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 Applicant’s claim for the benefit of a prior-filed application under 35 U.S.C. 119(e) or under 35 U.S .C. 120, 121, 365(c), or 386(c) is acknowledged. The present application is drawn fro m PCT/US2022/020385, filed 3/15/2022; and claims benefit under 35 U.S.C. 119(e) to U.S. Provisional application 63/161758, filed 3/16/2021. Status of Claims Claims 1-2, 4-5, 7-19, 21-24, 33-35, 45, 51 and 57-58 are pending and are being examined on the merits. Claim Objections Claims 19 and 21-22 are objected to because of the following informalities: The claims recite “the methods of claim s ”, whereby claims is plural but should be singular. Appropriate correction is required. 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. Claims FILLIN "Enter claim indentification information" \* MERGEFORMAT 23-24 , 33-35, 45, 51 and 57-58 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. Claims 23-24 recite the limitation wherein the antibody is administered before (claim 23) or after (claim 24) “the onset of one or more symptoms of the wound.” It is unclear what the symptoms of the wound are. The specifications do not define the symptoms of the wound. Are the symptoms of the wound different from the properties that define the wound? For example, would tissue damage, redness, swelling and/or pain, be considered symptoms of the wound, or the evidence of a wound, or both? Conversely, the symptoms of a wound might be considered to be further damage , insult or pathology that occurs in response to the presence of the wound for some duration, such that they are secondary symptoms to the primary pathology . Thus, the skilled artisan does not know whether the limitation of administering the antibody before onset of symptoms of the wound is referring to prophylactic administration before the wound has ever occurred, or refers to treating a chronic wound before the onset of secondary symptoms that arise in response to the chronic wound. As the metes and bounds of the claim are unclear, claims 23-24 are rejected for indefiniteness. Claims 33-35, 45 and 51 recite an antibody “comprising or consisting of” an amino acid sequence, whereby the amino acid sequence defines a CDR domain of an antibody (claims 33-35) or whereby the amino acid sequence defines the VH or VL domain of an antibody (claims 45 and 51). Applicants are directed to section 2111.03 of the MPEP regarding transitional phrases. The term “comprising” is inclusive or open-ended and does not exclude additional, unrecited elements; whereas “consisting of” excludes any element not specified in the claim. These terms are distinct alternatives, and encompass different limitations which may be in conflict with each other. That is, an embodiment “consisting of” is more limited than an embodiment “comprising”; and thus a skilled artisan would not know what the required limitations of the claim are. An antibody domain “comprising” the requisite amino acid sequences may also embody larger sequences encoding the specified domain, but would then be in conflict with a claim limited to an antibody domain “consisting of” the amino acid sequences, whereby any additional amino acid residues are not encompassed in the invention. Thus, an antibody domain sequence cannot be claimed as both “comprising or consisting of” a particular amino acid sequence, as these are distinctly different claim limitations regarding the amino acid sequence of the invention . A skilled artisan considering a particular amino acid sequence that comprises, but does not consist of, the claimed sequences is unsure of whether or not they are infringing on the claimed sequence(s) because the boundaries of claimed sequences are unclear . As the metes and bounds of the claim ed sequences are unclear, claim s 33-35, 45 and 51 are rejected as indefinite. Claims 57-58 depend from claim 51 but fail to rectify the indefiniteness issues and therefore are also rejected. Claim Rejections - 35 USC § 112 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. Claim FILLIN "Pluralize \“Claim\” if necessary, insert \“is\” or \“are\” as appropriate, and insert the claim number(s) which are under rejection." 16 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. 