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 December 3, 2025 is acknowledged. Claims 1-2, 5, 7, 12, 14, 16, 18-21, 23-24, 30, 32 and 34 are canceled. Claims 3-4, 6, 8-9, 11, 13, 15, 17, 22, 25-26, 29, 31, 33, 35-36 and 38-39 are amended. Claim 40 is newly added. Claims 3-4, 6, 8-11, 13, 15, 17, 22, 25-29, 31, 33, 35-39 and new claim 40 are pending in this application. Election was made without traverse in the reply filed on August 18, 2025.
3. Claims 3-4, 6, 8-11, 13, 15, 17, 22, 25-29, 31, 33 and 35-40 are under examination with respect to SEQ ID NOs: 34-35, 31, 41, 33 and 32 for HCDRs1-3 and LCDRs1-3, SEQ ID NOs:27 and 30 for VH and VL and SEQ ID NOs: 44 and 47 for HC and LC and multiple sclerosis in this office action.
4. Applicant’s arguments filed on December 3, 2025 have been fully considered but they are not deemed to be persuasive for the reasons set forth below.
Specification
5. The objection to the specification is withdrawn in response to Applicant’s arguments on p.9 of the response.
Claim Rejections/Objections Withdrawn
6. The objection to claims 1, 3-4, 6. 8, 13, 15, 21, 31 and 33 is withdrawn in response to Applicant’s amendment to the claims.
The rejection of claim 21 under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite is moot because the claim is canceled.
The rejection of claims 1-2 and 19-20 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 1-4, 6, 8-11, 13, 15, 17, 19-22, 25-29, 31, 33 and 35-39 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112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement is withdrawn in response to Applicant’s amendment to the claims and cancelation of claims 1-2 and 19-20.
The rejection of claims 1-2 and 19-20 under 35 U.S.C. 102(a)(1) and (a)(2) as being anticipated by Schwabe et al. (US2019040130) as evidenced by Piccio et al. (Brain, 2008; 131:3081-3091) and Ozturk et al. (Multiple Sclerosis 2010; 16:166-177) is moot because the claims are canceled.
Claim Rejections/Objections Maintained
In view of the amendment filed on December 3, 2025, the following rejections are maintained.
Claim Rejections - 35 USC § 112
7. 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 3-4, 6, 8-11, 13, 15, 17, 22, 25-29, 31, 33 and 35-40 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 ameliorating CPZ-induced pathology, enhancing myelin debris clearance based on reduced dMBP staining, increasing PDGFRa+ oligodendrocyte precursor cells (OPCs) density in the Corpus callosum and recruitment of OPCs to the Corpus callosum, promoting differentiation of OPC into mature oligodendrocytes, increasing SMI-31 expression in Trem2+/- mice with CPZ-induced demyelination and treated with an anti-TREM2 antibody 7E5 compared to the Trem2+/- mice treated with an isotype control antibody, does not reasonably provide enablement for a method for treating or preventing all forms of CNS demyelination diseases or promoting remyelination of one or more demyelination lesions in the CNS of an individual having all forms of CNS demyelination diseases using a structurally and functionally undefined agonist anti-TREM2 antibody 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.
Claims 3-4, 6, 8-11, 13, 15, 17, 22, 25-29, 31, 33 and 35-40 as amended are drawn to a method for promoting remyelination of one or more demyelination lesions in the CNS of an individual having a CNS demyelination disease, comprising administering to the individual a therapeutically effective amount of anti-TREM2 agonist antibody having recited SEQ ID NOs; 34-35, 31 and 41, 33 and 32 for HCDRs1-3 and LCDRs1-3 respectively or having SEQ ID NOs: 27 and 30 for VH and VL respectively or having SEQ ID NOs: 44 and 47 for HC and LC respectively.
The claims encompass methods of promoting remyelination in all forms of CNS demyelination diseases including multiple sclerosis (MS) using an anti-TREM2 agonist antibody having recited SEQ ID NOs; 34-35, 31 and 41, 33 and 32 for HCDRs1-3 and LCDRs1-3 respectively or having SEQ ID NOs: 27 and 30 for VH and VL respectively or having SEQ ID NOs: 44 and 47 for HC and LC respectively.
The specification provides insufficient guidance to enable a skilled artisan to practice the full scope of the claimed invention without undue experimentation because there is no well-established correlation between the animal model of TREM2+/-mice with CPZ-induced demyelination and different forms of CNS demyelination diseases caused by different mechanisms.
Response to Arguments
On p. 11-12 of the response, Applicant argues that the rejection has been overcome in view of amendment to the claims and administration of anti-TREM2 antibody 7E5 in TREM2+/-mice with CPZ-induced demyelination resulted in inducing DAP12 phosphorylation and TREM2 signaling in vitro and in vivo and promoting phosphorylated neurofilaments, recruiting oligodendrocyte precursor cells (OPCs) to the corpus callosum and differentiation of OPCs into mature oligodendrocytes and cites the specification show
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:
i. The specification provides no well-established correlation among different forms of CNS demyelination diseases caused by different mechanisms including mechanisms unrelated to TREM2.
As previously made of record, each type of animal models of CNS demyelination diseases caused by different mechanisms including MS only reflects part of pathogenesis of the disease as taught by Medina et al. (World J. Clin. Cases, 2024; 12:6361-6373, cited previously). Applicant obviously intended to treat and promote remyelination of demyelination in all forms of CNS demyelination diseases caused by all possible mechanism including those mechanisms unrelated to TREM2 using the claimed anti-TREM2 antibody.
