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 Status
Claims 1-20 are pending. Applicant’s election without traverse of acute asymptomatic seizures and 2-(4-isobutylphenyl)propionyl methansulfonamide and salts thereof (reparixin) in the reply filed on Feb. 23, 2026 is acknowledged. Claims 1, 2, 6-8, 11-16 and 20 are pending and subject to examination. Claims 3-5, 9-10 and 17-19 are withdrawn.
Claim Rejections – 35 USC § 112(b)
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.”
Claim 6 and 11 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 6 is directed towards the method of claim 1, wherein said CXCL8 inhibitor is a CXCR1 receptor inhibitor or a dual CXCR1 and CXCR2 receptor inhibitor. One of ordinary skill in the art cannot determine the metes and bounds of the claim because it is unclear what is a CXCR1 receptor or dual CXCR1 and CXCR2 receptor. CXCR1 and CXCR2 stand for C-X-C motif chemokine receptor 1 and C-X-C chemokine receptor 2, so a CXCR1 receptor is a C-X-C motif chemokine receptor 1 receptor, and it is unclear what that is because it could be referring to the CXCR1 itself or a receptor for CXCR1.
Claim 11 recites the limitation "the anti IL-8 antibodies" in line 3. There is insufficient antecedent basis for this limitation in the claim.
Claim 11 recites the limitation "the compounds of formula (I) and (II)" in the last line. There is insufficient antecedent basis for this limitation in the claim.
Claim Rejections – 35 USC § 112(d)
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 2 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 2 fails to further limit claim 1 upon which it depends because claim 2 merely recites a purpose or intended use of the method of claim 1, an effect which may or may not be desired or appreciated, as claim 1 does not require that the drug is administered to an individual “in need thereof.” (see MPEP § 2111.02). 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.
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) 1-2 and 12 is/are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Xu et al. (Brain Research Bulletin, 134 (2017), 91-98) (of record, cited in the last office action).
Claim 1 is directed towards a method for the prevention or treatment of seizures or the prevention of the onset of epilepsy or the progression of an established epilepsy in an individual, the method comprising administering a CXCL8 inhibitor, a pharmaceutically acceptable salt thereof or a prodrug thereof to the individual.
This claim reads on administering a CXCL8 inhibitor to an individual. The preamble is not further limiting to the claim because the individual is not an individual “in need thereof” (see MPEP § 2111.02).
Xu teaches a method for treating epilepsy comprising administering SB225002, an antagonist for CXCR2, the receptor for CXCL8 (interleukin 8) (i.e. SB225002 is a CXCL8 inhibitor):
C-X-C motif chemokine receptor 2 (CXCR2) is one of the most well characterized chemokine receptors and is a potential target for treating brain pathologies involving inflammatory processes, including epilepsy. However, the role of CXCR2 in epilepsy has not been investigated, and whether CXCR2 modulates seizure activity in temporal lobe epilepsy (TLE) remains unknown. In this study, we aimed to determine the potential role of CXCR2 in intractable TLE patients and in pilocarpine-induced epileptic mice. Here, through Western blotting and semi-quantitative immunohistochemistry, we detected that CXCR2 protein expression was up-regulated (by nearly 50%) in the temporal neocortex of TLE patients and in the hippocampus and adjacent temporal cortex of pilocarpine mice model. Double-label immunofluorescence and immunohistochemical analysis indicated that CXCR2 was expressed in neurons. To investigate the effect of the CXCR2 selective antagonist SB225002 on seizure activity, SB225002 was i.p. administered during the latency window of spontaneous recurrent seizures (SRSs). This treatment increased (by nearly 40%) the latency of SRSs and reduced (by nearly 50%) the frequency of SRSs during the chronic period of epilepsy. This study suggests that CXCR2 plays a critical role in modifying epileptic seizure activity and that CXCR2 blockade could be a potential molecular therapeutic target for epilepsy.
Xu, Abstract;
Clinical and experimental evidences indicate that inflammatory cytokines, including IL6 and IL8, are associated with the development of epilepsy (Youn et al., 2012, Pernhorst et al., 2013). IL6 and IL8 are secreted by brain cells and peripheral immune cells, and abnormal expression of these proteins has been detected in the cerebrospinal fluid and blood of epilepsy patients (Youn et al., 2012, Pernhorst et al., 2013, Ishikawa et al., 2015). Abnormal expression of IL6 and IL8 is indicative of active brain immuno-inflammatory responses in patients with epilepsy. IL6 and IL8 are the main ligands of CXCR2 (Manjavachi et al., 2010a, Manjavachi et al., 2010b, Semple et al., 2010), and the functions of IL6 and IL8 are mediated and regulated by CXCR2 signaling (Manjavachi et al., 2010a, Manjavachi et al., 2010b, Semple et al., 2010). Therefore, we assumed that CXCR2 might be related to TLE. The results of this study further support the association of CXCR2 with epilepsy.
