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
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on April 14, 2026 has been entered.
RESPONSE TO AMENDMENT
Status of Application/Amendments/claims
3. Applicant’s amendment filed April 14, 2026 is acknowledged. Claims 1-2, 5, 7, 9, 12, 14, 16, 18-21, 23-24, 30, 32, 34 and 39 are canceled. Claims 3 and 10 are amended. Claims 3-4, 6, 8, 10-11, 13, 15, 17, 22, 25-29, 31, 33, 35-38 and 40 are pending in this application. Election was made without traverse in the reply filed on August 18, 2025.
4. Claims 3-4, 6, 8, 10-11, 13, 15, 17, 22, 25-29, 31, 33, 35-38 and 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.
5. Applicant’s arguments filed on April 14, 2026 have been fully considered but they are not deemed to be persuasive for the reasons set forth below.
Claim Rejections/Objections Withdrawn
6. 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31, 33 and 35-40 under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, lack of scope of enablement is withdrawn in response to Applicant’s amendment to the claims and cancelation of claims 9 and 39.
The rejection of claims 9 and 39 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) is moot because the claims are canceled.
Claim Rejections/Objections Maintained
In view of the amendment filed on April 14, 2026, the following rejections are maintained.
Claim Rejections - 35 USC § 102
7. 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, 10-11, 13, 15, 17, 22, 25-29, 31, 33, 35-38 and 40 stand rejected under 35 U.S.C. 102(a)(1) and (a)(2) as being anticipated by Schwabe et al. (US20190040130) as evidenced by Kale (Eye and Brain 2016; 8:195-202), 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, 10-11, 13, 15, 17, 22, 25-29, 31, 33, 35-38 and 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, wherein the antibody promotes recruitment of oligodendrocyte precursor cells (OPCs) to one or more demyelination lesions in the CNS of the individual, and wherein the CNS demyelination disease includes optic neuritis, neuromyelitis optica (Devic’s disease) and other diseases recited in claim 3.
Response to Arguments
On p. 10-11 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, wherein the CNS demyelination disease includes optic neuritis, neuromyelitis optica (Devic’s disease) and other diseases recited in amended claim 3. ii) 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 does teach optic neuritis (see [0441]) because patients with multiple sclerosis accompanied with optic neuritis and also evidenced by Kale (see p. 195-197; Eye and Brain 2016; 8:195-202).
ii. 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 with optic neuritis, 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/optic neuritis 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 35-38 and 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 as in claims 36-37, 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 claim 38 (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/optic neuritis 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/optic neuritis 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” recited in claim 1, “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 10-11, 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 10-11, 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, 10-11, 13, 15, 17, 22, 25-29, 31, 33, 35-38 and 40 are anticipated by Schwabe et al. (US2019040130) as evidenced by Piccio and Ozturk.
Accordingly, the rejection of claims 3-4, 6, 8, 10-11, 13, 15, 17, 22, 25-29, 31, 33, 35-38 and 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, 10-11, 13, 15, 17, 22, 25-29, 31, 33, 35-38 and 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 and 41 of copending Application No. 17782127, or 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 in view of Schwabe et al. (US20190040130) and evidentiary references: Kale (2016), Piccio (2008) and Ozturk (2010) . The rejection is maintained for the reasons of record and the reasons set forth below.
Response to Arguments
On p. 11 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 No. 17916728 anticipates instant claims because the claims of the Application 17916728 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 CSF1R-deficient disease recited in copending Application No. 17782127 includes adult and pediatric leukoencephalopathy and the disease recited in copending application No. 17916728 incudes multiple sclerosis/optic neuritis), 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, 10-11, 13, 15, 17, 22, 25-29, 31, 33, 35-38 and 40 of the instant Application are not patentably distinct from claims 1-11, 15-17, 19, 21, 23, 25-31, 35 and 41 of the ‘127 Application or 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 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 and 41 of the ‘127 Application or 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.
Accordingly, the rejection of claims 3-4, 6, 8, 10-11, 13, 15, 17, 22, 25-29, 31, 33, 35-38 and 40 on the ground of nonstatutory double patenting as being unpatentable over claims 1-11, 15-17, 19, 21, 23, 25-31, 35 and 41 of copending Application No. 17782127, or 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 in view of Schwabe et al. (US20190040130) and evidentiary references: Piccio (2008) and Ozturk (2010) is maintained.
New Grounds of Rejection Necessitated by the Amendment
The following rejections are new grounds of rejections necessitated by the amendment filed on April 14, 2026.
Claim Rejections - 35 USC § 112
10. Claims 4, 17 and 33 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.
To provide adequate written description and evidence of possession of a claimed genus, the specification must provide sufficient distinguishing identifying characteristics of the genus. The factors to be considered include disclosure of complete or partial structure, physical and/or chemical properties, functional characteristics, structure/function correlation, methods of making the claimed product, or any combination thereof.
Claims 4, 17 and 33 encompass using a genus of anti-TREM2 agonist antibodies binding to a genus of TREM2 variants, a genus of anti-TREM2 bispecific agonist antibodies, a genus of anti-TREM2 multivalent agonist antibodies for promoting remyelination of one or more demyelination lesions in the CNS of an individual having a CNS demyelination disease including optic neuritis, neuromyelitis optica (Devic’s disease) and other diseases recited in claim 3.