However, the specification fails to provide a well-established correlation between the animal model of TREM2+/-mice with CPZ-induced demyelination and other forms of CNS demyelination diseases caused by different mechanisms unrelated to TREM2 and demyelination induced by CPZ shown in TREM2+/-mice with CPZ-induced demyelination.
The molecular mechanisms underlying CNS demyelination diseases are unclear (see p. 6361-6365; Medina et al., World J. Clin. Cases, 2024; 12:6361-6373). The specification provides insufficient guidance to demonstrate that administration of the claimed structurally and functionally undefined anti-TREM2 agonist antibody can treat MS and all other forms of CNS demyelination diseases because the reduced expression of TREM2 is not the only cause of CNS demyelination diseases. Several factors and genes are also involved in pathogenesis of CNS demyelination diseases including ageing, inflammation and immune response.
The specification fails to teach that other forms of CNS demyelination diseases caused by different mechanisms that are unrelated to TREM2 and CPZ-induced demyelination can be treated by the same drugs or same conditions, or would have the same effects as the animal model of TREM2+/-mice with CPZ-induced demyelination in response to the same drugs. The specification fails to provide sufficient guidance or evidence to demonstrate that all forms of CNS demyelination diseases caused by different mechanisms can be treated by the claimed anti-TREM2 agonist antibody because there is no well-established correlation between Trem2+/- mice with CPZ-induced demyelination and the pathogeneses or causes of other forms of CNS demyelination diseases caused by other mechanisms. Thus, it is unpredictable whether one treatment for one specific disorder can be applied to another disorder, indicating undue experimentation is required by a skilled artisan to perform while practice the claimed invention.
The scope of the claims must bear a reasonable correlation with the scope of enablement (In re Fisher, 166 USPQ 19 24 (CCPA 1970)). Without such guidance, it is unpredictable whether other forms of CNS demyelination diseases caused by different mechanisms can be treated by the claimed anti-TREM2 agonist antibody; and thus the experimentation left to those skilled in the art is extensive and undue. See Ex parte Forman, 230 USPQ 546 (Bd. Pat. App. & Int. 1986). Thus, the skilled artisan cannot readily make and use the claimed invention as currently claimed without further undue experimentation. Note that
“The ‘predictability or lack thereof' in the art refers to the ability of one skilled in the art to extrapolate the disclosed or known results to the claimed invention. If one skilled in the art can readily anticipate the effect of a change within the subject matter to which the claimed invention pertains, then there is predictability in the art. On the other hand, if one skilled in the art cannot readily anticipate the effect of a change within the subject matter to which that claimed invention pertains, then there is lack of predictability in the art. Accordingly, what is known in the art provides evidence as to the question of predictability. In particular, the court in In re Marzocchi, 439 F.2d 220, 223-24, 169 USPQ 367, 369-70 (CCPA 1971)” See MPEP § 2164.03
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 promoting remyelination of one or more demyelination lesions in the CNS of an individual having a CNS demyelination disease by the claimed anti-TREM2 agonist antibody.
Accordingly, the rejection of claims 3-4, 6, 8-11, 13, 15, 17, 22, 25-29, 31, 33 and 35-40 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 § 102
8. 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 3-4, 6, 8-11, 13, 15, 17, 22, 25-29, 31, 33 and 35-40 are rejected under 35 U.S.C. 102(a)(1) and (a)(2) as being anticipated by Schwabe et al. (US20190040130) as evidenced by Piccio et al. (Brain, 2008; 131:3081-3091) and Ozturk et al. (Multiple Sclerosis 2010; 16:166-177). The rejection is maintained for the reasons of record and the reasons set forth below.
Claims 3-4, 6, 8-11, 13, 15, 17, 22, 25-29, 31, 33 and 35-40 as amended are drawn to a method for promoting remyelination of one or more demyelination lesions in the CNS of an individual having a CNS demyelination disease, comprising administering to the individual a therapeutically effective amount of anti-TREM2 agonist antibody having recited SEQ ID NOs; 34-35, 31 and 41, 33 and 32 for HCDRs1-3 and LCDRs1-3 respectively or having SEQ ID NOs: 27 and 30 for VH and VL respectively or having SEQ ID NOs: 44 and 47 for HC and LC respectively.
Response to Arguments
On p. 13-15 of the response, Applicant argues that i) the rejection has been overcome in view of amendment to the claims; ii) Schwabe does not teach a method of promoting remyelination of one or more demyelination lesions in the CNS of an individual having a CNS demyelination disease comprising administering to the individual a therapeutically effective amount of an agonist antibody as recited in amended claims; and iii) Neither Piccio nor Ozturk cures the deficiencies of Schwabe because both references are silent about a method of promoting remyelination of one or more demyelination lesion in the CNS.
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 §2131-2131.01, Schwabe et al. (US2019040130) does teach the claimed method because:
i. Schwabe teaches a method of using the same material (i.e. anti-TREM2 agonist antibody comprising the same sequences for HC and LC; see the sequence alignment below; see para.[0027]; [0105]-[0128], [0261]; [0254]-[0279]; claim 40) and the same active step (i.e. administering to a subject in need thereof; see para. [0027]; [0375]) in the same patient population (i.e. multiple sclerosis, which is a demyelination disease in the CNS; see ([0439]-[0442]).