Xu, col. 1, p. 97.
Therefore, claim 1 is anticipated.
Claim 2 does not further limit the method of claim 1 because claim 1 and does not require that the drug is administered to a patient in need thereof and therefore is also anticipated for the reasons given in the rejection of claim 1.
Claim 12 is directed towards a pharmaceutical composition comprising the CXCL8 inhibitor and at least one inert pharmaceutically acceptable excipient. Xu teaches that the CXCL8 inhibitor is dissolved within 1% DMSO (an inert pharmaceutically acceptable excipient) for i.p. injection (Xu, p. 92, col. 2). Therefore, claim 12 is anticipated.
Claim(s) 1-2, 6, 13-14, and 20 is/are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Lopez-Gomez et al. (Neurological Sciences, Vol. 32, p. 1063-1067, May 2011) as evidenced by Kast et al. (British Journal of Neurology, Vol. 26, Issue 6, p. 813-817, May 2012) (of record, IDS dated Jan. 2, 2024).
Kast is cited to show an inherent disclosure by Lopez-Gomez (MPEP § 2131.01).
Claim 1 is directed towards a method for the prevention or treatment of seizures or the prevention of the onset of epilepsy or the progression of an established epilepsy in an individual, the method comprising administering a CXCL8 inhibitor, a pharmaceutically acceptable salt thereof or a prodrug thereof to the individual.
Lopez-Gomez teaches a method for the treatment of drug-resistant partial onset seizures comprising administering to a patient in need thereof 100 mg of dapsone per day:
Dapsone has shown anti-convulsive properties in animal models of epilepsy. In the present study, we tested the safety and tolerability of dapsone as adjunctive therapy in adult patients with drug-resistant partial-onset seizures. Twenty-two adult patients with drug-resistant partial-onset seizures were included. After a 3-month baseline period, patients received dapsone 100 mg per day, for a 3-month evaluation period. Plasma concentrations of anti-epileptic drugs (AEDs) did not significantly change during the study. No alteration of mean clinical laboratory values was observed. The reported adverse events were: mild methemoglobinemia (50%), headache (31.8%), pale ness (27.3%) and somnolence (4.5%).Sixteen of 22 patients reduced their seizure frequency in more than 50% as a result of dapsone treatment. Three subjects remained sei zure-free during the entire dapsone treatment period. This open-label study of adjunctive dapsone therapy at 100 mg/ day suggests that dapsone is safe, and well-tolerated in adults with drug-resistant partial-onset seizures.
Lopez-Gomez, Abstract.
While Lopez-Gomez does not teach that dapsone is a CXCL8 (interleukin-8) inhibitor, this is a known inherent property of dapsone that is responsible for its anti-seizure effects. For example, Kast teaches that “dapsone is operating to inhibit interleukin-8 (IL-8) function in its antiseizure role.” (Kast, p. 813, col. 1-2).
Therefore, claim 1 is anticipated.
Claim 2 does not further limit the method of claim 1 because claim 1 and does not require that the drug is administered to a patient in need thereof and therefore is also anticipated for the reasons given in the rejection of claim 1.
Claim 6 is directed towards the method of claim 1, wherein said CXCL8 inhibitor is a CXCR1 receptor inhibitor or a dual CXCR1 and CXCR2 receptor inhibitor.
Kast teaches that IL-8 receptors are CXCR1 and CXCR2 (Kast, p. 813, col. 2) and that dapsone is has a blinding effect on IL-8 receptors (i.e. is a dual CXCR1/2 receptor inhibitor) (Kast, p. 814, col. 2).
Therefore, claim 6 is anticipated.
Claim 13 is directed towards the method of claim 1, wherein the CXCL8 inhibitor is administered in combination with at least another drug, wherein said at least another drug is administered simultaneously, sequentially or separately.
Lopez-Gomez teaches that the dapsone is administered concomitantly with at least two anti-epileptic drugs (AEDs) (Lopez-Gomez, p. 1064, col. 2).
