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 .
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.
DETAILED ACTION
This action is in response to claim amendments filed 11/28/23. Claims 1-6, 11-12, 17-19, 23, 27-32, 65, and 76 are pending and under examination.
Claim Rejections - 35 USC § 112
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 2-6 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 a method of treating TBI. Claims 2-6 are directed to the administration window for the therapeutic, which is within a certain amount of time of “a brain injury”. This is not “the brain injury” or “the traumatic brain injury” and so, as written, the administration of the antibody occurs within a certain period of time of the patient suffering any brain injury, not just the TBI, which somehow treats a TBI. In one interpretation, the patient must already have TBI but the administration is after a second, unrelated brain injury. A second interpretation is that the administration can be after any brain injury even where the patient does not have TBI, but that administration will later treat a TBI should the patient eventually suffer TBI. A third interpretation is that “a brain injury” is meant to refer to the TBI in claim 1, though if this is the case the claim should read “the traumatic brain injury” to provide clear antecedent basis”.
Further note that claims 2, 4, and 5 recite “a brain injury”, claim 3 is “brain injury” (lacking any article), while claim 6 is “the brain injury”. Using “the brain injury” in claim 6 but not the previous claims adds further evidence that claims 2-5 are not meant to refer to TBI but to any brain injury as written, yet it is still unclear if this is in fact the case. The use of “the brain injury” in claim 6 also lacks clear antecedent basis because there is no “a brain injury” in claim 1. While it is suspected that “the brain injury” refers to “a traumatic brain injury”, consistent terminology should be used to provide clear antecedent basis.
Therefore, claims 2-6 are indefinite.
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.
The following is a quotation of pre-AIA 35 U.S.C. 112, fourth paragraph:
Subject to the following paragraph [i.e., the fifth paragraph of pre-AIA 35 U.S.C. 112], 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 76 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 76 is a kit, which depends from claim 1. However, claim 1 is a method of treating brain injury, the method steps themselves not being required by a kit. Further, the kit is for treating or preventing any brain injury, which is broader than treating (not preventing) specifically TBI. Thus, claim 76 does not contain all of the limitations from the claim upon which it depends.
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.
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.
Claim 76 is 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 TBI, does not reasonably provide enablement for preventing TBI. 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.
There are many factors considered when determining if the disclosure satisfies the enablement requirement and whether any necessary experimentation is undue. These factors include, but are not limited to: 1) nature of the invention, 2) breadth of claims, 3) amount of direction or guidance by the inventor, 4) relative skill of those in the art, 5) level of predictability in the art, 6) state of the prior art, 7) existence of working examples, and 8) quantity of the experimentation needed to make or use the invention. In re Wands, 858 F.2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988).
Where a composition is claimed with a particular use, that use must be evaluated for enablement (MPEP §2164.01(c)). In this case, Applicant claims a kit containing instructions regarding how to use the C1q antibody of claim 1 to prevent any and all brain injuries. This is use is not enabled and so the claim is not enabled for containing instructions on how to accomplish this non-enabled task.
The amount of direction in the specification is that brain injuries, specifically traumatic brain injury, may be treated with the claimed antibody. However, the specification does not contain any guidance regarding preventing brain injuries. Rather, with TBI, the art does not recognize any therapeutic which prevents a traumatic brain injury. The art suggests mechanical preventative, e.g., helmets, but does not suggest any drug or antibody which would prevent severe impact to the head from damaging the brain. Huber (2014; form 892) teaches that preventing TBI is desirable but has not yet been achieved. Rather, Huber focuses on ways to “prevent” secondary damage, specifically preventing the initial trauma from developing into a long-term neurodegenerative disease (abstract). Similarly, Guilhaume (2023; form 892) suggests research into therapeutics that “help prevent the secondary injury cascade after blast injury” (abstract). Thus, the “blast injury”—the brain injury—was not prevented and instead is being treated by attempting to mitigate secondary damage. The amount of experimentation is undue as the claims encompass the previously unattainable goal of full prevention of TBI regardless of the cause of said TBI while not providing evidence nor scientific reasoning as to why an antiC1q antibody would succeed where others failed. The claims then extend this to the prevention of any form of brain injury, which is equally unsubstantiated.
