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 .
Priority
This application filed on 01/12/2024 is a National Stage application under 35 U.S.C. 371 of International Application No. PCT/US2022/073718, filed 07/14/2022, which claims priority to U.S. Provisional Application No. 63/222,341 filed on 07/15/2021.
Information Disclosure Statement
The information disclosure statement (IDS) filed on 10/15/2020, complies with the provisions of 37 CFR 1.97, 1.98 and MPEP § 609. Accordingly, it has been placed in the application file and the information therein has been considered as to the merits, except where noted.
Status of the Application
The preliminary amendment filed on 09/16/2024, that amended claims 2, 5-6, 8, 10-11, 13, 15-17, 19-21 and 23-27 and canceled Claims 3-4, 7, 9, 12, 14, 18 and 28-33, is acknowledged.
Claims 1-2, 5-6, 8, 10-11, 13, 15-17, 19-27 are pending.
Rejections 35 U.S.C. 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.
Claim 22 is 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.
Pursuant to 35 U.S.C. 112(b), the claim must apprise one of ordinary skill in the art of its scope so as to provide clear warning to others as to what constitutes infringement. MPEP 2173.02(II); Solomon v. Kimberly-Clark Corp., 216 F.3d 1372, 1379, 55 USPQ2d 1279, 1283 (Fed. Cir. 2000).
The claims recite “a compound of Table 1 or a pharmaceutically acceptable salt thereof”. Table 1 recites in the specification page 12. Referencing to the structure of Tables 1 without reciting the structures in the claims render the claim indefinite. Where possible, claims are to be complete in themselves. Incorporation by reference to a specific figure or table "is permitted only in exceptional circumstances where there is no practical way to define the invention in words and where it is more concise to incorporate by reference than duplicating a drawing or table into the claim. Incorporation by reference is a necessity doctrine, not for applicant’s convenience." Ex parte Fressola, 27 USPQ2d 1608, 1609 (Bd. Pat. App. & Inter. 1993). Reference characters corresponding to elements recited in the detailed description and the drawings may be used in conjunction with the recitation of the same element or group of elements in the claims.
Claim Rejections - 35 USC § 112(d)
The following is a quotation of 35 U.S.C. 112(d):
(d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
Claim 21 is rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends.
Claim 1 recites a compound of formula I
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Claim 21 recites “the compound of claim 1 or a pharmaceutically acceptable salt thereof, wherein Y and B taken together form:
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The recitation
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is interpreted as explaining the structure highlighted with the square above. B is bonded to A2 and Y is bonded to N. However, claim 1 formula I includes a double bond between B and Y, whereas the structures of claim 21 do not include a double bond. The structure of compound 21 can be represented by claim 6 formula VII:
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Thus, claim 21 compounds does not read on formula I. As such claim 21 fails to further limit claim 1. Applicant may cancel the claim(s), amend the claim(s) to place the claim(s) in proper dependent form, rewrite the claim(s) in independent form, or present a sufficient showing that the dependent claim(s) complies with the statutory requirements.
Claim Rejections - 35 USC § 112 (a)
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 26 and 27 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for treating Leukemia, Lung cancer, Melanoma, Colon cancer, Breast cancer, Prostate cancer, Ovarian cancer, lymphoma, bladder cancer, Renal cancer, Pancreatic cancer, Stomach cancer, Liver cancer1, does not reasonably provide enablement for the treatment of the claimed scope of every type of cancer and all MAP4K1-dependent disorder. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims.
As a general rule, enablement must be commensurate with the scope of claim language. MPEP 2164.08 states, “The Federal Circuit has repeatedly held that “the specification must teach those skilled in the art how to use the full scope of the claimed invention without undue experimentation.” In re Wright, 999 F.2d 1557, 1561, 27 USPQ2d 1510, 1513 (Fed. Cir. 1993)”. The “use the full scope of the invention without undue experimentation” language was repeated in 2005 in Warner-Lambert Co. v. Teva Pharmaceuticals USA Inc., 75 USPQ2d 1865, and Scripps Research Institute v. Nemerson, 78 USPQ2d 1019 asserts: “A lack of enablement for the full scope of a claim, however, is a legitimate rejection.” The principle was explicitly affirmed most recently in Liebel-Flarsheim Co. v. Medrad, Inc. 481 F.3d 1371, 82 USPQ2d 1113; Auto. Tech. Int’l, Inc. v. BMW of N. Am., Inc., 501 F.3d 1274, 84 USPQ2d 1108 (Fed. Cir. 2007), Monsanto Co. v. Syngenta Seeds, Inc., 503 F.3d 1352, 84 U.S.P.Q.2d 1705 (Fed. Cir. 2007), and Sitrick v. Dreamworks, LLC, 516 F.3d 993, 85 USPQ2d 1826 (Fed. Cir. 2008).
