DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
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 1-7 and 9-11 are rejected under 35 U.S.C. 103 as being unpatentable over Tricaud et al. (US 2018/0140617) in view of Schutzer (US 2016/0187354) in view of Maccabee et al. (US 2016/0270709).
In re claim 1, Tricaud discloses method for treating demyelinating neuropathy of a patient [0001, 0018-0019] comprising:
placing a plurality of electrodes [0080] on a muscle area of the patient [0080];
acquiring, via the plurality of electrodes, a compound muscle action potential (CMAP) [0080] measure of muscle integrity in the muscle area of the patient [0080];
administering to the patient having the demyelinating neuropathy a therapeutically effective amount of at least one agent to treat the demyelinating neuropathy ([0019]: treatment is provided to patients with peripheral demyelinating diseases; [0038-0039]: dose of VDAC1 inhibitor is provided; [0115-0116]: VDAC1 inhibition increases myelin).
Tricaud fails to disclose
obtaining a biological sample of the patient;
inputting a conduction measure associated with a CMAP amplitude comprised in the CMAP measure into a regression model to determine a conduction measure that is within a demyelinating range defined by the regression model;
determining, from the biological sample of the patient, a biomarker activity measure of the patient that is above a predetermined threshold;
determining that the patient has a demyelinating neuropathy based at least in part on:
a) the conduction measure that is within the demyelinating range defined by the regression model, and
b) the biomarker activity measure that is above the predetermined threshold.
Regarding the limitations,
“obtaining a biological sample of the patient;
determining, from the biological sample of the patient, a biomarker activity measure of the patient that is above a predetermined threshold”,
Schutzer teaches diagnosing multiple sclerosis [0011] in a patient [0011], which is a common demyelinating disease [0004, 0046], and teaches
obtaining a biological sample [0013] of the patient [0011];
determining, from the biological sample of the patient, a biomarker ([0011]: any one of listed biomarkers; Table 1a-1c; any one of proteins; [0065]: biomarkers may be coupled with enzymes; [0075]) activity measure of the patient [0011] that is above a predetermined threshold ([0011]: biomarkers used to detect multiple sclerosis must be above a certain threshold to provide a positive indicator).
Schutzer further teaches that biomarkers indicate the presence of a disease [0056] and are used to identify metabolic pathways directed to a progression of the disease [0062], such as biomarkers to detect multiple sclerosis [0043-0044], which is characterized by demyelination.
It would have been obvious to someone of ordinary skill in the art at the time the instant invention was filed to modify the method for treating demyelinating neuropathy of a patient taught by Tricaud, to provide obtaining a biological sample of the patient and determining, from the biological sample of the patient, a biomarker activity measure of the patient that is above a predetermined threshold, as taught by Schutzer, because biomarkers indicate the presence of a disease and are used to identify metabolic pathways directed to a progression of the disease, such as multiple sclerosis, which is characterized by demyelination.
Regarding the limitations,
“inputting a conduction measure associated with a CMAP amplitude comprised in the CMAP measure into a regression model to determine a conduction measure that is within a demyelinating range defined by the regression model;
…determining that the patient has a demyelinating neuropathy based at least in part on:
a) the conduction measure that is within the demyelinating range defined by the regression model, and
b) the biomarker activity measure that is above the predetermined threshold”,
Maccabee teaches determining demyelinated nerve pathways [0020] and teaches
inputting a conduction measure ([0023]: conduction velocity) associated with a CMAP amplitude ([0021-0023]: CMAP would have a value i.e. an amplitude that allows for parameters such as conduction velocity to be measured) comprised in the CMAP measure into a regression model ([0064-0065]: regression analysis used to determine demyelinating regression boundary values for the CMAPs; fig. 9: step 904) to determine a conduction measure that is within a demyelinating range defined by the regression model ([0062-0065]: demyelinating boundary values are determined for the CMAPs and parameters derived from the CMAPs by the regression analysis; fig. 9);
determining a biomarker activity measure of the patient that is above a predetermined threshold ([0026-0028]: latencies are considered as biomarkers since they are objectively measured and a quantifiable characteristic of the demyelinating boundary; [0021]: latency determined at recording site after stimulation; [0005, 0022]);
determining that the patient has a demyelinating neuropathy based at least in part on:
a) the conduction measure that is within the demyelinating range defined by the regression model ([0064-0065]: conduction measure being within the demyelinating regression boundary values; [0062]:demyelinating boundary values determined for CMAPs; [0030]: boundaries used to diagnose demyelinating neuropathy), and
b) the biomarker activity measure that is above the predetermined threshold ([0034]: specific percents for latencies are used to define presence of peripheral nerve demyelination; [0026-0028]: clinician can use full history to detect peripheral neuropathy).
