DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application is being examined under the pre-AIA first to invent provisions.
The amendments and remarks filed 6/19/25 is acknowledged. Claims 1-5 have been amended. Claims 1-2 and 4-5 are pending and under examination.
Withdrawn Rejections
The objection to the specification for sequence disclosure deficiencies is withdrawn in light of Applicant’s amendment thereto. See paragraph 3, page 2 of the previous Office action.
The rejection of claim 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or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention, is withdrawn in light of Applicant’s cancelation of the claims. See paragraphs 6-7, page 4 of the previous Office action.
Maintained Rejections
Claim Rejections - 35 USC § 102
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 the appropriate paragraphs of pre-AIA 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(b) the invention was patented or described in a printed publication in this or a foreign country or in public use or on sale in this country, more than one year prior to the date of application for patent in the United States.
Claim(s) 1 and 4-5 is/are rejected under pre-AIA 35 U.S.C. 102(b) as being anticipated by Hanmei et al. (CN102205110 A, published October 5, 2011).
The instant claims are drawn to a method of treating or preventing rheumatoid arthritis with a polypeptide by a combination of downregulating inflammatory response and anti-angiogenesis, wherein the amino acid sequence of said polypeptide is: mPEG-SC20k-Ile-Val-Arg-Arg-Ala-Asp-Arg-Ala-Ala-Val-Pro-Gly-Gly-Gly-Gly-Arg-Gly-Asp (polypeptide IllI (SEQ ID NO: 3)).
CN102205110 A teach a polypeptide comprising the sequence mPEG-SC20k-Ile-Val-Arg-Arg-Ala-Asp-Arg-Ala-Ala-Val-Pro-Gly-Gly-Gly-Gly-Arg-Gly-Asp (polypeptide III) (See claim 1 and paragraphs 0009 and 0017-0018). CN102205110 A teach that the N end of polypeptide III is modified with PEG having a 20kD molecular weight (See paragraph 0020). Regarding the limitations “for use in a method for treatment or prevention of rheumatoid arthritis by a combination of downregulating inflammatory response and anti-angiogenesis”, “wherein said use involves the preparation of drugs for treatment or prevention of rheumatoid arthritis, wherein said drugs for treatment or prevention of rheumatoid arthritis contain an effective amount of salts acceptable to polypeptide III (SEQ ID NO: 3), or if necessary, pharmaceutically acceptable vectors or excipients”, and “wherein said use involves the preparation of drugs for treatment or prevention of rheumatoid arthritis, wherein said drugs for treatment or prevention of rheumatoid arthritis can be administered through a variety of routes, including hypodermic injection, intramuscular injection, intravenous injection, or drip, oral administration, including in the form of pills, capsules, and nasal spray”, the limitations are directed to the intended use of the polypeptide. A recitation of the intended use of the claimed invention must result in a structural difference between the claimed invention and the prior art in order to patentably distinguish the claimed invention from the prior art. If the prior art structure is capable of performing the intended use, then it meets the claim. In the instant case, the prior art teaches the claimed the same polypeptide recited in the instant claims, and therefore, would be capable of performing the intended use recited in the claim. Thus, CN102205110 A anticipate the claims.
ALIGNMENT:
Query Match 100.0%; Score 93; Length 18;
Best Local Similarity 100.0%;
Matches 18; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 IVRRADRAAVPGGGGRGD 18
||||||||||||||||||
Db 1 IVRRADRAAVPGGGGRGD 18
Applicant’s Arguments
Applicant argues that Hanmei does not teach the therapeutic use in rheumatoid arthritis via the combination of anti-inflammatory and anti-angiogenic mechanisms. Applicant argues that Hanmei does not teach or suggest the specific PEGYlation described in the present claims, using mPEG-SC with a molecular weight of approximately 20 kDa. Applicant argues that the intended use results in functional differences not present in the cited reference.