By way of background, four cases are of particular relevance to the question of enablement of a method of treating cancers broadly or even generally:
In In re Buting, 57 CCPA 777, 418 F.2d 540, 163 USPQ 689, the claim was drawn to “The method of treating a malignant condition selected from the group consisting of leukemias, sarcomas, adenocarcinomas, lymphosarcomas, melanomas, myelomas, and ascitic tumors” using a small genus of compounds. The Court decided that human testing “limited to one compound and two types of cancer” was not “commensurate with the broad scope of utility asserted and claimed”.
In Ex parte Jovanovics, 211 USPQ 907 the claims were drawn to “the treatment of certain specified cancers in humans” by the use of a genus of exactly two compounds, the N-formyl or N-desmethyl derivative of leurosine. Applicants submitted “affidavits, publications and data” for one of the compounds, and a dependent claim drawn to the use of that species was allowed. For the other, no data was presented, applicants said only that the other derivative would be expected to be less effective; claims to the genus were refused.
In Ex parte Busse, et al., 1 USPQ2d 1908, claims were drawn to “A therapeutic method for reducing metastasis and neoplastic growth in a mammal” using a single species. The decision notes that such utility “is no longer considered to be “incredible””, but that “the utility in question is sufficiently unusual to justify the examiner's requirement for substantiating evidence.” Note also that there is also a dependent claim 5 which specified “wherein metastasis and neoplastic growth is adenocarcinoma, squamous cell carcinoma, melanoma, cell small lung or glioma.” The decision notes that “even within the specific group recited in claim 5 some of the individual terms used actually encompass a relatively broad class of specific types of cancer, which specific types are known to respond quite differently to various modes of therapy.”
In Ex parte Stevens, 16 USPQ2d 1379 a claim to “A method for therapeutic or prophylactic treatment of cancer in mammalian hosts” was refused because there was “no actual evidence of the effectiveness of the claimed composition and process in achieving that utility.”
Pursuant to In re Wands, 858 F.2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988), one considers the following factors to determine whether undue experimentation is required:
(1) The breadth of the claims
(2) The nature of the invention
(3) The state of the prior art
(4) The level of one of ordinary skill
(5) The level of predictability in the art
(6) The amount of direction provided by the inventor
(7) The existence of working examples
(8) The quantity of experimentation needed to make or use the invention based on the content of the disclosure.
Some experimentation is not fatal; the issue is whether the amount of experimentation is “undue”; see In re Vaeck, 20 USPQ2d 1438, 1444.
The analysis is as follows:
(1) The breadth of the claims:
The presently claimed invention is directed to a method for treating a MAP4K1-dependent disorder or disease in a subject in need thereof, comprising administering to said subject an effective amount of the compound of any one of claim 1 or a pharmaceutically acceptable salt thereof, wherein said MAP4K1-dependent disease or disorder is a cancer, optionally wherein (1) the cancer comprises at least one cancer selected from the group consisting of colon cancer, pancreatic cancer, breast cancer, prostate cancer, lung cancer, ovarian cancer, cervical cancer, renal cancer, bladder cancer, stomach cancer, liver cancer, cancer of the head and neck, lymphoma, leukemia, and melanoma; and/or (2) the method further comprises administering an additional anti-cancer agent to said subject.
