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 .
Status of the Claims
Claims 25-38 are rejected
Information Disclosure Statement
All references from IDS filed on 12/12/2024 have been acknowledged and considered unless marked with a strikethrough.
Claim Rejections - 35 USC § 112(b)
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 33-35 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention. Specifically, Claim 33 recites the “said compound is compound A”, but includes an image of compound (I). Because compound A and compound (I) are defined different from one another throughout the instant application, the metes and bounds of claim 33 are unclear as to whether the claims requires the structure of compound A or the structure of compound (I). Claims 34-35 are included in the rejection as they depend from claim 33 and fail to cure the indefiniteness. To overcome the rejection, Examiner suggests replacing the structure currently recited in claim 33 with the structure of compound A.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
Claims 25, 28-29, 32-33, and 36-38 are rejected under 35 U.S.C. 103 as being unpatentable over KNIGHT (08 April 2010, ACS Med. Chem. Lett., 1, 39-43) in view of PARK (10 October 2017, Cancer Letters, 406, 47-53).
Knight teaches the discovery of GSK2126456, also known as omipalisib or, in the instant case, compound A, a highly potent and selective inhibitor of class 1 phosphoinositide 3-kindases (PI3Ks) and the mammalian target of rapamycin (mTOR).
Knight fails to teach inhibition of RAS proteins to treat proliferative diseases, such as lung cancer.
Park teaches the relationship between PI3K and mTOR signaling pathways and the activation of KRAS proteins. Park teaches that the constitutive activation of KRAS due to mutation leads to constant stimulation of the downstream PI3K/mTOR signaling pathways, which promote tumorigenesis (p. 47, ¶ 1, lines 10-13). Park later teaches that PI3K inhibitors are a useful current treatment option for various tumors including non-small cell lung cancer (NSCLC) (p. 51, ¶ 2, lines 1-2).
Prior to the filing of the instant application, a person having ordinary skill in the art (PHOSITA) following the teachings for Knight and Park would have found it prima facie obvious to have utilized a highly selective inhibitor for both mTOR and PI3K to reduce the activation of RAS proteins, thus leading to an inhibition of cellular proliferation. Thus, a PHOSITA would have been motivated to utilize compound A, omipalisib, to inhibit the activation of mutated RAS proteins through the inhibition of PI3K proteins.
Claim 25-38 are rejected under 35 U.S.C. 103 as being unpatentable over KNIGHT (08 April 2010, ACS Med. Chem. Lett., 1, 39-43) in view of PARK (10 October 2017, Cancer Letters, 406, 47-53) as applied to Claims 25, 28-29, 32-33, and 36-38 above, and further in view of SUNAGA (26 November 2021, Cancer, 13, 5956).
The combination of Knight and Park teach the utilization of omipalisib (to the instant case, compound A) to inhibit the activation of mutated RAS proteins through the inhibition of PI3K proteins.
The combination of Knight and Park fail to teach the specific mutations present in the RAS proteins.
Sunaga teaches of the RAS family, consisting of HRAS, NRAS and KRAS (p. 1, ¶ 1, lines 11-12) and teaches of common mutations in KRAS, with the G12C mutation being the most common in NSCLC, and the G12D and G12V mutations being the major subtypes in colorectal and pancreatic cancers (p. 2, ¶ 2, lines 5-7). Sunaga also teaches of KRAS G12C mutant patients acquiring resistance to a specific KRAS inhibitor, adagrasib, which binds to KRAS G12C/Y96C (p. 6, ¶ 1, lines 2-5).
Prior to the filing of the instant claims a PHOSITA following the teachings for Knight, Park and Sunaga would have found it prima facie obvious to have utilized omipalisib to have treated proliferative disease, such as NSCLC, with specific KRAS mutations with omipalisib, a compound shown to inhibit the activation of KRAS through PI3K. Thus, a PHOSITA would be motivated to treat proliferative disease, and specifically try to treat two specific mutations, KRAS G12C and KRAS G12C/Y96C, with omipalisib though the PI3K proteins, halting the activation of KRAS proteins.
Conclusion
Any inquiry concerning this communication or earlier communications from the examiner should be directed to EVAN G. THOMAE whose telephone number is (571)270-7609. The examiner can normally be reached 8:00 am - 4:30 pm.
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/E.G.T./Examiner, Art Unit 1623
/ADAM C MILLIGAN/Supervisory Patent Examiner, Art Unit 1623