Response to Arguments
Applicant’s arguments have been fully considered but they are not persuasive. In response to Applicant’s argument that the Hanmei does not teach the combination of anti-inflammatory and anti-angiogenic mechanisms, Hanmei teaches administering the same polypeptide to the same patient population required by the claims. Therefore, the properties of “antiangiogenic” and “anti-inflammatory” would inherently be present in the prior art method. "Products of identical chemical composition can not have mutually exclusive properties." In re Spada, 911 F.2d 705, 709, 15 USPQ2d 1655, 1658 (Fed. Cir. 1990). A chemical composition and its properties are inseparable. Therefore, if the prior art teaches the identical chemical structure, the properties applicant discloses and/or claims are necessarily present. Id
In response to Applicant’s argument that Hanmei does not teach the specific pegylation described in the claims, Hanmei teaches the same polypeptide (i.e., polypeptide III) as the polypeptide recited in the claims. Additionally, Hanmei explicitly teaches that the polypeptide is modified with mPEG. Thus, Hanmei teaches the specific peglyation required by the claims.
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 pre-AIA 35 U.S.C. 103(a) which forms the basis for all obviousness rejections set forth in this Office action:
(a) A patent may not be obtained though the invention is not identically disclosed or described as set forth in section 102, if the differences between the subject matter sought to be patented and the prior art are such that the subject matter as a whole would have been obvious at the time the invention was made to a person having ordinary skill in the art to which said subject matter 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 pre-AIA 35 U.S.C. 103(a) 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.
This application currently names joint inventors. In considering patentability of the claims under pre-AIA 35 U.S.C. 103(a), the examiner presumes that the subject matter of the various claims was commonly owned at the time any inventions covered therein were made absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and invention dates of each claim that was not commonly owned at the time a later invention was made in order for the examiner to consider the applicability of pre-AIA 35 U.S.C. 103(c) and potential pre-AIA 35 U.S.C. 102(e), (f) or (g) prior art under pre-AIA 35 U.S.C. 103(a).
Claims 1-2 and 4-5 is/are rejected under pre-AIA 35 U.S.C. 103(a) as being unpatentable over Li et al. (European Journal of Pharmacology, 2007; 567:166-170) in view of Xu et al. (CN 101143894 A, published March 19, 2008).
The instant claims are drawn to a method of treating or preventing rheumatoid arthritis with a polypeptide by a combination of downregulating inflammatory response and anti-angiogenesis, wherein the amino acid sequence of said polypeptide is: mPEG-SC20k-Ile-Val-Arg-Arg-Ala-Asp-Arg-Ala-Ala-Val-Pro-Gly-Gly-Gly-Gly-Arg-Gly-Asp (polypeptide IllI (SEQ ID NO: 3)).
Li et al. teach a recombinant human endostatin polypeptide for treating rheumatoid arthritis (See abstract and page 168). Li et al. teach that administration of endostatin in saline solution (carrier) (0.5 mg/kg and 2.5 mg/kg) to rats with adjuvant induced arthritis significantly attenuated right hind paw swelling compared to control mice (See pages 168-169). Li et al. teach that treatment with endostatin improved polyarthritic symptoms and blocked angiogenesis of synovial lining in adjuvant arthritis rats (See page 169).
Li et al. do not teach polypeptide III (SEQ ID NO: 3).
Zhu et al. teach the polypeptide, HM-3, is a potent RGD modified endostatin-derived polypeptide and is a potent angiogenesis inhibitor (See page 341). Zhu et al. teach that the polypeptide was modified at its N terminus with methoxy-polyethylene glycol-Succinimidyl Carbonate (SC-mPEG, molecular weight 20 kDa, named SCmPEG20k) (See page 341 and 342). It should be noted that HM-3 comprises the same amino acid sequence set forth in SEQ ID NO: 3 of the instant claims.