Applicant has not disclosed sufficient species for using the broad genus of anti-TREM2 agonist antibodies, the broad genus of bispecific anti-TREM2 agonist antibodies and multivalent anti-TREM2 agonist antibodies, the broad genus of anti-TREM2 agonist antibodies binding to aa 149-157 of SEQ ID NO:1, variants of TREM2, or one more amino acids recited in claim 20 or 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 for treating the broad genus of CNS demyelination diseases.
The specification only describes administration of anti-TREM2 7E5 antibody (SEQ ID NOs: 50 and 51 for VL and VH) to Trem2+/- mice with CPZ-induced demyelination results in 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, increasing differentiation of OPC into mature oligodendrocytes, and increasing SMI-31 expression in the Trem2+/- mice with CPZ-induced demyelination as compared to an isotype control antibody.
In making a determination of whether the application complies with the written description requirement of 35 U.S.C. 112, first paragraph, it is necessary to understand what Applicant is in possession of and what Applicant is claiming.
M.P.E.P. § 2163 instructs:
An invention described solely in terms of a method of making and/or its function may lack written descriptive support where there is no described or art-recognized correlation between the disclosed function and the structure(s) responsible for the function. . . .
An applicant may show possession of an invention by disclosure of drawings or structural chemical formulas that are sufficiently detailed to show that applicant was in possession of the claimed invention as a whole. . . .
An applicant may also show that an invention is complete by disclosure of sufficiently detailed, relevant identifying characteristics which provide evidence that applicant was in possession of the claimed invention, i.e., complete or partial structure, other physical and/or chemical properties, functional characteristics when coupled with a known or disclosed correlation between function and structure, or some combination of such characteristics.”
This standard has not been met in this case. From the specification, Applicant is in possession of using anti-TREM2 7E5 antibody (SEQ ID NOs: 50 and 51 for VL and VH) in 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, increasing differentiation of OPC into mature oligodendrocytes, and increasing SMI-31 expression in the Trem2+/- mice with CPZ-induced demyelination as compared to an isotype control antibody.
However, Applicant is not in possession of using other structurally and functionally undefined anti-TREM2 agonist antibodies binding to a genus of TREM2 variants, a genus of anti-TREM2 bispecific agonist antibodies, a genus of anti-TREM2 multivalent agonist antibodies for promoting remyelination of one or more demyelination lesions in the CNS of an individual having a CNS demyelination disease including optic neuritis, neuromyelitis optica (Devic’s disease) and other diseases recited in claim 3.
The specification provides no identification of any particular portion of the structure that must be conserved. The instant specification fails to provide sufficient descriptive information, such as definitive structural or functional features of the claimed genus of anti-TREM2 agonist antibodies binding to a genus of TREM2 variants, the genus of anti-TREM2 bispecific agonist antibodies, the genus of anti-TREM2 multivalent agonist antibodies for promoting remyelination of one or more demyelination lesions in the CNS of an individual having a CNS demyelination disease including optic neuritis, neuromyelitis optica (Devic’s disease) and other diseases recited in claim 3.
There is no description of the conserved regions which are critical to the function of the genus claimed. There is no description of the sites at which variability may be tolerated and there is no information regarding the relation of structure of other anti-TREM2 agonist antibodies binding to a genus of TREM2 variants, other anti-TREM2 bispecific agonist antibodies, other anti-TREM2 multivalent agonist antibodies for promoting remyelination of one or more demyelination lesions in the CNS of an individual having a CNS demyelination disease including optic neuritis, neuromyelitis optica (Devic’s disease) and other diseases recited in claim 3 or in 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, increasing differentiation of OPC into mature oligodendrocytes, and increasing SMI-31 expression in the Trem2+/- mice with CPZ-induced demyelination or even in treating a CNS demyelination disease.
Furthermore, the prior art does not provide compensatory structural or correlative teachings sufficient to enable one of skill to identify what other anti-TREM2 agonist antibodies binding to a genus of TREM2 variants, other anti-TREM2 bispecific agonist antibodies, other anti-TREM2 multivalent agonist antibodies might be. Since the common characteristics/features of other anti-TREM2 agonist antibodies binding to a genus of TREM2 variants, other anti-TREM2 bispecific agonist antibodies, other anti-TREM2 multivalent agonist antibodies 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-TREM2 agonist antibodies binding to a genus of TREM2 variants, other anti-TREM2 bispecific agonist antibodies, other anti-TREM2 multivalent agonist antibodies for treating the genus of CNS demyelination diseases.
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-TREM2 agonist antibodies binding to a genus of TREM2 variants, the genus of anti-TREM2 bispecific agonist antibodies, the genus of anti-TREM2 multivalent agonist antibodies for treating the genus of CNS demyelination diseases, 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.
Therefore, the claimed methods have 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.
Conclusion
11. NO CLAIM IS ALLOWED.
12. 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
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 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
June 27, 2026
/CHANG-YU WANG/Primary Examiner, Art Unit 1675
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