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
This application, 16/491,253, filed 09/05/2019 is a 371 (national stage entry) of PCT/JP2018/015363, International Filing Date: 04/12/2018 claims foreign priority to JP 2017-082167, filed 04/18/2017.
Status of Claims
Acknowledgement is made of the receipt and entry of the amendment to the claims filed on November 21, 2025. Claims 1-7 are currently pending and are examined in accordance to the elected species.
Action Summary
Claims 1-4 and 7 rejected under 35 U.S.C. 103(a) as being unpatentable over Hatakeyama, Oncology Reports 29, 911 – 916 (2013), in view of Hagiya, Photodiagnosis and Photodynamic Therapy, Volume 9, Issue 3, September 2012, Pages 204-214, Tamura, Drug Metab. Pharmacokinet. 22 (6): 428–440 (2007), Quan, Mol Pharmacol 72:1425–1439, 2007, and Studzian et al (Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, Volume 1853, Issue 8, August 2015, Pages 1759-1771), are maintained, but revisited and modified in light of the claim amendment.
Claims 5 and 6 are rejected under 35 U.S.C. 103(a) as being unpatentable over Hatakeyama (Oncology Reports 29, 911 – 916 (2013)) in view of Hagiya (Photodiagnosis and Photodynamic Therapy, Volume 9, Issue 3, September 2012, Pages 204-214), Tamura (Drug Metab. Pharmacokinet. 22 (6): 428–440 (2007)), Quan (Mol Pharmacol 72:1425–1439, 2007), and Studzian (Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, Volume 1853, Issue 8, August 2015, Pages 1759-1771), as applied to claims 1-4 and 7 in further view of Hatakeyam (EP 2 727 603 A1), are maintained.
Affidavit
The Declaration by Masahiro Ishizuka under 37 CFR 1.132 filed 11/21/2025 is insufficient to overcome the rejection of claims 1-7. The Declarant argues that the administration of 1mM ALA and 8 µM MiTMAB in a Caco-2 BCRP-Ko cell (human colon carcinoma cells with ABCG2 gene knocked out) exhibits the unexpected ability to increase accumulation of PpIX independent of ABCG2. In another word, the data indicates that MiTMAB (a dynamin inhibitor) inhibited PpIX efflux mediated by a mechanism other than ABCG2.
In response, the Declarant’s argument is not persuasive. Specifically, increase accumulation of PpIX independent of ABCG2, 1mM ALA and 8 µM MiTMAB, and colon carcinoma are not in the claim. Moreover, the claim broadly recites cancer, broadly recites 5-aminolevulinic acid (ALA), a derivative of 5-aminolevulinic acid (ALA), and a salt of 5-aminolevulinic acid (ALA), and dynamin inhibitor. Additionally, unexpected result does not show what the other mechanism is. And the other mechanism is not in the claim. However, the asserted unexpected ability to increase accumulation of PpIX independent of ABCG2 relates to a specific cancer (colon carcinoma and a specific dynamin inhibitor (MiTMAB), and 1mM ALA and 8 µM MiTMAB. Therefore, the asserted unexpecdted result is not commensurate in scope with the claim. Whether the unexpected results are the result of unexpectedly improved results or a property not taught by the prior art, the "objective evidence of nonobviousness must be commensurate in scope with the claims which the evidence is offered to support." In other words, the showing of unexpected results must be reviewed to see if the results occur over the entire claimed range. In re Clemens, 622 F.2d 1029, 1036, 206 USPQ 289, 296 (CCPA 1980) (See MPEP 716.02(d).)