CN101143894 A teach that although endostatin has attractive prospects, there are shortcomings that have limited its clinical use in humans: the targets of endostatin are unclear, the specificity and selectivity of blood vessels is not good enough, and the effect is limited, resulting in high dosage. CN101143894 A teaches that in the mouse models, the dose required is ten of milligrams/kilogram weight, which translates to a dose of at least a few grams humans. CN101143894 A teaches that such a large dose of the drug is bound to increase the likelihood of side effects of these drugs, resulting in difficulty with quality control, the scale of production, increased production costs and drug costs. CN101143894 A teaches that a good anti-angiogenic drug should be selective and improve the inhibition of angiogenesis drugs as a whole, done using only a low dose of the drug, it can achieve efficient inhibition of angiogenesis effect. CN101143894 A teach a modified endostatin peptide Ile-Val-Arg- Arg-Ala-Asp-Arg-Ala-Ala-Val-Pro-Gly-Gly-Gly-Gly-Arg-Gly-Asp (SEQ ID NO: 7) having improved anti-angiogenic effects, reduced side effects in vivo, and requiring lower dosage, thereby reducing costs for use as rheumatoid arthritis therapy. It should be noted that the polypeptide set forth in SE QID NO: 7 of the art is 100% identical to the polypeptide set forth in SEQ ID NO: 3. CN101143894 A teaches that the peptide can be modified with SC-mPEG (mono methoxy polyethylene glycol formyl succinimide) and the PEG can have a molecular weight range of 5000-30000 Da (See page 3). CN101143894 A teaches that the peptide is prepared in an expression vector and purified using HPLC (See page 3). CN101143894 A teaches that the peptide can be further modified to include PEG (See pages 1-2). CN101143894 A teach that the addition of the RGD motif to the endostatin peptide increases the binding affinity of the anti-angiogenic peptide to integrin, thereby resulting in a highly efficient angiogenesis inhibitor.
It would have been obvious to one of ordinary skill in the art at the time the invention was made to substitute the modified endostatin polypeptide HM-3 comprising SCmPEG20k for the full-length endostatin in the method of treating rheumatoid arthritis of Li et al. because Zhu et al. and CN101143894 A teach that the modified peptide has improved angiogenic effects and requires lower dosage. Given that CN101143894 A teach that full-length endostatin has limited effect, resulting in high dosage, it would be obvious to one of ordinary skill in the art to use the modified SCmPEG20k-HM-3 endostatin peptide, which offers the advantages of increased anti-angiogenic properties at lower doses and lower production cost, when treating rheumatoid arthritis. One of skill in the art would be motivated to use the modified SCmPEG20k-HM-3 endostatin peptide to treat rheumatoid arthritis because doing so would result in an improved angiogenic effect at lower doses and at a lower cost. One of ordinary skill in the art would have a reasonable expectation of success in treating rheumatoid arthritis with the modified SCmPEG20k-HM-3 endostatin peptide because both Zhu et al. and CN101143894 A teach that the peptide retains the anti-angiogenic properties of the full-length endostatin protein.
Additionally, KSR International Co. v. Teleflex Inc., 127 S. Ct. 1727, 1741 (2007), discloses that if a technique has been used to improve one method, and a person of ordinary skill would recognize that it would be used in similar methods in the same way, using the technique is obvious unless its application is beyond that person’s skill. KSR International Co. v. Teleflex Inc., 127 S. Ct. 1727, 1741 (2007) also discloses that “The combination of familiar element according to known methods is likely to be obvious when it does no more than yield predictable results”.
Thus, the combination of prior art references to arrive at the claimed invention provided a prima facie case of obviousness, absent evidence to the contrary.
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342
794
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Greyscale
SQ Sequence 18 AA;
Query Match 100.0%; Score 93; DB 12; Length 18;
Best Local Similarity 100.0%;
Matches 18; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 IVRRADRAAVPGGGGRGD 18
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Db 1 IVRRADRAAVPGGGGRGD 18
Applicant’s Arguments
Applicant argues that CN101143894 A acknowledges endostatin's "limited effect" in humans due to high dosage (page 9) but does not suggest HM-3 for rheumatoid arthritis. The prior art's focus on tumors provides no reason to apply HM-3 to arthritis, which involves distinct pathophysiology (synovial inflammation and angiogenesis). Applicant argues that the dual mechanism is unexpected. Applicant argues that the specification shows mPEG-SC20k-HM-3 inhibits NF-KB, TNF-a, and IL-6 while blocking angiogenesis (paragraph [0147]). Applicant argues that polypeptide III exhibits superior antirheumatoid arthritis activity and unexpected direct anti-inflammatory activity.