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 16 recites the method of claim 2 wherein the anti-ceramide antibody or antigen-binding fragment thereof is an “ antibody ” . Claim 2 recites administering an anti-ceramide antibody or antigen binding fragment thereof to the subject. The specifications (pg. 10, para. 0035) define the term “antibody” as referring to an immunoglobulin molecule which has two heavy chain polypeptides and two light chain polypeptides; and also encompasses “antigen-binding fragments thereof”. Thus the term “antibody” of claim 16 encompasses both a full length anti-ceramide antibody or an antigen-binding fragment thereof . Therefore claim 16 does not further limit the antibody or antigen-binding fragment thereof of claim 2. Examiner suggests applicants amend claim 16 to be drawn to the method of claim 2 wherein the anti-ceramide antibody is a full length antibody or immunoglobulin molecule. 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. Claims FILLIN "Insert the claim numbers which are under rejection." \d "[ 1 ]" 1-2, 7-12, 16-17 and 22-24 are rejected under 35 U.S.C. 102 FILLIN "Insert either \“(a)(1)\” or \“(a)(2)\” or both. If paragraph (a)(2) of 35 U.S.C. 102 is applicable, use form paragraph 7.15.01.aia, 7.15.02.aia or 7.15.03.aia where applicable." \d "[ 2 ]" (a)(1) and (a)(2) as being FILLIN "Insert either—clearly anticipated—or—anticipated—with an explanation at the end of the paragraph." \d "[ 3 ]" anticipated by FILLIN "Insert the prior art relied upon." \d "[ 4 ]" Rotolo et al., (US Patent 10,450,385; issued 10/22/2019) . Rotolo teaches anti-ceramide antibodies and methods for prevention or treatment of apoptosis in a subject by administering the anti-ceramide antibodies (abstract). In one aspect, the invention of Rotolo is directed to a method of treating Radiation GI Syndrome in a subject by administering an anti-ceramide antibody (col. 3, lines 23-27). Regarding the treatment of GI syndrome, Rotolo teaches “Radiation targets both the gastrointestinal microvasculat ure and intestinal stem cell compartments; dysfunction of the microvascular endothelium, detected as apoptosis at four hours following radiation represents a principle lesion leading to the GI syndrome,” (col. 8, lines 7-11). The lesions occur to crypt base columnar (CBC) cells, which are define d as a population of intestinal stem cells, which proliferate and differentiate incessantly, replenishing the physiologic loss of epithelial cells and maintaining the anatomical and functional integrity of the mucosa (col. 7, lines 62-67). Thus, Rotolo teaches that radiation therapy causes a “wound” to the GI, comprising lesions of the CBC cells, which lead to deterioration that represents GI syndrome; and that as the CBC cells naturally regenerate the anatomical and functional integrity of the mucosa, lesions to these cells also inhibit the “healing” of the tissue following radiation therapy. Rotolo teaches penetrating radiation (IR) was thought to kill cells by direct damage to DNA, but that apoptotic signaling can alternately be generated by the interaction of IR with cellular membranes. Ceramide mediated raft clustering is involved in IR-induced apoptosis and clonogenic cell death; and that it has long been accepted that the clonogenic compartment of the GI mucosa is the specific and direct target for radiation in inducing GI damage (col. 9, lines 1-11). Thus, the present application is directed to an anti-ceramide antibody (col. 9, lines 12-14). Rotolo teaches the methods of inhibiting apoptosis with an anti-ceramide antibody can also be used for treating or preventing graft versus host disease, before or after the onset of graft versus host disease, when a subject receives a transplant, including a bone marrow transplant (col. 16, lines 50-63). Treatment or prevention of graft versus host disease after a transplant in a subject is also an example of enhancing “wound healing” by administering an anti-ceramide antibody. For example, Figure 13 is an illustration that the anti-ceramide scFv , 6B5, protects mice from lethal acute graft versus host disease; whereby mice were scored weekly for GvHD-associated morbidity, including skin lesions (col. 5, lines 14-25; Fig. 13), and whereby mice treated with the antibody survived longer compared to control animals. Regarding the anti-ceramide antibody, Rotolo teaches the 6B5 anti-ceramide antibody comprises the VH of SEQ ID NO: 48 and the VL of SEQ ID NO: 8 (Fig. 6). Rotolo teaches the VH comprises the HCDRs of SEQ ID NOs: 1-3 respectively, and the VL comprises the LCDRs of SEQ ID NOs: 4-6, respectively (col. 53, claims 1-2). Rotolo SEQ ID NOs: 1 and 3-6 are identical to instant SEQ ID NOs: 1 and 3-6 respectively. The HCDR2 of Rotolo SEQ ID NO: 2 is YNYPRDGSTKYNEKF K G whereas the HCDR2 of the anti-ceramide antibody of instant SEQ ID NO: 44 (of claim 33) is YNYPRDGSTKYNEKF Q G. Thus, Rotolo teaches a variant embodiment of anti-ceramide antibodies; Rotolo does not teach the instantly