Therefore, claim 76 is not enabled for the full scope.
Claim Rejections - 35 USC § 101
35 U.S.C. 101 reads as follows:
Whoever invents or discovers any new and useful process, machine, manufacture, or composition of matter, or any new and useful improvement thereof, may obtain a patent therefor, subject to the conditions and requirements of this title.
Claim 65 rejected under 35 U.S.C. 101 because the claimed invention is directed to a judicial exception without significantly more.
Step 1: It must first be determined if the claim is to a statutory category and, if so, proceed to step 2A prong 1. Claim 65 is a method and falls within the statutory category of a process.
Step 2A, prong 1: Prong 1 requires the Examiner to evaluate whether the claim recites a judicial exception and, if so, proceed to prong 2. In this case, the claim recites “the risk of developing a brain injury is characterized based on the comparison of the amount or location of one or more of C1q, C1r, or C1s to the reference”. In other words, the claim is directed to the observation of the naturally occurring amount or location of these natural biomarkers and informing others of the relationship between these levels/locations and a risk (observation of a natural phenomenon).
Step 2A, prong 2: Prong 2 requires the Examiner to evaluate whether the claim recites additional elements that integrate the exception into a practical application of that exception and, if not, proceed to step 2B. In order to integrate the recited judicial exception into a practical application, the claim will apply, rely on, or use the judicial exception that imposes a meaningful limit such that the claim is more than a drafting effort to monopolize the judicial exception. Examiners evaluate integration by identifying additional elements in the claim beyond the judicial exception and evaluating those elements individually and in combination to determine whether they integrate the exception in to a practical application. Examples that have been found by the Courts in which the exception was not integrated into a practical application include:
Mere instructions to implement an abstract idea on a computer
Adding generic instructions that the judicial exception should be used ("apply it")
Adding insignificant extrasolution activity to the exception ("mere data gathering")
Generally linking the use of the exception to a particular technological environment or field of use
In this case, an antibody to the target is administered and detected. These are the necessary data gathering steps in order to observe the phenomenon. Once the necessary data is gathered, the data is “compared” (a mental step) and the claim warns others of the implications of that comparison. The characterization step is recited at a high level of generality. The characterization of risk is not claimed in any particular manner nor are there any limitations regarding the outcome of that characterization nor utilization of the characterization; this is not integration into a practical application as this is essentially “apply it”.
Step 2B: Where a claim does not integrate the exception, a claim may nevertheless be patent eligible, for example where additional elements are “significantly more” than the exception such that the additional elements were unconventional in combination. Considerations include whether or not the claim adds a specific limitation or combination of limitations that are not well-understood, routine, conventional activity in the field, which is indicative that an inventive concept may be present; or simply appends well-understood, routine, conventional activities previously known to the industry, specified at a high level of generality, to the judicial exception, which is indicative that an inventive concept may not be present. In this case, using antibodies to detect a biomarker is widely known, routine, and conventional. For example, see US 20170152309 (form 892) paragraph 50, which also uses anti-C1q antibodies to detect biomarkers. See also US 20120087861 (form 892) claim 18 (anti-tau antibodies for detecting tau and determining a diagnosis) and US 20150126396 (form 892) claims 1, 11, and 13-14 (tracer antibodies to bind biomarkers to determine a diagnosis).
Therefore, claim 65 is not patent eligible.
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 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 –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claim(s) 65 is rejected under 35 U.S.C. 102(a)(1-2) as being anticipated by Yednock (US 20170152309).
Regarding claim 65, Yednock teaches a method of determining a subject’s risk of developing a disease associated with complement activation comprising administering anti-C1q antibody coupled to a detectable label, detecting the label to determine the amount or location of C1q in the subject, and comparing this to a reference (e.g., claim 48).
