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 .1
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on Sept 25 2025 has been entered.
Status of Claims
Claims 1-4,6-13,15-21,23,25,28-33,35-37 and 39-52 are pending. Claims 6, 25, 28-30 and 48-52 are withdrawn. Claims 1-4,7-13,15-21,23,31-33,35-37 and 39-47 are rejected. The examined claims are directed to the process species comprising administering tonabersat2 to a subject having proliferative vitreoretinopathy.
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Note, as detailed by the non-final office action of Examiner Aguirre dated May 23 2024, Applicant elected the species of tonabersat for the treatment of subjects PVR. See below reproduction.
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New claims 48-52 are withdrawn as they are not directed to the elected species of method, treatment/prevention of PVR in a subject (claims 48-52) by administering tonabersat to the subject. In fact, claim 48 comprises further steps of identifying a subject with PVR, and measuring or visualizing EMT activity in the subject.
Claim Objections
Claims 6 and 25 are objected to because of the following informalities: Claims 6 and 25 are identified as “Withdrawn” but the text of the claim is missing. If claims 6 and 25 are considered to be merely withdrawn, the text of the claims must follow. If claims 6 and 25 are actually canceled, the claimed identifiers should be amended to “canceled.” Appropriate correction is required.
Response to Arguments
Applicant’s amendments to the specification, Paragraph 107, to correct the informalities therein have been fully considered and are persuasive. The objection to the specification has been withdrawn.
Applicant’s amendments to claims 1 and 20 to correct the informalities therein have been fully considered and are persuasive. The objection of claims 1 and 20 has been withdrawn.
Applicant’s amendments to claims 7-9 to correct the informalities therein have been fully considered and are persuasive. The objection of claims 7-9 has been withdrawn.
Applicant’s amendments to claim 3 to correct the informalities therein have been fully considered and are persuasive. The objection of claim 3 has been withdrawn.
Applicant's arguments filed 09/25/2025 with regard to the rejection of Claims 1, 2, 4, 7-21, 23, 26-27 and 31-40 under 35 USC §103 as obvious over Green WO 191, have been fully considered but they are not persuasive, see below obviousness rejections. See detailed response to Attorney arguments below the 103 rejection.
Claim Rejections - 35 USC § 103
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
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 1-4, 7-13, 15-21, 23, 31-33, 35-37 and 39-46 are rejected under 35 U.S.C. 103 as being unpatentable over Green et al. WO 2016/029191 A2 (pub. 25 Feb 2016) as evidenced by Pastor “Proliferative Vitreoretinopathy: An Overview SURVEY.” OF OPHTHALMOLOGY VOLUME 43 NUMBER 1 JULY-AUGUST 1998 (Year: 1998). Pastor is cited on the PTO-892 form.
Note, while the amended claims are rejected as being obvious over the same prior art, Green, these are new rejections as necessitated by amendment of claims 1 and 20 now directed to compounds of Formula I, and the particular subset of patients in need, to be treated for proliferative vitreoretinopathy.
Claim 1 is a method of treating a subject for proliferative vitreoretinopathy, comprising administering a hemichannel inhibitor to said subject in an amount effective to inhibit epithelial-mesenchymal transition activity, wherein the hemichannel inhibitor is a compound of Formula (I)
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wherein X, Y, R2, R3, R4, R5, R6, R7 and R8 and R9 are defined therein.
It is noted that tonabersat, falls within the scope of claims 1 and 4.
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Tonabersat has a structure of instant Formula (I),
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, wherein:
Y is C-R1,
R1 is acetyl,
R2 is hydrogen,
R3 and R4 are methyl,
R5 is hydroxy,
R6, R8 and R9 are hydrogen,
R7 is phenyl substituted with chloro and fluoro, and
X is oxygen.
Regarding the limitation of claims 1, 2 and 4 and the claimed hemichannel inhibitor compound of formula I (including tonabersat), Green et al. teach administering to a subject an effective amount of tonabersat. See paragraph 74. See also Example 9, where 1 mg/kg or 10 mg/kg tonabersat was injected into mice having retinal ischemia-reperfusion. (“A final blood Tonabersat concentration of 0.319 mM or 0.0319 mM was intended.”) According to Green, “Tonabersat is a very effective and direct hemichannel blocker” (para. 121), knocking down Cx43 in APRE-19 cells and causing internalization of the gap junctions/hemichannels (para. 117). As Green teaches the claimed and required effective amounts of tonabersat to inhibit EMT, Green discloses the required inhibition of EMT as claimed, as EMT activity would be inhibited at its taught doses. Specifically, Green teaches that “tonabersat may be administered orally once a day at a dose of approximately 2 mg to approximately 40 mg” (para. 482). With regard to the treatment of the claimed subject in need, for proliferative vitreoretinopathy, in amounts effective to inhibit epithelial-mesenchymal transition (EMT) activity, Green teaches tonabersat to treat patients afflicted with vitreoretinopathy (claim 67 and paragraph 43).
