, 51 J. Surgical Oncology 22-25 (1992). 5 Belani, Paclitaxel and Docetaxel Combinations in Non-Small Cell Lung Cancer, 117 Chest 144--151 (2000). 3 Appeal2014-004349 Application 13/012,433 particularly certain immunogen sequences, conjugates, and a spacer. See id. at 6 (citing Gevas '970 5:50-56, 7:3-10; Examples 1, 4; claim 11). Neither Gevas reference identifies non-small cell lung cancer as gastrin dependent, however (see id. at 5); for this, the Examiner turns to Zhou. As the Examiner explains, Zhou describes elevated serum gastrin levels in patients with various types of lung cancer: squamous cell carcinoma, adenocarcinoma, and small cell carcinoma (see id. at 6 (citing Zhou 25, Tables I, V)). Zhou also reports the decrease and return to normal of serum gastrin levels following surgical removal of the cancer, and teaches that the likely cause of high serum gastrin in lung cancer patients is the gastrin- producing property of the lung cancer cells. See id. at 6-7 (citing Zhou Abstract, 24, Fig. 1 ). Finally, the Examiner relies on Belani to teach using docetaxel, alone or in combination with other therapies, to treat patients with non-small cell lung cancer. Id. at 7 (citing Belani 146S). The Examiner concludes it would have been obvious to use the anti- G 17 immunogenic compositions as described in Gevas '628 and Gevas '970 to treat non-small cell lung cancers because of Zhou's teaching that patients with such cancers have significantly elevated serum levels of gastrin and Zhou's further teaching that these higher gastrin levels are probably due to the gastrin-producing properties of lung cancer cells. See Ans. 7-8 (citing Zhou Abstract). Appellants argue that there would have been no reasonable expectation of success from combining the references as claimed. Br. 6. Specifically, Appellants argue that Zhou teaches using gastrin levels as a diagnostic measure, not as a therapeutic target, and further that Zhou teaches only surgery, not immunotherapy. See id. at 7. Appellants dispute the 4 Appeal2014-004349 Application 13/012,433 Examiner's interpretation of the data in Zhou, accusing the Examiner of "improper unwarranted extrapolation," id. at 10, because much of the analysis in Zhou refers to lung cancer patients generally, including those afflicted with small cell cancer. See id. at 7-11. We have considered each of Appellants' attempts to discredit the Examiner's analysis of Zhou, and find ourselves unpersuaded. Although Zhou includes data for lung cancer patients generally, Zhou also includes a breakdown by cancer type. As the Examiner explains: Furthermore, Zhou et al disclose that there is a statistically significant difference (p<0.05) between squamous cell carcinoma and adenocarcinoma (see page 23, last paragraph). If the difference between squamous cell carcinoma (81.88Â±11.42 ng/L) and adenocarcinoma (134.44Â±14.28 ng/L) is statistically significant, the difference between normal subject (29.37Â±1.1 Ong/L) and adenocarcinoma (134.44Â±14.28 ng/L) would have been even more significant. Ans. 18 (discussing Zhou Tables I, V). Furthermore, Appellants' assertion that the "raw data concerning serum gastrin levels [are] non-informative" (Br. 9), because a few non-lung cancer patients had higher serum gastrin levels than the cancer patients, is not persuasive. One of ordinary skill in the art would not have needed the data to fit 100% to appreciate the correlation; as the Examiner points out, 41 of 4 7 of the non-small cell lung cancer patients "had significantly higher gastrin level compared to normal level." Ans. 18 (citing Zhou Tables I, V). Also, Zhou's teaching that the high serum gastrin level in lung cancer patients is likely due to the gastrin-producing properties of the lung cancer cells (see Ans. 19 (citing Zhou Abstract)) likewise applies to the patients with non-small cell lung cancer, as Zhou shows "the gastrin level of the 5 Appeal2014-004349 Application 13/012,433 cancer group (comprising 58 patients including 47 [non-small cell lung cancer] patients) returned to normal level on the 14th postoperative day," id. (citing Zhou Fig. 1 ). Accordingly, we are not persuaded that the Examiner erred in applying Zhou, or in combining Zhou with the other references in rejecting claim 1. As to the other pending claims, Appellants present a number of "[a ]dditional" arguments, see Br. 11-21, but the majority of these reiterate the same arguments regarding Zhou, which we have already found to be unpersuasive. As discussed above, Zhou describes both correlative and causal relationships between gastrin and lung cancer, including non-small cell lung cancers. One additional argument is made with regard to claim 5 (see Br. 14--15), which recites that "the lung cancer originated in the lung," (Br. 34 (Claims Appendix)). Appellants argue none of the references teaches or suggests such a cancer. We are also unpersuaded, as Zhou generally discusses "primary" cancers of the lung (see Zhou 22-23), and refers to metastases of these cancers in the lymph nodes (see id. at 23). As to claim 14 and its dependents, which recite administering docetaxel along with the anti-gastrin therapy, Appellants' arguments again focus on Zhou (and track the claim 1 arguments) (see Br. 19-21), not Belani's teaching of treating non-small cell lung cancer with docetaxel. Thus, for similar reasons as discussed above with respect to claim 1, we likewise are unpersuaded by Appellants' arguments that the Examiner erred in rejecting claims 2-5, 8- 14, or 16-19. 6 Appeal2014-004349 Application 13/012,433 B. Obviousness-Type Double Patenting The Examiner's rejection of claims 1-5, 8-14, and 16-19 for obviousness-type double patenting relies on claims 7 and 8 of Gevas '970, in view of the other references. See Ans. 9-12. Claims 7 and 8 of Gevas '970 recite: 7. A method for treating the growth of a gastrin-induced tumor in a patient by selectively neutralizing the peptide hormone G17 in vivo, which comprises administering to the patient anti-G17 antibodies which bind to an epitope located on the amino terminus of G17 so as to inhibit the binding of G17 to its physiological receptor on the tumor. 8. A method for the treatment of a gastrin-induced tumor in an animal, comprising administering to the animal an immunogen which is capable of eliciting a sufficient titer of antibodies in the animal which selectively bind to G17 so as to inhibit the binding of G17 to its physiological receptor on the tumor. Gevas '970 22:56----67. The Examiner's analysis of the combination of claims 7 and 8 of Gevas '970 with the other references is similar to the Examiner's analysis for theÂ§ 103 rejection. See Ans. 9-12. Likewise, Appellants' arguments regarding the obviousness-type double patenting rejection are very similar to those offered by Appellants regarding theÂ§ 103 rejection. See Br. 21-32; see also Ans. 20. Appellants correctly note that "a generic disclosure does not necessarily render obvious a particular species," Br. 22 (citing MPEP Â§ 2144.08), but this is not the sole basis for the Examiner's rejection. We find Appellants' arguments regarding obviousness-type double patenting unpersuasive for the same reasons discussed above regarding the Â§ 103 rejection. 7 Appeal2014-004349 Application 13/012,433 CONCLUSION For the reasons of record and as described herein, the Examiner's rejections of claims 1-5, 8-14, and 16-19 are affirmed. No time period for taking any subsequent action in connection with this appeal may be extended under 37 C.F.R. Â§ 1.136(a). AFFIRMED 8