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 .
Priority
The instant application is a 35 U.S.C. 371 national phase application and claims priority to International Application No. PCT/IB2022/057913 (filing date 08/24/2022), which claims the benefit of the prior-filed United States Provisional Patent Application No. 63/236,247, filing date 08/24/2021.
Status of Application/Claims
The preliminary amendment, filed 01/23/2025, is acknowledged. Claims 15-16, 18, 20-24, and 28-36 are canceled. Claims 5-14, 19, 25-26, and 37 are currently amended. Claims 1-14, 17, 19, 25-27, and 37 are currently pending and are examined on the merits herein.
Information Disclosure Statements
The information disclosure statements (IDSs) submitted on 05/03/2026 and 05/04/2026 have been fully considered by the examiner.
Specification
The use of the terms Q-Sense, Medoc, and Stoelting, which are trade names or marks used in commerce, has been noted in this application. The terms should be in all caps wherever they appear or, where appropriate, include a proper symbol indicating use in commerce such as ™, SM , or ® following the terms.
Although the use of trade names and marks used in commerce (i.e., trademarks, service marks, certification marks, and collective marks) are permissible in patent applications, the proprietary nature of the marks should be respected and every effort made to prevent their use in any manner which might adversely affect their validity as commercial marks.
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 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.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 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.
Claims 1-6, 14, and 25-27 are rejected under 35 U.S.C. 103 as being unpatentable over Melo-Carrillo, et al. Selective inhibition of trigeminovascular neurons by fremanezumab: A humanized monoclonal anti-CGRP antibody. Neurobiology of Disease (2017), 37:30, p.7149-7163 (herein referred to as Melo-Carrillo); in further view of Blumenfeld and Brin. Combination therapy with CGRP antagonists and clostridial derivatives—WO2020008402A2 (publication date: 09/01/2020; effective filing date: 05/07/2018; herein referred to as Blumenfeld); in further view of Lipton, et al. Cutaneous allodynia in the migraine population. Ann. Neurol. (2008), 63, p.148-158 (herein referred to as Lipton);and, as evidenced by Jedynak, et al. Shift from high-frequency to low-frequency episodic migraine in patients treated with galcanezumab: Results from two global randomized clinical trials. The J. of Headache and Pain (2021), 22:48, p.1-10 (publication date: 05/2021; herein referred to as Jedynak).
Melo-Carrillo teaches a method of selective inhibition of trigeminovascular neurons by fremanezumab, a humanized monoclonal anti-CGRP antibody (i.e., an anti-CGRP agent; instant claims 1 and 25-27) in a male and female rats (title; abstract). Melo-Carrillo teaches that CGRP monoclonal antibodies are capable of preventing migraine (see Significance Statement p.7149; instant claim 1). Melo-Carrillo teaches that the association between migraines and CGRP levels is well-established, and provides that levels of CGRP are increased in the blood and saliva during migraine attacks, that mice with increased expression of CGRP receptor exhibit photophobia, and that anti-migraine agents include suppressors of CGRP such as triptans, 5HT1D agonists, and anti-CGRP antibodies (abstract; p.7150, col.1, para.1). Melo-Carrillo teaches that humanized CGRP monoclonal antibodies are a new generation of drugs that reduce the availability of CGRP in migraineurs (i.e., in humans; instant claim 1) and were found to be effective in reducing the frequency of chronic migraine (p.7150, col.1, para.2; instant claim 1). Melo-Carrillo’s study was focused on examining the effects of anti-CGRP antibodies in migraine in anesthetized male and female rats that underwent spontaneous and evoked activity of high-threshold (HT) and wide-dynamic range (WDR) trigeminovascular neurons in the medullary and upper cervical dorsal horn. Melo-Carrillo also conceives that “…one would predict that, among migraine aura patients, responders to the prophylactic treatment of CGRP-mAb are likely to show no signs of cutaneous allodynia, a potential bio-marker of treatment success and a readily testable hypothesis” (i.e., which includes no allodynia at least 24, 48, or 72 hours; p.7161, col.2, para.2; instant claims 1, 5, and 6). Melo-Carrillo further teaches that CGRP-mAb inhibited naïve HT neurons, but not WDR trigeminovascular neurons, and that the inhibitory effects on the neurons were limited to their activation from the intracranial dura but not facial skin or cornea (p.7161, col.1, para.2; p.7161, col.2, para.2). Melo-Carrillo also teaches the particular relevance of interictal (i.e., post-ictal) cutaneous allodynia (instant claim 1): Melo-Carrillo teaches findings that “…raise the possibility that cutaneous allodynia in attacks preceded by aura is mediated by HT (high-threshold) neurons that are unresponsive to innocuous mechanical stimulation of the skin at baseline (i.e., interictally and before cortical spreading depression/CSD) but becomes mechanically responsive to brush after CSD”; and, that among migraine aura patients, responders to the prophylactic treatment of CGRP-mAb would show no signs of cutaneous allodynia, a potential biomarker of treatment success (p.7161, col.2, para.2).
