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 .
Application Status
2. Applicant's amendment and response, filed on March 3, 2026 has been reviewed by the examiner and entered of record in the file.
3. Claims 14, 15, 18 and 19 are amended. Claims 7-10 and 22-25 are canceled.
4. Claims 1, 3, 4, 11, 12, 14, 15, 18, 19, 26 and 27 are pending, under examination, and are the subject of this office action.
Previous Claim Rejections - 35 USC § 112(b)
5. Claims 18 and 19 were previously rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite regarding the recitation of “treating a disease responsive to inhibitors of the TGFb pathway…” which was confusing regarding the recitation of plural “inhibitors.” In view of Applicant’s amendatory changes to claim 18 such that it now recites “[a] method for treating a disease responsive to TGFb signaling inhibition…”, the previous indefiniteness rejection is overcome.
6. Claim 18 was also indefinite regarding the limitation, “wherein said method comprises administering an effective amount of a prodrug of the compound according to claim 14,” which was confusing because claim 14 specifically recites the prodrug form. In view of Applicant’s amendment to change the limitation to “a prodrug according to claim 14,” the previous indefiniteness rejection is overcome.
7. Accordingly, the previous rejections under 35 USC § 112(b) are withdrawn.
Previous Claim Rejections - 35 USC § 103
8. The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
9. Claims 1 and 11 are rejected under 35 U.S.C. 103 as being unpatentable over Beight et al., U.S. 2004/0106604 A1.
Claim 1 is drawn to a compound of Formula (I) or a pharmaceutically acceptable salt or solvate thereof:
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. Claim 11 is drawn to a pharmaceutical composition comprising an effective amount of a compound of claim 1 and at least one pharmaceutically acceptable carrier.
10. Beight et al. teach a genus of functionally related 2-(pyridine)-(5,6-dihydro-pyrrolo[1,2-b]-pyrazol)-quinoline derivatives that are TGFb inhibitors, having the same core structure that is instantly recited by Applicant, i.e., the genus of Formula (II) (see abstract and paragraph [0053]). Beight et al. specifically disclose the compound “ccccccccccccc” which is a stereoisomer of Applicant’s instant compound:
4-[2-(6-Methyl-pyridin-2-yl)-5,6-dihydro-4H-pyrrolo[- 1,2-b]pyrazol-3-yl]- quinolin-7-ol
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(i.e., the position isomer 7-hydroxy-quinoline, rather than Applicant’s 6-hydroxy-quinoline) (see page 16, paragraph [0415]).
Beight et al. go on to teach a pharmaceutical composition: “[t]he compositions of the present invention are therapeutically effective amounts of the TGF-b antagonists, noted above. The composition may be formulated with common excipients, diluents or carriers,” (paragraph [0962]).
11. Beight et al. do not teach a single disclosed compound or species that is 6-hydroxy substituted on the quinoline ring.
12. However, Beight et al. specifically teach a compound species which differs from Applicant’s compound only in the position of the hydroxy substituent on the quinoline ring. And, Beight et al. generically teach that a hydroxy substituent can occur in the 6-position or the 7-position of the quinoline ring of the compound of Formula (II) (see paragraph [0057]). Compounds which are position isomers (compounds having the same radicals in physically different positions on the same nucleus) are generally of sufficiently close structural similarity that there is a presumed expectation that such compounds possess similar properties. In re Wilder, 563 F.2d 457, 195 USPQ 426 (CCPA 1977). See also In re May, 574 F.2d 1082, 197 USPQ 601 (CCPA 1978) (stereoisomers prima facie obvious); Aventis Pharma Deutschland v. Lupin Ltd., 499 F.3d 1293, 84 USPQ2d 1197 (Fed. Cir. 2007) (5(S) stereoisomer of ramipril obvious over prior art mixture of stereoisomers of ramipril.)
13. Thus, one of skill in the art before the effective filing date of the claimed invention would have been motivated to prepare Applicant’s instant compound, because chemical compounds that are similar in structure and function are expected to have similar properties. In re Payne, 606 F.2d 303, 313, 203 USPQ 245, 254 (CCPA 1979). See In re Papesch, 315 F.2d 381, 137 USPQ 43 (CCPA 1963).
