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 .
Claim Status
Claims 1, 7, 9-10, 12 and 14–27 are pending. Claims 7 and 25 are withdrawn. Claims 1, 9–10, 12, 14-24 and 26-27 are rejected.
Response to Amendments/Arguments
Applicant’s amendments have overcome the 112b rejections of claims 17-22.
Applicant traverses the obviousness rejections over claims 1, 9–10, 12, 14-24 and 26-27 by suggesting that “it was only with the benefit of improper hindsight reasoning after reading Applicant’s own disclosure that a rejection was formulated.” Applicant maintains that “at most, the Examiner has identified the various parts of the claimed invention, but not an apparent reason for one of skill in the art to take the various alleged teachings in the cited art and combine various alleged teachings to arrive at the present claims.” The remarks filed 11/20/2025 do not provide any new substantive arguments on the merits of the claims which cover the same subject matter of the claim set filed 04/01/2025. Arguments on the alleged merits of the claims have been addressed in the office action dated 05/21/2025 and are presented again as follows:
[C]laims 1, 12 and 16 [] recite that the method comprises administering a therapeutically effective amount of a delta-tocotrienol compound that “binds to and reduces hCAS protein levels in cancerous or pre-cancerous tissues.” This new limitation does not distinguish the instant claims from the prior art. The fact that the inventor has recognized another advantage which would flow naturally from following the suggestion of the prior art cannot be the basis for patentability when the differences would otherwise be obvious. See Ex parte Obiaya, 227 USPQ 58, 60 (Bd. Pat. App. & Inter. 1985). The prior art teaches administering the same compound at the same dosages taught by Applicant such that the claimed result is a natural consequence.
Applicant traverses the 35 USC 103 rejections of the instant claims and asserts that claimed invention provides unexpected results. Applicant states that “the discovery of a molecule that not only had ‘high affinity for hCAS’ but also ‘induces the degradation of hCAS in cells’ was highly surprising and wholly unexpected from the prior art.” The fact that the prior art does not recognize that delta-tocotrienol is effective for modulating hCAS activity in order to treat pancreatic cancer does not support a conclusion of unexpected results. Both Ahsan et al. and Ling et al. provide an expectation that delta-tocotrienol would be useful in treating patients with pancreatic cancer regardless of the underlying mechanism. The secondary references of Stelma et al., Torrente et al., Jiang et al., and Husain et al. each provide a motivation for assaying the level of hCAS expression prior to treating cancer, with Jiang et al. and Husain et al. specifically providing connections between hCAS expression and pancreatic cancer. Accordingly, a person of ordinary skill could expect to encounter a patient population with subjects that are identified as having increased levels of hCAS expression. Both Ahsan et al. and Ling et al. identify delta-tocotrienol as a compound that is useful in treating cancer, such as pancreatic cancer, therefore a person of ordinary skill would be motivated to administer the compound to patients with the disease that are identified as having increased levels of hCAS expression as well as those who are not. The same rationale applies for Applicant’s second argument which alleges that the Examiner is using impermissible hindsight. Whether or not the instant claims are directed to only treating patients who are identified for hCAS overexpression, the instant method is obvious in view of combined prior art references which teach conducting an assay prior to treatment and administering the elected species to patients with pancreatic cancer generically.
Accordingly, the 35 USC 103 rejection of claims 1, 9-10, 12, 14-24 and 26-27 is maintained.
Election/Restrictions
Applicant’s elected species is not allowable therefore search and examination has been limited to claims embracing the elected species which are claims 1, 9–10, 12, 14-24 and 26-27. Claims 1, 9–10, 12, 14-24 and 26-27 have been examined to the extent that they are readable on the elected embodiment.
Claims 7 and 25 remain withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
Claims 1, 9-10, 12, 14 and 26 are rejected under 35 U.S.C. 103 as being unpatentable over WO 2010047663 A1 by Ling et al. in view of Ahsan et al. Pharmacological potential of tocotrienols: a review. Nutr Metab (Lond) 11, 52 (2014), in view of Stelma et al. Targeting nuclear transporters in cancer: Diagnostic, prognostic and therapeutic potential. IUBMB Life, 68: 268-280., of in view of Torrente et al. Identification of Cancer Related Genes Using a Comprehensive Map of Human Gene Expression. PLoS One. 2016;11(6):e0157484., and in further view of Jiang. Tumor Biol. (2016) 37:13077–13090.