Cancer is not a single disease, or a cluster of closely related disorders. There are hundreds of proliferative diseases, which have in common only some loss of controlled cell growth. Cancers are highly heterogeneous at both the molecular and clinical level, something seen especially in, for example, the cancers of the breast, brain, and salivary glands. They can occur in every part of the body. The specification and the art of record fail to disclose a validated marker or method for predicting a benefit from the instantly claimed compounds. Therefore, the scope of the diseases covered is deemed very broad, and cannot be considered enabled by the instant specification. In addition, treating a cancer encompasses thousands of anti-cancer/antitumor agents under the classes such as small molecular chemotherapy, antitumor antibiotic substance, a platinum-based agent etc. is deemed very broad, and cannot be considered enabled by the instant specification.
(2) The nature of the invention:
The present claims describe a method for treating every cancer, and every MAP4K1-dependent disorder or disease. That is; in order to be enabled to practice the present invention, the skilled artisan would have to accept that by administering a compound of Formula I to a cancer patient that such therapeutic objectives could actually be achieved. However, in light of the fact that the specification fails to provide the skilled artisan with any direction or guidance as to how the treatment of cancer in general could be achieved, or how all the species of Formula I dose or regimen will be selected for treating any particular kind of cancer, the present specification is viewed as lacking an enabling disclosure of the entire scope of the claimed invention.
(3) The state of the Prior Art:
The instant claims are directed to a method for treating a cancer by administering a compound of Formula I. However, as taught by Chakraborty (S. Chakraborty, et al. Ecancermedicalscience. 2012, 14;6:ed16, cited in the PTO-892), “the cure for cancer is like the Holy Grail since most of the existing treatments are not effective enough to provide full protection from this disease”. Chakraborty teaches that “in recent years the burgeoning of sophisticated genomic, proteomic and bioinformatics techniques has made it possible for us to get a glimpse of the intricate interplay of numerous cellular genes and regulatory genetic elements that are responsible for the manifestation of cancerous phenotypes. With the use of modern genomic technologies, we are now beginning to understand the enormous complexity of cancer, however, there are few success stories as far as the treatment of cancer is concerned, [Abstract]. Chakraborty teaches that the non-specific nature of cancer symptoms makes diagnosis difficult (let alone treatment and prevention). Chakraborty teaches examples of cancer with diagnosis difficulties include esophageal cancer, prostate cancer, and pancreatic cancer. [Page 3-4]. Moreover, Zafar (A. Zafar, et al. Med Res Rev. 2021;41:961–1021, cited in the PTO-892), teaches the challenges associated with neuroblastoma treatment. Zafar teaches that standard treatment in children all lead to relatively poor outcomes for NB treatment. It is also important to note that oncology drugs have the lowest LOA (likelihood of approval) from phase I (6.7%) compared with drugs used for other diseases (allergy, dermatology, urology, autoimmune disease, and ophthalmology).45 Complicating matters, the current treatments approved for NB have limited targeted specificity. [Page 964, 1st para.]. Numerous mechanisms have been proposed as methods of treating assorted cancers a selection of which follow. Cytotoxic agents could be applied directly to the tumor’s cells, directly killing them. Immunotherapy to stimulate the patient's immune system to attack cancer cells, either by immunization of the patient, in which case the patient's own immune system is trained to recognize tumor cells as targets, or by the administration of therapeutic antibodies as drugs, so the patient's immune system is recruited to destroy tumor cells by the therapeutic antibodies. Increasing the amount or activity of the body’s tumor suppressor genes, PTEN, APC and CD95, which can, for example, activate DNA repair proteins, suppress the Akt/PKB signaling pathway, or initiate apoptosis of cancer cells. Angiogenesis inhibitor strategies based on cutting off the blood supply that growing tumors need by shutting off the growth of new blood vessels by, for example, suppressing proliferation of endothelial cells or inducing apoptosis of endothelial cells.
A number of these approaches – and others as well – have produced anti-cancer drugs. However, despite high hopes for success, and a plausible theory why these should work for cancers generally, these approaches have yet to produce a drug which can claim such a goal.
Specifically, the prior art demonstrates that there never has been a compound capable of treating cancers generally. “The cancer therapy art remains highly unpredictable, and no example exists for efficacy of a single product against tumors generally.” A similar statement appears at In re Application of Hozumi et al., 226 USPQ 353: “In spite of the vast expenditure of human and capital resources in recent years, no one drug has been found which is effective in treating all types of cancer. Cancer is not a simple disease, nor is it even a single disease, but a complex of a multitude of different entities, each behaving in a different way”. There are compounds that treat a modest range of cancers, but no one has ever been able to determine how to get a compound to be effective against cancer generally, or even a majority of cancers.