First, the method in both Yednock and the instant claim is one of determining a risk. In other words, neither subject actually has a brain injury nor a disease associated with complement activation and so both methods are being performed on the same population. Second, the “wherein” clause in both Yednock and the instant claim describes what the data implies, i.e., it is not an additional step by the user but an inherent quality in the gathered data. Applicant's attention is directed to MPEP § 2112 (II), which states, "there is no requirement that a person of ordinary skill in the art would have recognized the inherent disclosure at the time of invention, but only that the subject matter is in fact inherent in the prior art reference. Schering Corp. v. Geneva Pharm. Inc., 339 F.3d 1373, 1377, 67 USPQ2d 1664, 1668 (Fed. Cir. 2003)." Furthermore, Integra Life Sciences I Ltd. v. Merck KGaA, 50 USPQ2d 1846 (DC SCalif, 1999) makes clear that a reference teaching a process may anticipate claims drawn to a method comprising the same process steps, despite the recitation of a different intended use in the preamble or the later discovery of a particular property of one of the starting materials or end products.
Finally, the instant specification does not provide any special definition for “brain injury”; however, the specification provides examples in the form of traumatic brain injury, hypoxic brain injury, brain infection, or stroke (e.g., p. 74 L8-9). Thus, the broadest reasonable interpretation of “brain injury” includes any damage to the brain by any cause. Yednock teaches that the disclosure is generally directed to synapse loss, specifically excessive synapse loss, which is within the broadest reasonable interpretation of a brain injury. Further, Yednock teaches many specific examples of this (paragraphs 37-38), including specific neurodegenerative diseases associated with the loss of synapses or nerve connections (paragraph 37). More broadly, Yednock teaches the increased expression of C1q “after brain injury” (paragraph 97) and that lowering complement is neuroprotective (paragraph 9). Thus, the diseases of Yednock associated with deteriorating brain tissue/nerves/synapses all meet the criteria of the instant “brain injury” and would have allowed the artisan to immediately envisage the methods of Yednock as ones treating/determining risk of “brain injury”.
Therefore, claim 65 is anticipated.
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.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 1-6, 11-12, 17-19, 23, 27-32, and 76 is/are rejected under 35 U.S.C. 103 as being unpatentable over Yednock (US 20170152309) in view of Muizelaar (IDS 11/28/23 citation CO) and further in view of Hammad (IDS 11/28/23 citation CF), McGonigal (form 892), and ScienceDaily (IDS 11/28/23 citation CA).
Regarding claim 1, Yednock teaches an antibody Fab fragment that binds to C1q (claim 1). Yednock teaches using an anti-C1q antibody to inhibit synapse loss, specifically excessive synapse loss. Further, Yednock teaches many specific examples of this (paragraphs 37-38), including specific neurodegenerative diseases associated with the loss of synapses or nerve connections (paragraph 37; claims 1, 31, 32, and 37) and ischemia-reperfusion injury (paragraph 38; 48; 101). In particular, Yednock notes that the complement factor is rapidly induced by “a variety of insults to the brain such as infection, ischaemia, and injury” (paragraph 164).
Yednock does not explicitly disclose TBI. The antibody of Yednock is a Fab, which is not a full-length antibody.
With respect to TBI, Yednock does not explicitly disclose TBI. However, Yednock does note the relevance of the inappropriate activation of the complement system in ischemia-reperfusion injury (paragraph 2). Further, Yednock teaches the anti-C1q therapy as treating “brain injury” (paragraph 9) as well as the increase of C1q after brain injury (paragraph 97).
Muizelaar teaches that traumatic brain injury is a brain injury (severe head injury). Muizelaar also teaches that TBI is an ischemia-reperfusion-type injury (title).
Hammad also teaches TBI is a brain injury: “TBI is defined as damage to the brain resulting from an external force that causes the brain to move quickly within the skull” (p.1 C1). Hammad also teaches the complement system plays a role in the inflammatory reaction, which is a primary contributor to the injury in TBI (abstract). Specifically, Hammad teaches that microglia exist in either the M1 state—which damages healthy cells—or the M2 state—which is associated with improved cellular survival and tissue repair—and that C1q “contributes to a shift towards the M1 phenotype” (p.2 C1).
One of ordinary skill in the art at the time of filing would have found it obvious to utilize the method of Yednock (administering anti-C1q antibody to treat brain injury) to treat TBI. TBI is a brain injury characterized by ischemia-reperfusion and deleterious activation of the complement system, while the method of Yednock is one of treating brain injury, in particular ischemia-reperfusion injuries and those which would benefit from inhibited C1q. Thus, while not explicitly naming TBI as the “brain injury”, one would have had a reasonable expectation of success in using Yednock’s method to treat TBI because Yednock teaches the method treats brain injury as well as pathologies present in TBI. This is further reinforced by Yednock’s discussion of the relevance of the complement system to ischemic injuries, while Muizelaar teaches that TBI is such an ischemic event and Hammad teaches the relevance of the complement system in TBI.