Therefore, claim 13 is anticipated.
Claim 14 is directed towards the method of claim 13, wherein the at least another drug is selected from benzodiazepines and AEDs. As shown in the rejection of claim 13, Lopez-Gomez teaches that the at least another drug(s) are AEDs. Therefore, claim 14 is anticipated.
Claim 20 is directed towards the method of claim 14, wherein the at least another drug is selected from diazepam, lorazepam, phenytoin and valproic acid (VPA).
Lopez-Gomez teaches that the AEDs include phenytoin and VPA:
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Potential interactions of dapsone with other AEDs were assessed by comparison of serum AED levels before and after dapsone administration. From all AEDs only topiramate and lamotrigine were not measured. Modifications in the dosing of any concomitant AED were not needed. There was no evidence that dapsone at 100 mg/day, interacted with concomitantly administered AED’s.
Lopez-Gomez, p. 1065, col. 1.
Therefore, claim 20 is anticipated.
1, 2, 6-8, 11-12 and 15 is/are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Sousa et al. (Clinics, Vol. 68, Issue 3, 2013, p. 391-394).
Claim 1 is directed towards a method for the prevention or treatment of seizures or the prevention of the onset of epilepsy or the progression of an established epilepsy in an individual, the method comprising administering a CXCL8 inhibitor, a pharmaceutically acceptable salt thereof or a prodrug thereof to the individual.
This claim reads on administering a CXCL8 inhibitor to an individual. The preamble is not further limiting to the claim because the individual is not an individual “in need thereof” (see MPEP § 2111.02).
Sousa teaches a method of attenuating ischemic injury and protecting against brain damage in ischemic stroke comprising administering reparixin, a CXCL1/2 allosteric antagonist/ CXCL8 inhibitor to an individual:
OBJECTIVE
Ischemic stroke may result from transient or permanent reductions of regional cerebral blood flow. Polymorphonuclear neutrophils have been described as the earliest inflammatory cells to arrive in ischemic tissue. CXCR1/2 receptors are involved in the recruitment of these cells. However, the contribution of these chemokine receptors during transient brain ischemia in mice remains poorly understood. In this work, we investigated the effects of reparixin, an allosteric antagonist of CXCR1/2 receptors, in a model of middle cerebral artery occlusion and reperfusion in mice.
METHODS
C57BL/6J male mice treated with reparixin or vehicle were subjected to a middle cerebral artery occlusion procedure 1 h after the treatment. Ninety minutes after ischemia induction, the monofilament that prevented blood flow was removed. Twenty-four hours after the reperfusion procedure, behavioral changes, including motor signs, were analyzed with the SmithKline/Harwell/Imperial College/Royal Hospital/Phenotype Assessment (SHIRPA) battery. The animals were sacrificed, and brain tissue was removed for histological and biochemical analyses. Histological sections were stained with hematoxylin and eosin, neutrophil infiltration was estimated by myeloperoxidase activity and the inflammatory cytokine IL-1β was measured by ELISA.
RESULTS
Pre-treatment with reparixin reduced the motor deficits observed in this model of ischemia and reperfusion. Myeloperoxidase activity and IL-1β were reduced in the reparixin-treated group. Histological analysis revealed that ischemic injury was also attenuated by reparixin pre-treatment.
CONCLUSIONS
Our results suggest that the blockade of the CXCR1/2 receptors by reparixin promotes neuroprotective effects by reducing the levels of polymorphonuclear infiltration in the brain and the tissue damage associated with middle cerebral artery occlusion and reperfusion.
Sousa, Abstract.
Therefore, claim 1 is anticipated.
Claim 2 does not further limit the method of claim 1 because claim 1 and does not require that the drug is administered to a patient in need thereof and therefore is also anticipated for the reasons given in the rejection of claim 1.
Claims 6-8, 11 and 15 read on the active agent reparixin and are anticipated for the reasons given in the rejection of claim 1.
Claim 12 is directed towards a pharmaceutical composition comprising the CXCL8 inhibitor and at least one inert pharmaceutically acceptable excipient. Sousa teaches that the reparixin is dissolved in saline (an inert pharmaceutically acceptable excipient) for subcutaneous injection (Sousa, p. 392, col. 1). Therefore, claim 12 is anticipated.
1, 2, 6-8, 11-12 and 15-16 is/are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Villa et al. (Molecular Medicine, Vol. 13, 2007, p. 125-133).