The anti-TREM2 agonist antibody disclosed by Schwabe comprises a HC comprising the amino acid sequence of SEQ ID NO: 201, which is 100% identical to instant SEQ ID NO:44, and a LC comprising the amino acid sequence of SEQ ID NO:214, which is 100% identical to instant SEQ ID NO:47 recited in claim 29, which comprises SEQ ID NOs: 34-35 and 31, and 41 and 33-32 for HVR-H1~H3 (HCDRs1-3) and HVR-L1~L3(LCDRs1-3) respectively recited in instant claim 3 or a VH comprising SEQ ID NO:27 and a VL comprising SEQ ID NO:30 recited in claim 22 (see the sequence alignment below; see para.[0027]; [0105]-[0128], [0261]; [0254]-[0279]; claim 40). Schwabe also teaches that that the anti-TREM2 antibody is a murine antibody, humanized antibody, bispecific antibody, multivalent antibody, a conjugate antibody or a chimeric antibody or a monoclonal antibody as in claim 17 (see para. [0053]-[0064]; [0285]-[0348]; [0306]) or that an antigen-binding fragment of an anti-TREM2 antibody is a Fab, Fab', Fab'-SH, F(ab')2, Fv or scFv fragment as in claim 25 (see para. [0024]; [0055]-[0060]), the anti-TREM2 antibody is of the IgG class including an IgGI,IgG2, IgG3, or IgG4 isotype, the IgM class, or the IgA class in claims 26-27 (see para. [0023]; [0130]-[0145], Table A), and wherein the antibody has a human IgGI isotype comprising amino acid substitutions in the Fc region at the residue positions P331S and E430G based on the EU numbering as in claim 28 (see para. [0023]; [0028]; [0465] Table A).
Schwabe teaches that the individual with MS is a human and/or comprises at least one copy of a functional TREM2 gene in claim 31, has a heterozygous or homozygous for a mutation in TREM2 gene in claim 33 (see para.[0401]-[0402]), which is also evidenced by Piccio et al. (p. 3084, 2nd col. last paragraph to p. 3088).
Schwabe teaches that the individual has or is at risk for a disease characteristic selected from the group consisting of myelin damage, one or more demyelination lesions in the CNS, inflammation in the CNS, one or more plaques in the CNS, loss of myelin sheaths, axonal damage, reduced OPCs, reduced OLs, reduced myelin debris clearance, axonal varicosities, axonal spheroids, gliosis, autofluorescent lipid-laden macrophages, axon destruction, and any combination thereof as in claims 35-40 (see para. [0440]), and also teach that the axonal damage and/or one or more demyelination lesions in the CNS include the white matter, the gray matter, or the corpus callosum of the CNS, which is evidenced by Ozturk et al. (see abstract; p. 167, 1st col).
Schwabe teaches that the individual has or is at risk for having a symptom selected from the group consisting of changes in sensation, pricking, numbness, muscle weakness, clonus, muscle spasms, difficulty in moving, difficulties with coordination, difficulties with balance, problems in speech, problems in swallowing, visual problems, fatigue, acute pain, chronic pain, bladder difficulties, bowel difficulties, cognitive impairment, depression, unstable mood, Uhthoffs phenomenon, Lhermitte's sign, and any combination thereof and wherein the demyelination disease is multiple sclerosis as in claims 38-39 (see para.[0441]).
Schwabe teaches the limitations “wherein the antibody enhances one or more TREM2 activities induced in the presence of myelin, and/or ii) the antibody induces one or more TREM2 activities selected from the group consisting of: i. TREM2 binding to DAP12; ii. DAP12 phosphorylation;…. increasing activity of one or more TREM2-dependent genes….comprise nuclear factor of activated T-cells (NFAT) transcription factors” recited in claims 6, 8 and 40 (see para.[0254]-[0279]).
ii. The references of Piccio and Ozturk are evidentiary references to evidence and further support that i. patients with MS comprises at least one copy of a functional TREM2 gene and including a heterozygous or homozygous for a mutation in TREM2 gene; ii the axonal damage and/or one or more demyelination lesions in the CNS in multiple sclerosis include the white matter, the gray matter, or the corpus callosum of the CNS.
iii. The intended result of “promoting remyelination of one or more demyelination lesions in the CNS of an individual” recited in the preamble of claim 3 is an inherent result of administration of an anti-TREM2 agonist antibody to the patients with MS because the material, the active step and the patient population disclosed in the Schwabe’s method are identical to instant claims. If the claimed method can promote remyelination of one or more demyelination lesions in the CNS of an individual, the Schwabe’s method can achieve the same intended result recited in the preamble of claim 3. Note that
“The claim preamble must be read in the context of the entire claim. …. If the body of a claim fully and intrinsically sets forth all of the limitations of the claimed invention, and the preamble merely states, for example, the purpose or intended use of the invention, rather than any distinct definition of any of the claimed invention' s limitations, then the preamble is not considered a limitation and is of no significance to claim construction. Pitney Bowes, Inc.v. Hewlett-Packard Co., 182 F.3d 1298, 1305, 51 USPQ2d 1161, 1165 (Fed. Cir.1999). See also Rowe v. Dror, 112 F.3d 473, 478, 42 USPQ2d 1550, 1553 (Fed. Cir.1997).