With respect to a “full-length antibody”, Yednock teaches using an antibody fragment, specifically a Fab. However, Yednock teaches throughout the document that the therapeutic mechanism of this Fab is that the antibody fragment binds and inhibits C1q, inhibiting the classical complement system (paragraphs 6; 32; 96).
McGonigal teaches the antibody M1, which binds and neutralizes C1q (p.3 C1). McGonigal teaches the M1 antibody was compared against a “non-specific isotype control IgG1 mAb”; since the isotype is defined by the Fc region, the M1 antibody is a full-length antibody. McGonigal tests the antibody in a mouse model for axonal injury as a result of inflammation mediated by the complement system (abstract). McGonigal demonstrates that the anti-C1q antibody M1 “attenuates [neuron] injury with a consequent neuroprotective effect” (abstract).
It would have been obvious at the time of filing that the anti-C1q antibody Fab of Yednock could be substituted with the anti-C1q antibody of McGonigal with predictable results. Both antibodies target and inhibit C1q, both documents describe the therapeutic benefits of inhibiting the classical complement pathway, and both documents describe the neuroprotective effect of these antibodies. Further, Yednock explicitly states that the antibody should bind the same C1q epitope as the M1 antibody (claim 7), which is the antibody of McGonigal, and suggests the Fab of Yednock has the identical CDRs (binding regions) of the M1 antibody (paragraph 24) and refers to the Fab as “M1 Fab” (paragraph 56), further providing a reasonable expectation that using the M1 antibody would achieve the same effects as Yednock since the antibody of Yednock is the McGonigal M1 antibody in a Fab format.
In summary, one of ordinary skill in the art would have known that the classical complement pathway can damage neurons (Hammad and Muizelaar) and that inhibiting the classical complement pathway by inhibiting specifically C1q is a desirable therapeutic outcome to protect neurons from such damage (Yednock and McGonigal). One of ordinary skill in the art would further have known that TBI is characterized by ischemia/reperfusion, leading to activation of the classical complement pathway which plays a role in the damage caused by TBI (Hammad and Muizelaar). One would have known that using an anti-C1q antibody is therapeutic for treating such ischemia- and complement-related conditions such as TBI (Yednock) and would have expected similar results using an antibody which demonstrates similar inhibition and neuroprotective properties (McGonigal), particularly as the antibody of Yednock is the Fab region of McGonigal’s M1 antibody, having the same CDRs and binding the same C1q epitope. Thus, the method of claim 1 as a whole would have been obvious.
Regarding claims 2-5, the claims are interpreted such that “brain injury” and “a brain injury” refer to “a traumatic brain injury” in claim 1. Yednock does not explicitly disclose treatment within the time frames claimed, i.e., a range of within the first 4 weeks of a brain injury to within six hours of a brain injury. However, “where the general conditions of a claim are disclosed in the prior art, it is not inventive to discover the optimum or workable ranges by routine experimentation.” In re Aller, 220 F.2d 454, 456, 105 USPQ 233, 235 (CCPA 1955). See MPEP §2144.05(II). “[I]t is a settled principle of law that a mere carrying forward of an original patented conception involving only change of form, proportions, or degree, or the substitution of equivalents doing the same thing as the original invention, by substantially the same means, is not such an invention as will sustain a patent, even though the changes of the kind may produce better results than prior inventions” (MPEP §2144.05(II)(A)).
Such is the case here. Where the only difference between the prior art and the instant claim is in an explicit timing requirement which represents no more than optimization of the prior art drug timing, such optimization would have been obvious. Further, as taught by ScienceDaily, “harmful changes to the brain’s synaptic connections occur within the first three minutes following a stroke” (title; summary) and indicates that while stroke can be treated “three hours after onset”, damage is occurring “almost immediately”. Thus, one of ordinary skill in the art at the time of filing would have found it obvious to administer treatment as soon after the injury as possible to limit the damage, making treatment within four weeks of the injury obvious. The same applies to “within six hours after [the TBI]”, as ScienceDaily teaches the damaging effects occur within minutes and suggests treatment should commence within three hours.
