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 .
DETAILED ACTION
RESPONSE TO AMENDMENT
Status of Application/Amendments/claims
2. Applicant’s amendment filed July 2, 2026 is acknowledged. Claims 3-4, 8-12, 14-18, 20, 23-28, 30-33, 35-91 are canceled. Claims 1, 13, 19, 21-22, 29 and 34 are amended. Claims 92-96 are newly added. Claims 1-2, 5-7, 13, 19, 21-22, 29, 34 and newly added claims 92-96 are pending in this application. Election was treated as without traverse in the reply filed on September 18, 2025.
3. Claims 1-2, 5-7, 13, 19, 21-22, 29, 34 and 92-96 are under examination with respect to anti-Gal3 antibody TB006, SEQ ID NOs: 31, 72, 113, 171, 222, 249, 298, 375, 449, 496, 540 and 622, and stroke in this office action.
4. Applicant’s arguments filed on July 2, 2026 have been fully considered but they are not deemed to be persuasive for the reasons set forth below.
Drawings
5. The objection to drawings/figures 1-9 and 13-17 is withdrawn in response to Applicant’s arguments on p. 16-17 of the response filed 07/02/2026.
Specification
6. The objection to the specification is withdrawn in response to Applicant’s amendment to the specification.
Claim Rejections/Objections Withdrawn
7. The objection to claims 1, 29, 35-36, 39-41, 43-44, 61, 66-68, 72, 79 and 90-91 is withdrawn in response to Applicant’s amendment to the claims.
The rejection of claims 1-2, 5-7, 10, 13, 19, 21-22, 29, 34 and 85-86 under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph
The rejection of claims 34 and 85-86 under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, lack of scope of enablement is moot because the claims are canceled.
The rejection of claims 34 and 85-86 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 is moot because the claims are canceled.
Claim Rejections/Objections Maintained
In view of the amendment filed on July 2, 2026, the following rejections are maintained.
Improper Markush Grouping
8. Claims 29 and 92-96 are rejected on the basis that it contains an improper Markush grouping of alternatives. See In re Harnisch, 631 F.2d 716, 721-22 (CCPA 1980) and Ex parte Hozumi, 3 USPQ2d 1059, 1060 (Bd. Pat. App. & Int. 1984). The rejection is maintained for the reasons of record and the reasons set forth below.
Briefly, the Markush grouping of different anti-Gal3 antibodies “TB001, TB006, 13A12.2E5, 14H10.2C9, 23H9.2E4, 2D10.2B2, 3B11.2G2, 15G7.2A7, F846C.1B2, F846C.1F5, F846C.1H12, F846C.2H3, 847.28D1, and F847C.21H6” recited in claim 29, the Markush grouping of different anti-Gal3 antibodies comprising different SEQ ID NOs: for VH-CDR1-3 and VL-CDR1-3 recited in claim 92, different SEQ ID NOs: for VH and VL recited in claims 93-96 are improper because the alternatives defined by the Markush grouping do not share both a single structural similarity and a common use for the following reasons:
The recited alternative species do not share a single structural similarity, as each species of anti-Gal3 antibody has a different chemical structure and comprises different amino acid sequences for VH-CDRs1-3 and VL-CDRs1-3; and VH and VL. Each antibody has a different binding activity or affinity to different epitopes. Thus, the antibodies do not share a single structural similarity or biological activity. Accordingly, they do not share a “single structural similarity” and a common use. See MPEP § 706.03(y).
Response to Arguments
On p. 17-18 of the response, Applicant argues that the recited anti-Gal3 antibodies binding to peptide 6, which share a common structural and functional feature.
Applicant's arguments have been fully considered but they are not persuasive. Here each recited alternative species does not share a single structural similarity, as each has different sequences for VH-CDRs1-3 and VL-CDRs1-3; and VH and V. Each antibody has a different sequence and a different biological activity, has a different binding activity or affinity to different epitopes or epitopes within a peptide comprising an amino acid sequence of SEQ ID NO:8, including fragments within SEQ ID NO:8. Thus, the recited antibodies do not share a single structural similarity or biological activity. The only structural similarity present is that they all are antibodies. The fact that the antibodies per se does not support a conclusion that they have a common single structural similarity because each antibody comprising different sequences and binding to peptide 6 alone is not correlated with a common activity of stroke.