Response to Arguments
Applicant’s arguments have been fully considered but they are not persuasive. In response to Applicant’s arguments against the deficiencies of CN101143894 A alone, the reference is not an anticipatory reference and was used in an obviousness rejection. Therefore, Applicant’s arguments against the deficiencies of CN101143894 A alone are not persuasive. one cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986).
In response to Applicant’s arguments that polypeptide III exhibits superior antirheumatoid arthritis activity and unexpected direct anti-inflammatory activity, the combination of references discloses the use of polypeptide III for treating rheumatoid arthritis. Therefore, the unexpected results demonstrated by Applicant would necessarily be present in the prior art method, and are not unexpected. Furthermore, Zhu et al. teach the polypeptide, HM-3, is a potent RGD modified endostatin-derived polypeptide and is a potent angiogenesis inhibitor. Therefore, the art already recognizes the antiangiogenic properties disclosed by Applicant. "Expected beneficial results are evidence of obviousness of a claimed invention, just as unexpected results are evidence of unobviousness thereof." In re Gershon, 372 F.2d 535, 538, 152 USPQ 602, 604 (CCPA 1967) (resultant decrease of dental enamel solubility accomplished by adding an acidic buffering agent to a fluoride containing dentifrice was expected based on the teaching of the prior art); Ex parte Blanc, 13 USPQ2d 1383 (Bd. Pat. App. & Inter. 1989) (Claims at issue were directed to a process of sterilizing a polyolefinic composition which contains an antioxidant with high-energy radiation. Although evidence was presented in appellant’s specification showing that particular antioxidants are effective, the Board concluded that these beneficial results would have been expected because one of the references taught a claimed antioxidant is very efficient and provides better results compared with other prior art antioxidants.
New Rejection Necessitated by Applicant’s Amendment
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 1-2 and 4-5 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 a method for treating rheumatoid arthritis with a polypeptide by a combination of downregulating inflammatory response and anti-angiogenesis, wherein said method comprises administering the polypeptide consisting of the amino acid sequence mPEG-SC20-Ile-Val-Arg-Arg-Ala-Asp-Arg-Ala-Ala-Val-Pro-Gly-Gly-Gly-Gly-Arg-Gly-Asp (polypeptide III (SEQ ID NO: 3)), does not reasonably provide enablement for preventing rheumatoid arthritis. 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.
The factors considered when determining if the disclosure satisfies the enablement requirement and whether any necessary experimentation is undue include, but are not limited to: 1) nature of the invention, 2) state of the prior art, 3) relative skill of those in the art, 4) level of predictability, 5) existence of working samples, 6) breadth of claims, 7) amount of direction or guidance by the inventor, and 8) quantity of experimentation needed to make or use the invention. In re Wands, 858 F.2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988).
1) Nature of the invention and 6) Breadth of the claims
The nature of the invention is a method of treating or preventing rheumatoid arthritis with a polypeptide by a combination of downregulating inflammatory response and anti-angiogenesis, wherein the amino acid sequence of said polypeptide is: mPEG-SC20k-Ile-Val-Arg-Arg-Ala-Asp-Arg-Ala-Ala-Val-Pro-Gly-Gly-Gly-Gly-Arg-Gly-Asp (polypeptide IllI (SEQ ID NO: 3)).
Therefore, the nature of the invention is a chemical case, wherein there is natural unpredictability in performance of certain species or sub-combinations other than those specifically enumerated; See MPEP 2163. Accordingly, it is the Office’s position that undue experimentation would be required to make and use the claimed polypeptide III for preventing rheumatoid arthritis, with a reasonable expectation of success, because it would not be predictable from the disclosure of any particular species what other species may or may not work; See MPEP 2164.03.