Regarding claim 6, inhibition of synapse loss is one means by which the treatment functions according to Yednock; see e.g., paragraphs 9, 166. Further, as the antibody of McGonigal inhibits the same target (C1q), is the parent antibody of the Yednock M1 Fab, and is also neuroprotective, these same results would be expected when using the M1 antibody.
Regarding claim 11, Yednock teaches these functions of the antibody (paragraph 31). Moreover, administering the same agent (anti-C1q antibody) to the same subject (one with a brain injury/synapse loss) must achieve the same results absent evidence to the contrary. McGonigal also teaches this result, teaching that anti-ganglioside antibodies pathogenically target nerve cells (p.2 C1; i.e., autoantibody) and that the M1 antibody prevents C1q from binding the anti-ganglioside antibody (autoantibody; p.3 C1). Yednock teaches the M1Fab has the same properties as the M1 antibody (paragraphs 22-24; figures 1 and 2).
Regarding claim 12, as above, administering the same agent (anti-C1q antibody) to the same subject (one with TBI/synapse loss) must achieve the same results.
Regarding claim 17, as above, administering the same agent (anti-C1q antibody) to the same subject (one with TBI/synapse loss) must achieve the same results. Further, Yednock teaches this is one of the mechanisms by which the method functions (paragraph 9: “neutralizing the activity of complement factors such as C1q”) as does McGonigal (p.3: “neutralizes C1q and thereby prevents binding”).
Regarding claim 18, see rejection of claim 11; for example, paragraph 31 of Yednock teaches the disruption of C1q binding to an autoantibody and C1q binding to C1r while McGonigal also teaches the antibody prevents C1q binding anti-ganglioside antibodies. Yednock teaches the M1 Fab has the same properties as the M1 antibody as discussed above.
Regarding claim 19, Yednock discloses the inhibition of the same biological activities, e.g., synapse loss (paragraph 32) while McGonigal teaches the antibody prevents activation of the classical complement cascade, i.e., activation pathway (p.3 C1).
Regarding claim 23, McGonigal teaches the antibody is monoclonal (p.3 C1: “monoclonal antibody M1”).
Regarding claim 27, Yednock teaches the antibody has a light chain of SEQ ID NO: 2. This sequence comprises SEQ ID NOs: 5, 6, and 7 within the HVR (CDR) of the chain. McGonigal does not disclose the CDRs of M1. However, there is ample evidence that the M1 antibody also comprises these claimed sequences. First, the sequence of M1 is inherent; whether others in the art knew the sequence or not at the time of filing, the M1 antibody necessarily had a sequence of amino acids. Second, as a practical matter, the Patent Office is not equipped to manufacture products by the myriad of processes put before it and then obtain prior art products and make physical comparisons therewith.” In re Brown, 459 F.2d 531, 535, 173 USPQ 685, 688 (CCPA 1972). In the same way, the Office is not equipped to obtain and sequence the M1 antibody to determine the variable domain sequences.
Nevertheless, Yednock teaches the M1 Fab is the Fab portion of the M1 antibody; Yednock teaches the Fab has the identical CDRs (binding regions) of the M1 antibody (paragraph 24) and refers to the Fab as “M1 Fab” (paragraph 56). Having the identical CDRs as M1 is sufficient evidence to conclude that the McGonigal antibody—which is M1—must have CDRs of instant SEQ ID NOs: 5-7 as taught by Yednock.
Regarding claim 28, the above reasoning is also true for the heavy chain. Yednock teaches the antibody has a heavy chain of SEQ ID NO: 1. This sequence comprises SEQ ID NOs: 9, 10, and 11 within the HVR (CDR) of the chain and, as Yednock teaches these are the same for antibody M1, the McGonigal antibody (M1) must also have these sequences.
Regarding claims 29 and 30, Yednock SEQ ID NO: 2 comprises a sequence 100% identical to instant SEQ ID NO: 37 as depicted below:
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A Fab includes the heavy and light chain variable regions of a full-length antibody (Yednock paragraphs 59-60). Thus, as above, the evidence suggests that the M1 Fab comprises the same VH and VL as M1, which supports the conclusion that M1 also comprises instant SEQ ID NO: 37.