Determining the scope and contents of the prior art. (See MPEP § 2141.01)
Ling et al. teach (title) “Use of tocotrienol composition for the prevention of cancer” and disclose the following on page 1, paragraph 0006:
the present invention refers to a method of preventing cancer or preventing the recurrence of cancer after undergoing a cancer treatment by administering a composition comprising or consisting of at least one of γ-tocotrienol or δ-tocotrienol, wherein the cancer is selected from the group consisting of melanoma, prostate cancer, colon cancer, liver cancer, bladder cancer, breast cancer and lung cancer.
Ascertainment of the differences between the prior art and the claims. (See MPEP § 2141.02)
Ling et al. disclose a method of preventing cancer recurrence after undergoing cancer treatment by administering delta-tocotrienol; however, the prior art does not disclose the method wherein the subject is identified as having increased levels of hCAS expression relative to a control. Additionally, Ling et al. do not disclose the method for preventing the recurrence of pancreatic cancer.
Finding of prima facie obviousness --- rationale and motivation (See MPEP § 2142-2143)
Ahsan et al. teach anti-cancer effects of tocotrienols. The prior art discloses (page 4, Col. 2, Anti-cancer effects):
[t]he anticancer properties of tocotrienols are well known and documented [60-76]. Tocotrienols not only suppress cancer-cell proliferation, but also induces apoptosis in cancer cells. It has been reported that γ- and δ-tocotrienols exhibit greater anticancer activity than α- or β-tocotrienols [76-78]. The mechanism of anticancer effects of tocotrienols has been worked out [5,79,80]. They exert anti-cancer activity on cancer cells by cell cycle arrest through induction of cell cycle inhibitory protein and decreased expression of cyclin dependent kinase [64,65,79]. Tocotrienols also work as an anticancer agent by inhibiting angiogenesis [81,82] or by enhancing immunity and inhibiting tumor cell migration [71]. Tocotrienol induces cell-cycle arrest and mitochondria-mediated apoptosis in human pancreatic cancer cells [68,70,75,83].
Further, Ahsan et al. report (page 5, Col. 1-2, Anti-cancer effects):
Husain et al. [97] has shown that oral administration of 100 mg/kg/d of d-tocotrienol to mice resulted in levels that were 10 times higher in pancreas than in subcutaneously implanted tumor tissue, suggesting that these compounds will have reasonable bioavailability for pancreatic tumor intervention [97]. In another study, they investigated the potential of the natural tocotrienols to inhibit pancreatic cancer and NF-kB activation in vitro and in vivo. In addition, they also investigated the potential of the most bioactive tocotrienol to augment gemcitabine activity in vitro and in vivo [98]. Their results show that d- and g-tocotrienol inhibited NF-kB activity, cell growth, cell survival, and tumor growth in nude mice. It was shown by them that d-tocotrienol augmented gemcitabine activity in vitro and in vivo. The results suggest that inhibition of NF-kB signaling by d-tocotrienol may be an effective approach for the prevention and treatment of pancreatic cancer.
Accordingly, a person of ordinary skill would have reasonably expected delta-tocotrienol to be useful in preventing cancer recurrence in patients who have previously had pancreatic cancer and would be motivated to administer the compound to said patients corresponding to instant claims 12 and 14.
Stelma et al. disclose (Abstract):
The Karyopherin superfamily is a major class of soluble transport receptors consisting of both import and export proteins. The trafficking of proteins involved in transcription, cell signalling and cell cycle regulation among other functions across the nuclear membrane is essential for normal cellular functioning. However, in cancer cells, the altered expression or localization of nuclear transporters as well as the disruption of endogenous nuclear transport inhibitors are some ways in which the Karyopherin proteins are dysregulated. The value of nuclear transporters in the diagnosis, prognosis and treatment of cancer is currently being elucidated with recent studies highlighting their potential as biomarkers and therapeutic targets.