The limitations “wherein the antibody promotes recruitment of oligodendrocyte precursor cells (OPCs) to one or more demyelination lesions in the CNS of the individual” “wherein the OPCs are PDGFRa positive” recited in claims 9-10, “wherein the antibody promotes: a. an increase of mature oligodendrocytes (OLs) in one or more demyelination lesions in the CNS of the individual; b. differentiation of OPCs into mature oligodendrocytes (OLs) in one or more demyelination lesions…. clearance of myelin debris in one or more demyelination lesions in the individual”, “wherein the mature OLs are OLIG2 and/or CNPase positive”, “wherein the phosphorylated neurofilaments are SMI-31 positive” recited in claims 11, 13 and 15 are in a wherein clause and are also inherent results of administration of an anti-TREM2 agonist antibody to the patients with MS. If the claimed method can result in the claimed features recited in claims 9-11, 13 and 15, the Schwabe’s method using the same material, the same active step in the same patient population can achieve the same features and results recited in claims 9-11, 13 and 15. Note that
In Hoffer v. Microsoft Corp., 405 F.3d 1326, 1329, 74 USPQ2d 1481, 1483 (Fed. Cir. 2005), the court held that when a “‘whereby’ clause states a condition that is material to patentability, it cannot be ignored in order to change the substance of the invention.” Id. However, the court noted (quoting Minton v.Nat’l Ass’n of Securities Dealers, Inc., 336 F.3d 1373, 1381, 67 USPQ2d 1614, 1620 (Fed. Cir. 2003)) that a “‘whereby clause in a method claim is not given weight when it simply expresses the intended result of a process step positively recited.’” Id.< See MPEP § 2111.04.
Thus, claims 3-4, 6, 8-11, 13, 15, 17, 22, 25-29, 31, 33 and 35-40 are anticipated by Schwabe et al. (US2019040130) as evidenced by Piccio and Ozturk.
Accordingly, the rejction of claims 3-4, 6, 8-11, 13, 15, 17, 22, 25-29, 31, 33 and 35-40 under 35 U.S.C. 102(a)(1) and (a)(2) as being anticipated by Schwabe et al. (US20190040130) as evidenced by Piccio and Ozturk is maintained.
Double Patenting
9. 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 3-4, 6, 8-11, 13, 15, 17, 22, 25-29, 31, 33 and 35-40 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-11, 15-17, 19, 21, 23, 25-31, 35, 39 and 41 of copending Application No. 17782127, claims 2-3, 5-6, 17, 22-23, 26, 32-34, 36-37, 39-40, 44, 46, 48, 51-52, 54-55, 57-59, 65, 69-70 and 86 of copending Application No. 17916728, or claims 1-2, 5-9, 11, 13, 23, 25, 27, 29-34, 39, 41, 44, 46-47, 51, 54, 67-68, and 79 of copending Application No. 18/806118. The rejection is maintained for the reasons of record and the reasons set forth below.
Response to Arguments
On p. 15-16 of the response, Applicant requests the provisional rejections be held in abeyance until allowable subject is indicated and Applicant would determine whether the non-statutory double patenting rejection is applicable.
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 §804 and MPEP §2131-2131.01, the method recited in the claims of the copending Application Nos. 11782127, 17916728 and 18806118 do anticipate instant claims because the claims of the Applications11782127, 17916728 and 18806118 use the same material (i.e. an anti-TRME2 agonist antibody comprising the same sequences), and the same active step (i.e. administering to a subject in need thereof) in the same patient population (i.e. the disease or the CSF1R-deficient disease recited in copending Applications includes myelin damage in the CNS, and MS), and thus would inherently result in the same results and features recited in the preamble of independent claims and dependent claims. Therefore, claims 3-4, 6, 8-11, 13, 15, 17, 22, 25-29, 31, 33 and 35-40 of the instant Application are not patentably distinct from claims 1-11, 15-17, 19, 21, 23, 25-31, 35, 39 and 41 of the ‘127 Application, claims 2-3, 5-6, 17, 22-23, 26, 32-34, 36-37, 39-40, 44, 46, 48, 51-52, 54-55, 57-59, 65, 69-70 and 86 of the ‘728 Application, or claims 1-2, 5-9, 11, 13, 23, 25, 27, 29-34, 39, 41, 44, 46-47, 51, 54, 67-68, and 79 of the ‘118 Application because instant claims 3-4, 6, 8-11, 13, 15, 17, 22, 25-29, 31, 33 and 35-40 are anticipated by claims 1-11, 15-17, 19, 21, 23, 25-31, 35, 39 and 41 of the ‘127 Application, claims 2-3, 5-6, 17, 22-23, 26, 32-34, 36-37, 39-40, 44, 46, 48, 51-52, 54-55, 57-59, 65, 69-70 and 86 of the ‘728 Application, or claims 1-2, 5-9, 11, 13, 23, 25, 27, 29-34, 39, 41, 44, 46-47, 51, 54, 67-68, and 79 of the ‘118 Application.
Accordingly, the rejection of claims 3-4, 6, 8-11, 13, 15, 17, 22, 25-29, 31, 33 and 35-40 on the ground of nonstatutory double patenting as being unpatentable over claims 1-11, 15-17, 19, 21, 23, 25-31, 35, 39 and 41 of copending Application No. 17782127, claims 2-3, 5-6, 17, 22-23, 26, 32-34, 36-37, 39-40, 44, 46, 48, 51-52, 54-55, 57-59, 65, 69-70 and 86 of copending Application No. 17916728, or claims 1-2, 5-9, 11, 13, 23, 25, 27, 29-34, 39, 41, 44, 46-47, 51, 54, 67-68, and 79 of copending Application No. 18/806118 is maintained.