Claim 1 is directed towards a method for the prevention or treatment of seizures or the prevention of the onset of epilepsy or the progression of an established epilepsy in an individual, the method comprising administering a CXCL8 inhibitor, a pharmaceutically acceptable salt thereof or a prodrug thereof to the individual.
This claim reads on administering a CXCL8 inhibitor to an individual. The preamble is not further limiting to the claim because the individual is not an individual “in need thereof” (see MPEP § 2111.02).
Villa teaches a method of improving neurological function and inhibiting long term inflammation following transient cerebral ischemia in an individual comprising administering to the individual reparixin:
Leukocyte infiltration is viewed as a pharmacological target in cerebral ischemia. We previously reported that reparixin, a CXCL8 receptor blocker that inhibits neutrophil infiltration, and related molecules can reduce infarct size in a rat model of transient middle cerebral artery occlusion (MCAO). The study aims were to compare the effects of reparixin in transient and permanent MCAO using varied treatment schedules and therapeutic windows to evaluate effects on long-term neurological deficits and late inflammatory response. Reparixin, administered for 1 to 3 days, 3.5 to 6 h after MCAO, ameliorates neurological function recovery and inhibits long-term inflammation. The infarct size reduction at 24 h, evaluated by TTC staining, is more pronounced in transient MCAO. MRI analysis identified a decrease in the progression of infarct size by reparixin that was more evident at 48 h in permanent MCAO, and was associated with a significantly improved recovery from long-term neurological deficits.
Villa, Abstract.
Therefore, claim 1 is anticipated.
Claim 2 does not further limit the method of claim 1 because claim 1 and does not require that the drug is administered to a patient in need thereof and therefore is also anticipated for the reasons given in the rejection of claim 1.
Claims 6-8, 11 and 15 read on the active agent reparixin and are anticipated for the reasons given in the rejection of claim 1.
Claim 16 is directed towards the method of claim 15, wherein said CXCL8 inhibitor is the lysine salt of reparixin. Villa teaches the lysine salt of reparixin (Villa, p. 126, col. 2). Therefore, claim 16 is anticipated.
Claim 12 is directed towards a pharmaceutical composition comprising the CXCL8 inhibitor and at least one inert pharmaceutically acceptable excipient. Villa teaches that the reparixin is dissolved in saline (an inert pharmaceutically acceptable excipient) for intravenous or subcutaneous injection (id.). Therefore, claim 12 is anticipated.
Nonstatutory 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 filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual 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/apply/applying-online/eterminal-disclaimer.
Claim 1, 2, 6-8, 11-16 and 20 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-8, 11, 17-21, 23 and 26 of copending Application No. 17/914,529 in view of Lopez-Gomez et al. (Neurological Sciences, Vol. 32, p. 1063-1067, May 2011) as evidenced by Kast et al. (British Journal of Neurology, Vol. 26, Issue 6, p. 813-817, May 2012) (of record, IDS dated Jan. 2, 2024).
Although the claims at issue are not identical, they are not patentably distinct because the present claims read on administering a CXCL8 antagonist to an individual, as do the claims of copending Application No. 17/914,529. Copending Application No. 17/914,529 also claims a method of administering reparixin and the lysine salt thereof. While copending Application No. 17/914,529 does not claim a method wherein the CXCL8 inhibitor is administered in combination with an AED such as VPA (dependent claims 14 and 20), one of ordinary skill in the art would have a reasonable expectation of success to administer the CXCL8 inhibitor in combination with an AED such as VPA because it is commonly known in the art to administer CXCL8 inhibitors in combination with AEDs, particularly phenytoin and VPA. For example, see the teachings of Lopez-Gomez above, presented in the 102 rejection of the claims over Lopez-Gomez, incorporated herein by reference.
This is a provisional nonstatutory double patenting rejection.
Claim 1, 2, 6-8, 11-16 and 20 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-17 of copending Application no. 18/996,270 in view of Villa et al. (Molecular Medicine, Vol. 13, 2007, p. 125-133) and Lopez-Gomez et al. (Neurological Sciences, Vol. 32, p. 1063-1067, May 2011) as evidenced by Kast et al. (British Journal of Neurology, Vol. 26, Issue 6, p. 813-817, May 2012) (of record, IDS dated Jan. 2, 2024).