Regarding altered expression of nuclear transporters, Stelma et al. state (page 272, paragraph 2):
The elevated expression of the Karyopherin proteins associates with the global dysregulation of protein transport and this has been observed in various types of cancer. Amongst all members of the Karyopherin family, XPO1, KPNB1, KPNA2 and CSE1L are the most frequently reported to be overexpressed in cancer (Table 1).
Paragraph [0060] of the instant specification describes hCAS protein as being synonymous with CSE1L.
Torrente et al. teach (title) “Identification of Cancer Related Genes Using a Comprehensive Map of Human Gene Expression”. Table 2 on page 13 of the prior art identifies CSE1L as one of the genes mapping to the top 100 probesets corresponding to genes which have been found in the Atlas of Genetics and Cytogenetics in Oncology and Haematology database to be related to cancer processes.
Accordingly, based on the involvement of CSE1L with cancer, a person having ordinary skill in the art would have been motivated to assay patients’ levels of the various transporters discussed by Stelma et al., including CSE1L. Further, Torrente’s identification of CSE1L as a gene candidate connected to cancer processes, irrespective of the tissue type would motivate one of ordinary skill to test for CSE1L/hCAS expression levels prior to treatment with delta-tocotrienol as taught by Ling et al. and Ahsan et al.
Jiang discloses (title) “CAS (CSE1L) signaling pathway in tumor progression and its potential as a biomarker and target for targeted therapy”. The prior art states (Abstract):
CSE1L (chromosome segregation 1-like protein), also named as CAS (cellular apoptosis susceptibility protein), is highly expressed in most cancer types. CSE1L/CAS is a multiple functional protein that plays roles in apoptosis, cell survival, chromosome assembly, nucleocytoplasmic transport, microvesicle formation, and cancer metastasis; some of the functions are explicitly correlated. CSE1L is also a cancer serum biomarker. The phosphorylation of CAS is regulated by the extracellular signal-regulated kinase (ERK). The RAS/RAF/MAPK/ERK signaling pathways are the essential targets of most targeted cancer drugs, thus serum phosphorylated CSE1L may be a potential biomarker for monitoring drug resistance in targeted therapy.
Regarding pancreatic cancer, Jiang et al. teach (page 13078, paragraph 1):
The chromosome 20q13 region is known to harbor amplifications in several cancers, and amplification of this chromosomal region is associated with the malignant progression of various cancer types including… pancreatic cancer [46], head and neck cancer [47], and myeloid cancer [48]. Moreover, amplification of chromosomal 20q was reported to be correlated with the aggressive phenotype, poor prognosis, and metastasis of cancer [49–51]. Brinkmann et al. reported that CSE1L gene maps on chromosome 20q13…
Accordingly, a person of ordinary skill in the art would have been motivated to test CAS/CSE1L gene expression levels prior to administration of treatment as CAS plays a role in cancer metastasis and maps on the chromosome 20q13 region, a region in which amplification has been associated with progression of pancreatic cancer as taught by Jiang.
Claims 1, 12, 14, 16-22 and 26 are rejected under 35 U.S.C. 103 as being unpatentable over WO 2010047663 A1 by Ling et al. in view of Ahsan et al. Pharmacological potential of tocotrienols: a review. Nutr Metab (Lond) 11, 52 (2014), in view of Husain et al. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2011 Apr 17-21; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl): Abstract nr 1667 and in further view of WO 2005013911 A2 by Sen et al.
Determining the scope and contents of the prior art. (See MPEP § 2141.01)
Ling et al. teach (title) “Use of tocotrienol composition for the prevention of cancer” and disclose the following on page 1, paragraph 0006:
the present invention refers to a method of preventing cancer or preventing the recurrence of cancer after undergoing a cancer treatment by administering a composition comprising or consisting of at least one of γ-tocotrienol or δ-tocotrienol, wherein the cancer is selected from the group consisting of melanoma, prostate cancer, colon cancer, liver cancer, bladder cancer, breast cancer and lung cancer.