Note that Green recites the broader class of vitreoretinopathy as a class to be treated and teaches the particular type, proliferative vitreoretinopathy as follows.
Pastor defines Proliferative vitreoretinopathy (PVR), an anomalous scarring process appearing with retinal detachment. See page 3, column 1. “Proliferative vitreoretinopathy can also be defined as the growth and contraction of cellular membranes within the vitreous cavity and on both retinal surfaces.” See page 3, column 1. “Clinically, PVR is characterized by the growth and contraction of cellular membranes within the hyaloid and the retina and on both retinal surfaces.” See page 3 column 2 bridging to page 4 column 1.
Green teaches various disorders to be treated with tonabersat include conditions such as “Serous detachment of the neurosensory retina . . . Retinal detachment occurs when subretinal fluid accumulates between the neurosensory retina and retinal pigment epithelium. . . [This includes a mechanism that] involves proliferative membranes on the surface of the retina or vitreous. These membranes can pull on the neurosensory retina causing a physical separation between the neurosensory retina and retinal pigment epithelium.” See paragraph 278.
Green, teaches the required elements of claim 1 with regard to the claimed compound of formula I (tonabersat) and treatment of vitreoretinopathy, specifically proliferative vitreoretinopathy (PVR) as evidenced by Pastor.
Prior to the filing of the instant application, a person having ordinary skill in the art (PHOSITA) following the teachings Green, as evidenced by Pastor, would have found it prima facie obvious to combine the prior art elements of Green (teaching treatment of vitreoretinopathy, spelling out the particular details of the proliferative species thereof, PVR, as evidenced by Pastor) according to known methods to yield predictable results.
Regarding claim 3, Green teaches the use of various organic molecules to inhibit gap junction or hemichannel currents, such as Peptide5, GAP19 and GAP26. See paragraph 180, among other multiple references.
Regarding the oral dosage amounts of claim 7 (10-200 mg per dose) and claim 8 (80-320 mg per day), Green teaches that “tonabersat may be administered orally once a day at a dose of approximately 2 mg to approximately 40 mg” (para. 482). Green also teaches that “[d]ata obtained from cell culture assays and animal studies can be used in formulating a range of dosages for use in humans. […] The dosage can be determined from the concentration of the amount administered, expected mass of the animal model tested (200-300 g per rat for adult Wistar rats) […].” (para. 477). For example, a PHOSITA would have deduced, based on Green’s teaching of administering 1 mg/kg of tonabersat (para. 593), that a 200-300 g adult Wistar rat can be administered a single daily dose of 200-300 mg of tonabersat. This range falls squarely within the range of claim 8 and touches the range of claim 7, and the tonabersat range of 2-40 mg overlaps with the range of claim 7. Since the claimed ranges overlap with the ranges of the prior art, a prima facie case of obviousness exists according to MPEP § 2144.05. Additionally, “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). A PHOSITA would have been motivated to select the disclosed range of 2-40 mg of oral tonabersat, or the range of 200-300 mg of tonabersat, for the purpose of optimizing the treatment method of administering tonabersat orally to treat the ocular disorders taught by Green.
Regarding claim 9 (0.2 mg/kg to 5 mg/kg per dose per day), Green teaches administering 1 mg/kg of tonabersat using an “in vivo model of retinal ischemia-reperfusion” (para. 593). This dosage would have informed a PHOSITA as to the proper dosage to use in an animal or human. See also Green para. 477 (“Data obtained from cell culture assays and animal studies can be used in formulating a range of dosages for use in humans.”).
Regarding claim 10, the intended “final blood Tonabersat concentration of 0.319 mM or 0.0319 mM” is equivalent to the concentration range of 319-31.9 µM, which overlaps the claimed circulating concentration range of 90-10 µM. Furthermore, Green teaches that tonabersat “is administered systemically […] such that the final circulating concentration is approximately 0.001 to approximately 150 micromolar, or higher […]” (para. 383). Since the claimed range both overlaps and is encompassed by the ranges of the prior art, a prima facie case of obviousness exists according to MPEP § 2144.05. Additionally, “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). A PHOSITA would have been motivated to select the disclosed range of 31.9-319 µM or the range 0.001-150 micromolar, for the purpose of optimizing the treatment method of using tonabersat.