Maccabee further teaches that the clinician may use a patient’s full history to detect peripheral neuropathy [0026], which would include checking for axonal range [0024-0025] for latency [0025-0028] and conduction velocity [0025, 0064-0065].
It would have been obvious to someone of ordinary skill in the art at the time the instant invention was filed to modify the method for treating demyelinating neuropathy of a patient yielded by the proposed combination, to provide inputting a conduction measure associated with a CMAP amplitude comprised in the CMAP measure into a regression model to determine a conduction measure that is within a demyelinating range defined by the regression model and determining that the patient has a demyelinating neuropathy based at least in part on: a) the conduction measure that is within the demyelinating range defined by the regression model, and b) the biomarker activity measure that is above the predetermined threshold, as taught by Maccabee, because the clinician may use a patient’s full history to detect peripheral neuropathy, which includes checking for axonal range for latency and conduction velocity.
In re claim 2, the proposed combination (all mapping directed to Tricaud unless otherwise stated) wherein the demyelinating neuropathy is a distal symmetric polyneuropathy ([0015]: distal symmetric polyneuropathy is known as nerve damage especially from diabetes; [0013]: neuropathy in hands and feet from diabetic neuropathies is considered distal symmetric polyneuropathy).
In re claim 3, the proposed combination (all mapping directed to Tricaud unless otherwise stated) wherein the demyelinating neuropathy is a peripheral neuropathy [0006, 0010].
In re claim 4, the proposed combination (all mapping directed to Tricaud unless otherwise stated) wherein the demyelinating neuropathy is a chronic inflammatory demyelinating polyneuropathy [0015-0016].
In re claim 5, the proposed combination fails to yield wherein the biological sample is urine.
Schutzer teaches wherein the biological sample is urine [0013].
Schutzer further teaches that although CSF may be used [0013], other biological samples may also be used [0013], such as urine [0013].
It would have been obvious to someone of ordinary skill in the art at the time the instant invention was filed to modify the method for treating demyelinating neuropathy of a patient yielded by the proposed combination, to provide wherein the biological sample is urine, as taught by Schutzer, because various biological samples may be used, such as urine.
In re claim 6, the proposed combination yields (all mapping directed to Schutzer unless otherwise stated) wherein the biomarker activity measure is a neuroinflammatory biomarker ([0102]: Nogo receptor is a type of neuroinflammatory biomarker that shows first-attack patients; [0011]: first- attack multiple sclerosis is detected by the Nogo receptor is multiple sclerosis is known as a neuroinflammatory disease [0046]), for substantially the same reasons as discussed in re claim 1 above.
In re claim 7, the proposed combination yields (all mapping directed to Schutzer unless otherwise stated) wherein the biomarker activity measure is an enzyme ([0065]: antibodies may be coupled to enzyme, see in re claim 1 above), for substantially the same reasons as discussed in re claim 1 above.
In re claim 9, the proposed combination (all mapping directed to Tricaud unless otherwise stated)wherein the muscle area comprises a nerve selected from
a tibial nerve [0080],
a peroneal nerve,
a median nerve,
an ulnar nerve,
a radial nerve, and
a sural nerve.
In re claim 10, the proposed combination (all mapping directed to Tricaud unless otherwise stated) wherein the plurality of electrodes comprises a surface electrode ([0080]: second pair of electrodes would comprise a surface).
In re claim 11, the proposed combination (all mapping directed to Tricaud unless otherwise stated) wherein the plurality of electrodes comprises a needle-based electrode [0080].
Claim 8 is rejected under 35 U.S.C. 103 as being unpatentable over Tricaud et al. (US 20180140617) in view of Schutzer (US 2016/0187354 in view of Maccabee et al. (US 2016/0270709) in view of Dennis et al. (US 2011/0105610).
In re claim 8, the proposed combination fails to yield wherein the biomarker activity measure is a secretory phospholipase 2 (sPLA2) enzyme.
Dennis teaches treating multiple sclerosis [0004] and teaches measuring a secretory phospholipase 2 (sPLA2) enzyme ([0074-0075]: sPLAS2 is measured in mice).
Dennis further teaches that the sPLA2 enzyme can set off demyelinating response [0073] and influences the progression of multiple sclerosis ([0075]: influences EAE, which is the animal version of multiple sclerosis [0071]).
It would have been obvious to someone of ordinary skill in the art at the time the instant invention was filed to modify the method for treating demyelinating neuropathy of a patient yielded by the proposed combination, to provide wherein the biomarker activity measure is a secretory phospholipase 2 (sPLA2) enzyme, as taught by Dennis, because the sPLA2 enzyme can set off a demyelinating response and influences the progression of multiple sclerosis.