New Rejection necessitated by claim amendment
Claim Rejections - 35 USC § 112
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 1-7 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention. The claim broadly recites the dynamin inhibitor is administered such that it suppresses ABCG2- independent export of PpIX in the cells. In other words, any administration route of any dynamin inhibitor. Said limitation is not supported by the specification as filed. Applicant pointed out support for said limitation at paragraphs [0073]-[0078]. However, the Examiner cannot find anywhere in the specification that teaches or decribes the dynamin inhibitor is administered such that it suppresses ABCG2- independent export of PpIX in the cells. he specification (the published application) at paragraph [0085] teaches from the measurement result of extracellular PpIX amount, it was shown that OcTMAB had an effect similar to ETC for suppressing PpIX extracellular export. Moreover, it was found that the use of OcTMAB in combination with ETC decreases the extracellular PpIX amount compared to when OcTMAB or FTC was administered alone. From these results, it was suggested that OcTMAB was possibly acting on an export mechanism different from ABCG2. First, OcTMAB is the only dynamin inhibitor mentioned in this paragraph. Second, just because OcTMAB can possibly act on export mechanism different from ABCB2 does not mean the dynamin inhibitor is administered such that it suppresses ABCG2- independent export of PpIX in the cells.
Maintained/Revisited/Modified Rejection
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 for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or non-obviousness.
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 and 7 are rejected under 35 U.S.C. 103(a) as being unpatentable over Hatakeyama, Oncology Reports 29, 911 – 916 (2013), in view of Hagiya, Photodiagnosis and Photodynamic Therapy, Volume 9, Issue 3, September 2012, Pages 204-214, Tamura, Drug Metab. Pharmacokinet. 22 (6): 428–440 (2007), Quan, Mol Pharmacol 72:1425–1439, 2007, and Studzian et al (Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, Volume 1853, Issue 8, August 2015, Pages 1759-1771). Hatakeyam and Tamura are cited in the IDS filed on 07/01/2022. (Hagiya and Quan are cited in the IDS filed on 10/31/2023. Studzian is cited as reference U).
Hatakeyama teaches 5-aminolevulinic acid (ALA, the elected compound of Formula (I); amended instant Claim 9)-mediated photodynamic therapy (PDT) (ALA-PDT) is a highly selective treatment for malignant cells and that ALA-PDT has the potential to develop into a novel therapeutic strategy for various types of cancer. Specifically, Hatakeyama teaches a method of photodynamic therapy and photodynamic diagnosis comprising administering to a human subject 5-ALA, irradiating a ray of light to a cancer site of the subject to excite PpIX and detecting fluorescence from the excited PpIX to detect and diagnose the present of cancer. (See Abstract; page 913, left column; and first paragraph of right column; Fig. 4B and 5A.) Moreover, Hatakeyama teaches the anti-tumor effect of ALA-PDT using various light emitting diodes (LEDs) in human colon cancer cells (HT-29 cell line) in vitro and in vivo (CRC-bearing mouse model, 250 mg/kg, ALA; taken to be an effective amount) (Abstract, Figure 5B). Furthermore, Hatakeyama teaches ALA-PDT and ALA-PDD using fluorescence laparoscopy may provide to be effective diagnostic and treatment modalities for colorectal cancer. (See page 915, first paragraph of right column.)
