DETAILED ACTION
The present application is a domestic application filed 05 October 2022, which is a continuation of PCT/US2021/026113, filed 07 April 2021, and claims priority to US Provisional Application No. 63/006,176, filed 07 April 2020.
The preliminary amendment filed 20 December 2022 is acknowledged. Claims 1-12, 14-16, 18, 21-29 and 33 are pending in the current application. Claims 15, 18, 21 and 23-28 are withdrawn as being drawn to a non-elected species, see below. Claims 1-12, 14, 16, 22, 29 and 33 are examined on the merits herein.
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 .
Election/Restrictions
Applicant's election with traverse of N-acetyllactosamine as the species of galectin-3 inhibitor in the reply filed on 22 October 2025 is acknowledged. The traversal is on the ground(s) that a search for publications relating to the elected species should reveal publications relating to the other species, and thus, would not impose a serious burden on the Office. This is not found persuasive because a search of each species requires separate and additional search queries, and consideration.
The requirement is still deemed proper and is therefore made FINAL.
Claims 15, 18 and 21, 23-28 are withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to a nonelected species, there being no allowable generic or linking claim. Applicant timely traversed the restriction (election) requirement in the reply filed on 22 October 2025.
While Applicant indicated the species reads on claims 1-12, 14, 16, 29 and 33, it is noted N-acetyllactosamine is a disaccharide comprising galactose: β-D-galactosyl-1,4-N-acetyl-D-glucosamine. Thus, claim 22 is not withdrawn.
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.
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.
Claim(s) 4-6 are rejected under 35 U.S.C. 103 as being unpatentable over Panjwani et al. (WO 2014/078655, cited in IDS submitted 20 December 2022) in view of Muntendam (US Patent Application Publication No. 2013/0029955, cited in IDS submitted 20 December 2022).
Panjwani et al. teach methods of using a pharmaceutical composition for inhibiting ocular angiogenesis or fibrosis, by inhibiting expression and/or activity of a galectin protein, including galectin-3 (abstract; claims 1 and 2). The composition comprises an effective amount of a carbohydrate to treat or prevent the ocular angiogenesis (claims 3, 4 and 52). The carbohydrate includes a compound of the general formula:
PNG
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192
404
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Greyscale
(claims 7 and 22). The compound is a derivative of N-acetyllactosamine, when R1 is N-acetylglucosamine (claims 9 and 23). The ocular angiogenesis/ocular fibrosis includes treating or preventing neovascular glaucoma (claim 53). Scar tissue formation in the eye (i.e. ocular fibrosis) can lead to the formation of preretinal and/or optic nerve head neovascularization (p.4:1-16). The composition can be formulated for an ocular delivery, to allow for various forms of ocular administration (p.18:27-30; and p.18-19, bridging para). The subject is a human (p.17:11-15). Factors determining the therapeutically effective amount include severity of the disease state and age (p.84:17-30).
Galectin-3 enhances vascularization in vivo (p.42:13-15). VEGF-A mediated angiogenesis is reduced in vitro by the addition of a dominant negative galectin-3, by a pan-galectin inhibitor (e.g. lactose), and by galectin-3 knockdown (p.42:16-18). Galectin-3 expression is developmentally regulated in the kidneys, and its expression level in pulmonary alveolar epithelial cells and hepatocytes is up-regulated following injury (p.73: lines 20-27). Panjwani et al. teach monitoring cornea opacity in mice treated with a galectin-3 inhibitor (p.106-108, examples 28 and 29).
While Panjwani et al. teach administering derivatives of N-acetyllactosamine, Panjwani et al. do not expressly disclose administering N-acetyllactosamine (present claim 16).
Muntendam teaches galectin-3 inhibitors includes carbohydrates, wherein the carbohydrate is N-acetyllactosamine (claim 5).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to administer N-acetyllactosamine to treat or prevent glaucoma.
The ordinary artisan would have been motivated to administer N-acetyllactosamine to treat or prevent glaucoma, because it is recognized as a galectin-3 inhibitor, wherein galectin-3 inhibitors are taught by Panjwani et al. for the treatment or prevention of ocular angiogenesis or fibrosis, including neovascular glaucoma. The ordinary artisan would have had a reasonable expectation of success because Panjwani et al. teach using galectin-3 inhibitors that are structural derivatives of N-acetyllactosamine for treating ocular conditions including neovascular glaucoma.
Thus, the claimed invention as a whole is prima facie obvious over the combined teaching of the prior art.