While the different antibodies are asserted to have the property of binding to peptide 6, they do not share a single structural similarity essential to this activity because each antibody with different sequences for VH-CDRs1-3 and VL-CDRs1-3; and VH and V and has a different biological activity or a different binding activity or affinity to different epitopes or epitopes within a peptide comprising an amino acid sequence of SEQ ID NO:8, including fragments within SEQ ID NO:8 as evidenced by the data shown in Examples 7-8 (see p. 145-148 and Figures 10-11) and as admitted by Applicant at p. 143, [0462] of the specification filed 07/02/2026, “Clones IMT001(TB001) and F847C.21H6” exhibited mutual competitive binding for Ga3 but did not prevent binding of the rest of the clones….Clones IMT006(TB006)….exhibited mutual competitive binding for Gal3, but did not prevent binding of the rest of the clones….” . There is no evidence of record to establish that it is clear from their very nature that the recited different antibodies with different sequences for VH-CDRs1-3 and VL-CDRs1-3; and VH and VL share a “single structural similarity” and “a common use”. See MPEP § 706.03(y).
Following this analysis, the claims are rejected as containing an improper Markush grouping. Accordingly, the rejection of claims 29 and 92-96 on the basis that it contains an improper Markush grouping of alternatives is maintained.
Claim Rejections - 35 USC § 112
9. The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 1-2, 5-7, 13, 19, 21-22, 29, 34 and 92-96 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 pre-AIA the applicant regards as the invention. The rejection is maintained for the reasons of record and the reasons set forth below.
Response to Arguments
On p. 18-19 of the response, Applicant argues that: i) the rejection has been overcome in view of amendment to the claims and ii) the recited antibody designations correspond to specific antibodies disclosed in the specification including their structure features and sequences.
Applicant's arguments have been fully considered but they are not found persuasive. Contrary to Applicant' s arguments, the examiner asserts that based on MPEP§2171-MPEP§2173, claims 1-2, 5-7, 13, 19, 21-22, 29, 34 and 92-96 are indefinite because:
i. The limitation “…reduces loss of locomotor dysfunction…..in the subject as compared to locomotor dysfunction……or any combination thereof” recited in claim 1 is not clear. It is not clear which and what level and/or which and what subject is used for comparison in order to determine the claimed effects of “reduces loss of locomotor dysfunction…in the subject”. The term “reduce” is not defined by the claim and the specification does not provide a standard for ascertaining the requisite degree, and thus a skilled artisan would not be reasonably apprised of the scope of the invention. Applicant fails to set forth the metes and bounds of what is encompassed within the definition of “…reduces loss of locomotor dysfunction…..in the subject as compared to locomotor dysfunction……or any combination thereof” recited in claim 1. Since the metes and bounds are unknown, a skilled artisan cannot envision what would be considered as “…reduces loss of locomotor dysfunction…..in the subject as compared to locomotor dysfunction……or any combination thereof” recited in claim 1. Thus, the claim is indefinite.
ii. Regarding claim 29, the terms “TB001, TB006, 12G5.D7, 13A12.2E5, 14H10.2C9, 15F10.2D6, 19B5.2E6,…….20H5.A3-VH6VL1, 20H5.A3-VH6VL3” recited in claim 29 without a reference to a precise amino acid sequence identified by a proper SEQ ID NO: or providing a full name for abbreviated names. Without identification of property or combination of properties which are unique to and, therefore, definitive of the instant recitations, the metes and bounds of the claims remain undetermined. Further, the use of laboratory designations only to identify a particular molecule renders the claims indefinite because different laboratories may use the same laboratory designations to define completely distinct molecules. The rejection can be obviated by amending the claims to specifically and uniquely identify “TB001, TB006, 12G5.D7, 13A12.2E5, 14H10.2C9, 15F10.2D6, 19B5.2E6,…….20H5.A3-VH6VL1, 20H5.A3-VH6VL3” recited in claim 29.
iii. The rest of claims are indefinite as depending from an indefinite claim.
Accordingly, the rejection of claims 1-2, 5-7, 13, 19, 21-22, 29, 34 and 92-96 under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite is maintained.