Ascertainment of the differences between the prior art and the claims. (See MPEP § 2141.02)
Ling et al. disclose a method of preventing cancer recurrence after undergoing cancer treatment by administering delta-tocotrienol; however, the prior art does not teach the method for preventing recurrence of pancreatic cancer. Further, the prior art does not disclose the method wherein the subject is identified as having increased levels of hCAS expression relative to a control or wherein the level of hCAS protein is assayed prior to treatment.
Finding of prima facie obviousness --- rationale and motivation (See MPEP § 2142-2143)
Ahsan et al. teach anti-cancer effects of tocotrienols. The prior art discloses (page 4, Col. 2, Anti-cancer effects):
[t]he anticancer properties of tocotrienols are well known and documented [60-76]. Tocotrienols not only suppress cancer-cell proliferation, but also induces apoptosis in cancer cells. It has been reported that γ- and δ-tocotrienols exhibit greater anticancer activity than α- or β-tocotrienols [76-78]. The mechanism of anticancer effects of tocotrienols has been worked out [5,79,80]. They exert anti-cancer activity on cancer cells by cell cycle arrest through induction of cell cycle inhibitory protein and decreased expression of cyclin dependent kinase [64,65,79]. Tocotrienols also work as an anticancer agent by inhibiting angiogenesis [81,82] or by enhancing immunity and inhibiting tumor cell migration [71]. Tocotrienol induces cell-cycle arrest and mitochondria-mediated apoptosis in human pancreatic cancer cells [68,70,75,83].
Further, Ahsan et al. report (page 5, Col. 1-2, Anti-cancer effects):
Husain et al. [97] has shown that oral administration of 100 mg/kg/d of d-tocotrienol to mice resulted in levels that were 10 times higher in pancreas than in subcutaneously implanted tumor tissue, suggesting that these compounds will have reasonable bioavailability for pancreatic tumor intervention [97]. In another study, they investigated the potential of the natural tocotrienols to inhibit pancreatic cancer and NF-kB activation in vitro and in vivo. In addition, they also investigated the potential of the most bioactive tocotrienol to augment gemcitabine activity in vitro and in vivo [98]. Their results show that d- and g-tocotrienol inhibited NF-kB activity, cell growth, cell survival, and tumor growth in nude mice. It was shown by them that d-tocotrienol augmented gemcitabine activity in vitro and in vivo. The results suggest that inhibition of NF-kB signaling by d-tocotrienol may be an effective approach for the prevention and treatment of pancreatic cancer.
Accordingly, a person of ordinary skill would have reasonably expected delta-tocotrienol to be useful in preventing cancer recurrence in patients who have previously had pancreatic cancer as well as in ongoing treatment of pancreatic cancer and would be motivated to administer the compound to said patients, corresponding to instant claims 1, 12, 14, 16 and 26.
Husain et al. disclose (title) “Abstract 1667: In vitro and in vivo validation of CSE1L/hCAS as a potential molecular target in pancreatic cancer”. Specifically, the prior art teaches (Results) “[p]ancreatic ductal carcinomas (PCA) were hCAS strongly positive. Normal pancreatic ducts (ND) were hCAS weakly positive. hCAS KD-MiaPaCa-2 tumor growth was retarded in mice compared to Scr-MiaPaCa-2 tumors. hCAS KD-MiaPaCa-2 tumors showed hCAS depletion, lower proliferative index, increased caspase-3 immunostaining and PARP1 cleavage.” Husain et al. conclude (Conclusion) “[t]his is the first report of hCAS expression in human pancreatic cancer. Our data suggest that hCAS is a regulator of cell proliferation, cell cycle regulation and apoptosis. hCAS may represent a potential chemopreventive and therapeutic target for human pancreatic cancer.”
Accordingly, a person of ordinary skill in the art would have been motivated to test hCAS expression levels prior to treating pancreatic cancer with delta-tocotrienol in the teachings of Ling et al. and Ahsan et al. as hCAS is a potential molecular target in pancreatic cancer taught by Husain et al. (corresponding to instant claims 1, 12 and 16).