Claim 12 is rejected under 35 U.S.C. 103 as being unpatentable over Tricaud et al. (US 20180140617) in view of Schutzer (US 2016/0187354 in view of Maccabee et al. (US 2016/0270709) in view of Cohen et al. (US 2014/0038927).
In re claim 12, the proposed combination fails to yield wherein the needle-based electrode is selected from a group consisting of
needle-based electrodes comprising a monopolar needle electrode,
a concentric needle electrode, and
a single-fiber needle electrode.
Cohen teaches providing therapy for neurological disorders [0011] , including multiple sclerosis [0013], and teaches using monopolar needle electrodes [0448].
Cohen further teaches that monopolar needle electrodes can be used for both stimulation and recording [0448], as well as for measuring CMAP signal [0448].
It would have been obvious to someone of ordinary skill in the art at the time the instant invention was filed to modify the method for treating demyelinating neuropathy of a patient yielded by the proposed combination, to provide wherein the needle-based electrode is a monopolar needle electrode, as taught by Cohen, because monopolar needle electrodes can be used for both stimulation and recording, as well as for measuring CMAP signal.
Claims 13-19 are rejected under 35 U.S.C. 103 as being unpatentable over Tricaud et al. (US 20180140617) in view of Schutzer (US 2016/0187354 in view of Maccabee et al. (US 2016/0270709) in view of Ishida et al. (US 2021/0269516).
In re claim 13 , regarding the limitation, “wherein the demyelinating neuropathy is a chronic inflammatory demyelinating polyneuropathy”, see in re claim 4 above.
The proposed combination fails to yield wherein the at least one agent is an immune modulator agent.
Ishida teaches an agent [0001] for treating peripheral neuropathies [0001, 0132] including demyelinating polyneuropathy [0132], and teaches wherein
demyelinating neuropathy [0132] is a chronic inflammatory demyelinating polyneuropathy [0132] and
at least one agent is an immune modulator agent ([0138]: anti-RGMa neutralizing antibodies to treat symptoms associated with peripheral neuropathies; [0148-0154]).
Ishida further teaches that the immune modulator agent has an effect on pain symptoms [0138] associated peripheral neuropathies [0009].
It would have been obvious to someone of ordinary skill in the art at the time the instant invention was filed to modify the method for treating demyelinating neuropathy of a patient yielded by the proposed combination, to provide wherein the at least one agent is an immune modulator agent, as taught by Ishida, because the immune modulator agent has an effect on pain symptoms associated with peripheral neuropathies.
In re claim 14, regarding the limitation, “wherein the demyelinating neuropathy is a chronic inflammatory demyelinating polyneuropathy”, see in re claim 4 above.
The proposed combination fails to yield wherein the at least one agent is selected from a group consisting of
immunoglobulin,
glucocorticoid, and
plasma.
Ishida teaches wherein the at least one agent is selected from a group consisting of
immunoglobulin [0119-0120],
glucocorticoid, and
plasma.
Ishida further teaches that the antibodies may be derived from immunoglobulins from non-human animals [0119] and an antibody binds to an epitope [0063], which bind to RGMa proteins [0086-0088] and treat peripheral neuropathies [0001] by inhibiting RGMa activity [0001]
It would have been obvious to someone of ordinary skill in the art at the time the instant invention was filed to modify the method for treating demyelinating neuropathy of a patient yielded by the proposed combination, to provide wherein the at least one agent is immunoglobulin, as taught by Ishida, because the antibodies may be derived from immunoglobulins from non-human animals and used to treat peripheral neuropathies.
In re claim 15, regarding the limitation, “wherein the demyelinating neuropathy is a chronic inflammatory demyelinating polyneuropathy”, see in re claim 4 above.
The proposed combination fails to yield wherein the at least one agent is selected from a group consisting of
azathioprine,
cyclophosphamide,
cyclosporine,
etanercept,
interferon alpha-2a,
interferon beta-1a,
mycophenolate mofetil,
methotrexate,
rituximab, and
tacrolimus.
Ishida teaches wherein the at least one agent is methotrexate [0114].
Ishida further teaches that treating peripheral neuropathy comprises administrating an effective amount of an RGMa inhibiting substance ([0050]: “treating a peripheral neuropathy, which comprises administering an effective amount of an RGMa inhibiting substance to a mammal”), and that methotrexate is an example of a low molecular weight compound [0114], which are bound to anti-RGMA antibodies [0110, 0117].