The specification does not provide written description for preventing rheumatoid arthritis. The specification demonstrates that the polypeptide having the amino acid sequences set forth in SEQ ID NO: 3 treats rheumatoid arthritis, as shown by reduced paw swelling, reduced joint swelling, and reduced clinical score compared to the model control in the CIA and AIA animal models. However, the specification does not demonstrate that the polypeptide has the function of preventing rheumatoid arthritis. The term "prevent" is defined as to keep from occurring or happening; however, the specification does not show that the polypeptides keep rheumatoid arthritis from occurring. It should be noted that in both models of rheumatoid arthritis, disease is induced and then the individual polypeptides are administered. Preventing would necessarily mean that an individual would be given the claimed polypeptide, and such administration would ensure that the patient did not develop rheumatoid arthritis. However, the polypeptide is never administered before the onset of disease to show that the polypeptides prevent the development of rheumatoid arthritis in the CIA and AIA animal models. Thus, the models provide guidance regarding the use of the polypeptides to treat rheumatoid arthritis, but not for prevention of arthritis.
(5) The state of the prior art and (7) The predictability or unpredictability of the art
The state of the art regarding treating and preventing rheumatoid arthritis is discussed by Machold (Best Practice and Research Clinical Rheumatology, 2010; 24:353-361). Machold teaches that advances in treatment of rheumatoid arthritis have made it possible to influence signs and symptoms as well as the course of joint destruction; however cure (the absence of signs and symptoms without further treatment) is still relatively rare, observable in at most, 20% of the patients (See abstract). Machold teaches that "cure" of a disease means that, after a period of absence of health, the affected individual regains full health without continuous treatment (See page 354). Machold teaches that RA is a chronic inflammatory disease whose cause is still unknown but appears to be multifactorial and progresses with cumulative damage to joints and sometimes, soft tissue and internal organs. Machold teaches that in this framework, "cure" appears to have a low probability of occurring (See page 354). Machold teaches that prevention has several stages: “primary prevention” refers to methods designed to avoid the occurrence of disease or impairment; “secondary prevention” refers to methods directed to those identified within the target populations at risk and thus refers to early diagnosis and treatment to shorten illness episodes and limit disease sequelae; “tertiary prevention” involves both treatment of the identified problem or disease and restoration of the individual to a full state of functioning within the targeted population (See page 354). Machold teaches that secondary and tertiary prevention imply that some limited amount of impairment might remain, and thus, are the more likely scenarios when discussing outcomes of intervention in rheumatoid arthritis (See page 354). Machold teaches that the bulk of the literature on RA implies, even if only minimal disease activity is reached, most patients appear to be in need of at least some amount of treatment (See page 354). Machold teaches much less clarity exists whether sufficiently aggressive treatment which has resulted in remission may be withheld, given that the proportion of patients that continue to do well without treatment (and thus would be considered cured from RA) is rather low (See page 358). Thus, the reference demonstrates that it is unlikely that any therapeutic agent "prevents" rheumatoid arthritis.
Further underscoring the unpredictability in treating rheumatoid arthritis, Allaart et al. (Clinical and Experimental Rheumatology, 2006; 6(Suppl. 43):77-82) discuss four different treatment strategies for patients with early rheumatoid arthritis. Allaart et al. teach that 508 patients with newly diagnosed RA were randomized to four different treatment strategies: 1. sequential monotherapy, 2. step up to combination therapy (both starting with methotrexate), 3. initial combination therapy with methotrexate, sulphasalazine, and a tapered high dose of prednisone, and 4. initial combination therapy with methotrexate and infliximab (See page 77). Allaart et al. teach that 80% of all patients achieved the goal of DAS ≤ 2.4, and 42% reached clinical remission (DAS < 1.6) (See page 77). Allaart et al. teach that initial combination therapy, either with prednisone (group 3) or with infliximab (group 4), resulted in earlier improvement in functional ability, more continuous clinical remission (DAS < 1.6), and less joint damage progression than initial monotherapy (groups 1 and 2) (See page 77). Allaart et al. teach that patients receiving combination therapy were able to switch to monotherapy after two years of treatment (See page 80). It should be noted that Allaart et al. does not demonstrate that any patient is “cured" from RA or that RA is prevented. Allaart et al. teach that the focus of treatment is prevention of structural damage and functional declines and demonstrates that this is achieved with combination therapy. This reference underscores the fact that even with well-established therapies, prevention of rheumatoid arthritis is unlikely. Furthermore, it should be noted that the best treatment for rheumatoid arthritis are combination therapies. Given the teachings of the art, one would not readily recognize preventing rheumatoid arthritis with a single polypeptide monotherapy as required by the instant claims.