Conclusion
10. NO CLAIM IS ALLOWED.
11. The prior art made of record and not relied upon is considered pertinent to applicant's disclosure.
Sequence alignments
US2019040130 (under the 102 rejection) teaches a method of treating injury and demyelination in demyelination diseases in the CNS including MS using the claimed anti-TREM2 agonist antibody (see the sequence alignment below).
SEQ ID NO:44
BGB58142
(NOTE: this sequence has 9 duplicates in the database searched)
ID BGB58142 standard; protein; 452 AA.
XX
AC BGB58142;
XX
DT 21-MAR-2019 (first entry)
XX
DE Anti-TREM2 antibody HC region-mutant huIgG1 PSEG, SEQ ID 201.
XX
KW TREM2 protein; alzheimers disease; amnesia; antibody;
KW antibody production; antibody therapy; antiinflammatory; cancer;
KW cognitive disorder; colitis; cytostatic; dementia;
KW frontotemporal dementia; gastrointestinal-gen.; heavy chain;
KW immunoglobulin G1; immunoglobulin gamma 1; immunosuppressive;
KW multiple sclerosis; mutein; neuroprotective; nootropic;
KW prophylactic to disease; spinal cord injury; therapeutic;
KW traumatic brain injury; triggering receptor expressed on myeloid cells-2;
KW ulcerative colitis; vulnerary.
XX
OS Homo sapiens.
OS Unidentified.
OS Chimeric.
OS Synthetic.
XX
CC PN US2019040130-A1.
XX
CC PD 07-FEB-2019.
XX
CC PF 03-AUG-2018; 2018US-00054680.
XX
PR 03-AUG-2017; 2017US-0541019P.
PR 27-FEB-2018; 2018US-0636095P.
XX
CC PA (ALEC-) ALECTOR LLC.
XX
CC PI Schwabe T, Brown E, Kong P, Tassi I, Lee S, Rosenthal A;
CC PI Pejchal R, Nielson NP;
XX
DR WPI; 2019-13815K/17.
XX
CC PT New antibody useful in pharmaceutical composition for preventing,
CC PT reducing risk, or treating individual having disease, disorder or injury
CC PT including dementia, frontotemporal dementia, Alzheimer's disease,
CC PT cognitive deficit and memory loss.
XX
CC PS Claim 13; SEQ ID NO 201; 264pp; English.
XX
CC The present invention relates to a novel anti-triggering receptor
CC expressed on myeloid cells-2 (TREM2) antibody useful for preparing a
CC pharmaceutical composition. The pharmaceutical composition is used for
CC preventing, reducing risk or treating individual having disease, disorder
CC or injury includes dementia, frontotemporal dementia, Alzheimer's
CC disease, Nasu-Hakola disease, cognitive deficit, memory loss, spinal cord
CC injury, traumatic brain injury, multiple sclerosis, chronic colitis,
CC ulcerative colitis and cancer. The invention further provides: a nucleic
CC acid sequence encoding the antibody; a vector comprising the nucleic acid
CC ; an isolated host cell comprising the vector; a method of producing the
CC antibody that binds to TREM2; and an antibody comprising fragment
CC crystallizable (Fc) region. The present sequence represents a anti-TREM2
CC antibody heavy chain region (HC) comprising a mutant human immunoglobulin
CC gamma 1 (huIgG1 PSEG) P331S/E430G, which is used in the invention for
CC treating the above mentioned diseases.
XX
SQ Sequence 452 AA;
Query Match 100.0%; Score 2407; Length 452;
Best Local Similarity 100.0%;
Matches 452; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 QVQLVQSGAEVKKPGASVKVSCKASGYAFSSQWMNWVRQAPGQRLEWIGRIYPGGGDTNY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 QVQLVQSGAEVKKPGASVKVSCKASGYAFSSQWMNWVRQAPGQRLEWIGRIYPGGGDTNY 60
Qy 61 AGKFQGRVTITADTSASTAYMELSSLRSEDTAVYYCARLLRNQPGESYAMDYWGQGTLVT 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 AGKFQGRVTITADTSASTAYMELSSLRSEDTAVYYCARLLRNQPGESYAMDYWGQGTLVT 120
Qy 121 VSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVL 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 121 VSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVL 180
Qy 181 QSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPEL 240
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 181 QSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPEL 240
Qy 241 LGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREE 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 241 LGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREE 300
Qy 301 QYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPS 360
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 301 QYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPS 360
Qy 361 RDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDK 420
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 361 RDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDK 420
Qy 421 SRWQQGNVFSCSVMHGALHNHYTQKSLSLSPG 452
||||||||||||||||||||||||||||||||
Db 421 SRWQQGNVFSCSVMHGALHNHYTQKSLSLSPG 452
SEQ ID NO:47
BGB58155
(NOTE: this sequence has 11 duplicates in the database searched)
ID BGB58155 standard; protein; 219 AA.
XX
AC BGB58155;
XX
DT 21-MAR-2019 (first entry)
XX
DE Anti-TREM2 antibody LC region-mutant huIgG1 PSEG, SEQ ID 214.
XX
KW TREM2 protein; alzheimers disease; amnesia; antibody;
KW antibody production; antibody therapy; antiinflammatory; cancer;
KW cognitive disorder; colitis; cytostatic; dementia;
KW frontotemporal dementia; gastrointestinal-gen.; immunoglobulin G1;
KW immunoglobulin gamma 1; immunosuppressive; light chain;
KW multiple sclerosis; mutein; neuroprotective; nootropic;
KW prophylactic to disease; spinal cord injury; therapeutic;
KW traumatic brain injury; triggering receptor expressed on myeloid cells-2;
KW ulcerative colitis; vulnerary.