Although the claims at issue are not identical, they are not patentably distinct because the present claims read on administering a CXCL8 antagonist to an individual, as do the claims of copending Application No. 18/996,270, which are particularly towards a powder pharmaceutical composition comprising reparixin and related methods of use. Claim 17 of 18/996,270 is directed towards a method for the treatment or prevention of seizures in an individual, the method comprising administering a pharmaceutical composition comprising reparixin to the subject, similar to the instant claims. While 18/996,270 does not claim a lysine salt of reparixin, one of ordinary skill in the art would have a reasonable expectation of success to administer the lysine salt of reparixin because it is commonly known in the art for the treatment of neurological conditions. For example, see the teachings of Villa above in the 102 rejection of the claims, incorporated herein by reference.
While copending Application No. 18/996,270 does not claim a method wherein the CXCL8 inhibitor is administered in combination with an AED such as VPA (dependent claims 14 and 20), one of ordinary skill in the art would have a reasonable expectation of success to administer the CXCL8 inhibitor in combination with an AED such as VPA because it is commonly known in the art to administer CXCL8 inhibitors in combination with AEDs, particularly phenytoin and VPA. For example, see the teachings of Lopez-Gomez above, presented in the 102 rejection of the claims over Lopez-Gomez, incorporated herein by reference.
Claim 1, 2, 6-8, 11-16 and 20 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-17 of copending Application no. 18/996,171 in view of Villa et al. (Molecular Medicine, Vol. 13, 2007, p. 125-133) and Lopez-Gomez et al. (Neurological Sciences, Vol. 32, p. 1063-1067, May 2011) as evidenced by Kast et al. (British Journal of Neurology, Vol. 26, Issue 6, p. 813-817, May 2012) (of record, IDS dated Jan. 2, 2024).
Although the claims at issue are not identical, they are not patentably distinct because the present claims read on administering a CXCL8 antagonist to an individual, as do the claims of copending Application No. 18/996,171, which are particularly towards a liquid suspension pharmaceutical composition comprising reparixin and related methods of use. Claim 17 of 18/996,171 is directed towards a method for the treatment or prevention of seizures in an individual, the method comprising administering a pharmaceutical composition comprising reparixin to the subject, similar to the instant claims. While 18/996,171 does not claim a lysine salt of reparixin, one of ordinary skill in the art would have a reasonable expectation of success to administer the lysine salt of reparixin because it is commonly known in the art for the treatment of neurological conditions. For example, see the teachings of Villa above in the 102 rejection of the claims, incorporated herein by reference.
While copending Application No. 18/996,171 does not claim a method wherein the CXCL8 inhibitor is administered in combination with an AED such as VPA (dependent claims 14 and 20), one of ordinary skill in the art would have a reasonable expectation of success to administer the CXCL8 inhibitor in combination with an AED such as VPA because it is commonly known in the art to administer CXCL8 inhibitors in combination with AEDs, particularly phenytoin and VPA. For example, see the teachings of Lopez-Gomez above, presented in the 102 rejection of the claims over Lopez-Gomez, incorporated herein by reference.
Claims 1, 2, 6-8, 11-16 and 20 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-19 of U.S. Patent No. 11,660,291 B2 in view of in view of Villa et al. (Molecular Medicine, Vol. 13, 2007, p. 125-133) and Lopez-Gomez et al. (Neurological Sciences, Vol. 32, p. 1063-1067, May 2011) as evidenced by Kast et al. (British Journal of Neurology, Vol. 26, Issue 6, p. 813-817, May 2012) (of record, IDS dated Jan. 2, 2024).
Although the claims at issue are not identical, they are not patentably distinct because the present claims read on administering a CXCL8 antagonist to an individual, as do the claims of U.S. Patent No. 11,660,291 B2. While U.S. Patent No. 11,660,291 B2 does not claim a method wherein the CXCL8 inhibitor is administered in combination with an AED such as VPA (dependent claims 14 and 20), one of ordinary skill in the art would have a reasonable expectation of success to administer the CXCL8 inhibitor in combination with an AED such as VPA because it is commonly known in the art to administer CXCL8 inhibitors in combination with AEDs, particularly phenytoin and VPA. For example, see the teachings of Lopez-Gomez above, presented in the 102 rejection of the claims over Lopez-Gomez, incorporated herein by reference.
While U.S. Patent No. 11,660,291 B2 does not claim a lysine salt of reparixin, one of ordinary skill in the art would have a reasonable expectation of success to administer the lysine salt of reparixin because it is commonly known in the art for the treatment of neurological conditions. For example, see the teachings of Villa above in the 102 rejection of the claims, incorporated herein by reference.
