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 Claims
Claims 1-4, 7, 12-14, 20, 32, and 47 are pending in the instant application.
Claims 5-6, 8-11, 15-19, 21-31, and 33-46 have been canceled.
Domestic Benefit
Applicant has claimed domestic benefit to Application Nos. 63/124,669, 63/214,736, 63/277,555, and 63/288,035 filed on December 11th, 2020, June 24th, 2021, November 9th, 2021, and November 24th, 2021, respectively. Claims 1-4, 7, 12-14, 20, 32, and 47 application are fully supported by Application No. 63/124,669 and will be evaluated with an effective filing date of December 11th, 2020.
Information Disclosure Statement
The Information Disclosure Statements filed on September 26th, 2023 and October 10th, 2024 have been fully considered by the examiner, except where marked with a strikethrough.
Specification
Applicant is reminded of the proper content of an abstract of the disclosure.
In chemical patent abstracts for compounds or compositions, the general nature of the compound or composition should be given as well as its use, e.g., “The compounds are of the class of alkyl benzene sulfonyl ureas, useful as oral anti-diabetics.” Exemplification of a species could be illustrative of members of the class. For processes, the type of reaction, reagents and process conditions should be stated, generally illustrated by a single example unless variations are necessary.
Drawings
Acknowledgement is made of the drawings received June 6th, 2023. These drawings are acceptable.
Claim Rejections - 35 USC § 112
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 1-4, 7, 12-14, 32, and 47 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 lung cancer, esophageal cancer, and colorectal cancer, does not reasonably provide enablement for treatment of cancer in general. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the invention commensurate in scope with these claims.
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 and (8) The quantity of experimentation needed to make or use the invention based on the content of the disclosure.
Nature of the invention:
The invention is drawn to a method of treating cancer comprising administering a compound of Formula I in combination with a KRAS inhibitor.
Breadth of the invention:
The scope of the claimed invention is very broad, as it is drawn to the treatment of any cancer, in general. This encompasses a myriad of conditions with distinct etiologies.
State of the prior art and predictability in the art:
No compound has ever been found to treat cancers of all types generally. Since this assertion is contrary to what is known in medicine, proof must be provided that this revolutionary assertion has merits. The existence of such a “silver bullet” is contrary to our present understanding of oncology. The state of the art is not indicative of any pharmaceutical agents that are useful in the treatment of cancer generally. At Page 1004, Cecil Textbook of Medicine states that “each specific type has unique biologic and clinical features that must be appreciated for proper diagnosis, treatment and study”. Different types of cancers affect different organs and have different methods of growth and harm to the body. Also see In re Buting, 163 USPQ 689 (CCPA 1969), wherein ‘evidence involving a single compound and two types of cancer, was held insufficient to establish the utility of the claims directed to disparate types of cancers’. Thus, it is beyond the skill of oncologists today to get an agent to be effective against cancers 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 figure out 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. This is because it is now understood that there is no “master switch” for cancers generally; cancers arise from a bewildering 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 (an estimated at least 20% are of viral origin e.g. Human papillomavirus, EBV, Hepatitis B and C, HHV-8, HTLV-1 and other retroviruses, and quite possibly Merkel cell polyomavirus, and there is some evidence that CMV is a causative agent in glioblastoma), exposure to chemicals such as tobacco tars, excess alcohol consumption (which causes hepatic cirrhosis, an important cause of HCC), ionizing radiation, and unknown environmental factors.
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 for a compound that treats all types of cancer. Likewise, In re Cartright, 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 Applicant’s 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.