Sen et al. teach (title) “Protective and Therapeutic Uses for Tocotrienols”. The prior art discloses (Abstract):
[t]herapeutic and prophylactic agents comprising tocotrienols, and methods of using the same are provided for the treatment of and the prevention of the onset of stroke and other disorders and diseases associated with elevated glutamate levels, and the effects of lipoxygenases such as the enzyme 12-lipoxygenase.
Further, Sen et al. state “[t]ocotrienol is disclosed herein to have an inhibitory effect on the function of 12-LOX. Thus, tocotrienols are indicated as pharmaceutical agents for treatment of melanoma and other cancers” (page 9, lines 22-25).
Regarding instant claims 17, 18 and 22 Sen et al. state (page 4, lines 3-9):
[a]s used in accordance with the methods of the present invention, tocotrienol compositions are administered to subjects, as needed, on a daily basis in single or multiple doses from about 1 to about 1000 mg per dose. Preferably the doses for adults are about 600 mg and are administered from 1 to 3 times per day. A preferred mode of administration is orally in the form of gel caps. The tocotrienols used according to the methods are selected from the group consisting of α-tocotrienol, β-tocotrienol, γ-tocotrienol, δ-tocotrienol, derivatives of these, and mixtures of one or more of these.
With regards to overlapping ranges, MPEP 2144.05(I) states:
In the case where the claimed ranges "overlap or lie inside ranges disclosed by the prior art" a prima facie case of obviousness exists. In re Wertheim, 541 F.2d 257, 191 USPQ 90 (CCPA 1976);
Accordingly, the overlapping range taught by Sen et al. renders the 400mg to 1600mg dosage range disclosed in instant claims 17 prima facie obvious. Further, the 400mg dosage of instant claim 19 and the 800mg dosage of instant claim 20, are embraced by the prior art’s disclosed range of “about 1 to about 1000mg per dose”.
With regard to the limitation in claims 1, 12 and 16 wherein the method comprises administering a therapeutically effective amount of a delta-tocotrienol compound that “binds to and reduces hCAS protein levels in cancerous or pre-cancerous tissues,” this new limitation does not distinguish the instant claims from the prior art. The fact that the inventor has recognized another advantage which would flow naturally from following the suggestion of the prior art cannot be the basis for patentability when the differences would otherwise be obvious. See Ex parte Obiaya, 227 USPQ 58, 60 (Bd. Pat. App. & Inter. 1985). The prior art teaches administering the same compound at the same dosages taught by Applicant such that the claimed result is a natural consequence.
Instant claim 21 is directed towards the method of preventing cancer recurrence and/or anti-cancer treatment maintenance wherein δ-tocotrienol is administered for 6 months. A person of skill would have been motivated to administer the compound for extended periods of time to reduce the likelihood of recurrence.
Claims 9-10, 15, 23 and 27 are rejected under 35 U.S.C. 103 as being unpatentable over WO 2010047663 A1 by Ling et al., Ahsan et al. Pharmacological potential of tocotrienols: a review. Nutr Metab (Lond) 11, 52 (2014), Husain et al. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2011 Apr 17-21; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl): Abstract nr 1667 and WO 2005013911 A2 by Sen et al. as applied to claims 1, 12, 14, 16-22 and 26 above, and further in view of US 20040102421 A1 by Ames et al.
Ling et al., Ahsan et al., Husain et al., and Sen et al. teach a combined method of identifying a patient with high hCAS expression and administering delta-tocotrienol to prevent pancreatic cancer recurrence or treat pancreatic cancer however the prior art does not teach the method wherein an NSAID or COX-2 inhibitor is co-administered.
Ames et al. disclose (page 9, claim 1):
[a] medicament comprising predetermined amounts of a phytyl substituted chromanol and an inhibitor of prostaglandin E2 (PGE2) formation, wherein: said medicament is in unit dosage form suitable for pharmaceutical administration; said phytyl substituted chromanol is selected from the group consisting of gamma-tocopherol, delta-tocopherol, gamma-tocotrienol and delta-tocotrienol; and said PGE2 inhibitor is selected from the group consisting of an omega-3 fatty acid cyclooxygenase substrate and a non-steroidal anti-inflammatory drug (NSAID) cyclooxygenase inhibitor.