Claim Rejections - 35 USC § 112
10. 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 1-2, 5-7, 13, 19, 21-22, 29, 34 and 92-96 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for reducing loss of locomotor activity, increasing latency to fall and distance traveled, reducing microhemorrhage, reducing activated microglia and reducing activated astrocytes in an animal model of intracerebral hemorrhage (ICH) stroke after treatment with mTB001 (comprising SEQ ID NOs: 27, 71, 112, 170, 221 and 248 for VH-CDRs1-3 and VL-CDRs1-3 respectively or SEQ ID NOs: 297 and 374 for VH and VL respectively) as compared to wild type control mice, does not reasonably provide enablement for a method for treating stroke in a subject in need thereof comprising administering a structurally and functionally undefined anti-Gal3 antibody or binding fragment thereof to the subject as broadly claimed. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims. The rejection is maintained for the reasons of record and the reasons set forth below.
Briefly Applicant is enabled for reducing loss of locomotor activity and increasing latency to fall and distance traveled (figures 23A-D), reducing microhemorrhage based on Prussian Blue-positive area (Figures 24A-D), reducing activated microglia and astrocytes based on 1ba1 positive immunostaining (Figures 25A-B) in an animal model of intracerebral hemorrhage (ICH) stroke by intraperitoneal administration of mTB001 at 10mg/kg for 8 doses twice in a week to the animal model of ICH stroke compared to wild type control mice, wherein the mTB001 comprises SEQ ID NOs: 27, 71, 112, 170, 221 and 248 for VH-CDRs1-3 and VL-CDRs1-3 respectively, or SEQ ID NOs: 297 and 374 for VH and VL respectively. However, the specification provides no-well established structural and functional relationship or correlation between mTB001 and structurally and functionally undefined anti-Gal3 antibodies including elected TB006 anti-Gal3 antibody (corresponding sequences: SEQ ID NOs: 31, 72 and 113, and SEQ ID NOs:171, 222 and 249 for HCDRs1-3 and LCDRs1-3 respectively; SEQ ID NOs: 298 and 375 for VH and VL respectively; SEQ ID NOs: 449 and 496 for HC and LC respectively; and SEQ ID NOs: 540 and 622 VH and VL DNA sequences). It is unpredictable whether all the claimed Gal3 antibodies including elected TB006 anti-Gal3 antibody have the same activity as mTB001 in reducing loss of locomotor activity and increasing latency to fall and distance traveled (figures 23A-D), reducing microhemorrhage based on Prussian Blue-positive area (Figures 24A-D), reducing activated microglia and astrocytes based on 1ba1 positive immunostaining (Figures 25A-B) in the animal model of ICH stroke treated with mTB001 compared to wild type control mice because Allumette-Hebert et al. (J. Neurosci. 2012; 32:10383-10395) teach that disruption of the galectin-3 gene in a galectin-3 knock-out mouse (Gal-3KO) resulted in significantly altering microglia activation and induces ~4-fold decrease in microglia proliferation and that defective microglia activation/proliferation was further associated with significant “increase” in the size of ischemic lesion, ~2-fold increase in the number of apoptotic neurons, and a marked deregulation of the IGF-1 levels, suggesting that Galectin-3 is required for resident microglia activation and proliferation in response to ischemic injury (see abstract). The specification provides insufficient guidance to enable one of skill in the art to practice the full scope of the claimed invention without undue experimentation because there is no well-established structural and functional relationship or correlation between the claimed Gal3 antibody including TB006 (elected) and the mTB001 anti-Gal3 antibody in recovering locomotor activity deficit and increasing latency to fall and distance traveled, reducing microhemorrhage based on Prussian Blue-positive area, reducing activated microglia and astrocytes based on 1ba1 positive immunostaining in the animal model of ICH stroke treated with mTB001 compared to wild type control mice or even treating stroke.
Response to Arguments
On p. 22-24 of the response, Applicant argues that: i) the claims are directed to methods of treatment, not antibodies; ii) the claimed methods are enabling because the specification provides support for the claimed methods in view of Ands factors, and cites para [0637] and examples 1, 6, 7, 9 and 12 and Genetech v. Novo Nordisk in support of the arguments.