14. Regarding the comprehensive of the genus of compounds disclosed by Beight et al., a reference may be relied upon for all that it would have reasonably suggested to one having ordinary skill the art, including nonpreferred embodiments. Merck & Co. v. Biocraft Laboratories, 874 F.2d 804, 10 USPQ2d 1843 (Fed. Cir.), cert. denied, 493 U.S. 975 (1989). And, in this case, when the species is clearly named, the species claim is anticipated no matter how many other species are additionally named. Ex parte A, 17 USPQ2d 1716 (Bd. Pat. App. & Inter.1990) (The claimed compound was named in a reference which also disclosed 45 other compounds. The Board held that the comprehensiveness of the listing did not negate the fact that the compound claimed was specifically taught. The Board compared the facts to the situation in which the compound was found in the Merck Index, saying that "the tenth edition of the Merck Index lists ten thousand compounds. In our view, each and every one of those compounds is described' as that term is used in 35 U.S.C. § 102(a), in that publication."). Id. at 1718. See also In re Sivaramakrishnan, 673 F.2d 1383, 213 USPQ 441 (CCPA 1982).
As such, claims 1 and 11 are prima facie obvious.
15. Claims 3, 4, and 12 remain rejected under 35 U.S.C. 103 as being unpatentable over Beight et al., U.S. 2004/0106604 A1, as applied to claims 1 and 11, above, in view of Herbertz et al., Drug Design, Development and Therapy 2015, and Luangmonkong et al., British Journal of Pharmacology 2017.
Claims 1 and 11 are addressed in detail, above.
Claim 3 is drawn to a method of treating a disease responsive to TGFb signaling inhibition selected from the group consisting of liver cancer, liver metastatic cancer, cirrhosis, hepatic steatosis, breast cancer, breast cancer resistant to anti-HER2 therapy, breast carcinoma, breast adenocarcinoma, metastatic colorectal cancer, and pancreatic ductal adenocarcinoma, comprising administering an effective amount of a compound of claim 1 to a subject in need thereof.
16. Beight et al. teach a genus of TGFb inhibitors that embrace Applicant’s instantly recited compound, and specifically disclose the compound “ccccccccccccc” which is a stereoisomer of Applicant’s instant compound: 4-[2-(6-Methyl-pyridin-2-yl)-5,6-dihydro-4H-pyrrolo[- 1,2-b]pyrazol-3-yl]-quinolin-7-ol
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. And, Beight et al. generically teach that a hydroxy substituent can occur in the 6-position or the 7-position of the quinoline ring of the compound of Formula (II) (see paragraph [0057]).
17. Beight et al. suggest the use of said genus of TBFb inhibitors for the treatment of cancer [paragraph [0961]), but are silent to the administration of said compounds for the treatment of liver cancer, liver metastatic cancer, cirrhosis, hepatic steatosis, breast cancer, breast cancer resistant to anti-HER2 therapy, breast carcinoma, breast adenocarcinoma, metastatic colorectal cancer, and pancreatic ductal adenocarcinoma.
18. Yet, Herbertz et al. teach the small molecule inhibitor of the TGF-β receptor I kinase, galunisertib,
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, which is similar in structure to the Beight et al. TBFb inhibitor compound “ccccccccccccc.” Herbertz et al. teach that galunisertib has antitumor activity in tumor-bearing animal models such as breast cancer, colon cancer (i.e., colorectal cancer), and hepatocellular carcinoma, (i.e., liver cancer), (see abstract). Herbertz et al. additionally suggest the use of galunisertib in pancreatic cancer, i.e., “[g]alunisertib was able to block the renewal of cancer stem cells isolated from pancreatic cancers and was additive in the combination with a Hedgehog inhibitor,” (see page 4492, right column, under “Pancreatic cancer”) and breast cancer resistant to anti-HER2 therapy (page 4493, right column, under “Breast cancer”). And, Luangmonkong et al. suggest galunisertib for the treatment of liver fibrosis, wherein cirrhosis is end-stage liver fibrosis, (see abstract and page 3115, right column, under “Conclusion”).