The attempts to find compounds to treat the various cancers arguably constitute the single most massive enterprise in all of pharmacology. This has not resulted in finding any treatment for tumors generally, and the existence of such a single treatment for cancer is contrary to our present understanding in oncology. This is because it is now understood that there is no “master switch” for cancers generally; cancers arise from an exceptionally wide variety of differing mechanisms. Even the most broadly effective antitumor agents are only effective against a small fraction of the vast number of different cancers known. This is true in part because cancers arise from a wide variety of sources, primarily a wide variety of failures of the body's cell growth regulatory mechanisms, but also such external factors such as viruses, exposure to environmental chemicals (e.g. tobacco tars, alcohol, toxins), ionizing radiation, and unknown environment factors.
The claims also directed to a method of treating all MAP4K1-dependent disorders or diseases. Neither the specification nor the state of the prior art listed the full scope of the MAP4K1-dependent disorders and the diseases. In an example, Chuang (H. Chuang et al. Advances in Immunology, Academic Press, 2016, VL-129, PP 277-314, cited in the PTO-892) teaches that the physiological roles of MAP4Ks in immunity and inflammation are largely unknown until recent studies using biochemical approaches and knockout mice. MAP4Ks regulate immune responses through novel targets. HPK1 inhibits T-cell receptor (TCR) signaling and B-cell receptor signaling via inducing phosphorylation/ubiquitination of SLP-76 and BLNK, respectively. Chuang teaches MAP4Ks correlated with autoimmune diseases such as psoriatic arthritis, systemic lupus erythematosus, rheumatoid arthritis, adult-onset Still's disease; systemic inflammation, cancer, as well as type 2 diabetes. [Abstract]. Chuang draws connection between some conditions and MAP4K, however, Chuang does not teach treatment of these condition by administering a MAP4K1 inhibitor, nor the prior art teach treatment of MAP4K1-dependent conditions by administering an inhibitor of MAP4K1. For example, Eisenberg (R. Eisenberg, J Autoimmun. 2009 May-Jun;32(3-4):223-30) teaches “No new therapy for systemic lupus erythematosus has been approved. In the last decade, the development of several novel compounds has been pursued for lupus, but so far nothing has been proven to be effective.” [Abstract]. Eisenberg described the difficulty of finding treatment for systemic lupus erythematosus including complexity of the disease itself; the lack of reliable outcome measures; our limited understanding of the pathogenesis of the disease; the propensity of lupus patients to have bad outcomes and to react to medicines in unusual ways; the heterogeneity of the patient population; the unpredictable course of disease in individual patients; and the lack of reliable biomarkers. [abstract].
Accordingly, there is substantive “reason for one skilled in the art to question the objective truth of the statement of utility or its scope” (In re Langer, 183 USPQ 288, 297), specifically, the scope of covering cancer generally.
Similarly, In re Novak, 134 USPQ 335, 337-338, says “unless one with ordinary skill in the art would accept those allegations as obviously valid and correct, it is proper for the examiner to ask for evidence which substantiates them.” There is no such evidence in this case. Likewise, In re Cortright, 49 USPQ2d 1464, states: “Moreover, we have not been shown that one of ordinary skill would necessarily conclude from the information expressly disclosed by the written description that the active ingredient” does what the specification surmises that it does. That is exactly the case here. Moreover, even if applicants’ assertion that cancer in general could be treated with these compounds were plausible, which it is not, that “plausible” would not suffice, as was stated in Rasmusson v. SmithKline Beecham Corp., 75 USPQ2d 1297, 1301: “If mere plausibility were the test for enablement under section 112, applicants could obtain patent rights to “inventions” consisting of little more than respectable guesses as to the likelihood of their success.”
(4) The skill of those in the art:
The skill of those in the art is expected to be high, requiring advanced training in chemistry, medicine, or pharmacology.