Regarding claim 11, Green’s Example 9 teaches administering tonabersat by injection.
Regarding claims 12-13 (administering tonabersat orally), Green teaches that “tonabersat may be administered orally once a day at a dose of approximately 2 mg to approximately 40 mg” (para. 482).
Regarding claim 15 (drawn to inducing or promoting closure of a hemichannel), claim 16 (drawn to blocking, inhibiting, or decreasing hemichannel opening), and claim 17 (drawn to triggering, inducing or promoting internalization of a hemichannel), these claims are drawn to properties or characteristics inherent to administering the hemichannel inhibitor of claim 1, which in this case is tonabersat. See, e.g., specification paragraph 58 and Green Figure 11 (“Tonabersat internalizes and down regulates Cx43 GJ plaques”) for evidence.
Regarding claim 18 and the preventing PVR as an aspect, a PHOSITA would have found it obvious to administer tonabersat to a subject to prevent proliferative vitreoretinopathy, because it is characterized by the prior art conditions “serious detachment of the neurosensory retina, RPE detachment, hemorrhages (subretinal pigment epithelial, subretinal, intraretinal or pre-retinal, including breakthrough bleeding into the vitreous), piretinal, intraretinal, subretinal or sub-pigment epithelial scar/glial tissue or fibrin-like deposits, retinal fibrosis, retinal angiomatous proliferations and retinochoroidal anatastamosis” (Green claim 67). Green also teaches using the compounds to treat “vitreoretinopathy” (para. 43) and “rhegmatogenous retinal detachment” (para. 278), wherein proliferative vitreoretinopathy “is a severe blinding complication of rhegmatogenous retinal detachment” according to Applicant’s admitted prior art (specification para. 8). Therefore, a PHOSITA would have found it obvious to use tonabersat to treat a subject having proliferative vitreoretinopathy, and the PHOSITA would have had a reasonable expectation of success, due to Green’s teaching that tonabersat is capable of treating the ocular conditions listed above, which include symptoms and causes of proliferative vitreoretinopathy.
Regarding claim 19 (wherein the subject is human), Green teaches treating human hCMEC cells with tonabersat (para. 116) and also that “the term ‘subject’ […] refers to any mammal, including humans” (para. 231); therefore a PHOSITA would have found it obvious to select a human as the subject to which tonabersat is administered.
Regarding claims 20 (where tonabersat is said to prevent or inhibit EMT activity at risk for having or having proliferative vitreoretinopathy (PVR) as claimed in claim 1), and claim 21 (connexin 43 hemichannel inhibitor), claim 23 (tonabersat), and claim 43 (directed to a method of solely preventing PVR in a subject), Green teaches a method of administering a therapeutically effective amount of tonabersat (a small molecule inhibitor) to a subject (e.g., claim 67 and Example 9). Since tonabersat is a Cx43 hemichannel inhibitor and inhibiting Cx43 inherently inhibits EMT activity as evidenced by the specification in paragraph 14 (“anti-hemichannel compounds can be used to inhibit EMT”), the method of administering tonabersat would inherently inhibit EMT. Similarly, a PHOSITA would recognize inhibition and/or treatment of EMT such as proliferative vitreoretinopathy, would necessarily prevent EMT activity in a patient at risk of having or having PVR as claimed. With regard to the preventing and inhibiting aspects of EMT activity in a patient with PVR), Green teaches in some aspects of this invention, its use of “treatment” refers to “[d]esirable effects of treatment include, but are not limited to preventing occurrence or recurrence of a disease, disorder or condition. . . “, etc. See paragraph 223.
See also above discussion of claim 1 where a method of treating PVR with tonabersat, as evidenced by Pastor) is detailed above. Prior to the filing of the instant application, a person having ordinary skill in the art (PHOSITA) following the teachings Green, as evidenced by Pastor, would have found it prima facie obvious to combine the prior art elements of Green (teaching treatment of vitreoretinopathy, spelling out the particular details of the proliferative species thereof, PVR, as evidenced by Pastor) according to known methods to yield predictable results.
Regarding claim 31 directed to tonabersat, Green teaches tonabersat, see above.
Regarding claim 32 (administering tonabersat orally), Green teaches that “tonabersat may be administered orally once a day at a dose of approximately 2 mg to approximately 40 mg” (para. 482).
Regarding claim 33, Green’s Example 9 teaches administering the tonabersat once on the day of the experiment (i.e., once per day).