Recently, Wu et. al. (“Small-molecule inhibitors, immune checkpoint inhibitors, and more: FDA- approved novel therapeutic drugs for solid tumors from 1991 to 2021; Journal of Hematology & Oncology, 15, 143, 2022; hereinafter referred to as Wu), at the Abstract, discloses that between 1991 and 2021 there have been 228 new cancer drugs approved by the U.S. Food and Drug Administration of which 120 of these are drawn to the treatment of solid tumors alone. At Page 5, Table 1 Wu teaches that there are 21 different approved drugs for treating lung cancers, some of which have cellular targets. At Page 10, Table 2, Wu teaches breast cancer has 22 different drugs that have varied cellular targets and are indicated for different types of breast cancer. At Page 17, Table 4, Wu teaches there are 17 different drugs available to treat different forms of gastrointestinal cancers. At Page 38, Figure 12, Wu summarizes the protein structure of some cellular targets and the binding site of their respective drugs. Taken together, Wu teaches that no single therapeutic has ever been identified as a treatment for all forms of cancer; and closer examination of Figure 12 provides a logical explanation. As highlighted in Figure 12, molecular protein targets implicated in different cancers (e.g. EGFR for lung cancer in Table 1, VEGFR2 for gastric cancer in Table 4) have different three-dimensional protein structures, different active sites, and therefore require different drugs with the right shape and chemical groups in order to bind the target active site and have an effect in treating cancer. In other words, there is no one size fits all approach to treating cancer simply for the reason that no single molecule will have the shape and chemical functional groups necessary to bind and modulate all modular targets of cancer, all of which have varied shapes. It is commonly known in the pharmaceutical arts that shape dictates function wherein drugs which have a shape complimentary to the protein target will bind and have an effect (this is often referred to simplistically as a “Lock and Key” model). Given the varied shape of protein targets in cancer (e.g. EGFR and VEGFR2), it is pure fantasy to speculate that a single drug with a single three dimensional shape will bind all protein targets implicated in cancer therapy and have an effect in treating all forms of the disease. As such, at present the “silver bullet” drug therapy to treat all forms of cancer is elusive and such a therapy is not recognized in the art where the reality is that different forms of cancer require different drug therapies.
Level of ordinary skill in the art:
An ordinary artisan in the area of drug development would have experience in synthesizing chemical compounds for particular activities. The synthesis of new drug candidates, while complex, is routine in the art. The process of finding new drugs that have in vitro activity against a particular biological target (i.e., receptor, enzyme, etc.) is well known. Additionally, while high throughput screening assays can be employed, developing a therapeutic method, as claimed, prior to synthesizing and testing compounds is generally not well-known or routine, given the complexity of certain biological systems.
The amount of direction provided and working examples:
Beginning at Page 38 of the instant specification, Example 1 sufficiently discloses the efficacy of the claimed combination as recited in instant Claim 1 in inhibiting cell proliferation in the NCI-H358 and NCI-H2122 cell lines. Each of these are lung cancer cell lines.
Example 2 further discloses the efficacy of the aforementioned combination in decreasing viability of the KYSE-410 cell line, an esophageal cancer cell line.
Examples 3-7 further support the efficacy of the claimed combination in treating lung cancer and esophageal cancer.
Beginning at Page 50 of the instant specification, Example 8 discloses the result of the claimed combination in treating colorectal cancer in a mouse model.
Examples 9-11 provide additional support of the efficacy of the claimed combination in treating colorectal and lung cancers.
Taken together, the Applicant has sufficiently disclosed the efficacy of the disclosed combination in treating lung cancer, esophageal cancer, and colorectal cancer. These limited examples, however, are insufficient to guide a person having ordinary skill in the art to a method of treating other cancers. Doing so would require undue experimentation, as suitable cell lines/and or models must be identified and/or developed to determine the efficacy of treatment with the claimed combination, and a person having ordinary skill in the art would need to deploy these models, with no assurance of success.
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 that Applicant is not enabled for treating cancers in general beyond lung cancer, esophageal cancer, and colorectal cancer.
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.
Claim 12 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.
Claim 12 recites the limitation "third MAPK pathway inhibitor". There is insufficient antecedent basis for this limitation in the claim, as Claim 1, from which Claim 12 depends is silent with respect to limitations specifying inhibition of the MAPK pathway.
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 1-4, 7, 13-14, 20, 32, and 47 are rejected under 35 U.S.C. 103 as being unpatentable over Fu et. al. (US 2020/0277308 A1; cited on Applicant’s Information Disclosure statement filed September 26th, 2023; hereinafter referred to as Fu) in view of Pelaia et. al. (“Effects of statins and farnesyl transferase inhibitors on ERK phosphorylation, apoptosis and cell viability in non-small lung cancer cells”, Cell Prolif. 2012; hereinafter referred to as Pelaia).