While Melo-Carrillo conceives of anti-CGRP preventative/prophylactic treatment in humans, Melo-Carrillo does not teach a method of preventive treatment in human patients specifically. However, in addition to the animal study provided by Melo-Carrillo in the context of solving the problem of migraine in humans, Blumenfeld also specifically teaches anti-CGRP agent-mediated treatment of migraine in human patients specifically (see below).
Blumenfeld teaches that “Migraine is a common neurological disorder that affects up to 16% of the adult population in Western countries. It is characterized by attacks, often of disabling headache, which can be associated with sensory, visual, or language (aura), associated symptoms such as nausea and/or vomiting, phonophobia, and photophobia, as well as dizziness and cognitive symptoms” (p.1, [0002]). Claim 3 of Blumenfeld recites the following: “A method for treating, preventing, alleviating or reducing the frequency of occurrence of migraine or a symptom of migraine in a patient in need thereof, comprising administering to the patient an antagonist of calcitonin gene-related peptide (CGRP-antagonist; i.e., an anti-CGRP agent), wherein said patient is concurrently undergoing treatment with a clostridial derivative” (p.34). Blumenfeld additionally teaches treatments for post-ictal headaches (p.44, claim 113). Blumenfeld teaches that the CGRP antagonist may be ubrogepant, atogepant, erenumab, epitinezumab, or rimegepant (i.e., gepants; i.e., anti-CGRP antagonists; i.e., anti-CGRP receptor antibodies; p.3, [0003]; p.34, claim 11; instant claim 25-26); or, may be an anti-CGRP antibody or an antigen-binding fragment thereof (p.3, [0007]; p.44, claim 116). Additionally, Blumenfeld teaches treatment using monoclonal antibodies, human monoclonal antibodies, or antigen-binding fragments thereof (p.1, [0002]). Claims 95 and 96 of Blumenfeld teach that the method may be for when the migraine is either a chronic or episodic migraine (p.42; instant claims 2 and 4). Blumenfeld further teaches that the prevention and treatment is for human patients (p.22, [0135]; see also claims and Examples; instant claim 1).
It would have been prima facie obvious for one of ordinary skill in the art before the effective filing date to combine the teachings of Melo-Carrillo with the teachings of Blumenfeld by modifying a method of preventative/prophylactic treatment for chronic and/or episodic migraine via administration of an anti-CGRP agent (taught by Melo-Carrillo) such as a gepant that is ubrogepant, atogepant, erenumab, epitinezumab, or rimegepant, ubrogepan (taught by Blumenfeld), or an anti-CGRP antagonist antibody (taught by Melo-Carrillo) to human patients (taught by Blumenfeld) by using the method to treat human subjects who do not exhibit post-ictal allodynia (taught by Melo-Carrillo), in order to receive the benefit of higher responsiveness to preventative treatment for chronic and/or episodic migraine. One of ordinary skill in the art would have a reasonable expectation of success because both Melo-Carrillo and Blumenfeld teach treatment of chronic and/or episodic migraine by administering anti-CGRP agents, including gepants anti-CGRP antibodies; Melo-Carrillo and Blumenfeld each teach prophylactic treatment; and, Blumenfeld teaches anti-CGRP agent administration in human patients. As evidenced by Jedynak, “high frequency episodic migraine” encompasses individuals exhibiting 8-14 migraine headaches per month; “HFEM”), which is an intermediate stage between “low-frequency episodic migraine” individuals exhibiting 4-7 migraine headache days/month and “chronic migraine” sufferers (title; abstract). Thus, one of ordinary skill would also have a reasonable expectation of success in treating human HFEM individuals (instant claim 3).