XX
OS Homo sapiens.
OS Unidentified.
OS Chimeric.
OS Synthetic.
XX
CC PN US2019040130-A1.
XX
CC PD 07-FEB-2019.
XX
CC PF 03-AUG-2018; 2018US-00054680.
XX
PR 03-AUG-2017; 2017US-0541019P.
PR 27-FEB-2018; 2018US-0636095P.
XX
CC PA (ALEC-) ALECTOR LLC.
XX
CC PI Schwabe T, Brown E, Kong P, Tassi I, Lee S, Rosenthal A;
CC PI Pejchal R, Nielson NP;
XX
DR WPI; 2019-13815K/17.
XX
CC PT New antibody useful in pharmaceutical composition for preventing,
CC PT reducing risk, or treating individual having disease, disorder or injury
CC PT including dementia, frontotemporal dementia, Alzheimer's disease,
CC PT cognitive deficit and memory loss.
XX
CC PS Claim 13; SEQ ID NO 214; 264pp; English.
XX
CC The present invention relates to a novel anti-triggering receptor
CC expressed on myeloid cells-2 (TREM2) antibody useful for preparing a
CC pharmaceutical composition. The pharmaceutical composition is used for
CC preventing, reducing risk or treating individual having disease, disorder
CC or injury includes dementia, frontotemporal dementia, Alzheimer's
CC disease, Nasu-Hakola disease, cognitive deficit, memory loss, spinal cord
CC injury, traumatic brain injury, multiple sclerosis, chronic colitis,
CC ulcerative colitis and cancer. The invention further provides: a nucleic
CC acid sequence encoding the antibody; a vector comprising the nucleic acid
CC ; an isolated host cell comprising the vector; a method of producing the
CC antibody that binds to TREM2; and an antibody comprising fragment
CC crystallizable (Fc) region. The present sequence represents a anti-TREM2
CC antibody light chain region (LC) comprising a mutant human immunoglobulin
CC gamma 1 (huIgG1 PSEG) P331S/E430G, which is used in the invention for
CC treating the above mentioned diseases.
XX
SQ Sequence 219 AA;
Query Match 100.0%; Score 1137; Length 219;
Best Local Similarity 100.0%;
Matches 219; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 DVVMTQSPDSLAVSLGERATINCRSSQSLVHSNRYTYLHWYQQKPGQSPKLLIYKVSNRF 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DVVMTQSPDSLAVSLGERATINCRSSQSLVHSNRYTYLHWYQQKPGQSPKLLIYKVSNRF 60
Qy 61 SGVPDRFSGSGSGTDFTLKISRVEAEDVGVYYCSQSTRVPYTFGQGTKLEIKRTVAAPSV 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 SGVPDRFSGSGSGTDFTLKISRVEAEDVGVYYCSQSTRVPYTFGQGTKLEIKRTVAAPSV 120
Qy 121 FIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSL 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 121 FIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSL 180
Qy 181 SSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC 219
|||||||||||||||||||||||||||||||||||||||
Db 181 SSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC 219
US17/782127 (US20230024528) (under the ODP rejection) teaches a method of treating injury and demyelination in demyelination diseases in the CNS including MS using the claimed anti-TREM2 agonist antibody (see the sequence alignment below).
SEQ ID NO:44
Sequence 44, US/17782127
Publication No. US20230024528A1
GENERAL INFORMATION
APPLICANT: ALECTOR LLC
TITLE OF INVENTION: METHODS OF USE OF ANTI-TREM2 ANTIBODIES
FILE REFERENCE: 73502-20032.00
CURRENT APPLICATION NUMBER: US/17/782,127
CURRENT FILING DATE: 2022-06-02
PRIOR APPLICATION NUMBER: PCT/US2020/063339
PRIOR FILING DATE: 2020-12-04
PRIOR APPLICATION NUMBER: US 63/005,110
PRIOR FILING DATE: 2020-04-03
PRIOR APPLICATION NUMBER: US 62/944,298
PRIOR FILING DATE: 2019-12-05
NUMBER OF SEQ ID NOS: 145
SEQ ID NO 44
LENGTH: 452
TYPE: PRT
ORGANISM: Artificial Sequence
FEATURE:
OTHER INFORMATION: Synthetic Construct
Query Match 100.0%; Score 2407; Length 452;
Best Local Similarity 100.0%;
Matches 452; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 QVQLVQSGAEVKKPGASVKVSCKASGYAFSSQWMNWVRQAPGQRLEWIGRIYPGGGDTNY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 QVQLVQSGAEVKKPGASVKVSCKASGYAFSSQWMNWVRQAPGQRLEWIGRIYPGGGDTNY 60
Qy 61 AGKFQGRVTITADTSASTAYMELSSLRSEDTAVYYCARLLRNQPGESYAMDYWGQGTLVT 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 AGKFQGRVTITADTSASTAYMELSSLRSEDTAVYYCARLLRNQPGESYAMDYWGQGTLVT 120
Qy 121 VSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVL 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 121 VSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVL 180
Qy 181 QSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPEL 240
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 181 QSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPEL 240
Qy 241 LGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREE 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 241 LGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREE 300
Qy 301 QYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPS 360
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 301 QYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPS 360
Qy 361 RDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDK 420
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 361 RDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDK 420
Qy 421 SRWQQGNVFSCSVMHGALHNHYTQKSLSLSPG 452
||||||||||||||||||||||||||||||||
Db 421 SRWQQGNVFSCSVMHGALHNHYTQKSLSLSPG 452
SEQ ID NO:47
Sequence 47, US/17782127
Publication No. US20230024528A1
GENERAL INFORMATION
APPLICANT: ALECTOR LLC
TITLE OF INVENTION: METHODS OF USE OF ANTI-TREM2 ANTIBODIES
FILE REFERENCE: 73502-20032.00
CURRENT APPLICATION NUMBER: US/17/782,127
CURRENT FILING DATE: 2022-06-02