19. Thus, it would have been obvious to one of skill in the art before the effective filing date of the claimed invention to modify Herbertz et al. and/or Luangmonkong et al. and substitute Applicant’s instantly recited TGFb inhibitor for galunisertib in the treatment of breast cancer, colon cancer, hepatocellular carcinoma, (i.e., liver cancer), pancreatic cancer, or liver cirrhosis, with a reasonable expectation of success. And, as noted by the court in In re Font, 675 F.2d 297 (CCPA 1982), an express suggestion to substitute one equivalent component (i.e., an equivalent TGFb inhibitor) for another is not necessary to render such substitution obvious. In the instant case, (1) the prior art element of Herbertz et al. and/or Luangmonkong et al. perform the function specified in the claim with only insubstantial differences; (2) the claimed component (i.e., 4-[2-(6-methyl-pyridin-2-yl)-5,6-dihydro-4H-pyrrolo[- 1,2-b]pyrazol-3-yl]-quinolin-6-ol and its function was known/suggested by the art (i.e., Beight et al. teach the TGFb inhibitor 4-[2-(6-methyl-pyridin-2-yl)-5,6-dihydro-4H-pyrrolo[- 1,2-b]pyrazol-3-yl]-quinolin-7-ol); (3) a person of ordinary skill in the art would have recognized the interchangeability of the elements and could have substituted one known element (TGFb inhibitor) for another; and (4) the results of the substitution would have been predictable, i.e., a reasonable expectation success in the treatment of breast cancer, colon cancer, hepatocellular carcinoma, (i.e., liver cancer), pancreatic cancer, or liver cirrhosis in a subject in need thereof.
As such, claim 3 is prima facie obvious.
Claim 4 is drawn to claim 3, further comprising administering chemotherapy, a targeted cancer therapy, immunotherapy, and/or an immune checkpoint inhibitor.
Claim 12 is drawn to claim 11, further comprising an immunotherapeutic agent or chemotherapeutic agent.
20. Beight et al. additionally teach the treatment of cancer comprising administering the TGFb signaling inhibitor in combination with another anti-cancer therapy (paragraph [0960]).
21. And, Herbertz et al. additionally teach that, “[g]alunisertib is being investigated either as monotherapy or in combination with standard antitumor regimens (including nivolumab) in patients with cancer with high unmet medical needs such as glioblastoma, pancreatic cancer, and hepatocellular carcinoma,” (see abstract). Herbertz et al. go on to teach galunisertib with targeted cancer therapy in the treatment of hepatocellular carcinoma: “the combination of sorafenib and galunisertib has demonstrated an additive effect in immune-competent C57BL6/ASV-B mice,135 a murine model that spontaneously develops HCC as a result of SV40 antigen overexpression in the liver” (page 4491, right column, last paragraph). Herbertz et al. suggest the combination of galunisertib and chemotherapy in pancreatic cancer, “[i]n a xenograft model, LY2109761 was reported to have antitumor activity in combination with gemcitabine. This observation was confirmed using galunisertib,” (page 4492, right column, under “Pancreatic cancer”).
22. Thus, one of skill in the art would have been motivated to substitute Applicant’s instantly recited TGFb inhibitor for galunisertib, and combine said TGFb inhibitor (in the form of a compound or pharmaceutical composition) with a chemotherapeutic agent, a targeted cancer therapy, or immunotherapy, as guided by Herbertz et al., to achieve an additive effect in the treatment of cancer in a subject in need thereof.
As such, claims 4 and 12 are prima facie obvious.
23. Claims 14, 15 and 26 are rejected under 35 U.S.C. 103 as being unpatentable over Beight et al., U.S. 2004/0106604 A1, as applied to claims 1 and 11, above, further in view of Sun et al., Chemical Reviews 2018.
Claims 1 and 11 are addressed in detail, above.
Claim 14 is drawn to a prodrug of a compound of claim 1, according to formula (II) or formula (IV), or a pharmaceutically acceptable salt thereof, (more specifically, a prodrug according to formula (III):
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(claim 15)). Claim 26 is drawn to a pharmaceutical composition comprising a compound of claim 14.
24. Beight et al. teach a genus of TGFb inhibitors that embrace Applicant’s instantly recited compound, and specifically disclose the compound “ccccccccccccc” which is a stereoisomer of Applicant’s instant compound: 4-[2-(6-Methyl-pyridin-2-yl)-5,6-dihydro-4H-pyrrolo[- 1,2-b]pyrazol-3-yl]-quinolin-7-ol, and its pharmaceutical composition thereof. And, Beight et al. generically teach that a hydroxy substituent can occur in the 6-position or the 7-position of the quinoline ring of the compound of Formula (II) (see paragraph [0057]).
Beight et al. teach prodrugs thereof in paragraph [0027], but do not teach the recited prodrug compounds according to formula (III).
25. However, Sun et al. teach lignin derived monomers possessing favorable pharmacological activity that are commonly employed cleavable moieties for preparing prodrugs:
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, wherein the arrow points to the same monomer employed as a cleavable group at the hydroxyl moiety for prodrug activation in Applicant’s instant compound of formula (III) (see page 662, lines 6-8 and page 647, Figure 30).