The combination of Melo-Carrillo and Blumenfeld teaches the prevention and treatment of migraine in human subjects by administering an anti-CGRP agent. Melo-Carrillo further teaches that patients who respond to prophylactic treatment include those that do not exhibit cutaneous allodynia (p.7161, col.2, para.2). The combination of Melo-Carrillo/Blumenfeld does not specifically teach a method of determining whether a subject exhibits post-ictal allodynia and/or hyperalgesia (instant claim 1).
Lipton teaches about cutaneous allodynia (CA) in the migraine population and validation of a questionnaire for assessing CA (title). Lipton teaches that allodynia is a marker of central sensitization and a proposed risk factor for progression to chronic migraine; and, that CA has significant implications for our understanding of the pathophysiology of migraine attacks, for treatment implications, and for assessing prognosis (p.148, col.1, para.1). Lipton teaches assessment of cutaneous allodynia using several questionnaires, including quantitative sensory testing (QST; p.148, col.1, para.2 – col.2, para.2; instant claim 14), which can be used for assessing hot and cold allodynia (p.179, col.1, para.1). Lipton also teaches that assessment of mechanical allodynia is performed by brushing the skin; and that Von Frey hair filaments have been used to assess static mechanical/pressure allodynia (p.179, col.1, para.1). Lipton teaches that their psychometric analysis confirms that CA can be considered as a quantitative trait that is consistent with clinical impressions of allodynia. Lipton teaches that some patients do not develop allodynia at all (p.154, col.1, para.2). Lipton teaches that, “…if CA predicts response to triptan therapy, knowing whether a patient has allodynia has clinical implications,” citing Burstein (p.157, col.1, para.2; also, see next paragraph).
It would have been prima facie obvious for one of ordinary skill in the art before the effective filing date to further combine the teachings of Melo-Carrillo/Blumenfeld with the teachings of Lipton by modifying the method of preventative treatment in humans by administering an anti-CGRP agent to a subject that does not exhibit allodynia at least 24, 48, or 72 hours by using QST for assessing and determining whether a subject exhibits hot, cold, and/or mechanical allodynia, to arrive at the instantly claimed invention and in order to receive the benefit that subjects who have been determined not to exhibit allodynia have better treatment responses (taught by Melo-Carrillo). One of ordinary skill in the art would have a reasonable expectation of success because Lipton teaches determination of allodynia in subjects and the rationale that the presence of allodynia impacts clinical treatment; and, because Melo-Carrillo teaches that patients that do not exhibit allodynia are better responders to anti-CGRP treatment.
Claim 7 is rejected under 35 U.S.C. 103 as being unpatentable over the combination of Melo-Carrillo, Blumenfeld, and Lipton, (as evidenced by Jedynak) as applied to claim 1, above; and, further in view of Jakubowski, et al. Exploding vs. imploding headache in migraine prophylaxis with Botulimun toxin A. Pain, 2006, 125, p.286-295 (herein referred to as Jakubowski).
The combination of Melo-Carrillo, Blumenfeld, and Lipton, (as evidenced by Jedynak) teaches a method for determination of cutaneous allodynia at least 24, 48, or 72 hours into the post-ictal phase and the preventative treatment of migraine in human subjects who do not exhibit signs of allodynia by administering an anti-CGRP agent as applied to instant claim 1 above.
The combination of Melo-Carrillo/Blumenfeld/Lipton does not teach a heat pain threshold of below 41ºC and/or a cold pain threshold of above 20ºC and/or a mechanical pain threshold of below 30g for skin indentation with calibrated von Frey hairs (instant claim 7).