Regarding claims 31 and 32, Yednock SEQ ID NO: 1 comprises a sequence 100% identical to instant SEQ ID NO: 33 as depicted below:
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For the same reasons above, M1 comprises instant SEQ ID NO: 33.
Regarding claim 76, Yednock teaches the antibody M1 Fab that binds to C1q (claim 1) and McGonigal teaches M1 also binds C1q. The M1 antibody meets the limitations of a full-length antibody that inhibits C1q. Yednock also teaches this antibody in combination with a package insert containing instructions (claim 47), which would have made it obvious to one of ordinary skill in the art to include such instructions with the therapeutic M1 antibody of McGonigal for the same purpose.
See MPEP §2111.05 describing the considerations for “descriptive material”. In this case, there is no functional relationship between the package insert and the antibody in the same way that “in a kit containing a set of chemicals and a printed set of instructions for using the chemicals, the instructions are not related to that particular set of chemicals. In re Ngai, 367 F.3d at 1339”. In other words, the actual instructions do not alter the function of the antibody nor vice versa. Thus, the limitation “for using…” does not distinguish the instant kit from the prior art kit as this merely relates to what is printed on the insert, which shares no functional relationship to the antibody.
Therefore, claims 1-6, 11-12, 17-19, 23, 27-32, and 76 would have been obvious.
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 USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The 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/process/file/efs/guidance/eTD-info-I.jsp.
Claims 1-6, 11-12, 17-19, 23, 27-32, 65, and 76 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-20 of U.S. Patent No. 10723788 in view of Muizelaar and further in view of Hammad, McGonigal, and ScienceDaily. Although the claims at issue are not identical, they are not patentably distinct from each other because the reference claims are directed to an antibody with the same VH/VL regions as the instant antibody (claims 30 and 32), differing only in the instant antibody being a full-length antibody while the reference antibody is a Fab. However, McGonigal teaches the M1 antibody achieves the same results and inhibits the same target as that of the reference Fab, making substituting the monoclonal full-length antibody of McGonigal a predictable substitution. The reference document also claims a kit with the antibody and the written instructions (claim 7). There are no method claims in the reference patent. See the decisions in Sun Pharmaceuticals v Eli Lily Fed Cir July 28, 2010; Geneva v GlaxoSmithKline 349, F.3d 1373; and Pfizer v Teva 518 F3d 1353 supporting the Office’s use of disclosed utilities of compositions when applying double patenting rejections to method claims. The utility disclosed in ‘788 for these antibodies is both in treatment of synapse loss as well as determining risk for such (see discussion of ‘309 above, which is the PgPub of the reference patent).
Given this utility, it would have been obvious that the full-length version of the reference antibody could be predictably used to treat TBI within 6 hours based on the teachings of Muizelaar, Hammad, McGonigal, and ScienceDaily as discussed above and incorporated herein.
Claims 1-6, 11-12, 17-19, 23, 27-32, 65, and 76 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-19 of U.S. Patent No. 11999779 in view of Muizelaar and further in view of Hammad, McGonigal, and ScienceDaily. Although the claims at issue are not identical, they are not patentably distinct from each other because the reference claims are directed to inhibiting synapse loss using an antibody (SEQ ID NOs: 1 and 2) with the same claimed functions. Thus, the reference claimed antibody differs from the instant antibody only in the instant antibody being a full-length antibody while the reference antibody is a Fab. However, McGonigal teaches the M1 antibody achieves the same results and inhibits the same target as that of the reference Fab, making substituting the monoclonal full-length antibody of McGonigal a predictable substitution. Given the reference claims a method of treating any C1q mediated disease where the classical complement pathway is activated (claim 6), inflammatory disease (claim 13) and inhibiting synapse loss (claim 1), it would have been obvious that the full-length version of the reference antibody could be predictably used to treat TBI within 6 hours based on the teachings of Muizelaar, Hammad, McGonigal, and ScienceDaily as discussed above and incorporated herein.
