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 .
DETAILED ACTION
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 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.
Status of Claims
Claims 18-23 are pending and examined on merits in this office action.
Claim Rejections - 35 USC § 112
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 18-23 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for pre-AIA the inventor(s), at the time the application was filed, had possession of the claimed invention.
Claim 18 and claims dependent thereon are directed to treat an individual with dry AMD that is at risk of developing wet AMD based on detection of either a at least 20% increase or a 20% decrease of anyone of the autoantibody recited in step (ii) as compared to a control value. However, throughout the specification, a determination of an individual as a risk of developing from dry AMD to wet AMD using a single autoantibody selected from anyone of the recited auto-antibody has not been clearly been established in the specification. As for example, specification teaches that one of the most prominently changed reactivity is against alpha-synuclein but Alpha-synuclein is known from other neurodegenerative diseases. Others are heat shock proteins (e.g. HSP 10) and also Annexin V, which plays a major role in apoptotic processes. Specification also teaches that several other biomarkers including HSP10, MAPK3, Annexin-V and alpha-synuclein are associated with various other diseases including neurodegenerative diseases. Claim 20 is directed to is directed to determination of individual suffers from Dry AMD or wet AMD from either of the increased or decreased content of autoantibodies against OGFR in various types of samples from a subject. Note that the recitation “Dry and/or wet AMD” includes either of Dry or Wet AMD and thus either of increase or decrease of 20% compared to control of autoantibody to OGFR provides detection of Wet AMD in the subject. Throughout the specification, determination of dry AMD or wet AMD in a subject by detecting at least 20% increase or 10% decrease in autoantibody against OGFR only has not clearly been established. Contrary to claim’s recitation, Fig. 3 of the specification teaches pattern of increase and pattern of decrease of several biomarker (not only one) (autoantibodies) for the determination of either dry AMD or WET AMD and moreover, the sample as disclosed in the specification is a blood sample, not the various types of samples (as for example, tissue sample, cerebrospinal fluid or retinal fluid) as encompassed by the claims. There are no working examples in which autoantibodies were detected in any of the other body fluids as encompassed by the claims. Furthermore, as evidenced from Mollick et al (Cancer immune 2003) melanoma, prostrate, breast or ovarian cancer patients have antibodies to OGFR (see abstract) and thus increase of OGFR only in a subject cannot be attributed to risk of developing wet AMD absent substantiated by confirmation with other biomarker that providing indication of developing from dry AMD to wet AMD.
Throughout the specification, it is the increase and/or decrease of some selected autoantibody, not only a single autoantibody wherein the pattern shows some autoantibodies increased by 20% (upregulation of immunoreactivity) and some decreased by 20% (down regulation of immunoreactivity) which is indicative of Dry AMD or Wet AMD compared with a control from a healthy subject. Correlation of increase or decrease of a single autoantibody has not been clearly established or clearly correlated to only Dry AMD or Wet AMD, which as described above many of the claimed biomarker are associated with various other diseases including various other neurodegenerative diseases including cancer.
Example of determination based only on immunoreactivity only with a single antigen has not been clearly been disclosed and even if a determination based on only on a single autoantibody has been disclosed, the disclosure would not be considered a representation of determination with all the autoantibody selected individually.
To provide adequate written description and evidence of possession of a claimed genus, the specification must provide sufficient distinguishing identifying characteristics of the genus. The factors to be considered include disclosure of complete or partial structure, physical and/or chemical properties, functional characteristics when coupled with a known or disclosed structure/function correlation, methods of making the claimed product, or any combination thereof.
Accordingly, it is deemed that the specification fails to provide adequate written description and clear guidance for a determination of an individual as suffering from Dry AMD or Wet AMD using a single autoantibody selected from anyone of the recited autoantibody as encompassed by the claim has not been clearly established in the specification and the specification does not reasonable convey to one skilled in the relevant art that the inventor(s), at the time the application was filed, had possession of the entire scope of the claimed invention.