At Page 18, Table 1, entry 31, Fu teaches the following compound:
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This compound is the compound of Formula I as recited at instant Claim 1.
At Page 108, Fu teaches this compound has an IC50 of 4.2 nM against SHP2.
At Page 7, Paragraph 0115, Fu teaches a method of treating a disease treatable by inhibition of SHP2. Further, Fu teaches the suitable diseases include lung and colon cancer.
Fu recites this compound at Claims 1 and 21. At Claim 29, Fu teaches a method of treating a disease treatable by inhibition of SHP comprising administering a compound of Claim 1, and at Claim 30 specifies such diseases include lung and colon cancer.
Fu does not teach administering the compound of Formula I with a KRAS inhibitor as a method to treat lung, esophageal, and/or colorectal cancer.
At Page 558, First Column, last Paragraph Pelaia teaches R115777 is tipifarnib.
At Page 557, first Paragraph, Pelaia teaches the aim of this study was to investigate the effects of R115777 on two cultures of non-small lung cancer cells, adenocarcinoma (GLC-82) and squamous (CALU-1). Further, at Page 557, under “Results and conclusion”, Pelaia teaches R115777 exerts anti-proliferative activity in both GLC-82 and CALU-1 cell lines.
Taken together, this obviates instant Claims 1, 7, 20, and 47, as Fu teaches administration of a compound of Formula I for the treatment of lung cancer, and Pelaia teaches administration of tipifarnib, a KRAS inhibitor recited at instant Claim 7, for the treatment of lung cancer. As such, it would have been prima facie obvious for a person having ordinary skill in the art to administer a combination of a compound of Formula I with a KRAS inhibitor, in this case tipifarnib, as both were known in the art to be efficacious in treating lung cancer. Per MPEP 244.06, I. “"It is prima facie obvious to combine two compositions each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose.... [T]he idea of combining them flows logically from their having been individually taught in the prior art." In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980) (citations omitted)”.
Regarding Claims 2-4, Pelaia teaches at Page 558, First Column, Second Paragraph, that “Carcinogenic mutations of KRas that stabilize the GTP-bound active conformation of this G-protein (thus being responsible for its constitutive activation), have been detected in about 20% of lung cancers, with relevant predominance occurring in the adenocarcinoma subtype of NSCLC.”
While Fu in view of Pelaia is silent regarding the specific mutations of KRAS present in the cancer cells suitable for treatment by a compound of Formula I and/or tipifarnib, treating cancers with these mutations will naturally flow from the method made obvious by the prior art (see above rejection), since the same compounds (a compound of Formula I and tipifarnib) are being administered to treat the same conditions, i.e. lung cancer. In other words, products of identical or similar composition cannot exert mutually exclusive properties when administered under the same or similar circumstances.
In other words, though the prior art is silent regarding treating cancers with the specific mutations recited, by practicing the method made obvious by the prior art, administering a combination of a compound of Formula I and tipifarnib, one will also be treating lung cancer with the mutations recited in Claims 2-4, even though the prior art was not aware of it.
Apparently, Applicant has discovered a new property or advantage of treating cancers with specific KRAS mutations of the method made obvious by the prior art.
MPEP 2145, II. states “The fact that Applicant 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”. Ex parte Obiaya, 227 USPQ 58, 60.
Regarding Claims 13-14 and 32, Fu teaches at Page 57, Paragraph 0543, that compounds of the invention are suitable for oral administration and can be provided in tablets containing about 1.0 to about 1000 mg, can be administered in single or multiple doses, and a suitable dosage level may be from about 0.1 to about 250 mg/kg per day. Per MPEP 2144.05, I., “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); In re Woodruff, 919 F.2d 1575, 16 USPQ2d 1934 (Fed. Cir. 1990)”.
Claim 12 is rejected under 35 U.S.C. 103 as being unpatentable over Fu in view of Pelaia in further view of Keating (“Afatinib: A Review of Its Use in the Treatment of Advanced Non-Small Cell Lung Cancer”, Adis Drug Evaluation, 2014; hereinafter referred to as Keating).