claimed anti-ceramide antibodies. Regarding claims 1-2 , Rotolo teaches a method for treating a Radiation GI Syndrome in a subject, whereby the GI Syndrome is characterized by radiation-induced lesions of CBC cells, and thus anticipates the method of treating a wound of instant claim 1 . As the lesioned CBC cells promote natural replacement of the damaged GI tissue, the method for preventing apoptosis of the CBC cells in response to radiation anticipates the method for enhancing wound healing of instant claim 2 . Regarding claims 7-8 and 22 , Rotolo teaches the anti-ceramide antibody may be administered topically or intravenously (col. 16, lines 64-66; col. 17 line 2). Thus the method of Rotolo anticipates instant claims 7-8 and 22 . Regarding claims 9-12 , Rotolo teaches the anti-ceramide antibody may be administered as a single dose or bolus, as a continuous infusion, or as multiple doses which may be administered daily, weekly or monthly (col. 18, lines 7-15). Thus, the various administration regimens of Rotolo anticipate instant claims 9-12 . Regarding claim 1 6 -1 7 , Rotolo teaches the antibody may be a full length antibody or an antigen-binding fragment thereof, including an scFv (col. 6, lines 50-55; col 12, lines 19-25). Thus the full length antibody or the scFv antibody fragment of Rotolo anticipates instant claims 1 6 -1 7 . Regarding claims 23-24 , Rotolo teaches administering the anti-ceramide antibody for mitigation of cell death (i.e., a lesion or wound) in GI syndrome. Rotolo teaches the antibody may be administered after the penetrating radiation which causes the lesions and GI syndrome, or before exposure of the subject to penetrating radiation (col. 16, lines 25-50). Thus, the methods of Rotolo anticipate instant claims 23-24 . Claim Rejections - 35 USC § 103 The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action: A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made. Claims FILLIN "Insert the claim numbers which are under rejection." \d "[ 1 ]" 1-2, 4-5, 7-19 and 21-24 are rejected under 35 U.S.C. 103 as being unpatentable over FILLIN "Insert the prior art relied upon." \d "[ 2 ]" Rotolo et al., (US Patent 10,450,385; issued 10/22/2019) , Ojeh et al., (Int. J. Mol. Sci., 2015, 16) , and Gold et al., (from IDS of 9/15/2023; WO 2010027802; published 3/11/2010) , as evidenced by US '971 (from IDS of 9/15/2023; US20150216971; published 8/6/2015) . The reasons why Rotolo et al. anticipates claims 1-2, 7-12, 16-17 and 22-24 are described above. However, Rotolo et al. does not teach wherein the wound is a chronic or diabetic wound (re. claims 4-5), whereby the treatment is administered at various stages of the wound healing process (re. claims 13-15), or whereby the treatment includes measures of wound healing (re. claims 18-19 and 21). Specifically, Rotolo et al. teaches that anti-ceramide antibodies prevent the apoptosis of CBC stem cells, thus preventing the GI lesions which lead to GI syndrome following radiation stress. Rotolo teaches that ceramide mediated raft clustering is involved in IR-induced apoptosis and clonogenic cell death (col. 9, lines 7-8). US ‘971, also from Rotolo, elaborates further on this mechanism. US ‘971 discusses the damage of stem cell clonogens (SCCs) as autonomous lesions leading to irreversible tissue injury (pg. 4, para. 0046). US ‘971 teaches radiation stress activates endothelial ASMase , c a talyzing ceramide generation on the external plasma membrane of mouse and human endothelium to initiate apoptotic signaling. US ‘971 teaches that attenuation of intestinal endothelial apoptosis by genetic inactivation of ASMase-mediatd ceramide generation enhances SCC survival, facilitating repair of crypt damage and rescue of animals from GI lethality (pg. 5, para. 0046). Further, that ceramide rich platforms (CRPs) are amenable to pharmacologic inactivation, specifically pharmacologic inhibition of CRP formation with an antibody to ceramide attenuated endothelial damage, enhanced crypt stem cell clonogen survival, and thereby increased tissue regeneration, even following lethal radiation doses (pg. 5, para. 0047). Taken together, Rotolo and US ‘971 teach that anti-ceramide antibodies can inhibit the CRPs that result from ASMase -mediated ceramide generation, and in doing so prevent apoptosis of CBC stem cells, allowing them to regenerate radiation stress-induced lesions and GI tissue regeneration. Ojeh et al. teaches the role of stem cells in skin regeneration, wound healing and their clinical application. Ojeh teaches that skin compartments, epidermis, and hair follicles house st e m cells that are