Claim(s) 1-3, 7-12, 14, 16, 22, 29 and 33 are rejected under 35 U.S.C. 103 as being unpatentable over Panjwani et al. and Muntendam as applied to claims 4-6 above, and further in view of Belmares et al. (Clinical Anatomy, 2018, vol. 31, pp. 1031-1049, cited in IDS submitted 20 December 2022).
Panjwani et al. teach as discussed above.
Panjwani et al. do not expressly disclose treating retinal damage in a subject suffering from glaucoma (present claims 1, 7, 8).
Muntendam teaches as discussed above.
Belmares et al. teach glaucoma is associated with fibrotic changes in the optic nerve head and trabecular meshwork (abstract). Belmares et al. found galectin-3 was increased in the optic nerve head of glaucomatous eyes. Glaucoma is often associated with elevated intraocular pressure (IOP), due to glaucomatous damage to trabecular meshwork tissues (p.1039, Discussion). “In all forms of glaucoma, there is progressive pathologic damage to the optic nerve head, which compromises retinal ganglion cell axons as they exit the eye to form the optic nerve” (p.1039, Discussion). In a mouse model of optic nerve damage, an increase in galectin-3 expression was observed (p.1046, second para). Galectin-3 expression has been reported in animal optic nerve head studies, as well as in retinal tissue (p.1034, right column, first para). Belmares et al. teach “the effect potential of aging in the ONH should be minimized with our use of age-matched donors” (p.1046, first para).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to treat a subject having glaucoma and retinal nerve damage.
In addition to the reasons above, one having ordinary skill in the art would have been motivated to select and treat a subject having glaucoma and retinal nerve damage, because according to Belmares et al., optic nerve damage progresses in all forms of glaucoma. The ordinary artisan would have been motivated to administer a galectin-3 inhibitor to a subject to treat retinal nerve damage and suffering from glaucoma, because Belmares et al. found galectin-3 was increased in the optic nerve head of glaucomatous eyes, and Panjwani et al. teach the administration of galectin-3 inhibitors to treat an advanced form of glaucoma known as neovascular glaucoma. Since galectin-3 was increased in the optic nerve head of glaucomatous eyes, the ordinary artisan would have been further motivated to select a subject to receive the galectin-3 inhibitor if the patient has elevated intraocular levels of galectin-3 because they would be expected to be the most responsive to treatment with a galectin-3 inhibitor.
Additionally, the ordinary artisan would have been motivated to select a subject if the patient has elevated blood plasma levels of galectin-3, because Panjwani et al. teach galectin-3 expression is developmentally regulated in the kidneys, and its expression level in pulmonary alveolar epithelial cells and hepatocytes is up-regulated following injury.
One having ordinary skill in the art would have been motivated to monitor the subject’s response to the galectin-3 inhibitor to evaluate therapeutic benefit, because Panjwani et al. teach monitoring cornea opacity in mice treated with a galectin-3 inhibitor.
The ordinary artisan would have been motivated to administer N-acetyllactosamine, because it is recognized as a galectin-3 inhibitor, wherein galectin-3 inhibitors are taught by Panjwani et al. for the treatment or prevention of ocular angiogenesis or fibrosis, including neovascular glaucoma. The ordinary artisan would have had a reasonable expectation of success because Panjwani et al. teach using galectin-3 inhibitors that are structural derivatives of N-acetyllactosamine.
One having ordinary skill in the art would have been motivated to further determine if the subject has retinal nerve damage due to elevated intraocular pressure as recited in claim 7 and/or determining if the subject’s eye has elevated intraocular pressure as recited in claim 9, because Belmares et al. teach glaucoma is “often associated with elevated IOP” and “in all forms of glaucoma, there is progressive pathologic damage to the optic nerve head”.
One having ordinary skill in the art would have been motivated to treat an adult human, because Panjwani et al. teach formulating the composition for human use wherein factors determining the therapeutically effective amount include severity of the disease state and age. Additionally, Belmares et al. teach “the effect potential of aging in the ONH should be minimized with our use of age-matched donors” (p.1046, first para). The prior art as a whole suggest humans to be treated include aging individuals, such as adults. Thus, one having ordinary skill in the art would have been motivated to treat adults.
The recitation “wherein the method achieves at least a 25% reduction in the volume of retinal nerve damage” in claim 2 necessarily occurs upon performing the positively recited step of claim 1. The same rational applies to claim 3.
Thus, the claimed invention as a whole is prima facie obvious over the combined teaching of the prior art.
Conclusion
In view of the rejections to the pending claims set forth above, no claim is allowed.
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/BAHAR CRAIGO/
Primary Examiner
Art Unit 1699