Applicant's arguments have been fully considered but they are not found persuasive. Contrary to Applicant's arguments, the examiner asserts that based on MPEP §2164, MPEP §§2164.01-2164.06(b) & 2164.08, the specification provides insufficient guidance to enable a skilled artisan to practice the full scope of the claimed invention without undue experimentation because of the following:
i. There is no well-established structural and functional relationship or correlation between the claimed Gal3 antibody or binding fragments thereof and the mTB001 anti-Gal3 antibody in recovering locomotor activity deficit and increasing latency to fall and distance traveled, reducing microhemorrhage based on Prussian Blue-positive area, reducing activated microglia and astrocytes based on 1ba1 positive immunostaining in the animal model of ICH stroke treated with mTB001 compared to wild type control mice or even in treating stroke.
There is no well-established structural and functional relationship or correlation between the claimed Gal3 antibody including TB006 (elected) or binding fragments thereof and the mTB001 anti-Gal3 antibody in recovering locomotor activity deficit and increasing latency to fall and distance traveled, reducing microhemorrhage based on Prussian Blue-positive area, reducing activated microglia and astrocytes based on 1ba1 positive immunostaining in the animal model of ICH stroke treated with mTB001 compared to wild type control mice or even in treating stroke.
As previously made of record, Allumette-Hebert et al. (J. Neurosci. 2012; 32:10383-10395) teach that disruption of the galectin-3 gene in a galectin-3 knock-out mouse (Gal-3KO) resulted in significantly altering microglia activation and induces ~4-fold decrease in microglia proliferation and that defective microglia activation/proliferation was further associated with significant “increase” in the size of ischemic lesion, ~2-fold increase in the number of apoptotic neurons, and a marked deregulation of the IGF-1 levels, suggesting that Galectin-3 is required for resident microglia activation and proliferation in response to ischemic injury (see abstract).
It is unpredictable whether all the claimed Gal3 antibodies have the same activity as mTB001 in reducing loss of locomotor activity and increasing latency to fall and distance traveled (figures 23A-D), reducing microhemorrhage based on Prussian Blue-positive area (Figures 24A-D), reducing activated microglia and astrocytes based on 1ba1 positive immunostaining (Figures 25A-B) in the animal model of ICH stroke treated with mTB001 compared to wild type control mice. Thus, a skilled artisan cannot contemplate how to use the claimed invention, indicating undue experimentation is required by the skilled artisan to perform while practicing the claimed invention.
ii. There is no well-established structural and functional relationship or correlation between the elected TB006 anti-Gal3 antibody and the mTB001 anti-Gal3 antibody in recovering locomotor activity deficit and increasing latency to fall and distance traveled, reducing microhemorrhage based on Prussian Blue-positive area, reducing activated microglia and astrocytes based on 1ba1 positive immunostaining in the animal model of ICH stroke treated with mTB001 compared to wild type control mice or even in treating stroke.
As admitted by Applicant at p. 143, [0462] of the specification filed 07/02/2026, “Clones IMT001(TB001) and F847C.21H6 exhibited mutual competitive binding for Ga3 but did not prevent binding of the rest of the clones…. …..IMT006(TB006)….exhibited mutual competitive binding for Gal3, but did not prevent binding of the rest of the clones….” .
It is unpredictable whether the elected TB006 anti-Gal3 antibody has the same activity as mTB001 in reducing loss of locomotor activity and increasing latency to fall and distance traveled (figures 23A-D), reducing microhemorrhage based on Prussian Blue-positive area (Figures 24A-D), reducing activated microglia and astrocytes based on 1ba1 positive immunostaining (Figures 25A-B) in the animal model of ICH stroke treated with mTB001 compared to wild type control mice. Thus, a skilled artisan cannot contemplate how to use the claimed invention, indicating undue experimentation is required by the skilled artisan to perform while practicing the claimed invention.
iii. The specification provides insufficient description as to what other common structures or sequences and features are required by the claimed genus of anti-Gal3 antibodies including TB006 in order to preserve the activity of mTB001 in reducing loss of locomotor activity and increasing latency to fall and distance traveled, reducing microhemorrhage based on Prussian Blue-positive area, reducing activated microglia and astrocytes based on 1ba1 positive immunostaining in the animal model of ICH stroke treated with mTB001 compared to wild type control mice or even in treating stroke. Thus, it is unpredictable whether TB006 or other Gal3 antibodies can be used in the claimed method of treating stroke, indicating undue experimentation is required by a skilled artisan to perform while practicing the claimed invention.