Hatakeyama does not teach dynamin inhibitor OctMAB
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Hagiya teaches the ALA-based photocytotoxicity was found to be well correlated with intracellular PpIX levels, which suggests that certain enzymes and/or transporters involved in ALA-induced PpIX production are critical determinants. We found that high expression of the peptide transporter PEPT1 (ALA influx transporter) and low expression of the ATP-binding cassette transporter ABCG2 (porphyrin efflux transporter) determined ALA-induced PpIX production and cellular photosensitivity in vitro. (See Abstract.) Moreover, Hagiya teaches ALA-based photocytotoxicity-resistant NKPS cells contained the lowest level of PpIX. TMK-1, KKLS, and MKN28 cells had moderate levels of intracellular PpIX located between the PpIX levels observed for MKN45 and NKPS cells. (See Figures 1A and 1B.) Hagiya teaches the ALA-based photocytotoxicity—resistant TMK-1 cell line had the highest level of ABCG2 protein with a low level of PEPT1 protein. These results suggest that both ALA influx mediated by PEPT1 and PpIX efflux by ABCG2 are critical factors in terms of cellular sensitivity to ALA-based photocytotoxicity. (See page 207, fight column, first paragraph.) Additionally, Hagiya teaches the contribution of ABCG2 to the cellular resistance to ALA-based photocytotoxicity was determined and it was assumed that high levels of ABCG2 in these cells might contribute to ALA-PDT resistance owing to its function of facilitating PpIX efflux from those cells. By suppression of ABCG2 expression, intracellular PpIX level was increased by 2.5-fold in NKPS cells after treatment with ABCG2-specific siRNA and ALA and suppression of ABCG2 expression in NKPS cells resulted in a 3-fold increase in the sensitivity to ALA-based photocytotoxicity in terms of the IC50 value (see page 208, left column, first paragraph bridging page 208, right column, first paragraph.) Furthermore, Hagiya teaches the efficacy of ALA-PDT is considered to depend on the intracellular concentration of PpIX that can produce cytotoxic singlet oxygen and other ROS via photoactivation reactions. (See page 206, right column, last paragraph.)
In sum, Hagiya reported that the balance between the protein expression level of PEPT1, which is a peptide transporter that is involved in the uptake of ALA into cells, and the expression level of ATP binding cassette subfamily G member 2 (ABCG2), which is a drug-resistant transporter involved in the elimination of PpIX, was correlated with the levels of PpIX accumulation in several gastric cancer cell lines. Hagiya also showed that inhibition of ABCG2 suppresses the extracellular excretion of PpIX and increase its intracellular accumulation. Hagiya strongly suggest that ABCG2 plays an important role in PpIX excretion.
Tamura ABCG2 genetic variants, i.e., V12M, Q141K, S441N, and F489L, as well as the wild type (WT) in Flp-In-293 cells were expressed to examine the hypothesis. Cells expressing S441N and F489L variants exhibited high levels of both cellularly accumulated pheophorbide a and photosensitivity, when those cells were incubated with pheophorbide a and irradiated with visible light. To further elucidate the significance of ABCG2 in cellular porphyrin homeostasis, we observed cellular accumulation and compartmentation of porphyrin and pheophorbide a by means of a new fluorescence microscopy technology, and found that accumulation of porphyrin and pheophorbide a in the cytoplasm compartment was maintained at low levels in Flp-In-293 cells expressing ABCG2 WT, V12M, or Q141K. When ABCG2 was inhibited by imatinib or novobiocin, however, those cells became sensitive to light. Based on these results, it is strongly suggested that certain genetic polymorphisms and/or inhibition of ABCG2 by drugs can enhance the potential risk of photosensitivity. (See Abstract.)
In sum, Tamura teaches accumulation of porphyrin and pheophorbide in the cytoplasm compartment was maintained at low levels in cells expressing ABCG2 WT and when ABCG2 was inhibited, those cells became sensitive to light and can enhance photosensitivity.