26. As such, one of skill in the art would reasonably consider employing the teachings of Sun et al. to prepare a prodrug of compound 4-[2-(6-Methyl-pyridin-2-yl)-5,6-dihydro-4H-pyrrolo[- 1,2-b]pyrazol-3-yl]-quinolin-7-ol of Beight et al., and its stereoisomer 4-[2-(6-Methyl-pyridin-2-yl)-5,6-dihydro-4H-pyrrolo[- 1,2-b]pyrazol-3-yl]-quinolin-6-ol, comprising the same cleavable moiety recited in formula (III) of Sun et al., in order to obtain a pharmacologically inactive compound that is converted to an active drug upon administration, thus resulting in the practice of claims 14 and 15.
27. One of skill in the art would have been motivated to prepare a pharmaceutical composition comprising said prodrug, as guided by Beight et al: “[t]he compositions of the present invention are therapeutically effective amounts of the TGF-b antagonists, noted above. The composition may be formulated with common excipients, diluents or carriers,” (paragraph [0962]).
As such, claims 14, 15 and 26 are prima facie obvious.
28. Claims 18, 19, and 27 are rejected under 35 U.S.C. 103 as being unpatentable over Beight et al., U.S. 2004/0106604 A1, as applied to claims 1 and 11, above, in view of Sun et al., Chemical Reviews 2018, as applied to claims 14, 15 and 26, above, and further in view of Herbertz et al., Drug Design, Development and Therapy 2015, and Luangmonkong et al., British Journal of Pharmacology 2017.
Claims 1, 14 and 26 are addressed in detail, above.
Claim 18 is drawn to a method of treating a disease responsive to TGFb signaling inhibition selected from the group consisting of liver cancer, liver metastatic cancer, cirrhosis, hepatic steatosis, breast cancer, breast cancer resistant to anti-HER2 therapy, breast carcinoma, breast adenocarcinoma, metastatic colorectal cancer, and pancreatic ductal adenocarcinoma, comprising administering an effective amount of a prodrug of the compound of claim 14 to a subject in need thereof.
29. Beight et al. in view of Sun et al. suggest a prodrug of TGFB inhibitor compound 4-[2-(6-Methyl-pyridin-2-yl)-5,6-dihydro-4H-pyrrolo[- 1,2-b]pyrazol-3-yl]-quinolin-6-ol, comprising the same cleavable moiety recited in formula (III) of Sun et al., and Beight et al. suggest the use of said genus of TBFb inhibitors for the treatment of cancer (paragraph [0961]).
30. However the combined prior art does not teach the treatment of liver cancer, liver metastatic cancer, cirrhosis, hepatic steatosis, breast cancer, breast cancer resistant to anti-HER2 therapy, breast carcinoma, breast adenocarcinoma, metastatic colorectal cancer, and pancreatic ductal adenocarcinoma comprising administering said prodrug.
31. Yet, Herbertz et al. teach the small molecule inhibitor of the TGF-β receptor I kinase, galunisertib,
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, which is similar in structure to the Beight et al. TBFb inhibitor compound “ccccccccccccc” and its stereoisomer, 4-[2-(6-Methyl-pyridin-2-yl)-5,6-dihydro-4H-pyrrolo[- 1,2-b]pyrazol-3-yl]-quinolin-6-ol. Herbertz et al. teach that galunisertib has antitumor activity in tumor-bearing animal models such as breast cancer, colon cancer (i.e., colorectal cancer), and hepatocellular carcinoma, (i.e., liver cancer), (see abstract). Herbertz et al. additionally suggest the use of galunisertib in pancreatic cancer, i.e., “[g]alunisertib was able to block the renewal of cancer stem cells isolated from pancreatic cancers and was additive in the combination with a Hedgehog inhibitor,” (see page 4492, right column, under “Pancreatic cancer”) and breast cancer resistant to anti-HER2 therapy (page 4493, right column, under “Breast cancer”). And, Luangmonkong et al. suggest galunisertib for the treatment of liver fibrosis, wherein cirrhosis is end-stage liver fibrosis, (see abstract and page 3115, right column, under “Conclusion”).