(6) The amount of direction or guidance by the inventor; (7) The existence of working examples
The specification teaches that the therapeutic effect of polypeptides I-III were investigated in the mouse collagen-induced arthritis (CIA) model and adjuvant induced arthritis (AIA ) in rats. The specification teaches that polypeptides I-III show an immunoprotective effect on CIA mouse models, as demonstrated by significantly reduced paw swelling, reduced joint swelling, and reduced clinical score compared to the model control (See tables 1, 3, and 5). The specification teaches that polypeptides I-III show an immunoprotective effect in the AIA model, as demonstrated by significantly reduced paw swelling, reduced joint swelling, and reduced clinical score compared to the model control (See tables 2, 4, and 6).
Applying the above test to the facts of record, it is determined that 1) no declaration under 37 C.F.R. 1.132 or other relevant evidence has been made of record establishing the amount of experimentation necessary, 2) insufficient direction or guidance is presented in the specification with respect to making and using the claimed polypeptide for preventing rheumatoid arthritis, 3) the relative skill of those in the art is commonly recognized as quite high (post-doctoral level). One of skill in the art would require guidance, in order to make or use the claimed polypeptide for treating rheumatoid arthritis. Without proper guidance, the experimentation to is undue.
The Applicant has not provided sufficient guidance to enable one of skill in the art to make and use the claimed invention in a manner reasonably correlated with the scope of the claims broadly including preventing rheumatoid arthritis with the claimed polypeptide III. The scope of the claims must bear a reasonable correlation with the scope of enablement (In re Fisher, 166 USPQ 19 24 (CCPA 1970). Without such guidance, preventing rheumatoid arthritis with the claimed polypeptide is unpredictable and the experimentation left those skilled in the art is unnecessarily and improperly, extensive and undue. See Amgen Inc v Chugai Pharmaceutical Co Ltd. 927 F 2d 1200, 18 USPQ2d 1016 (Fed. Cir. 1991) at 18 USPQ2d 1026-1027 and Ex parte Forman, 230 U.S.P.Q. 546(Bd. Pat=. App & int. 1986).
In view of all of the above, one of skill in the art would be forced into undue experimentation to practice the claimed invention, and thus, the claimed invention does not satisfy the requirements of 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph.
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 1-2 and 4-5 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.
Claim 1 is indefinite because the claim does not recite an active step. Although the preamble specifies that the claim is for treating or preventing rheumatoid arthritis, and the body specifies the sequence of the polypeptide, the claim does not include a positively recited active step (i.e., administering the polypeptide). It is recommended that Applicant amend the claim to recite “A method for treating rheumatoid arthritis with a polypeptide by a combination of downregulating inflammatory response and anti-angiogenesis, wherein said method comprises administering the polypeptide consisting of the amino acid sequence mPEG-SC20-Ile-Val-Arg-Arg-Ala-Asp-Arg-Ala-Ala-Val-Pro-Gly-Gly-Gly-Gly-Arg-Gly-Asp (polypeptide III (SEQ ID NO: 3)”. The dependent claims do not cure the deficiencies of claim 1, and thus, are included in the rejection. Clarification and/or correction is required.
Claim Status
No claims are allowed.
Conclusion
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
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/SANDRA CARTER/Examiner, Art Unit 1674
/VANESSA L. FORD/Supervisory Patent Examiner, Art Unit 1674
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