Quan teaches dynamin is a GTPase enzyme involved in membrane constriction and fission during endocytosis. Phospholipid binding via its pleckstrin homology domain maximally stimulates dynamin activity. We developed a series of surface-active small-molecule inhibitors, such as myristyl trimethyl ammonium bromide (MiTMAB) and octadecyl trimethyl ammonium bromide (OcTMAB), and we now show MiTMAB targets the dynamin-phospholipid interaction. MiTMAB inhibited dynamin GTPase activity. These small molecule inhibitors rapidly and reversibly block multiple forms of endocytosis with no acute cellular damage. (See Abstract.) Moreover, Quan teaches Endocytosis in eukaryotic cells services the uptake of extracellular material and the recycling of membrane components. Multiple forms of endocytosis exist that regulate a variety of different cellular processes, such as regulation of cell surface receptor expression and signaling, cell fate determination, cell migration, antigen presentation, and synaptic transmission. (See page 1425, left and right column under the Abstract Section.) Quan reported that because exocytosis and endocytosis are coupled in two models for neuronal exocytosis and endocytosis, it is first necessary to determine the effects on exocytosis of any potential inhibitor, before determining its effect on endocytosis. A block in the former will nonspecifically inhibit the latter, masking any specific endocytic effect. The results reveal that MiTMAB blocks exocytosis in chromaffin cells by reducing Ca2+ entry via an intracellular site of action, presumably Ca2+ channels. (See page 1434, right and left column.) Quan teaches another well-characterized endocytic route is synaptic vesicle endocytosis (SVE), in which the role of dynamin I has been well established. In these systems, exocytosis and endocytosis are highly regulated and coupled; thus, blocking one route interferes with the other. (See page 1437, left column, second paragraph.) Lastly, Quan teaches dynamin is a 96-kDa GTPase enzyme involved in membrane constriction and fission during RME and SVE. At a late stage of the process, dynamin assembles into rings to form a collar or helix around the neck of the invaginating vesicles. Upon GTP hydrolysis the vesicle is pinched from the plasma membrane by a conformational twist in the dynamin helix. Dynamin is also needed for many, but not all, forms of clathrin-independent endocytosis, such as phagocytosis, caveolae internalization, and endocytosis of cytokine receptors in non-neuronal cells, and for fast/rapid endocytosis in neurons and neuroendocrine cells. (See page 1426, left column, second paragraph.)
In sum, Quan teaches myristyl trimethyl ammonium bromide (MiTMAB) is a dynamin inhibitor that disrupts receptor-mediated endocytosis (RME, which is the same as clathrin-mediated endocytosis that involves dynamin) and synaptic vesicle endocytosis by targeting the dynamin-phospholipid interaction. It inhibits the GTPase activity of dynamin, preventing the formation of clathrin-coated vesicles and subsequent endocytosis. MiTMAB can also inhibit exocytosis. Inhibition of exocytosis in neuronal cells can be expected to inhibit exocytosis in other cells because the fundamental molecular machinery and processes involved in exocytosis are largely conserved across different eukaryotic cell types.
Studzian teaches high expression of ABCG2 in cancer cells can lead to increased binding of the 5D3 antibody, which then triggers endocytosis of the ABCG2 protein. This process involves the antibody binding to an external epitope on ABCG2, causing a conformational change that facilitates internalization through both clathrin-dependent and caveolin-independent pathways. ABCG2, a metabolite and xenobiotic transporter located at the plasma membrane (predominantly in barrier tissues and progenitor cells), undergoes a direct progressive endocytosis process from plasma membrane to intracellular compartments upon binding of 5D3 monoclonal antibody. ABCG2 is endocytosed by a mixed mechanism: partially via a rapid, clathrin-dependent pathway and partially in a cholesterol-dependent, caveolin-independent manner. (See Abstract.) Moreover, Studzian teaches Dynamin is a GTPase that plays a crucial role in endocytosis, the process by which cells internalize substances from their surroundings. ABCG2, a transporter protein, can be internalized through endocytosis in some cases. One study found that treatment with dynasore, a dynamin inhibitor, completely blocked the internalization (endocytosis) of ABCG2, resulting in its exclusive localization on the cell membrane. This suggests a direct link between dynamin's activity and ABCG2's ability to be endocytosed. While the study mentioned above suggests a direct link, it also notes that dynamin is involved in both clathrin-dependent and clathrin-independent endocytosis, and other inhibitors of varying specificity also had an effect on ABCG2 endocytosis. This implies that ABCG2 internalization might involve dynamin as a key, but not the only, player. In conclusion, evidence suggests that blocking dynamin with inhibitors like dynasore can indeed block the endocytosis of ABCG2. This highlights a potential interplay between these two proteins in cellular trafficking and function. (See Highlights Section, third and fourth paragraphs of the left column of pate 1767; third paragraph of the left column of page 1767.) Furthermore, Studzian teaches the putative degradation event by lysosomes could be quasi-totally inhibited (the decrease in ABCG2 amount was no longer statistically significant) by dynasore, a general inhibitor of multiple endocytotic pathways (via dynamin inhibition), suggesting a full dependence of observed decrease in ABCG2 amount on opsonization-mediated endocytosis. (See right column of first paragraph of page 1765.) In essence, dynamin inhibitors can inhibit ABCG2 activity indirectly by disrupting the normal endocytosis and trafficking process of ABCG2, leading to its degradation and ultimately decreasing its ability to efflux substances out of the cell.