Jakubowski teaches Botulinum toxin injection as an alternative approach to prophylactic migraine treatment (abstract; p286, col.1, para.1). Jakubowski teaches procurement of patient history followed by QST assessment of pain thresholds to thermal and mechanical stimuli of the skin, and cites key references in the field: Fruhstorfer et al, 1976; Yarnitsky, 1997; and, Burstein et al., 2006 (p.287, col.2, para.5). Jakubowski teaches that pain thresholds for heat, cold, and mechanical skin stimuli are in the following ranges and also cites the following references: heat, between 42–47ºC (Lindblom, 1994); cold, 5–18ºC (Lindblom, 1994; Harrison and Davis, 1999); and mechanical, 75–281g (Strigo et al., 2000). Jakubowski also sets the following criteria for which a patient is considered to exhibit allodynia: below 40ºC for heat, above 20ºC for pain, and below 30g for skin indentation (p.288, col.1, para.5; instant claim 7).
It would have been prima facie obvious for one of ordinary skill in the art before the effective filing date to combine the teachings of Melo-Carrillo/Blumenfeld/Liptonwith the teachings of Jakubowski by modifying the method of determination of allodynia and anti-CGRP agent administration (taught by Melo-Carrillo/Blumenfeld/Lipton) by using the heat, cold, and mechanical pain stimuli threshold criteria for allodynia (taught by Jakubowski) to arrive at the instantly claimed invention, because the combination of teachings in the prior art would allow one of ordinary skill to receive the benefit that using the QST allodynia thermal and mechanical threshold criteria allows for identification of patients who do not exhibit allodynia (taught by Jakubowski) at least 24, 48, or 72 hours post-ictally. One of ordinary skill in the art would have a reasonable expectation of success because Lipton and Jakubowski teach QST assessment of allodynia; Lipton teaches that assessment of mechanical allodynia is performed by brushing the skin using Von Frey hair filaments; and, Jakubowski teaches the heat, cold, and mechanical stimuli threshold ranges for healthy and allodynic patients.
Claim 19 is rejected under 35 U.S.C. 103 as being unpatentable over the combination of Melo-Carrillo, Blumenfeld, and Lipton, (as evidenced by Jedynak) as applied to claim 1 above; and, further in view of Iyengar, et al. The role of calcitonin gene-related peptide in peripheral and central pain mechanisms including migraine. Pain, 2017, 158, p.543-559 (herein referred to as Iyengar); in further view of Maleki, et al. Ictal and interictal brain activation in episodic migraine: Neural basis for extent of allodynia. PLoS One (01/04/2021), 16:1, p.1-19 (herein referred to as Maleki); and, in further view of Iyengar, et al. CGRP and the trigeminal system in migraine. J. of Head and Face Pain, p.659-681 (herein referred to as Aurora).
The combination of Melo-Carrillo, Blumenfeld, and Lipton (as evidenced by Jedynak) teaches a method for determination of cutaneous allodynia at least 24, 48, or 72 hours into the post-ictal phase and the preventative treatment of migraine in human subjects who are determined to not exhibit signs of allodynia by administering an anti-CGRP agent as applied to instant claim 1 above.
The combination of Melo-Carrillo/Blumenfeld/Lipton does not teach that the subject exhibits cephalic allodynia but not extracephalic allodynia (instant claim 19).
Maleki teaches that migraine attacks are associated with symptoms of allodynia which can be localized (cephalic) or generalized (extracephalic) (abstract). Maleki teaches that he functional magnetic resonance imaging (fMRI) findings provide direct evidence for the view that in migraine patients who are allodynic during the ictal phase of their attacks, the spinal trigeminal nucleus and posterior thalamus become hyper-responsive (sensitized)–to the extent that they mediate cephalic and extracephalic allodynia, respectively (abstract).
Iyengar teaches the role of CGRP in peripheral and central pain mechanisms in migraine (title). Iyengar taches that CGRP is a 37-amino acid peptide found primarily in the C and Aδ sensory fibers arising from the dorsal root and trigeminal ganglia, as well as the central nervous system; that CGRP is a pronociceptive neuromediator, both at
somatic and cephalic sites (p.554, col.2, para.1); that CGRP is upregulated in conditions of inflammatory and neuropathic pain (abstract); that CGRP is believed to contribute to the development of central sensitization and enhanced pain (p.548, col.1, para.2); that CGRP is a critical component for the pathogenesis of migraine (p.543, col.2, para.1); and, that recent successful clinical studies have shown that blocking the function of CGRP can alleviate migraine (abstract). Iyengar further teaches that animal studies suggest that the development of widespread allodynia with migraine is due to development of central sensitization, and teaches that imaging studies with migraine patients using functional magnetic resonance imaging scans with recent blood-oxygenation-level dependent (BOLD) signals indicated a sensitization of the thalamus associated with extracephalic allodynia (p.549, col.1, para.2).