Regarding claim 35 (drawn to inducing or promoting closure of a hemichannel), claim 36 (drawn to blocking, inhibiting, or decreasing hemichannel opening), and claim 37 (drawn to triggering, inducing or promoting internalization of a hemichannel), these claims are drawn to properties or characteristics inherent to administering the hemichannel inhibitor of claim 1, which in this case is tonabersat. See, e.g., specification paragraph 58 and Green Figure 11 (“Tonabersat internalizes and down regulates Cx43 GJ plaques”) for evidence.
Regarding claim 39 and a human subject, Green also teaches that “[d]ata obtained from cell culture assays and animal studies can be used in formulating a range of dosages for use in humans.” (para. 477).
Regarding claims 40-42 and 44-45, Green teaches tonabersat, see above.
Regarding claim 46 and a method of preventing PVR in a subject in need with connexin 43 hemichannel inhibitors, such as Peptide 5, GAP19 and GAP26, as discussed above, Green teaches the treatment of PVR as discussed above, where it teaches the Peptide 5, GAP19 and GAP26 as hemichannel inhibitors and gap junction inhibitors as claimed and required for the treatment of PVR. See paragraph 180 specifically, as well as numerous references to these three organic molecules throughout.
Claim 1-4,7-13,15-21,23,31-33,35-37 and 39-47 are rejected under 35 U.S.C. 103 as being unpatentable over Green as evidenced by Pastor in view of Coutinho et al. Xentry-Gap19 inhibits Connexin43 hemichannel opening especially during hypoxic injury Drug Deliv Transl Res (2020) 10:751–765 in view of Idrees et al. Proliferative Vitreoretinopathy: A Review Int Ophthalmol Clin. 2019 ; 59(1): 221–240.
As discussed above, claims 1-4,7-13,15-21,23,31-33,35-37 and 39-46 are rejected as being obvious over Green as evidenced by Pastor but Green does not teach XG19 as particular species to treat PVR.
As discussed above, Green teaches a method of treating an EMT modulated disease, PVR by use of Peptide 5, GAP19 and GAP26 as discussed above, but does not teach the species of claim 47, XG19..
Where claim 47 requires XG19, Coutinho teaches the XG19 (Xentry-Gap19), blocked pathological hemichannel opening. See abstract. Under hypoxic conditions, increased expression of the plasma membrane proteoglycan Syndecan-4 was targeted by Xentry (the cell penetrating peptide of XG19), leading to even greater XG19 uptake leading to higher inhibition of ATP release and greater cell survival. Coutinho suggests that XG19, which is targeted specifically to hypoxic cells, can efficiently and safely block Cx43 HC and could therefore be a novel treatment for hypoxic and inflammatory diseases. See abstract. While Coutinho suggests treatment of a subject in need, the administration of XG19 in amounts therapeutically effective to treat a subject suffering from hypoxic/inflammatory diseases, it does not teach treatment of a disease, disorder or condition characterized in part by pathological or unwanted EMT activity, such as Proliferative vitreoretinopathy (PVR).
However, a PHOSITA would predictably have a reasonable expectation to treat PVR with a Cx43 HC inhibitor such as XG19 as taught in the prior art.
Idrees teaches “two primary events occur that act as the initiating factors of the potential PVR cascade. These events are the breakdown of the blood-retinal barriers and retinal hypoxia.” See page 3, Section Pathophysiology. The rationale to support the prima facie case of obvious are the prior art elements (where retinal hypoxia is a initiating factor for PVR cascade) combined with known methods (use of XG19 that specifically targets hypoxic cells, efficiently/safely blocks Cx43 HC as a treatment of hypoxic diseases) so to predictably arrive at the claimed invention by PHOSITA.
RESPONSE TO ATTORNEY ARGUMENTS:
The Attorney response states blocking the EMT of RPE cells will be an efficient way to prevent PVR and there is no currently available drug to prevent it. The Attorney response states Green merely states vitreoretinopathy and NOT proliferative vitreoretinopathy, (PVR) a specific type of vitreoretinopathy as detailed therein (RPE glial migration into the vitreous cavity/retinal surfaces etc., as per Yang et al. Nat Rev Mol Cell Biol. 2020, Jun 21 (6) 341-352.
In response, the obviousness rejection is now directed to be over Green as evidenced by Pastor. With regard to the treatment of the claimed subject in need, for proliferative vitreoretinopathy, in amounts effective to inhibit epithelial-mesenchymal transition (EMT) activity, Green teaches tonabersat to treat patients afflicted with vitreoretinopathy (see claim 67 and paragraph 43.
Note that Green recites the broader class of vitreoretinopathy as a class to be treated and teaches the particular type, proliferative vitreoretinopathy as follows.