It would have been prima facie obvious to one of ordinary skill in the art, before the effective filing date of the claimed invention, to administer a combination of 5-aminolevulinic acid (5-ALA) by performing PDT on the subject, (Hatakeyama) with the very potent dynamin inhibitor compound OctMAB or MITMAB (Quan) to improve the efficacy or the photosensitivity of the 5-ALA in a subject having a cancer cell type in which PpIX is not sufficiently accumulated for PDT in order to effectivity diagnose and treat colon cancer. One would have been motivated to improve the efficacy and the photosensitivity of 5-ALA by adding the dynamin inhibitor in this case OctMAB or MiTMAB because Hagiya teaches that the balance between the protein expression level of PEPT1, which is a peptide transporter that is involved in the uptake of ALA into cells, and the expression level of ATP binding cassette subfamily G member 2 (ABCG2), which is a drug-resistant transporter involved in the elimination of PpIX, was correlated with the levels of PpIX accumulation in several gastric cancer cell lines and also showed that ABCG2 inhibitors suppress the extracellular excretion of PpIX and increase its intracellular accumulation, because Tamura teaches that depending on the cancer cell type or the degree of malignancy, there are some cells where one member of the ABC transporter family, ABCG2, of which the substrate is porphyrins such as PpIX, is highly expressed, thus causing PpIX to be exported into the cytoplasm, and PpIX is not sufficiently accumulated, and because Quan teaches a series of surface-active small-molecule inhibitors, such as myristyl trimethyl ammonium bromide (MiTMAB) and octadecyltrimethyl ammonium bromide (OcTMAB) can rapidly and reversibly block multiple forms of endocytosis with no acute cellular damage, and also because Studzian teaches blocking dynamin with inhibitors like dynasore can indeed block the endocytosis of ABCG2, where ABCG2 endocytosis is dynamin-dependent and proceeds via early endosome. Therefore, one would reasonably expect that by blocking the dynamin-dependent pathway, potentially using dynamin inhibitors like MiTMAB or OctMAB, could lead to the accumulation of protoporphyrin IX (PpIX) by indirectly inhibiting the ABCG2 transporter or the ABCG2 transporter endocytosis, consequently enhancing photodynamic diagnosis (PDD) by suppressing PpIX efflux in a subject with cancer that overexpresses ABCG2 with success.
Accordingly, the fact that the method taught by Hatakeyama, Hagiya, Tamura, Quan, and Hatakeyam in combination teaches the same dynamin inhibitor as claimed, i.e. MitMAB, suppression of ABCG2-independent export of PpIX in the cells would naturally flow from the teaching of the same dynamin inhibitor claimed. The fact that the inventor has recognized another advantage which would flow naturally from following the suggestion of the prior art cannot be the basis for patentability when the differences would otherwise be obvious. See Ex parte Obiaya, 227 USPQ 58, 60 (Bd. Pat. App. & Inter. 1985).
The combination of Hatakeyama and Joshi are silent with respect to the administration regimen of ALA and OctMAB or MiTMAB; i.e., concurrently, or, administering ALA prior to or after OctMAB or MiTMAB (instant Claims 10 and 11).