Aurora teaches the role of CGRP in trigeminal system and pathophysiology in migraine (title). Aurora teaches that the trigeminal ganglion neurons provide the connection between the periphery, stemming from the interface between
the primary afferent fibers of the trigeminal ganglion and the meningeal vasculature and the central terminals in the trigeminal nucleus caudalis; and, that the neuropeptide CGRP is abundant in trigeminal ganglion neurons, and is released from the peripheral nerve and central nerve terminals as well as being secreted within the trigeminal ganglion (abstract). Aurora teaches that blocking sensitization of the trigeminal
nerve by attenuating CGRP activity in the periphery may be sufficient to block a migraine attack (abstract). Aurora further teaches that it is generally accepted that anti-CGRP therapeutics most likely act peripherally to relieve migraine attacks since small-molecule CGRP receptor antagonists and the anti-CGRP antibodies have very little ability to cross the blood-brain barrier (i.e., BBB; p.668, col.1, para.2). Thus, as extracephalic allodynia involves the thalamus in the brain and anti-CGRP antibodies have little ability to cross the BBB, it would be expected that cephalic rather than extracephalic subjects would be more responsive to treatment.
It would have been prima facie obvious for one of ordinary skill in the art before the effective filing date to further combine the teachings of Melo-Carrillo/ Blumenfeld/Lipton with the teachings of Maleki, Iyengar, and Aurora by modifying the method of preventative treatment comprising administering an anti-CGRP agent (taught by Melo-Carrillo/Blumenfeld/Lipton) to subjects that exhibit cephalic allodynia rather than extracephalic allodynia (taught by the combination of Melaki, Iyengar, and Aurora) to arrive at the instantly claimed invention in order to receive the benefit that subjects with cephalic allodynia would be expected to have a better response to an anti-CGRP agent (taught by Aurora). One of ordinary skill would have a reasonable expectation of success because Iyengar teaches that CGRP is a 37-amino acid peptide found primarily in the C and Aδ sensory fibers arising from the dorsal root and trigeminal ganglia, as well as the central nervous system; Maleki teaches the involvement of the thalamus (in the brain) in extracephalic but not cephalic allodynia; and Aurora teaches that anti-CGRP therapeutics most likely act peripherally to relieve migraine attacks since small-molecule CGRP receptor antagonists and the anti-CGRP antibodies have very little ability to cross the blood-brain barrier.
Claims 8-13 are rejected under 35 U.S.C. 103 as being unpatentable over the combination of Melo-Carrillo, Blumenfeld, and Lipton,(as evidenced by Jedynak) as applied to claim 1above; and, further in view of Bennett, et al. Alleviation of mechanical and thermal allodynia by CGRP8-37 in a rodent model of chronic central pain. Pain, 2000, 86, p.163-175 (herein referred to as Bennett).
The combination of Melo-Carrillo, Blumenfeld, Lipton, (as evidenced by Jedynak) teaches a method for determination of cutaneous allodynia at least 24, 48, or 72 hours into the post-ictal phase and the preventative treatment of migraine in human subjects who exhibit cephalic allodynia but not extracephalic allodynia by administering an anti-CGRP agent as applied to instant claim 1 above.
The combination of Melo-Carrillo/Blumenfeld/Lipton does not teach that the subject exhibits heat allodynia in the absence of both cold and mechanical allodynia (instant claim 8); both heat and cold allodynia in the absence of mechanical allodynia (instant claim 9); heat and mechanical allodynia in the absence of cold allodynia (instant claim 10); cold allodynia in the absence of both heat and mechanical allodynia (instant claim 11); both cold and mechanical allodynia in the absence of heat allodynia (instant claim 12); or, mechanical allodynia in the absence of both heat and cold allodynia (instant claim 13).