Claim 11 on page 9 specifies the medicament wherein the PGE2 inhibitor is cyclooxygenase-2 (COX-2) selective inhibitor corresponding to instant claims 9, 10, 15, 23 and 27. Table 1 on page 3 discloses aspirin as a suitable NSAID cyclooxygenase inhibitor.
Claim 13 (page 9) of the prior art discloses a method of inhibiting inflammation comprising the medicament. Ames et al. further disclose “[t]hese subject medicaments can also be used to treat and prevent chronic diseases associated with inflammation such as cancer and cardiovascular disorders” (page 1, paragraph 0008).
Accordingly, a person of ordinary skill in the art would be motivated to modify the method of preventing cancer reoccurrence taught by Ling et al., or the method of treating pancreatic cancer taught by Ahsan to include administration of aspirin disclosed by Ames et al. for improved cancer treatment outcomes in the combined method.
Claim 24 is rejected under 35 U.S.C. 103 as being unpatentable over WO 2010047663 A1 by Ling et al., Ahsan et al. Pharmacological potential of tocotrienols: a review. Nutr Metab (Lond) 11, 52 (2014), Husain et al. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2011 Apr 17-21; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl): Abstract nr 1667 and WO 2005013911 A2 by Sen et al. as applied to claims 1, 12, 14, 16-22 and 26 above, and further in view of U.S. Pat. No. 6,440,737 by Freier.
Ling et al., Ahsan et al., Husain et al., and Sen et al. teach a combined method of identifying a patient with high hCAS expression and administering delta-tocotrienol to prevent pancreatic cancer recurrence or treat pancreatic cancer; however, the combined references are silent to administering an additional compound that reduces hCAS levels.
Freier teaches the methods of using antisense compounds to modulate the expression of cellular apoptosis susceptibility gene and the treatment of its associated diseases (Abstract). Specifically, the prior art discloses (Col. 13, lines 56-66):
For therapeutics, an animal, preferably a human, suspected of having a disease or disorder which can be treated by modulating the expression of cellular apoptosis susceptibility gene is treated by administering antisense compounds in accordance with this invention. The compounds of the invention can be utilized in pharmaceutical compositions by adding an effective amount of an antisense compound to a suitable pharmaceutically acceptable diluent or carrier. Use of the antisense compounds and methods of the invention may also be useful prophylactically, e.g., to prevent or delay infection, inflammation or tumor formation, for example.
Freier further specifies that inhibition or a decrease in expression is the preferred form of modulation (Col. 3, lines 45-40). Accordingly, a person of ordinary skill in the art would have been motivated to modify the combined treatment method to administer the antisense compounds of Freier because hCAS is strongly positive in pancreatic cancers and hCAS is a potential molecular target in pancreatic cancer taught by Husain et al.
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 conflicting claims 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); 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 nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) 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 www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 12, 14-16, 23-24, and 26-27 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-14 of U.S. Patent No. 8846653 and claims 1-9 of U.S. Patent No. 8288369 in view of WO 2010047663 A1 by Ling et al. in view of Ahsan et al. Pharmacological potential of tocotrienols: a review. Nutr Metab (Lond) 11, 52 (2014), WO 2005013911 A2 by Sen et al., Husain et al. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2011 Apr 17-21; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl): Abstract nr 1667, US 20040102421 A1 by Ames et al. and U.S. Pat. No. 6,440,737 by Freier.
Although the claims at issue are not identical, they are not patentably distinct from each other because claim 1 of each patent discloses a method of treating pancreatic cancer by administering delta-tocotrienol which serves as the basis of a rejection under 35 USC 103. The teachings and rationale of Ling et al., Ahsan et al., Husain et al. and Freier relative to instant claims 12, 14-16, 23-24, and 26-27 are incorporated here by reference. The instant claims are deemed to be variants of the subject matter of U.S. Patent Nos. 8846653 and 8288369 for the same reasons as under 35 USC 103.
Conclusion
THIS ACTION IS MADE FINAL. Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
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/A.A.C./Examiner, Art Unit 1626
/MATTHEW P COUGHLIN/Primary Examiner, Art Unit 1626