It would have been obvious to someone of ordinary skill in the art at the time the instant invention was filed to modify the method for treating demyelinating neuropathy of a patient yielded by the proposed combination, to provide wherein the at least one agent is methotrexate, as taught by Ishida, because treating peripheral neuropathy comprises administrating an effective amount of an RGMa inhibiting substance, which includes methotrexate.
In re claim 16, regarding the limitation, “wherein the demyelinating neuropathy is a distal symmetric polyneuropathy”, see in re claim 2 above.
The proposed combination fails to yield wherein at least one agent is an antidepressant agent.
Ishida teaches wherein
demyelinating neuropathy is a distal symmetric polyneuropathy [0139] and
at least one agent is an antidepressant agent [0153].
Ishida further teaches that antidepressants can be used with anti-pain agents [0153] to treat peripheral neuropathies [0151].
It would have been obvious to someone of ordinary skill in the art at the time the instant invention was filed to modify the method for treating demyelinating neuropathy of a patient yielded by the proposed combination, to provide wherein at least one agent is an antidepressant agent, as taught by Ishida, because antidepressants can be used with anti-pain agents to treat peripheral neuropathies.
In re claim 17, regarding the limitation, “wherein the demyelinating neuropathy is a distal symmetric polyneuropathy”, see in re claim 2 above.
The proposed combination fails to yield wherein the at least one agent is an antiepileptic agent.
Ishida teaches wherein the at least one agent is an antiepileptic agent [0153].
Ishida further teaches that antiepileptic drugs can be used with anti-pain agents [0153] to treat peripheral neuropathies [0151].
It would have been obvious to someone of ordinary skill in the art at the time the instant invention was filed to modify the method for treating demyelinating neuropathy of a patient yielded by the proposed combination, to provide wherein the at least one agent is an antiepileptic agent, as taught by Ishida, because antiepileptic drugs can be used with anti-pain agents to treat peripheral neuropathies.
In re claim 18, regarding the limitation, “wherein the demyelinating neuropathy is a peripheral neuropathy”, see in re claim 3 above.
The proposed combination fails to yield wherein at least one agent is an antidepressant agent.
Ishida teaches wherein
demyelinating neuropathy is a peripheral neuropathy [0151, 0050] and
at least one agent is an antidepressant agent [0153].
Ishida further teaches that antidepressants can be used with anti-pain agents [0153] to treat peripheral neuropathies [0151].
It would have been obvious to someone of ordinary skill in the art at the time the instant invention was filed to modify the method for treating demyelinating neuropathy of a patient yielded by the proposed combination, to provide wherein at least one agent is an antidepressant agent, as taught by Ishida, because antidepressants can be used with anti-pain agents to treat peripheral neuropathies.
In re claim 19, regarding the limitation, “wherein the demyelinating neuropathy is a peripheral neuropathy”, see in re claim 3 above.
Regarding the limitation, “wherein the at least one agent is an antiepileptic agent”, see in re claim 17 above.
Claim 20 is rejected under 35 U.S.C. 103 as being unpatentable over Tricaud et al. (US 20180140617) in view of Schutzer (US 2016/0187354 in view of Maccabee et al. (US 2016/0270709) in view of Schultz et al. (US 2014/0038949).
In re claim 20, regarding the limitation, “wherein the demyelinating neuropathy is a peripheral neuropathy”, see in re claim 3 above.
The proposed combination fails to yield wherein at least one agent is an opioid-based agent.
Schultz teaches stimulating increased myelination of nerves in a subject [0006] to treat a patient having a demyelinating disease [0007], wherein at least one agent is an opioid-based agent [0007].
Schultz further teaches that various agents may be administered to a patient [0007], including an opioid receptor modulator [0007] to treat the demyelinating disease [0007].
It would have been obvious to someone of ordinary skill in the art at the time the instant invention was filed to modify the method for treating demyelinating neuropathy of a patient yielded by the proposed combination, to provide wherein at least one agent is an opioid-based agent, as taught by Schultz, because various agents may be administered to a patient, including an opioid receptor modulator to treat the demyelinating disease
Conclusion
The prior art made of record and not relied upon is considered pertinent to applicant’s disclosure:
Li et al. (US 2018/0036311) discloses treating demyelinating diseases (abstract) and measuring CMAP amplitudes [0078] before [0078] and after treatment [0078], and teaches obtaining biological samples [0112-0113].
Contact
Any inquiry concerning this communication or earlier communications from the examiner should be directed to RUMAISA R BAIG whose telephone number is (571)270-0175. The examiner can normally be reached Mon-Fri: 8am- 5pm.
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/RUMAISA RASHID BAIG/Examiner, Art Unit 3796
/DAVID HAMAOUI/SPE, Art Unit 3796