Pastor defines Proliferative vitreoretinopathy (PVR), an anomalous scarring process appearing with retinal detachment. See page 3, column 1. “Proliferative vitreoretinopathy can also be defined as the growth and contraction of cellular membranes within the vitreous cavity and on both retinal surfaces.” See page 3, column 1. “Clinically, PVR is characterized by the growth and contraction of cellular membranes within the hyaloid and the retina and on both retinal surfaces.” See page 3 column 2 bridging to page 4 column 1.
Green teaches various disorders to be treated with tonabersat include conditions such as “Serous detachment of the neurosensory retina . . . Retinal detachment occurs when subretinal fluid accumulates between the neurosensory retina and retinal pigment epithelium. . . [This includes a mechanism that] involves proliferative membranes on the surface of the retina or vitreous. These membranes can pull on the neurosensory retina causing a physical separation between the neurosensory retina and retinal pigment epithelium.” See paragraph 278.
Green, teaches the required elements of claim 1 with regard to the claimed compound of formula I (tonabersat) and treatment of vitreoretinopathy, specifically proliferative vitreoretinopathy (PVR) as evidenced by Pastor.
The Attorney response states there is no basis to suggest that someone of ordinary skill (a PHOSITA) reviewing the 7 conditions would have immediately concluded the compounds to inhibit connexin hemichannels with a hemichannel modulator (tonabersat) would modulate EMT as claimed by Applicant’s invention. The Attorney response states it is potent evidence that this was not readily apparent to any of the four named inventors on the of the Green et al. application, who are far beyond those of ordinary skill (Professor Green also being an inventor of the currently described and claimed inventions in the present application).
In response, as detailed above, Green recites the broader class of vitreoretinopathy as a class to be treated and teaches the particular type, proliferative vitreoretinopathy as follows. Pastor defines Proliferative vitreoretinopathy (PVR), an anomalous scarring process appearing with retinal detachment. See page 3, column 1. “Proliferative vitreoretinopathy can also be defined as the growth and contraction of cellular membranes within the vitreous cavity and on both retinal surfaces.” See page 3, column 1. “Clinically, PVR is characterized by the growth and contraction of cellular membranes within the hyaloid and the retina and on both retinal surfaces.” See page 3 column 2 bridging to page 4 column 1.
Green teaches various disorders to be treated with tonabersat include conditions such as “Serous detachment of the neurosensory retina . . . Retinal detachment occurs when subretinal fluid accumulates between the neurosensory retina and retinal pigment epithelium. . . [This includes a mechanism that] involves proliferative membranes on the surface of the retina or vitreous. These membranes can pull on the neurosensory retina causing a physical separation between the neurosensory retina and retinal pigment epithelium.” See paragraph 278.
Green, teaches the required elements of claim 1 with regard to the claimed compound of formula I (tonabersat) and treatment of vitreoretinopathy, specifically proliferative vitreoretinopathy (PVR) as evidenced by Pastor.
Additionally, while Applicant argues it was the first to discover the role of EMT to treat PVR, it is pointed out that claim 1 and the other independent claimed method recite AND require an effective amount of a compound of formula I (tonabersat) to inhibit EMT activity. Claims 7-9 recite doses of compounds of formula I noted to be orally effective amounts to activate EMT, and as detailed above, these amounts are taught by Green as detailed above, so as to achieve circulating amounts of tonabersat that ranges from about 10 micromolar to about 90 micromolar. Claim 10 is taught by Green as detailed above. As Green teaches the claimed and required effective amounts of tonabersat to inhibit EMT, Green discloses the required inhibition of EMT as claimed, as EMT activity would be inhibited at its taught doses. Specifically, Green teaches that “tonabersat may be administered orally once a day at a dose of approximately 2 mg to approximately 40 mg” (para. 482).
Conclusion and Correspondence
In conclusion, no claims are allowed. Any inquiry concerning this communication or earlier communications from the examiner should be directed to WILLIAM LEE whose telephone number is (571)270-3876. Examiner can normally be reached M-F.
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Adam C. Milligan can be reached at (571) 270-7674. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/WILLIAM Y LEE/Examiner, Art Unit 1623
/ADAM C MILLIGAN/Supervisory Patent Examiner, Art Unit 1623
1 This application, filed on March 2, 2022, claims priority to NZ 773493, filed on March 2, 2021. Receipt is acknowledged of certified copies of papers required by 37 CFR 1.55.
2 Gemichannel inhibitor N-[(3S,4S)-6-acetyl-3-hydroxy-2,2-dimethyl-3,4-dihydrochromen-4-yl]-3-chloro-4-fluorobenzamide (tonabersat) elected with traverse in the reply filed on March 13, 2024
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