32. Thus, it would be obvious to one of skill in the art to modify Herbertz et al. and/or Luangmonkong et al. and substitute Applicant’s instantly recited TGFb inhibitor prodrug for galunisertib in the treatment of breast cancer, colon cancer, hepatocellular carcinoma, (i.e., liver cancer), pancreatic cancer, or liver cirrhosis, with a reasonable expectation of success. And, as noted by the court in In re Font, 675 F.2d 297 (CCPA 1982), an express suggestion to substitute one equivalent component (i.e., an equivalent TGFb inhibitor) for another is not necessary to render such substitution obvious. In the instant case, (1) the prior art element of Herbertz et al. and/or Luangmonkong et al. perform the function specified in the claim with only insubstantial differences; (2) the claimed component (i.e., a prodrug of 4-[2-(6-methyl-pyridin-2-yl)-5,6-dihydro-4H-pyrrolo[- 1,2-b]pyrazol-3-yl]-quinolin-6-ol and its function was known/suggested by the art (i.e., Beight et al. teach the TGFb inhibitor 4-[2-(6-methyl-pyridin-2-yl)-5,6-dihydro-4H-pyrrolo[- 1,2-b]pyrazol-3-yl]-quinolin-7-ol and Sun et al. suggest the recited prodrug); (3) a person of ordinary skill in the art would have recognized the interchangeability of the elements and could have substituted one known element (TGFb inhibitor) for another; and (4) the results of the substitution would have been predictable, i.e., a reasonable expectation success in the treatment of breast cancer, colon cancer, hepatocellular carcinoma, (i.e., liver cancer), pancreatic cancer, or liver cirrhosis in a subject in need thereof.
As such, claim 18 is prima facie obvious.
Claim 19 is drawn to claim 18, further comprising administering chemotherapy, a targeted cancer therapy, immunotherapy, and/or an immune checkpoint inhibitor.
Claim 27 is drawn to claim 26, further comprising an immunotherapeutic agent or chemotherapeutic agent.
33. Beight et al. additionally teach the treatment of cancer comprising administering the TGFb signaling inhibitor in combination with another anti-cancer therapy (paragraph [0960]).
34. And, Herbertz et al. additionally teach that, “[g]alunisertib is being investigated either as monotherapy or in combination with standard antitumor regimens (including nivolumab) in patients with cancer with high unmet medical needs such as glioblastoma, pancreatic cancer, and hepatocellular carcinoma,” (see abstract). Herbertz et al. go on to teach galunisertib with targeted cancer therapy in the treatment of hepatocellular carcinoma: “the combination of sorafenib and galunisertib has demonstrated an additive effect in immune-competent C57BL6/ASV-B mice,135 a murine model that spontaneously develops HCC as a result of SV40 antigen overexpression in the liver” (page 4491, right column, last paragraph). Herbertz et al. suggest the combination of galunisertib and chemotherapy in pancreatic cancer, “[i]n a xenograft model, LY2109761 was reported to have antitumor activity in combination with gemcitabine. This observation was confirmed using galunisertib,” (page 4492, right column, under “Pancreatic cancer”).
35. Thus, one of skill in the art would have been motivated to substitute Applicant’s instantly recited TGFb inhibitor prodrug for galunisertib, and combine said TGFb inhibitor (in the form of a compound or pharmaceutical composition) with a chemotherapeutic agent, a targeted cancer therapy, or immunotherapy, as guided by Herbertz et al., to achieve an additive effect in the treatment of cancer in a subject in need thereof.
As such, claims 19 and 27 are prima facie obvious.
Response to Arguments
36. Applicant traverses the previous obviousness rejection of claims 1 and 11 over Beight et al., and of claims 3, 4, and 12 over Beight et al. in view of Herbertz and Luangmonkong, and of claims 14, 15 and 26 over Beight et al., in view of Sun, and of claims 18, 19 and 27 over Beight et al., in view of Sun, and further in view of Herbertz and Luangmonkong. Applicant argues the following points:
(i) Applicant argues that the positional isomer taught by Beight et al. is introduced in the instant Specification as "reference compound 338" at page 27, lines 8-13, and used it for experimental comparison to the claimed compound of formula (I),
Applicant argues that Figure 13 shows how the claimed compound of formula (I) “exhibits a large improvement of therapeutic activity and blocks liver metastasis formation to a much larger extent than galunisertib and, unexpectedly, also in comparison with reference compound 4-[2-(methyl-pyridin-2-yl) 5,6-dihydro-4H-pyrrolo[1,2-b]pyrazol-3-yl]-quinolin-7-ol, (reference compound 338)” (page 3 of Applicant’s remarks). Applicant argues that Figure 17 shows that the claimed compound of formula (I) “exhibits a large improvement of therapeutic activity and blocks liver metastasis formation to a much larger extent than compound 338,” (page 3 of Applicant’s remarks).