indispensable for skin homeostasis and regeneration; and that these stem cells contribute to wound repair, resulting in restoration of tissue integrity and function of damaged tissue. Unsuccessful wound healing processes often lead to non-healing wounds; such chronic wounds are caused by depletion of stem cells and a variety of other cellular and molecular mechanisms, many of which are poorly understood (abstract). Ojeh teaches that a number of factors can cause a delay in wound healing including venous or arterial insufficiency, and diabetes (pg. 25477, para. 2). Ojeh teaches that in response to injury, stem cells from the hair follicle and IFE contribute towards re-epithelialization of wounds (pg. 25479, section 2.2). Ojeh teaches that fate-mapping experiments demonstrated that K15-positive hair follicle bulge stem cells transiently contribute to wound re-epithelialization in full-thickness wounds in mice so o n after injury but were lost from the epidermis several weeks later, suggesting that stem cells from the hair follicle are not mandatory for the ling-term upkeep of the IFE but contribute during wound healing. Ojeh highlights efforts to evaluate the feasibility and potential healing capacity of autologous scalp follicular grafts transplanted into the wound bed of chronic leg ulcers as a therapeutic strategy for chronic wound healing, whereby such efforts enhanced wound healing compared to controls (section 2.2, pg. 25480, para. 1). Thus, Ojeh teaches that underlying condition such as diabetes, as well as other factors that deplete stem cells, promote unsuccessful wound healing process, resulting in chronic wounds , and that efforts to increase stem cells at the wound can promote wound healing . It would have been obvious to one of skill in the art to modify the method of administering anti-ceramide antibodies for the treatment of GI lesions , to instead administer anti-ceramide antibodies for the treatment of diabetic or chronic wounds. One would have been motivated to do so given the knowledge that protecting stem cells from apoptosis would enhance wound healing, as taught by Ojeh et al. There would have been a reasonable expectation for success given that ASMase mediates formation of ceramide rich platforms (CRP) which induce apoptosis of the CBC stem cells in GI endothelium, and that anti-ceramide antibodies attenuate the ceramide-mediated apoptosis of CBS stem cells, as taught by Rotolo et al and US ‘971 . Thus the invention was prima facie obvious to one of skill in the art at the time the invention was made. Regarding claims 4-5 , t he modified methods of Rotolo and Ojeh , as evidenced by US ‘971 , comprising administering an anti-ceramide antibody to a wound to inhibit apoptosis of stem cells to enhance wound healing of chronic wounds or chronic wounds in diabetic patients make obvious instant claims 4-5 . However, the combination of Rotolo and Ojeh do not teach whereby the treatment is administered at various stages of the wound healing process (re. claims 13-15), or whereby the treatment includes measures of wound healing (re. claims 18-19 and 21). Gold teaches the art of treating diabetic wounds (title). Gold teaches that wound healing occurs in four phases: coagulation, inflammation, proliferation and remodeling (pg. 1, lines 14-15). Gold teaches chronic wound healing does not proceed normally through the four healing stages, rather defects in the healing process result in inflammatory excess, thereby continuing the inflammation stage that prevents the proper healing of the wound (pg. 2, lines 8-17). Gold teaches that chronic wounds are a common and serious complication of diabetes (pg. 2, lines 18-19). Gold teaches diabetic wounds exhibit impairments in the remodeling of the dermis and are hypocellular, hypovascular , and show impaired ability to form granulation tissue; and that many of these problems are related to the effects that diabetes has on cellular functioning, including impaired fibroblasts (pg. 3, lines 14-21). Thus, Gold teaches that diabetic wounds encompass chronic wounds, and vice versa; and that such deficiencies in wound healing are due to impairments in the inflammatory stage processes of wound healing, including a deficiency in cell migration and proliferation which are critical to neovascularization and angiogenesis. Gold teaches a method of treating chronic diabetic wounds by administering calreticulin (pg. 98, claims 1-2). Gold teaches calreticulin induces the migration of bone-derived mesenchymal stem cells, termed fibrocytes, as well as keratinocytes, fibroblasts, monocytes and macrophages (pg. 92, Example 22, lines 