PRIOR APPLICATION NUMBER: PCT/US2020/063339
PRIOR FILING DATE: 2020-12-04
PRIOR APPLICATION NUMBER: US 63/005,110
PRIOR FILING DATE: 2020-04-03
PRIOR APPLICATION NUMBER: US 62/944,298
PRIOR FILING DATE: 2019-12-05
NUMBER OF SEQ ID NOS: 145
SEQ ID NO 47
LENGTH: 219
TYPE: PRT
ORGANISM: Artificial Sequence
FEATURE:
OTHER INFORMATION: Synthetic Construct
Query Match 100.0%; Score 1137; Length 219;
Best Local Similarity 100.0%;
Matches 219; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 DVVMTQSPDSLAVSLGERATINCRSSQSLVHSNRYTYLHWYQQKPGQSPKLLIYKVSNRF 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DVVMTQSPDSLAVSLGERATINCRSSQSLVHSNRYTYLHWYQQKPGQSPKLLIYKVSNRF 60
Qy 61 SGVPDRFSGSGSGTDFTLKISRVEAEDVGVYYCSQSTRVPYTFGQGTKLEIKRTVAAPSV 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 SGVPDRFSGSGSGTDFTLKISRVEAEDVGVYYCSQSTRVPYTFGQGTKLEIKRTVAAPSV 120
Qy 121 FIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSL 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 121 FIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSL 180
Qy 181 SSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC 219
|||||||||||||||||||||||||||||||||||||||
Db 181 SSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC 219
US17/916728 (US20230183341) (under the ODP rejection) teaches a method of treating injury and demyelination in demyelination diseases in the CNS including MS using the claimed anti-TREM2 agonist antibody (see the sequence alignment below).
SEQ ID NO:44
Sequence 44, US/17916728
Publication No. US20230183341A1
GENERAL INFORMATION
APPLICANT: ALECTOR LLC
TITLE OF INVENTION: METHODS OF USE OF ANTI-TREM2 ANTIBODIES
FILE REFERENCE: 73502-20035.00
CURRENT APPLICATION NUMBER: US/17/916,728
CURRENT FILING DATE: 2022-10-03
PRIOR APPLICATION NUMBER: PCT/US2021/025626
PRIOR FILING DATE: 2021-04-02
PRIOR APPLICATION NUMBER: US 63/079,810
PRIOR FILING DATE: 2020-09-17
PRIOR APPLICATION NUMBER: US 63/005,130
PRIOR FILING DATE: 2020-04-03
NUMBER OF SEQ ID NOS: 145
SEQ ID NO 44
LENGTH: 452
TYPE: PRT
ORGANISM: Artificial Sequence
FEATURE:
OTHER INFORMATION: Synthetic Construct
Query Match 100.0%; Score 2407; Length 452;
Best Local Similarity 100.0%;
Matches 452; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 QVQLVQSGAEVKKPGASVKVSCKASGYAFSSQWMNWVRQAPGQRLEWIGRIYPGGGDTNY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 QVQLVQSGAEVKKPGASVKVSCKASGYAFSSQWMNWVRQAPGQRLEWIGRIYPGGGDTNY 60
Qy 61 AGKFQGRVTITADTSASTAYMELSSLRSEDTAVYYCARLLRNQPGESYAMDYWGQGTLVT 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 AGKFQGRVTITADTSASTAYMELSSLRSEDTAVYYCARLLRNQPGESYAMDYWGQGTLVT 120
Qy 121 VSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVL 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 121 VSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVL 180
Qy 181 QSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPEL 240
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 181 QSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPEL 240
Qy 241 LGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREE 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 241 LGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREE 300
Qy 301 QYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPS 360
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 301 QYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPS 360
Qy 361 RDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDK 420
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 361 RDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDK 420
Qy 421 SRWQQGNVFSCSVMHGALHNHYTQKSLSLSPG 452
||||||||||||||||||||||||||||||||
Db 421 SRWQQGNVFSCSVMHGALHNHYTQKSLSLSPG 452
SEQ ID NO:47
Sequence 47, US/17916728
Publication No. US20230183341A1
GENERAL INFORMATION
APPLICANT: ALECTOR LLC
TITLE OF INVENTION: METHODS OF USE OF ANTI-TREM2 ANTIBODIES
FILE REFERENCE: 73502-20035.00
CURRENT APPLICATION NUMBER: US/17/916,728
CURRENT FILING DATE: 2022-10-03
PRIOR APPLICATION NUMBER: PCT/US2021/025626
PRIOR FILING DATE: 2021-04-02
PRIOR APPLICATION NUMBER: US 63/079,810
PRIOR FILING DATE: 2020-09-17
PRIOR APPLICATION NUMBER: US 63/005,130
PRIOR FILING DATE: 2020-04-03
NUMBER OF SEQ ID NOS: 145
SEQ ID NO 47
LENGTH: 219
TYPE: PRT
ORGANISM: Artificial Sequence
FEATURE:
OTHER INFORMATION: Synthetic Construct
Query Match 100.0%; Score 1137; Length 219;
Best Local Similarity 100.0%;
Matches 219; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 DVVMTQSPDSLAVSLGERATINCRSSQSLVHSNRYTYLHWYQQKPGQSPKLLIYKVSNRF 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DVVMTQSPDSLAVSLGERATINCRSSQSLVHSNRYTYLHWYQQKPGQSPKLLIYKVSNRF 60
Qy 61 SGVPDRFSGSGSGTDFTLKISRVEAEDVGVYYCSQSTRVPYTFGQGTKLEIKRTVAAPSV 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 SGVPDRFSGSGSGTDFTLKISRVEAEDVGVYYCSQSTRVPYTFGQGTKLEIKRTVAAPSV 120
Qy 121 FIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSL 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 121 FIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSL 180
Qy 181 SSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC 219
|||||||||||||||||||||||||||||||||||||||
Db 181 SSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC 219
US18/806118 (US20250084165) (under the ODP rejection) teaches a method of treating injury and demyelination in demyelination diseases in the CNS including MS using the claimed anti-TREM2 agonist antibody (see the sequence alignment below).