Response to argument
Applicant's arguments and amendments filed 04/06/2026 have been fully considered and but are not persuasive to overcome the rejection under 35 USC 112 (a).
Applicant argued that Applicant discovered the surprising effect that one can predict if a patient having dry AMD is at risk of developing wet AMD based on specific individual antigens or specific groups/patterns of antigens. This is clearly noted in paragraphs [0068-0076] and paragraphs [0106]-[0111] of the instant Specification. For at least these reasons, the rejections of independent claim 18 and those claims depending therefrom should be withdrawn.
The above arguments have fully been considered but are not found persuasive. The claim recites “identifying the individual as being at risk of developing wet AMD if the amount of at least one antibody (note that at least one antibody includes only one antibody) in the pattern of autoantibodies (i.e. all the autoantibodies detected in the control) is increased by at least 20% or decreased by at least 20% compared to control values”. So, in fact, the claim encompasses predicting risk of developing wet AMD based on detection of increase or decrease by 20% of only one of the autoantibodies either from Group A or Group B autoantibodies, which does not have a clear descriptive support in the specification. As claimed and as addressed in the rejection, claim 18 and dependent claims thereon are directed to treating an individual having dry AMD with a VEGF antagonist after individual being determined at a risk of developing to wet AMD, wherein the determination is based on detection of either a at least 20% increase or a 20% decrease of anyone of the autoantibody recited in step (ii) as compared to a control value. As described in the rejection, a determination of an individual as a risk of developing from dry AMD to wet AMD from the 20% increase or decrease of a single autoantibody selected from anyone of the recited auto-antibody has not been clearly been established in the specification. Specification teaches that one of the most prominently changed reactivity is against alpha-synuclein but Alpha-synuclein is known from other neurodegenerative diseases. Others are heat shock proteins (e.g. HSP 10) and also Annexin V, which plays a major role in apoptotic processes. Specification also teaches that several other biomarkers including HSP10, MAPK3, Annexin-V and alpha-synuclein are associated with various other diseases including neurodegenerative diseases. Fig. 3 discloses at least 20% increase of autoantibody to OGFR in a subject from dry AMD and the 20% increase in autoantibody to OGFR only does not provide any indication that the subject is at risk of developing wet AMD as there is no clear data establish the result. Regarding claim 20, , throughout the specification, determination of Dry AMD or Wet AMD in a subject by detecting at least 20% increase or 10% decrease in autoantibody against OGFR only has not clearly been established. Contrary to claim’s recitation, Fig. 3 of the specification teaches pattern of increase and pattern of decrease of several biomarker (autoantibodies) for the determination of either dry AMD or WET AMD and moreover, the sample as disclosed in the specification is a blood sample, not the various types of samples (as for example, tissue sample, cerebrospinal fluid or retinal fluid) as encompassed by the claims. There are no working examples in which autoantibodies were detected in any of the other body fluids as encompassed by the claims. Furthermore, as evidenced from Mollick et al (Cancer immune 2003) melanoma, prostrate, breast or ovarian cancer patients have antibodies to OGFR (see abstract) and thus increase of OGFR only in a subject cannot be attributed to risk of developing wet AMD absent substantiated by confirmation with other biomarker that providing indication of developing from dry AMD to wet AMD.
Conclusion
THIS ACTION IS MADE FINAL. 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.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to SHAFIQUL HAQ whose telephone number is (571)272-6103. The examiner can normally be reached on Mon-Fri 8-4:30.
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, Gregory S. Emch can be reached on 571-272-8149. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of an application may be obtained from the Patent Application Information Retrieval (PAIR) system. Status information for published applications may be obtained from either Private PAIR or Public PAIR. Status information for unpublished applications is available through Private PAIR only. For more information about the PAIR system, see http://pair-direct.uspto.gov. Should you have questions on access to the Private PAIR system, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative or access to the automated information system, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
/SHAFIQUL HAQ/Primary Examiner, Art Unit 1678
Prosecution Insights