10-20). Gold teaches the effects of calreticulin administration on wound healing can be compared to control, whereby calrecticulin enhances wound healing, decreases the overall surface area of the wound and decreases the time it takes to achieve 50% decrease in overall wound healing (pg. 12, lines 7-12; Figures 12-14). It would have been obvious to apply the administration protocols and methods of measuring wound healing of chronic diabetic wounds of Gold et al. to the methods of Rotolo and Ojeh . One would have been motivated to do so given that comparing the surface area of the treated wound to a control wound provides a measure of the effectiveness of the treatment, as taught by Gold et al. There would have been a reasonable expectation for success as Gold also teaches treatment of chronic diabetic wounds with an alternative agent that enhances wound healing in the same manner (i.e. reducing the surface area of the wound) as the combination of Rotolo and Ojeh . Therefore its obvious for the skilled artisan to implement the same administration protocols and measures of wound healing to methods of administering a substitute agent for the same purposes. Regarding claims 13-15 , the methods of Rotolo and Ojeh , comprising administering an anti-ceramide antibody to enhance stem cell survival and chronic wound healing are described above. Gold teaches that wound healing occurs in four stages, coagulation, inflammation, proliferation and remodeling. Gold teaches that chronic diabetic wounds are characterized by an excessive inflammation stage and that recruitment of fibroblasts and stem cells promote the wound healing moving beyond the inflammation stage. Thus, it is obvious to the skilled artisan that the anti-ceramide antibody treatment of Rotolo and Ojeh can be applied during the inflammatory stage, the proliferative stage or the remodeling stage. Thus, the combination of Rotolo, Ojeh and Gold make obvious instant claims 13-15 . Regarding claims 18-19 and 21 ; Gold teaches a method for enhancing wound healing whereby the healing is compared to a control wound , is measured by a decrease in surface area of the wound, and is measured by the time it takes to achieve 50% decrease in surface area of the wound (Figures 12-14). Thus, Gold makes obvious providing such comparative measures of effectiveness in a method of treating a chronic diabetic wound. As the methods of Rotolo and Ojeh comprise administering an anti-ceramide antibody for the treatment of chronic diabetic wounds, the effectiveness of the anti-ceramide antibody at closing the wound are properties that are inherent to the anti-ceramide antibody of Rotolo et al. Thus, the combination of Rotolo, Ojeh and Gold make obvious instant claims 18-19 and 21 . Claim Rejections - 35 USC § 103 Claim s FILLIN "Pluralize claim, if necessary, and then insert the claim number(s) which is/are under rejection." \d "[ 1 ]" 1-2, 7-12, 16-17, 22-24, 33-35, 45, 51 and 57-58 are rejected under 35 U.S.C. 103 as being obvious over FILLIN "Insert the prior art reference." \d "[ 2 ]" Rotolo et al., (US Patent 10,450,385; issued 10/22/2019) and Kolesnick et al., (WO 2021/188770, with priority to 3/18/2020) . The applied reference (specifically Kolesnick et al. ) has a common FILLIN "Insert—assignee--, --applicant--, or—joint inventor--." \d "[ 3 ]" Assignee and Inventor with the instant application. Based upon the earlier effectively filed date of the reference, it constitutes prior art under 35 U.S.C. 102(a)(2). This rejection under 35 U.S.C. 103 might be overcome by: (1) a showing under 37 CFR 1.130(a) that the subject matter disclosed in the reference was obtained directly or indirectly from the inventor or a joint inventor of this application and is thus not prior art in accordance with 35 U.S.C.102(b)(2)(A); (2) a showing under 37 CFR 1.130(b) of a prior public disclosure under 35 U.S.C. 102(b)(2)(B); or (3) a statement pursuant to 35 U.S.C. 102(b)(2)(C) establishing that, not later than the effective filing date of the claimed invention, the subject matter disclosed and the claimed invention were either owned by the same person or subject to an obligation of assignment to the same person or subject to a joint research agreement. See generally MPEP § 717.02. The reasons why Rotolo et al. anticipates claims 1-2, 7-12, 16-17 and 22-24 are described above. However, Rotolo et al. does not teach whereby the anti-ceramide antibodies comprise the CDRs, or VH and VL sequences of instant claims 33-35, 45, 51 or 57-58. Kolesnick et al. teaches anti-ceramide antibodies , and method for preventing cell death in a subject in need thereof (abstract). Kolesnick teaches the anti-ceramide antibodies may be used to treat cell death in patients with graft versus host disease, radiation disease, GI syndrome and autoimmune disease (pg. 44, para. 0166). Kolesnick teaches that radiation leads to dysfunction in the gastrointestinal microvasculature and intestinal stem cell compartments, including lesions in the CBC cells (pg. 44, para. 0167); and that ceramide mediated raft clustering is involved in clonogenic cell death (pg. 44, para. 0168). Kolesnick teaches the present disclosure is directed to a method for the mitigation of cell death comprising administering an effective amount of anti-ceramide antibody (pg. 45, para. 0169). Regarding the anti-ceramide antibodies, Kolesnick teaches the antibodies may comprise an HCDR1 of SEQ ID NO: 1, an HCDR2 of SEQ ID NOs: 3-6, and an HCDR3 of SEQ ID NO: 7. Kolesnick teaches the LCDRs 1-3 of SEQ ID NOs: 8-10 (pg. 21, Table 1). The HCDRs of Kolesnick SEQ ID NOs: 1-7 are 100% identical in amino acid sequence identity to instant SEQ ID NOs: 1, 44-47 and 3, respectively. The LCDRs of Kolesnick SEQ ID NOs: 8-10 are 100% identical to instant SEQ ID NOs: 4-6, respectively. Thus, Kolesnick teaches anti-ceramide antibodies comprising the identical CDR amino acid sequences to the instantly claimed antibodies. Further, Kolesnick teaches the VH of the antibody may be SEQ ID NO: 18 or 20 and the VL may be SEQ ID NO: 22 (pg. 25, Table 2). The VHs of Kolesnick SEQ ID NOs: 18 and 20 are 100% identical to the VHs of instant SEQ ID NOs: 49 and 51, respectively; and the VL of Kolesnick SEQ ID NO: 22 is 100% identical to the VL of instant SEQ ID NO: 53. Thus, Kolesnick teaches anti-ceramide antibodies comprising the identical VH and VL of the instant claimed antibodies. It would have been obvious to one of skill in the art to substitute the anti-ceramide antibodies of Kolesnick et al. in the methods of treating GI lesions comprising administering anti-ceramide antibodies of Rotolo et al. One would have been motivated to do so in order to treat the GI lesions induced by CRP-mediated apoptosis of GI CBC cells, as taught by Rotolo et al. There would have been a reasonable expectation for success given that alternative variant anti-ceramide antibodies also treat the CRP-mediated GI lesions, as taught by Kolesnick et al. Thus, it is prima facie obvious to substitute one known element for another to obtain predictable results (see MPEP section 2143(I)(B)). In this case the known anti-ceramide antibody variants are being substituted in the same methods to produce the same results. Regarding claims 33-35 ; Kolesnick teaches anti-ceramide antibodies comprising the HCDRs that are identical to instant SEQ ID NOs: 1, 44-47 and 3; as well as LCDRs that are identical to instant SEQ ID NOs: 4-6 (see Table 1, para. 0101). Specifically Kolesnick teaches HCDR2 may be SEQ ID NOs: 3 or 4, which are 100% identical to the variant HCDR2 of instant SEQ ID NOs: 44 and 45, respectively. Thus, the combination of Rotolo and Kolesnick make obvious instant claims 33-35 . Regarding claims 45 and 51 , Kolesnick teaches the VH may be SEQ ID NOs: 18 or 20 and the VL may be SEQ ID NO: 22 (see Table 2, para. 0118), which are 100% identical to the VH of instant SEQ ID NOs: 49 and 51, respectively, and the VL of instant SEQ ID NO: 53. Thus, the combination of Rotolo and Kolesnick make obvious instant claims 45 and 51 . Regarding claims 57-58 ; Kolesnick teaches the 6B5 antibodies may be humanized (pg. 51, Example 1, para. 0188; pg. 90, claim 77) and may be scFv fragments (pg. 90, claim 80). Thus, the combination of Rotolo and Kolesnick make obvious instant claims 57-58 . 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 . Claims FILLIN "Pluralize \“Claim\” if necessary, insert \“is\” or \“are\” as appropriate, and insert the claim number(s) which are under rejection." 1-2, 7-12, 16-17, 22-24, 33-35, 45, 51 and 57-58 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims FILLIN "Pluralize \“Claim\” if necessary, insert \“is\” or \“are\” as appropriate, and insert the claim number(s) of the copending application.." 1-2, 10, 43-44, 77, 80-81, 84, 93-94, 97-98 and 100-102 of copending Application No. FILLIN "Insert the number of the reference copending application." 