Therefore, in view of the breadth of the claims, the lack of guidance in the specification, the limited examples, the unpredictability of inventions, and the current status of the art, undue experimentation would be required by one of skill in the art to perform in order to practice the full scope of the claimed invention as it pertains to a method for treating stroke by the claimed anti-Gal3 antibody.
Accordingly, the rejection of claims 1-2, 5-7, 13, 19, 21-22, 29, 34 and 92-96 under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, lack of scope of enablement is maintained.
Claim Rejections - 35 USC § 112
11. Claims 1-2, 5-7, 13, 19, 21-22, 29, 34 and 92-96 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 pre-AIA the inventor(s), at the time the application was filed, had possession of the claimed invention. The rejection is maintained for the reasons of record and the reasons set forth below.
Claims 1-2, 5-7, 13, 19, 21-22, 29, 34 and 92-96 encompass treating stroke using a genus of anti-Gal3 antibody or a genus of binding fragment thereof binding to a peptide on Gal3 comprising an amino acid sequence according to SEQ ID NO:8. The claimed genus of anti-Gal3 antibodies encompass structurally and functionally undefined anti-Gal3 antibodies. The claimed genus of binding fragments thereof include structurally and functionally undefined fragments within the claimed genus of anti-Gal3 antibodies. The limitation “an amino acid sequence according to SEQ ID NO:8” includes any fragments within SEQ ID NO:8
Briefly Applicant has not disclosed sufficient species of using the broad genus of anti-Gal3 antibodies or the broad genus of binding fragment thereof for treating stroke. The specification fails to provide a well-established structural and functional relationship or correlation between the claimed genus of anti-Gal3 antibodies including TB006 and mTB001 in reducing loss of locomotor activity and increasing latency to fall and distance traveled, reducing microhemorrhage based on Prussian Blue-positive area, reducing activated microglia and astrocytes based on 1ba1 positive immunostaining in the animal model of ICH stroke treated with mTB001 compared to wild type control mice.
The specification provides insufficient description as to what other common structures or sequences and features are required by the claimed genus of anti-Gal3 antibodies including elected TB006 or the claimed genus of binding fragments in order to preserve the activity of mTB001 in reducing loss of locomotor activity and increasing latency to fall and distance traveled, reducing microhemorrhage based on Prussian Blue-positive area, reducing activated microglia and astrocytes based on 1ba1 positive immunostaining in the animal model of ICH stroke treated with mTB001 compared to wild type control mice or even in treating or preventing stroke. The prior art does not provide compensatory structural or correlative teachings sufficient to enable one of skill to identify what other anti-Gal3 antibodies or what binding fragments thereof having the same activity as mTB001 might be. Since the common characteristics/features of other anti-Gal3 antibodies including elected TB006 and the genus of binding fragments thereof are unknown, a skilled artisan cannot envision the functional correlations of the genus with the claimed invention. Accordingly, in the absence of sufficient recitation of distinguishing identifying characteristics, the specification does not provide adequate written description of using the genus of anti-Gal3 antibodies and the genus of binding fragments in the claimed for treating stroke.
Response to Arguments
On p. 20-22 of the response, Applicant argues that: i) the claims are directed to methods of treating stroke using anti-Gal3 antibodies, not antibodies themselves as compositions of matter. ii)the specification identified peptide 6 of Gal3 (SEQ ID NO:8) as a therapeutically relevant epitope and at least 15 anti-Gal3 antibodies binding to the peptide 6 (see para. [0637]), and showed that TB001 and TB006 achieve the claimed treatment-related outcomes in stroke models and cites Examples 1, 6, 7, 9 and 12 in support of the arguments. Applicant further cites Teva Pharmaceuticals, Intl. v. El Lilly and Co. in support of the arguments.