(5) The level of predictability in the art:
With specific reference to cancer, Ex parte Kranz, 19 USPQ2d 1216, 1219 notes the “general unpredictability of the field [of] …anti-cancer treatment.” In re Application of Hozumi et al., 226 USPQ 353 notes the “fact that the art of cancer chemotherapy is highly unpredictable”. More generally, the invention is directed toward medicine and is therefore physiological in nature. The complexity of inflammation and autoimmune conditions as taught by Chaung and Eisenberg indicates the unpredictability of these conditions. It is well established that “the scope of enablement varies inversely with the degree of unpredictability of the factors involved,” and physiological activity is generally considered to be an unpredictable factor. See In re Fisher, 427 F.2d 833, 839, 166 USPQ 18, 24 (CCPA 1970).
With this in mind the level of predictability in the art is sufficiently low that even with hundreds of successful examples of chemotherapy there has yet to be shown any single method of treating the vast scope of cancers known. The level of unpredictability in the art renders the scope of instant claim to be not enabled.
(6) The amount of direction provided:
While the treatment of cancer is discussed in broad terms, the necessary specifics, i.e. dosing, therapeutic index, contraindications, interaction between the claimed compound with other antitumor agents, toxicity etc., are completely absent. And while the anti-cancer agent therapy is discussed in board term the, only inhibition of MAP4K1 assay is discussed. The limited assays do very little to provide the necessary information, and, in light of the immense diversity of types of cancers and their varied reactions to treatment, and complexity of inflammation and autoimmune conditions, the guidance provided is very limited.
(7) Working examples:
The examples of the treatment of cancer are limited inhibition of MAP4K1 assays. For example, the specification provides IC50 on 70 species of the claim 1 genus of Formula I, and very limited IL-2 Primary T Cell EC50. Example 6 describes in vivo study comprises administering a compound of Formula I to C57BL/6 mice to evaluate the effect of the compound on tumor size. No results are shown. The specification only provides example of the effect of the claimed compound on inhibiting MAP4K1. The exceptional diversity of cancers, inflammation and autoimmune disorders and diseases, and the treatment of them, is not well represented by these examples. It is well known that there is no single treatment that works for all kinds of cancers and all inflammation and autoimmune conditions, so the experimentation required, based on solely limited cell line assays to practice the instant invention would be egregious.
(8) The quantity of experimentation needed:
Given the fact that, historically, the development of new cancer drugs has been difficult and time consuming, and treatment of all MAP4K-dependent conditions has been difficult, and especially in view of the above factors, the quantity of experimentation needed is expected to be great. However, the quantity needed to expand limited cell line assays as a working example provided in the instant specification to a viable treatment for the claimed scope of cancer or tumor is untenable.
MPEP 2164.01(a) states, “A conclusion of lack of enablement means that, based on the evidence regarding each of the above factors, the specification, at the time the application was filed, would not have taught one skilled in the art how to make and/or use the full scope of the claimed invention without undue experimentation. In re Wright, 999 F.2d 1557, 1562, 27 USPQ2d 1510, 1513 (Fed. Cir. 1993).” That conclusion is clearly justified here.
Allowable subject Matter
Claims 1-2, 5-6, 8, 10-11, 13, 15-17, 19-20, 23-25 are allowed.
Reasons for Allowance
The following is an examiner’s statement of reasons for allowance:
The closest prior art is considered to be J. Brubaker et al. (WO 2021/146370 A1, 07/22/2021 (Effective filing date 01/14/2021), Brubaker, cited in the IDS dated 10/15/2024).
Brubaker teaches MAP4K1 inhibitors of Formula I, or a pharmaceutically acceptable salt thereof. Brubaker teaches compound 3 as species of Formula I, [page 14, Table 1]:
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Brubaker’s above compound reads on instantly claimed compound of formula I, wherein A1 is N; A2 is CH; Y is CR6 and R6 is C1-5 alkyl; X is OR3 and R3 is C1-3 alkyl, B is N; and differs from the instantly claimed compound of formula I, for example compound 4 (page 13 of instant specification), in the highlighted region, as depicted in the below table:
[Brubaker’s compound 3]
[Instant claimed compound 4]
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In order to arrive at a compound falling within the instant claim 1 compound of Formula I, for example, instant claimed compound 4 above, one of ordinary skill in the art would have to modify Brubaker’s compound 3 above and replace the highlighted NH2, with OH to arrive at compound of instant claimed compound 4. However, Brubaker’s disclosure does not provide sufficient guidance and motivation to one of ordinary skill in the art to perform the functional modifications to arrive at the instantly claimed compounds. One of ordinary skill in the art would have no motivation to switch the O and N position of Brubaker’s compounds to arrive at a compound of instant formula I. Therefore, Brubaker’s does not anticipate or render the instantly claimed compound of Formula I obvious.