17/912,286 in view of FILLIN "Insert the secondary reference." Rotolo et al., (US Patent 10,450,385; issued 10/22/2019) . Application ‘286 claims anti-ceramide antibodies comprising the HCDRs 1-3 of SEQ ID NOs: 1, 3 and 7 and LCDRs 1-3 of SEQ ID NOs: 8-10; or wherein the HCDR2 is SEQ ID NO: 4 (claims 1-2 and 112 ); or whereby the antibody comprises the VH and VL of SEQ ID NOs: 18 and 22, respectively, or that of SEQ ID NOs: 20 and 22 (claim s 10(iv)(x) and 43-44 ). The HCDRs of SEQ ID NOs: 1, 3-4, and 7 are 100% identical to instant SEQ ID NOs: 1, 44-45, and 3, respectively; and the LCDRs of SEQ ID NOs: 8-10 are 100% identical to instant SEQ ID NOs: 4-6, respectively. App. ‘286 VH of SEQ ID NOs: 18 and 20 are identical to the instant VH of SEQ ID NOs: 49 and 51, respectively; and the VL of SEQ ID NO: 22 is identical to instant VL of SEQ ID NO: 53. Application ‘286 also claims wherein the anti-ceramide antibody is humanized (claim 77), a scFv fragment (claims 80-81), wherein the VL is carboxy-terminal to the VH of the scFv (claim 84) . App ‘286 also claims polynucleotides encoding the scFv , vectors and host cells comprising the polynucleotides, and methods of making the antibody (claims 97-100). App ‘286 claims methods of inhibiting apoptosis (claim 101), wherein the apoptosis is associated with GVHD, radiation or GI syndrome (claims 102-103); wherein the antibody is administered topically or IV (claim 106); wherein the subject has been exposed to penetrating radiation (claim 107), wherein the antibody is administered within 24 hours after exposure to penetrating radiation (claim 108), whereby the subject has GVHD resulting from a transplant (claim 110) and wherein the transplant is a bone marrow transplant (claim 111). Rotolo et al. teaches administering anti-ceramide antibodies to treat, prevent or enhance healing of wounds, specifically lesions of the GI CBC stem cells, as described above. It would have been obvious to one of skill in the art to substitute the anti-ceramide antibodies of app ‘286 in the methods of treating GI lesions comprising administering anti-ceramide antibodies of Rotolo et al. One would have been motivated to do so in order to treat the GI lesions induced by CRP-mediated apoptosis of GI CBC cells, as taught by Rotolo et al. There would have been a reasonable expectation for success given that alternative variant anti-ceramide antibodies also treat GI lesions, as claimed by app ‘286. Thus, it is prima facie obvious to substitute one known element for another to obtain predictable results (see MPEP section 2143(I)(B)). In this case the known anti-ceramide antibody variants are being substituted in the same methods to produce the same results. The methods of Rotolo makes obvious methods of administering anti-ceramide antibodies to treat a treat a wound or enhance wound healing of claims 1-2, 7-12, 16-17, 22-24 , as described above; app ‘286 makes obvious the specific anti-ceramide antibodies of claims 33-35, 45, 51 and 57-58 . Thus the combination of Rotolo and app ‘286, whereby the specific anti-ceramide antibodies of ‘286 are used in the methods of Rotolo make obvious instant claims 1-2, 7-12, 16-17, 22-24 , 33-35, 45, 51 and 57-58 for the same reasons as described above . This is a provisional nonstatutory double patenting rejection. Note that application 17/912,286 was allowed on 2/23/2026, but has not issued. Claim s FILLIN "Pluralize \“Claim\” if necessary, insert \“is\” or \“are\” as appropriate, and insert the claim number(s) which are under rejection." 1-2, 4-5, 7-19, 21-24, 33-35, 45, 51 and 57-58 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claim s FILLIN "Pluralize \“Claim\” if necessary, insert \“is\” or \“are\” as appropriate, and insert the claim number(s) of the copending application.." 1-2, 10, 43-44, 77, 80-81, 84, 93-94, 97-98 and 100-102 of copending Application No. FILLIN "Insert the number of the reference copending application." 17/912,286 in view of FILLIN "Insert the secondary reference." Rotolo et al., (US Patent 10,450,385; issued 10/22/2019) , Ojeh et al., (Int. J. Mol. Sci., 2015, 16) , and Gold et al., (from IDS of 9/15/2023; WO 2010027802; published 3/11/2010) , as evidenced by US '971 (from IDS of 9/15/2023; US20150216971; published 8/6/2015) The reasons why the combination of application ‘286 and Rotolo make obvious the methods of claims 1 -2, 7-12, 16-17, 22-24 , 33-35, 45, 51 and 57-58 are described above. However, Rotolo does not teach methods for enhancing wound healing wherein the wound is a chronic or diabetic wound, wherein the antibody is administered during different stages of wound healing, or wherein the method comprises measuring the effectiveness of wound healing versus a control wound, of instant claims 4-5, 13-15, 18-19 and 21. US ‘971 evidences that it is an inherent property of the methods of Rotolo to that anti-ceramide antibodies protect stem cells from ASMase /CRP mediated apoptosis. Ojeh teaches methods of increasing stem