As stated above, Fu in view of Pelaia obviates the limitations recited at instant Claim 1, from which instant Claim 12 depends.
Fu in view of Pelaia does not teach further administering a third MAPK pathway inhibitor.
At Page 207, under “Abstract”, Keating teaches Afatinib, recited as a suitable MAPK pathway inhibitor at Page 14, Paragraph 0098 of the instant specification, is approved for the treatment of non-small cell lung cancer.
Per MPEP 2144.06, I., “"It is prima facie obvious to combine two compositions each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose.... [T]he idea of combining them flows logically from their having been individually taught in the prior art." In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980).”
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 1-4, 7, 12, 14, and 47 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 7, 14, 38, and 60 of copending Application No. 18/256,089 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of the instant application and the reference application are drawn to a method of treating cancer comprising administering a compound of Formula I as recited at instant Claim 1.
The claims of the reference application differ from the instant application in that Claim 1 of the reference application recites the limitation that the compound of Formula I is administered in combination with an EFGR inhibitor. Claim 7 of the reference application recites a list of suitable EGFR inhibitors. In the instant application, Claim 12 is drawn to administration of a compound of Claim 1, a KRAS inhibitor, and a third MAPK pathway inhibitor. The list of suitable MAPK pathway inhibitors includes, for example, afatinib and lapatinib, both of which are recited as suitable EGFR inhibitors at Claim 7 of the reference application. Thus, a method of treating cancer comprising administration of a compound of Formula I, a KRAS inhibitor, and a third MAPK pathway inhibitor as instantly recited reads on the method recited at least Claim 1 of the reference application, as the term “comprising” allows for additional components to be present as part of the application. Therefore, these claims are not patentably distinct.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 1-4, 7, 12-14, 32, and 47 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 60, 63-70, 75-78, and 84-88 of copending Application No. 18/256,090 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of the instant application and the reference application are drawn to a method of treating cancer comprising administering a compound of Formula I as recited at instant Claim 1.
The claims of the reference application differ from the instant application in that Claim 60 of the reference application recites the limitation that the compound of Formula I is administered in combination with an MEK inhibitor. Claims 69-70 of the reference application recites a list of suitable MEK inhibitors, including, for example binimetinib and trametinib. In the instant application, Claim 12 is drawn to administration of a compound of Claim 1, a KRAS inhibitor, and a third MAPK pathway inhibitor. The list of suitable MAPK pathway inhibitors includes, for example, binimetinib and trametinib, both of which are recited as suitable MEK inhibitors at Claims 69-70 of the reference application. Thus, a method of treating cancer comprising administration of a compound of Formula I, a KRAS inhibitor, and a third MAPK pathway inhibitor as instantly recited reads on the method recited at least Claim 60 of the reference application, as the term “comprising” allows for additional components to be present as part of the application. Therefore, these claims are not patentably distinct.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 1-4, 7, 12-14, 32, and 47 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 5-6, 9-11, 19, 21, and 24 of copending Application No. 18/572,412 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of the instant application and the reference application are drawn to a method of treating cancer comprising administering a compound of Formula I as recited at instant Claim 1.
The claims of the reference application differ from the instant application in that Claim 1 of the reference application recites the limitation that the compound of Formula I is administered in combination with an inhibitor of CDK 4/6. In the instant application, Claim 12 is drawn to administration of a compound of Claim 1, a KRAS inhibitor, and a third MAPK pathway inhibitor. At Page 14, Paragraph 0098, the instant specification sates the third MAPK inhibitor can target CDK4 and CDK6. Thus, a method of treating cancer comprising administration of a compound of Formula I, a KRAS inhibitor, and a third MAPK pathway inhibitor as instantly recited reads on the method recited at least Claim 1 of the reference application, as the term “comprising” allows for additional components to be present as part of the application. Therefore, these claims are not patentably distinct.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Conclusion
Claims 1-4, 7, 12-14, 20, 32, and 47 are rejected.
No claim is allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to DANIEL JOHN BURKETT whose telephone number is (703)756-5390. The examiner can normally be reached Monday - Friday.
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/D.J.B./ Examiner, Art Unit 1624
/JEFFREY H MURRAY/ Supervisory Patent Examiner, Art Unit 1624