Any comments considered necessary by applicant must be submitted no later than the payment of the issue fee and, to avoid processing delays, should preferably accompany the issue fee. Such submissions should be clearly labeled “Comments on Statement of Reasons for Allowance.”
Conclusion
Claims 1-2, 5-6, 8, 10-11, 13, 15-17, 19-20 and 23-25 are allowed. Claims 21, 22, 26 and 27 are rejected.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to MANAHIL MIRGHANI ALI ABDALHAMEED whose telephone number is (571)272-1242. The examiner can normally be reached M-F 7:30 am - 5:00 pm.
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) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, James H Alstrum-Acevedo can be reached at 571-272-5548. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/M.M.A./Examiner, Art Unit 1622
/JAMES H ALSTRUM-ACEVEDO/Supervisory Patent Examiner, Art Unit 1622
1 The connection of MAP4K1 inhibition and the enabled MAP4K1 cancers is taught by Ling, Faia, Chuang, Yang, Li, Pavese, Wei, Mahadevan, Wang, X. Li, O. Wang and Chen. Ling (Q. Ling, et al. eBioMedicine, 2021; 69, cited in the PTO-892) teaches the connection between inhibition of MAP4K1 and leukemia. Faia (K. Faia, et al. Abstract 1717: Cancer Res 1 July 2021; 81 (13_Supplement): 1717, cited in the PTO-892) teaches the connection between inhibition of MAP4K1 and lung cancer. Tripathi (R. Tripathi, et al. Nat Commun 11, 5463 (2020)) teaches the connection between inhibition of MAP4K1 and Melanoma. Chuang (H. Chuang, et al. J Biomed Sci 26, 82, 2019, cited in the PTO-892) teaches the connection between inhibition of MAP4K1 and Liver cancer and lung cancer. Yang (H. Yang, et al. Molecular and Cellular Biology 2006, 26(4), 1297–1306, cited in the PTO-892) teaches the connection between inhibition of MAP4K1 and Colon cancer. Li (Y. Li et al. International Journal of Molecular Medicine, 2016, 38: 803-811, cited in the PTO-892) teaches the connection between inhibition of MAP4K1 and Breast cancer. Pavese (J. Pavese, et al. PLOS ONE, 2014, 9(7): e102289, cited in the PTO-892) teaches the connection between inhibition of MAP4K1 and prostate cancer. Wei (Z. Wei, et al. Cancer Science, 2009, 100: 1408-1413, cited in the PTO-892) teaches the connection between inhibition of MAP4K1 and Ovarian cancer. Mahadevan (D. Mahadevan, et al. Mol Cancer Ther 1 2005; 4 (12): 1867–1879, cited in the PTO-892) teaches the connection between inhibition of MAP4K1 and lymphoma. Wang (Y. Wang et al, Molecular Medicine Reports 2012, 5: 260-265, cited in the PTO-892) teaches the connection between inhibition of MAP4K1 and bladder cancer. X. Li (X. Li et al. J. Cancer Res. Clin. Oncol. 2012, 138, 529–535, cited in the PTO-892) teaches the connection between inhibition of MAP4K1 and Renal cancer. O. Wang (O. Wang, et al. PLoS ONE 2016, 11(3): e0152300, cited in the PTO-892) teaches the connection between inhibition of MAP4K1 and Pancreatic cancer. Chen (Y. Chen, et al. Cell Death Differ, 2019, 26, 1346–1364, cited in the PTO-892) teaches the connection between inhibition of MAP4K1 and Stomach cancer. You (D. You D, et al. J Immunother Cancer. 2021 Jan;9(1):e001402, cited in the IDS dated 10/15/2024) teaches inhibition of MAP4K1 inhibition and enhancing immune response.
Prosecution Insights