Applicant's arguments have been fully considered but they are not found persuasive. Contrary to Applicant's arguments, the examiner asserts that based on MPEP §2163, MPEP §§2163.01-2163.03, the specification fails to provide sufficient description or information or evidence to demonstrate that Applicant is in possession of using the claimed genus of anti-Gal3 antibodies and the claimed genus of binding fragments thereof for treating stroke because:
i. There is no well-established structural and functional relationship or correlation between the claimed genus of anti-Gal3 antibodies or elected TB006 and mTB001 shown in Examples in reducing loss of locomotor activity and increasing latency to fall and distance traveled, reducing microhemorrhage based on Prussian Blue-positive area, reducing activated microglia and astrocytes based on 1ba1 positive immunostaining in the animal model of ICH stroke treated with mTB001 compared to wild type control mice or even in treating stroke.
As admitted by Applicant at p. 143, [0462] of the specification filed 07/02/2026, “Clones IMT001(TB001) and F847C.21H6 exhibited mutual competitive binding for Ga3 but did not prevent binding of the rest of the clones…. …..IMT006(TB006)….exhibited mutual competitive binding for Gal3, but did not prevent binding of the rest of the clones….” .
The specification fails to teach the detailed structures and sequences and characteristics for the claimed genus of anti-Gal3 antibodies and the claimed genus of binding fragments thereof including any fragments within the claimed structurally and functionally undefined anti-Gal3 antibodies. The specification also fails to provide sufficient description or evidence to demonstrate that Applicant is in possession of using the claimed genus of anti-Gal3 antibodies and the claimed genus of binding fragments thereof including any fragments within the claimed structurally and functionally undefined anti-Gal3 antibodies for treating stroke.
The specification's general reference to “an anti-Gal3 antibody or binding fragment thereof” does not clearly suggest a particular sequence of structurally and functionally undefined anti-Gal3 antibody or binding fragment thereof that bind to a peptide on Gal3 comprising an amino acid sequence of SEQ ID NO:8” that can be used for treating stroke because the structural and functional relationship or correlation between the claimed genus of anti-Gal3 antibodies and binding fragments thereof and mTB001 is unknown. The structure and function of mTB001 is also different from those of elected TB006 as admitted by Applicant (see p. 143, [0462] of the specification filed 07/02/2026). As such, he/she cannot possibly have possessed using the entire genus for treating stroke in view of MPEP§2161.01 and 2163 and Amgen, Inc. v. Sanofi, 872 F.3d 1367 (Fed. Cir. 2017).
ii. The specification provides insufficient description as to what other common structures or sequences and features are required by the claimed genus of anti-Gal3 antibodies including TB006 in order to preserve the activity of mTB001 in reducing loss of locomotor activity and increasing latency to fall and distance traveled, reducing microhemorrhage based on Prussian Blue-positive area, reducing activated microglia and astrocytes based on 1ba1 positive immunostaining in the animal model of ICH stroke treated with mTB001 compared to wild type control mice or even in treating stroke.
Furthermore, the prior art does not provide compensatory structural or correlative teachings sufficient to enable one of skill to identify what other anti-Gal3 antibodies having the same activity as mTB001 might be. Since the common characteristics/features of other anti-Gal3 antibodies including elected TB006 are unknown, a skilled artisan cannot envision the functional correlations of the genus with the claimed invention in view of Burgess et al. (J of Cell Bio. 1990, 111:2129-2138, cited previously), Bowie et al. (see col 2, p. 1306, Bowie et al. Science, 1990, 247:1306-1310, cited previously), Pawson et al. (see p. 445 the second column, first paragraph, Pawson et al. 2003, Science 300:445-452, cited previously), Alaoui-lsmaili et al. (see p. 502, right col., 2th paragraph; Alaoui-lsmaili et al., Cytokine Growth Factor Rev. 2009; 20:501-507, cited previously) and Guo et al. (see p. 9207, left col., 2th paragraph, Guo et al., PNAS 2004; 101:9205-9210, cited previously).
Accordingly, in the absence of sufficient recitation of distinguishing identifying characteristics, the specification does not provide adequate written description of the genus of anti-Gal3 antibodies and the claimed genus of binding fragments thereof that can be used in the claimed for treating or preventing stroke.
Based on MPEP § 2161.01 and §2163, “to satisfy the written description requirement, a patent specification must describe the claimed invention in sufficient detail that one skilled in the art can reasonably conclude that the inventor had possession of the claimed invention. See, e.g., Moba, B.V. v. Diamond Automation, Inc., 325 F.3d 1306, 1319, 66 USPQ2d 1429, 1438 (Fed. Cir. 2003); Vas-Cath, Inc. v. Mahurkar, 935 F.2d at 1563, 19 USPQ2d at 1116”.