cell viability to enhance wound healing in chronic diabetic skin wounds. Gold et al. teaches methods of enhancing wound healing in chronic and/or diabetic wounds comprising administering an agent that increases the viability of stem cells during the wound healing process, whereby the methods make obvious adding additional steps of measuring and comparing the enhanced healing of the wound surface area versus a control wound. The combination of Rotolo, US ‘971, Ojeh and Gold make obvious instant claims 4-5, 13-15, 18-19 and 21, as described above, and which is incorporated here in full. App ‘286 teaches the identical anti-ceramide antibodies of instant claims 33-35, 45, 51 and 57-58. Therefore the combination of app ‘286, Rotolo, US ‘971, Ojeh and Gold make obvious instant claims 1 -2, 4-5, 7 -19, 2 1 -24 , 33-35, 45, 51 and 57-58 . This is a provisional nonstatutory double patenting rejection. As described above, Rotolo et al. and US ‘971 teach methods comprising administering an anti-ceramide antibody for inhibiting ASMase -ceramide/CRP-mediated apoptosis of tissue regenerating stem cells, regardless of the various stressors that induce the lesions (e.g., radiation stress, GVHD stress, inflammation stress or autoimmune stress). Ojeh teaches stem cells are critical for wound healing, including methods of administering stem cell grafts to enhance wound healing of chronic or diabetic epithelial ulcers. Gold teaches methods of enhancing wound healing of chronic, diabetic wounds on skin, whereby the method comprises administering an agent that increases the viability of stem cells during the wound healing process, and whereby the methods of Gold et al. make obvious adding additional steps of measuring and comparing the enhanced healing of the wound surface area versus a control wound. Together, Rotolo, US ‘971, Ojeh and Gold make obvious a method of administering anti-ceramide antibodies to treat, or enhance healing, of a wound. Therefore, any co-pending application or issued patent that claims anti-ceramide antibodies or methods of administering anti-ceramide antibodies makes obvious instant claims 1-2, 4-5, 7-19 and 21-24 which are broadly drawn to methods of administering anti-ceramide antibodies for the purpose of treating, preventing or enhancing wound healing. Instant claims 33-3 5, 45, 51 and 57-58 limit the anti-ceramide antibodies to the species recited in the claims; and it would not be obvious to a skilled artisan to arrive at the specific species of anti-ceramide antibodies recited in claims 33-3 5, 45, 51 and 57-58 or their use in methods of treating , preventing or enhancing wound healing . Claims 1-2, 4-5, 7-19 and 21-24 are rejected (in the case of issued patents), or provisionally rejected (in the case of pending applications) over the listed claims of the following U.S. Patents and pending applications, in view of Rotolo et al., (US Patent 10,450,385; issued 10/22/2019) , Ojeh et al., (Int. J. Mol. Sci., 2015, 16) , and Gold et al., (from IDS of 9/15/2023; WO 2010027802; published 3/11/2010) , as evidenced by US '971 (from IDS of 9/15/2023; US20150216971; published 8/6/2015) . Below is a Table listing patents and/ or co-pending applications , which name a common inventor, and which claim generic anti-ceramide and/or methods of administering anti-ceramide antibodies , whereby the claims would make obvious, over Rotolo, US ‘971, Ojeh and Gold, instant claim s 1-2, 4-5, 7-19 and 21-24 , for the same reasons why Rotolo, US ‘971, Ojeh and Gold make obvious the instant claims as described above. U.S. Patent or co-pending U.S. application Claims Comment 8562993 1-6 Methods of treatment with anti-ceramide antibodies 9592238 1-8 2A2 anti-ceramide antibodies and pharmaceutical compositions 11207329 1-6 Methods of inhibiting cell death by CRP formation by administering 2A2 anti-ceramide antibodies 12121525 1-4 Anti-ceramide antibodies, compositions, methods of treating GI syndrome or GVHD 18/892240 1-9 Methods of treating GVHD, GI syndrome with anti-ceramide antibodies 10722577 1-9 Methods of treating GI damage with anti-ceramide antibodies and other agents. 10450385 1-4 Anti-ceramide antibodies 11447572 1-13 Methods of inhibiting apoptosis with anti-ceramide antibodies; GI syndrome, GVHD 18/790647 1-5 Anti-ceramide antibodies, methods of making, methods of inhibiting apoptosis 10975169 1-19 Methods of treating or preventing diabetic retinopathy with anti-ceramide antibodies 17/763989 153 Methods of treating or preventing diabetic retinopathy with anti-ceramide antibodies Conclusion No claims are allowed. 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