SEQ ID NO:44
Sequence 44, US/18806118
Publication No. US20250084165A1
GENERAL INFORMATION
APPLICANT: ALECTOR LLC (en)
TITLE OF INVENTION: METHODS OF USE OF ANTI-TREM2 ANTIBODIES (en)
FILE REFERENCE: 73502-20041.01
CURRENT APPLICATION NUMBER: US/18/806,118
CURRENT FILING DATE: 2024-08-15
NUMBER OF SEQ ID NOS: 180
SEQ ID NO 44
LENGTH: 452
TYPE: PRT
FEATURE:
NAME/KEY: REGION
LOCATION: 1..452
QUALIFIERS: note = Synthetic Construct
FEATURE:
NAME/KEY: source
LOCATION: 1..452
QUALIFIERS: mol_type = protein
organism = synthetic construct
Query Match 100.0%; Score 2407; Length 452;
Best Local Similarity 100.0%;
Matches 452; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 QVQLVQSGAEVKKPGASVKVSCKASGYAFSSQWMNWVRQAPGQRLEWIGRIYPGGGDTNY 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 QVQLVQSGAEVKKPGASVKVSCKASGYAFSSQWMNWVRQAPGQRLEWIGRIYPGGGDTNY 60
Qy 61 AGKFQGRVTITADTSASTAYMELSSLRSEDTAVYYCARLLRNQPGESYAMDYWGQGTLVT 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 AGKFQGRVTITADTSASTAYMELSSLRSEDTAVYYCARLLRNQPGESYAMDYWGQGTLVT 120
Qy 121 VSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVL 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 121 VSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVL 180
Qy 181 QSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPEL 240
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 181 QSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPEL 240
Qy 241 LGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREE 300
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 241 LGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREE 300
Qy 301 QYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPS 360
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 301 QYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPS 360
Qy 361 RDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDK 420
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 361 RDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDK 420
Qy 421 SRWQQGNVFSCSVMHGALHNHYTQKSLSLSPG 452
||||||||||||||||||||||||||||||||
Db 421 SRWQQGNVFSCSVMHGALHNHYTQKSLSLSPG 452
SEQ ID NO:47
Sequence 47, US/18806118
Publication No. US20250084165A1
GENERAL INFORMATION
APPLICANT: ALECTOR LLC (en)
TITLE OF INVENTION: METHODS OF USE OF ANTI-TREM2 ANTIBODIES (en)
FILE REFERENCE: 73502-20041.01
CURRENT APPLICATION NUMBER: US/18/806,118
CURRENT FILING DATE: 2024-08-15
NUMBER OF SEQ ID NOS: 180
SEQ ID NO 47
LENGTH: 219
TYPE: PRT
FEATURE:
NAME/KEY: REGION
LOCATION: 1..219
QUALIFIERS: note = Synthetic Construct
FEATURE:
NAME/KEY: source
LOCATION: 1..219
QUALIFIERS: mol_type = protein
organism = synthetic construct
Query Match 100.0%; Score 1137; Length 219;
Best Local Similarity 100.0%;
Matches 219; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 DVVMTQSPDSLAVSLGERATINCRSSQSLVHSNRYTYLHWYQQKPGQSPKLLIYKVSNRF 60
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 DVVMTQSPDSLAVSLGERATINCRSSQSLVHSNRYTYLHWYQQKPGQSPKLLIYKVSNRF 60
Qy 61 SGVPDRFSGSGSGTDFTLKISRVEAEDVGVYYCSQSTRVPYTFGQGTKLEIKRTVAAPSV 120
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 SGVPDRFSGSGSGTDFTLKISRVEAEDVGVYYCSQSTRVPYTFGQGTKLEIKRTVAAPSV 120
Qy 121 FIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSL 180
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 121 FIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSL 180
Qy 181 SSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC 219
|||||||||||||||||||||||||||||||||||||||
Db 181 SSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC 219
12. 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.
13. 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 on Monday-Thursday, 7:00am-5:30pm 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 on 571-272-0911. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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Chang-Yu Wang
January 10, 2026
/CHANG-YU WANG/Primary Examiner, Art Unit 1675