Bennett teaches CGRP is produced in small diameter neurons in the dorsal root ganglion (DRG) which give rise to unmyelinated (C) and thinly myelinated (Aδ), and that this subpopulation of primary afferent fibers has been implicated in the transmission of pain, temperature sensation, and other modalities including noxious and non-noxious mechanical stimuli (p.163, col.2, para.1). Bennett provides a listing of studies supporting that the observation that CGRP is involved in nociceptive behavior is supported by several experiments that support a role for CGRP in thermal and mechanical hyperalgesia as well as some studies that show administration of CGRP antagonists inhibits both thermal and mechanical nociception (p.164, col.1, para.1). Maleki’s study additionally teaches alleviation of both mechanical and thermal allodynia, including both cold and heat allodynia, by administering a CGRP antagonist (title; abstract; p.166, col.2, para.2; p.169, col.1, para.1; p.170, col.2, para.2; p.172, col.1, para.1; instant claims 8-13).
It would have been prima facie obvious for one of ordinary skill in the art before the effective filing date to further combine the teachings of Melo-Carrillo/Blumenfeld/ Lipton/Burstein/Toriyama/Alpuente/Iyengar with the teachings of Bennett by modifying the method of preventative treatment with an anti-CGRP agent (taught by Melo-Carrillo/Blumenfeld/Lipton/Burstein/Toriyama/Alpuente/Iyengar) to comprise treating a subject exhibiting thermal cold and/or thermal heat and/or mechanical allodynia (taught by Bennett) to arrive at the instantly claimed invention and in order to receive the benefit that thermal cold, thermal heat, and mechanical allodynia can be alleviated with an anti-CGRP agent (taught by Bennett). One of ordinary skill in the art would have a reasonable expectation of success because Bennett teaches that CGRP8-37 is an anti-CGRP agent/antagonist, Lipton teaches that allodynia is a marker of central sensitization, and Iyengar teaches that CGRP contributes to central sensitization, and Bennett teaches alleviation of cold allodynia, heat allodynia, and mechanical allodynia using a CGRP antagonist. Thus, the anti-CGRP agent would be expected to preventatively treat subjects recited in each of instant claims 8-13, which recite the various combinations of thermal and mechanical allodynia experienced by subjects.
Claims 17 and 37 are rejected under 35 U.S.C. 103 as being unpatentable over the combination of Melo-Carrillo, Blumenfeld, and Lipton (as evidenced by Jedynak) as applied to claim 1above; and, further in view of American Headache Society. Choosing the right preventive treatment. Headache Research Library, online 10/22/2020, p.1-6 (herein referred to as AHS).
The combination of Melo-Carrillo, Blumenfeld, Lipton (as evidenced by Jedynak) teaches a method for determination of allodynia at least 24, 48, or 72 hours into the post-ictal phase and the preventative treatment of migraine in human subjects who do not exhibit signs of allodynia by administering an anti-CGRP agent as applied to instant claim 1 above.
The combination of Melo-Carrillo/Blumenfeld/Lipton does not teach that the anti-CGRP agent is administered while the subject is migraine free (instant claim 37).
AHS teaches that preventative treatments can give patients an opportunity to experience more pain-free days by limiting migraine attacks before they occur (p.4, para.1), and therefore before the acute phase and when the patient is migraine-free (instant claims 17 and 37). AHS teaches that good candidates for preventative treatment are individuals who are diagnosed with chronic or episodic migraine (p.4, para.2). AHS also teaches that preventative treatments include CGRP antibodies (p.5.para.4)
It would have been prima facie obvious for one of ordinary skill in the art before the effective filing date to combine the teachings of Melo-Carrillo/Blumenfeld/Lipton with the teachings of AHS by modifying the method of determination of allodynia and anti-CGRP agent administration (taught by Melo-Carrillo/Blumenfeld/Lipton) by administering the anti-CGRP agent while the patient is migraine-free (taught by AHS) to arrive at the instantly claimed invention, in order to receive the benefit that treating patients while they are migraine-free provides patients the opportunity to experience more pain-free days by limiting migraine attacks. One of ordinary skill in the art would have a reasonable expectation of success because AHS teaches that preventative treatments include CGRP antibodies for subjects with chronic or episodic migraine.
Conclusion
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/JAMI MICHELLE GURLEY/Examiner, Art Unit 1647
/JOANNE HAMA/Supervisory Patent Examiner, Art Unit 1647