Claims 1, 2, 6-8, 11-16 and 20 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6 of U.S. Patent No. 12,133,843 B2 in view of in view of Lopez-Gomez et al. (Neurological Sciences, Vol. 32, p. 1063-1067, May 2011) as evidenced by Kast et al. (British Journal of Neurology, Vol. 26, Issue 6, p. 813-817, May 2012) (of record, IDS dated Jan. 2, 2024).
Although the claims at issue are not identical, they are not patentably distinct because the present claims read on administering a CXCL8 antagonist to an individual, as do the claims of U.S. Patent No. 12,133,843 B2. U.S. Patent No. 12,133,843 B2 also claims a method of administering reparixin and the lysine salt thereof (patent claims 3-4). While U.S. Patent No. 12,133,843 B2 does not claim a method wherein the CXCL8 inhibitor is administered in combination with an AED such as VPA (dependent claims 14 and 20), one of ordinary skill in the art would have a reasonable expectation of success to administer the CXCL8 inhibitor in combination with an AED such as VPA because it is commonly known in the art to administer CXCL8 inhibitors in combination with AEDs, particularly phenytoin and VPA. For example, see the teachings of Lopez-Gomez above, presented in the 102 rejection of the claims over Lopez-Gomez, incorporated herein by reference.
Claims 1, 2, 6-8, 11-16 and 20 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-16 of U.S. Patent No. 12,268,671 B2 in view of in view of Lopez-Gomez et al. (Neurological Sciences, Vol. 32, p. 1063-1067, May 2011) as evidenced by Kast et al. (British Journal of Neurology, Vol. 26, Issue 6, p. 813-817, May 2012) (of record, IDS dated Jan. 2, 2024).
Although the claims at issue are not identical, they are not patentably distinct because the present claims read on administering a CXCL8 antagonist to an individual, as do the claims of U.S. Patent No. 12,268,671 B2. U.S. Patent No. 12,268,671 B2 also claims a method of administering reparixin and the lysine salt thereof (patent claims 7-8). While U.S. Patent No. 12,268,671 B2 does not claim a method wherein the CXCL8 inhibitor is administered in combination with an AED such as VPA (dependent claims 14 and 20), one of ordinary skill in the art would have a reasonable expectation of success to administer the CXCL8 inhibitor in combination with an AED such as VPA because it is commonly known in the art to administer CXCL8 inhibitors in combination with AEDs, particularly phenytoin and VPA. For example, see the teachings of Lopez-Gomez above, presented in the 102 rejection of the claims over Lopez-Gomez, incorporated herein by reference.
Claims 1, 2, 6-8, 11-16 and 20 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-20 of U.S. Patent No. 11,291,641 B2 in view of in view of Villa et al. (Molecular Medicine, Vol. 13, 2007, p. 125-133) and Lopez-Gomez et al. (Neurological Sciences, Vol. 32, p. 1063-1067, May 2011) as evidenced by Kast et al. (British Journal of Neurology, Vol. 26, Issue 6, p. 813-817, May 2012) (of record, IDS dated Jan. 2, 2024).
Although the claims at issue are not identical, they are not patentably distinct because the present claims read on administering a CXCL8 antagonist to an individual, as do the claims of U.S. Patent No. 11,291,641 B2. While U.S. Patent No. 11,291,641 B2 does not claim a method wherein the CXCL8 inhibitor is administered in combination with an AED such as VPA (dependent claims 14 and 20), one of ordinary skill in the art would have a reasonable expectation of success to administer the CXCL8 inhibitor in combination with an AED such as VPA because it is commonly known in the art to administer CXCL8 inhibitors in combination with AEDs, particularly phenytoin and VPA. For example, see the teachings of Lopez-Gomez above, presented in the 102 rejection of the claims over Lopez-Gomez, incorporated herein by reference.
While U.S. Patent No. 11,291,641 B2 does not claim a lysine salt of reparixin, one of ordinary skill in the art would have a reasonable expectation of success to administer the lysine salt of reparixin because it is commonly known in the art for the treatment of neurological conditions. For example, see the teachings of Villa above in the 102 rejection of the claims, incorporated herein by reference.
Conclusion
No claim is found to be allowable.
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/HEATHER DAHLIN/Examiner, Art Unit 1629