Vas-Cath Inc. v. Mahurkar, 19USPQ2d 1111, clearly states “applicant must convey with reasonable clarity to those skilled in the art that, as of the filing date sought, he or she was in possession of the invention. The invention is, for purposes of the ‘written description' inquiry, whatever is now claimed.” (See page 1117.) The specification does not “clearly allow persons of ordinary skill in the art to recognize that [he or she] invented what is claimed.” (See Vas-Cath at page 1116).
As discussed above, the skilled artisan cannot envision the detailed chemical structure of the encompassed genus of anti-Gal3 antibodies, binding fragments thereof that can be used for treating stroke, and therefore conception is not achieved until reduction to practice has occurred, regardless of the complexity or simplicity of the method of isolation. Adequate written description requires more than a mere statement that it is part of the invention and reference to a potential method of isolating it. The compound itself is required. See Fiers v. Revel, 25 USPQ2d 1601 at 1606 (CAFC 1993) and Amgen Inc. v. Chugai Pharmaceutical Co. Ltd., 18 USPQ2d 1016. One cannot describe what one has not conceived. See Fiddes v. Baird, 30 USPQ2d 1481 at 1483 and Centocor v. Abbott, 636 F.3d1341 (Fed. Cir. 2011) and AbbVie v. Janssen, 759 F.3d 1285 (Fed. Cir.2014). One cannot describe what one has not conceived. See Fiddes v. Baird, 30 USPQ2d 1481 at 1483.
Therefore, the claimed method has not met the written description provision of 35 U.S.C. §112, first paragraph. Applicant is reminded that Vas-Cath makes clear that the written description provision of 35 U.S.C. §112 is severable from its enablement provision (see page 1115). Applicant is directed to the Guidelines for the Examination of Patent Applications Under the 35 U.S.C. 112, ¶ 1 "Written Description" Requirement. See MPEP § 2161.01 and 2163.
Accordingly, the rejection of claims 1-2, 5-7, 13, 19, 21-22, 29, 34 and 92-96 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 is maintained.
Conclusion
12. NO CLAIM IS ALLOWED.
13. The prior art made of record and not relied upon is considered pertinent to applicant's disclosure.
NCT05156827 (published 2022-07-26; a study to assess the efficacy, safety and pharmacokinetics of TB006 in participants with Acute ischemic Stroke (see p. 1) discloses a method of evaluating the efficacy, safety and pharmacokinetics of TB006 antibody in patients with acute ischemic stroke, wherein the patients will receive intravenous 3 infusion of 4000mg TB006 one every 28 days (Q28D) (p.6).
Mosleh et al. (Biomarker Insights; 2018;13:1-10. DOI:10.1177/1177271918771969) teach that Galectin-3 KO mice showed reduced myocardial macrophage infiltration after acute MI and that Galectin-3 levels were higher in patients with early systolic dysfunction, and predicted 3-month major adverse cardiovascular event (see abstract).
Hemadou et al. (J. Am. Heart Assco. 2021; 10:e016287. DOI:10.1161/JAHA.120.016287) teach that P3 scFv-Fc-2c specifically targeted atherosclerotic plaques in the Apoe−/− mouse model (see abstract).
Fontayne et al. (US11091552, issued Aug 17, 2021, priority Oct 5, 2018) teach a method of treating atherosclerosis by administering to a subject in need thereof an anti-Gal3 antibody at multiple doses including 0.05mg comprising a VH having the sequence of SEQ ID NO:1 and a VL having the sequence of SEQ ID NO:2 (col. 13-14, claims 1-17).
14. 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.
15. Any inquiry concerning this communication or earlier communications from the examiner should be directed to CHANG-YU WANG whose telephone number is (571)272-4521. The examiner can normally be reached Monday-Thursday, 7:00am-5:00pm EST.
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, Jeffrey Stucker can be reached at 571-272-0911. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
Chang-Yu Wang
September 21, 2026
/CHANG-YU WANG/Primary Examiner, Art Unit 1675
Prosecution Insights