Claims 1-6, 11-12, 17-19, 23, 27-32, 65, and 76 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-28 of U.S. Patent No. 9708394 in view of Muizelaar and further in view of Hammad, and ScienceDaily. Although the claims at issue are not identical, they are not patentably distinct from each other because the reference claims are directed to a full-length antibody meeting the criteria of the most specific anti-C1q antibodies of the instant claims (see reference claims 1(b), 2, 3). The instant methods are not claimed in the reference patent. However, see the decisions in Sun Pharmaceuticals v Eli Lily Fed Cir July 28, 2010; Geneva v GlaxoSmithKline 349, F.3d 1373; and Pfizer v Teva 518 F3d 1353 supporting the Office’s use of disclosed utilities of compositions when applying double patenting rejections to method claims. The utility disclosed in ‘394 for these antibodies is both in treatment of synapse loss as well as determining risk for such (see e.g., C34, C55). Given this utility, it would have been obvious that the full-length version of the reference antibody could be predictably used to treat TBI within 6 hours based on the teachings of Muizelaar, Hammad, and ScienceDaily as discussed above and incorporated herein.
Claims 1-6, 11-12, 17-19, 23, 27-32, 65, and 76 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-30 of U.S. Patent No. 10227398 in view of Muizelaar and further in view of Hammad, and ScienceDaily. Although the claims at issue are not identical, they are not patentably distinct from each other because the reference claims are directed to inhibiting synapse loss using a full-length antibody (SEQ ID NOs: 1 and 2) with the same claimed functions, meeting the criteria of the most specific anti-C1q antibodies of the instant claims (claims 30 and 32). Given the reference claims a method of treating any C1q mediated disease where the classical complement pathway is activated (claim 6), inflammatory disease (claim 13) and inhibiting synapse loss (claim 1), it would have been obvious that the full-length version of the reference antibody could be predictably used to treat TBI within 6 hours based on the teachings of Muizelaar, Hammad, and ScienceDaily as discussed above and incorporated herein.
Claims 1-6, 11-12, 17-19, 23, 27-32, 65, and 76 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-21 of U.S. Patent No. 10590190 in view of Muizelaar and further in view of Hammad, and ScienceDaily. Although the claims at issue are not identical, they are not patentably distinct from each other because the reference claims are directed to a full-length antibody meeting the criteria of the most specific anti-C1q antibodies of the instant claims (claims 30 and 32; see reference claims 1(b), 2, 3). The instant methods are not claimed in the reference patent. However, see the decisions in Sun Pharmaceuticals v Eli Lily Fed Cir July 28, 2010; Geneva v GlaxoSmithKline 349, F.3d 1373; and Pfizer v Teva 518 F3d 1353 supporting the Office’s use of disclosed utilities of compositions when applying double patenting rejections to method claims. The utility disclosed in ‘394 for these antibodies is both in treatment of synapse loss as well as determining risk for such (see e.g., C34, C55). Given this utility, it would have been obvious that the full-length version of the reference antibody could be predictably used to treat TBI within 6 hours based on the teachings of Muizelaar, Hammad, and ScienceDaily as discussed above and incorporated herein.
Claims 1-6, 11-12, 17-19, 23, 27-32, 65, and 76 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-30 of U.S. Patent No. 10316081 in view of Muizelaar and further in view of Hammad, and ScienceDaily. Although the claims at issue are not identical, they are not patentably distinct from each other because the reference claims are directed to an antibody meeting the criteria of the most specific anti-C1q antibodies of the instant claims (claims 30 and 32; see reference claims 1(b), 2, 3). The instant methods are not claimed in the reference patent. However, see the decisions in Sun Pharmaceuticals v Eli Lily Fed Cir July 28, 2010; Geneva v GlaxoSmithKline 349, F.3d 1373; and Pfizer v Teva 518 F3d 1353 supporting the Office’s use of disclosed utilities of compositions when applying double patenting rejections to method claims. The utility disclosed in ‘394 for these antibodies is both in treatment of synapse loss as well as determining risk for such (see e.g., C34, C55). Given this utility, it would have been obvious that the full-length version of the reference antibody could be predictably used to treat TBI within 6 hours based on the teachings of Muizelaar, Hammad, and ScienceDaily as discussed above and incorporated herein.
Conclusion
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/Adam Weidner/ Primary Examiner, Art Unit 1675