However, the sequence of administration of the elected compound of Formula (I) (ALA) and the elected dynamin inhibitor (OctMAB) or MiTMAB as recited in instant claims are amenable to the type of analysis set forth in MPE 2144.04 (IV): Ex parte Rubin, 128 USPQ 440 (Bd. App. 1959) and also in re Burhans, 154 F.2d 690, 69 USPQ 330 (CCPA 1946), where the court found that the selection of any order of performing process steps is prima facie obvious in the absence of new or unexpected results. As such, applying the same logic to the instant method claims, one of ordinary skill in the art would have a reasonable expectation that administering ALA-PDT and OctMAB/MiTMAB, concurrently or in any sequence would result in the same outcome of killing a cancer cell; absent a showing of a surprising or unexpected result. It is noted that the language “prior to or after” does not limit the administration regimen to any specific time period and allows for administering one compound immediately before or immediately after the other compound.
Acknowledgement is made of the receipt and entry of Applicant’s remarks/arguments filed on November 21, 2025.
The vast majority of arguments presented in this response filed on 11/21/2025 have been previously addressed. It is emphasized that the instant rejection has been maintained in the Non-Final Rejection mailed on 08/21 /20201. A response to these arguments can be found in this Office Actions. Newly presented arguments are addressed below.
However, Applicant’s argument using the declaration appears to be the same argument presented in the Affidavit section above, Therefore, the same response applies.
Claims 5 and 6 are rejected under 35 U.S.C. 103(a) as being unpatentable over Hatakeyama (Oncology Reports 29, 911 – 916 (2013)) in view of Hagiya (Photodiagnosis and Photodynamic Therapy, Volume 9, Issue 3, September 2012, Pages 204-214), Tamura (Drug Metab. Pharmacokinet. 22 (6): 428–440 (2007)), Quan (Mol Pharmacol 72:1425–1439, 2007), and Studzian (Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, Volume 1853, Issue 8, August 2015, Pages 1759-1771), as applied to claims 1-4 and 7 in further view of Hatakeyam (EP 2 727 603 A1).
The teachings of Hatakeyama, Hagiya, Tamura, Quan, and Hatakeyam have been discussed in the above rejection.
Hatakeyama, Hagiya, Tamura, Quan, and Hatakeyam collectively do not teach ALA derivatives selected from the group consisting of ALA methyl ester, ALA ethyl ester, ALA propyl ester, ALA butyl ester, Page 3 ALA pentyl ester and ALA hexyl ester.
Hatakeyam teaches a method of photodynamic therapy and photodynamic diagnosis comprising a composition comprising photosensitizing agent such as 5-ALA, ALA methyl ester, ALA ethyl ester, ALA propyl ester, ALA butyl ester, ALA pentyl ester, followed by irradiation with excitation light at a wavelength of 480 to 580 nm. (See Abstract.)
It would have been prima facie obvious to one of ordinary skill in the art at the time the invention was filed to replace the 5-ALA taught by Hatakeyama with the derivatives taught by Hatakeyam to give Applicant’s claimed invention. One would be motived by the fact that the 5-ALA and the derivatives thereof claimed are art-recognized photosensitizing agents. One would reasonably expect the substitution or replacement to be functionally and structurally equivalent.
Applicant’s argument
Applicant argues for at least the same reasons discussed above, Applicant respectfully submits that the combined teachings of Hatakeyama, Hagiya, Tamura, and Quan do not teach or suggest the method of independent claim 1, or claims depending therefrom. Tanaka is cited in the Office Action for teaching ALA derivatives. (Office Action, page 12). However, Tanaka fails to remedy the deficiencies of Hatakeyama, Hagiya, Tamura, and Quan.
Response to Argument
In response, Applicant’s argument is not found persuasive for the same reason established in the above Response to argument section. Therefore, Tanaka clearly remedies the deficiencies of Hatakeyama, Hagiya, Tamura, and Quan.
Conclusion
Claims 1-7 are not allowed.
THIS ACTION IS MADE FINAL. Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
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/JEAN P CORNET/Primary Examiner, Art Unit 1628