37. Applicant's arguments have been fully considered but they are not persuasive. It is well settled that a showing of unexpected results is generally sufficient to overcome a prima facie case of obviousness. In re Albrecht, 514 F.2d 1389 (CCPA 1975). In the instant case, Applicant has appropriately compared the claimed compound with that of the closest prior art (Beight et al) and demonstrated unexpectedly beneficial results of the claimed compound over compound 338 of Beight et al for inhibiting liver metastasis formation (Figures 13 and 17). However, although the evidence establishes unexpected results, Applicant is reminded that according to MPEP 716.02(d), the "objective evidence of nonobviousness must be commensurate in scope with the claims which the evidence is offered to support." The instant claims are not limited to Applicant’s alleged unexpected results, which compare the administration of the claimed compound of formula (I) relative to the administration of compound 338 of Beight et al., for blocking liver metastasis in the treatment of metastatic liver disease, including liver cancer, liver metastatic cancer, and/or cirrhosis in a subject in need thereof.
(ii) Applicant alleges that the increased potency of the claimed compound of formula (I) was unexpected as Li et al. teaches away from the introduction of electron-donating groups such as the hydroxyl featured in the 6-position by the compound of formula (I), i.e., there is nothing objectively reasonable about considering Beight and positioning the hydroxyl group at the 6-position of the quinoline moiety, as claimed herein in claim 1, and expecting that said compound could successfully treat a disease responsive to TGF3 signaling inhibition.
38. Applicant's arguments have been fully considered but they are not persuasive. Beight et al. teach that the 6-position of the quinoline ring can be substituted by electron withdrawing groups, including a hydroxy substituent (see paragraphs [0053]-[0057]), i.e., a hydroxy substitution can occur in the 6-position OR the 7-position of the quinoline ring of the compound of Formula (II) (see paragraph [0057]). Therefore one skilled in the art would recognize the interchangeability of the position of the hydroxy substituent on the pyridyl ring employed by Beight et al., and would have been motivated to substitute the instant 6-hydroxy substitution for the 7-hydroxy substitution, with a reasonable expectation of success.
And, regarding Applicant’s argument that Li et al. teach away from the instant claimed compound of formula (I), disclosed examples and preferred embodiments do not constitute a teaching away from a broader disclosure or nonpreferred embodiments. In re Susi, 440 F.2d 442, 169 USPQ 423 (CCPA 1971). "A known or obvious composition does not become patentable simply because it has been described as somewhat inferior to some other product for the same use." In re Gurley, 27 F.3d 551, 554, 31 USPQ2d 1130, 1132 (Fed. Cir. 1994) (The invention was directed to an epoxy impregnated fiber-reinforced printed circuit material. The applied prior art reference taught a printed circuit material similar to that of the claims but impregnated with polyester-imide resin instead of epoxy. The reference, however, disclosed that epoxy was known for this use, but that epoxy impregnated circuit boards have "relatively acceptable dimensional stability" and "some degree of flexibility," but are inferior to circuit boards impregnated with polyester-imide resins. The court upheld the rejection concluding that applicant’s argument that the reference teaches away from using epoxy was insufficient to overcome the rejection since "Gurley asserted no discovery beyond what was known in the art." 27 F.3d at 554, 31 USPQ2d at 1132.). Furthermore, "[t]he prior art’s mere disclosure of more than one alternative does not constitute a teaching away from any of these alternatives because such disclosure does not criticize, discredit, or otherwise discourage the solution claimed…." In re Fulton, 391 F.3d 1195, 1201, 73 USPQ2d 1141, 1146 (Fed. Cir. 2004).
Claim Objections
39. Claim 15 was previously objected to for missing a period at the end of the claim. In view of Applicant’s amendment to add a period to the end of the claim, the previous obviousness rejection is withdrawn.
Conclusion
40. Claims 1, 3-4, 11, 12, 14, 15, 18, 19, 26 and 27 are pending in the application and all claims are rejected. No claim is presently allowed.
41. THIS ACTION IS MADE FINAL. Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to JANET L COPPINS whose telephone number is (571)272-0680. The examiner can normally be reached Monday-Friday 8:30AM-5PM EST.
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/JANET L COPPINS/Examiner, Art Unit 1628 /AMY L CLARK/Supervisory Patent Examiner, Art Unit 1628
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