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. Election/Restrictions Applicant’s election without traverse of the invention of Group I, drawn to a conjugate comprising an anti-transferrin receptor ( TfR ) VHH molecule in the reply filed on 12/05/2025 is acknowledged. Applicant further elect a conjugate comprising 1) the VHH clone B8V32 having the CDRs of SEQ ID NOs: 674, 6, and 7 and reportedly present in the SEQ ID NOs: 578, 682, 684, and 703, 2) a nucleic acid such as siRNA as the therapeutic compound, and 3) an antibody or fragment of an antibody, provisionally Fc fragments. The elected anti- TfR VHH molecule was found to be free of the prior art; therefore, the Election of Species requirement for the anti- TfR VHH species has been withdrawn. In particular, the search was expanded to include VHH molecules comprising the CDR combinations specifically recited in claim 2. The VHH chains defined by the CDR combinations recited in claim 2 have been found to be free of the prior art. Accordingly, the full-length VHH chains recited in claims 3-8 comprising any of the CDR combinations recited in claim 2 are also free of the prior art. In the interest of compact prosecution, the Restriction Requirement between the inventions of Groups I and II (method of treating) has also been withdrawn. Claims 1 -20 and 22 are examined on the merits in the present Office Action. Claim Rejections - 35 USC § 112 The following is a quotation of the first paragraph of 35 U.S.C. 112(a): (a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention. The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112: The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention. Written Description Claims 1 , 7, 9- 20, and 22 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention. C laim 1 allows the CDRs of different anti- transferrin receptor ( TfR ) VHH clones and variants thereof to be interchanged , yet there is no evidence that CDRs from structurally distinct VHH clones can be interchanged without negatively impacting binding affinity as it does not appear that each clone is a variant/mutant of a single starting clone. Further, there is no guidance provided in the specification regarding how CDRs from different VHH clones can be interchanged such that binding to transferring receptor is maintained. Claims 7, 9-18 and 22 incorporate limitations of claim 1 but do not cure the deficiencies of claim 1 and thus are also rejected. The guidelines for the Examination of Patent Applications Under the 35 U.S.C. 112, § 1 "Written Description" Requirement make clear that if a claimed genus does not show actual reduction to practice for a representative number of species, then the Requirement may be alternatively met by reduction to drawings, or by disclosure of relevant, identifying characteristics, i.e., structure or other physical and or chemical properties, by functional characteristics coupled with a known or disclosed correlation between function and structure, or by a combination of such identifying characteristics, sufficient to show the applicant was in possession of the genus ( MPEP 2163). In The Regents of the University of California v. Eli Lilly (43 USPQ2d 1398-1412) 19 F. 3d 1559, the court held that disclosure of a single member of a genus (rat insulin) did not provide adequate written support for the claimed genus (all mammalian insulins). In this same case, the court also noted: “A definition by function, as we have previously indicated, does not suffice to define the genus because it is only an indication of what the gene does, rather than what it is. See Fiers , 984 F.2d at 1169-71, 25 USPQ2d at 1605-06 (discussing Amgen). It is only a definition of a useful result rather than a definition of what achieves that result. Many such genes may achieve that result. The description requirement of the patent statute requires a description of an invention, not an indication of a result that one might achieve if one made that invention. See In re Wilder, 736 F.2d 1516, 1521, 222 USPQ 369, 372-73 (Fed. Cir. 1984) (affirming rejection because the specification does “little more than outlin [e] goals appellants hope the claimed invention achieves and the problems the invention will hopefully ameliorate."). Accordingly, naming a type of material generally known to exist, in the absence of knowledge as to what that material consists of, is not a description of that material.” The court has further stated that “Adequate written description requires a precise definition, such as by structure, formula, chemical name or physical properties, not a mere wish or plan for obtaining the claimed chemical invention.” Id. at 1566, 43 USPQ2d at 1404 (quoting at 1171, 25 USPQ2d at 1606). Also see (CAFC 2002). Enzo- Biochem v. Gen-Probe Fiers , 984 F.2d 01-1230. Claim 1 is broadly drawn to a conjugate compound comprising one or more VHH molecules and at least one therapeutic compound or vehicle comprising such a therapeutic compound, wherein the CDR from multiple structurally distinct VHH clones can be interchanged. Thus, the claim encompasses numerous possible CDR combinations beyond the specific parental clones and variants disclosed in the specification. The specification describes the generation of VHH antibodies through extensive screening and optimization. A llama-derived VHH library was constructed and more than 2,000 clones were screened for TfR binding, with approximately 450 clones selected for further sequencing and comparison. Additional variants were generated through site-directed mutagenesis, CDR substitutions, humanization strategies, and deep mutational scanning, followed by further rounds of screening. With additional library screening rounds, hundreds of more clones were evaluated to identify antibodies with suitable binding and functional properties (Example III) . While the specification discloses numerous sequences of different VHH clones and variants thereof that target transferrin receptor, the specification does not demonstrate or provide evidence CDRs from different VHH clones can be interchanged with each other without substantially impacting the ability of the resulting VHH antibody to bind to transferrin receptor as it does not appear that each clone are variants/mutants of a single starting clone. Nor does the specification provide any guidance for predicting which CDR combinations from different VHH clones would be operable across the claim scope. Without further guidance , artisans could not readily determine which CDRs of different anti- TfR VHH clones and variants thereof can be interchanged such that binding affinity for transferrin receptor is maintained . Additionally, given the number of CDR combinations possible, claim 1 encompass es anti- Tfr VHH molecules. not presently disclosed in specification; and there is no evidence provided in the specification of other nanobodies comprising CDR combinations not presently disclosed but encompassed by the claims that have the functional property of binding to transferrin receptor . Claims 7, 9- 20 , and 22 incorporate limitations of claim 1 but do not cure the deficiencies of claim 1 and thus are also rejected. Therefore, the claimed genus of anti- TfR VHH antibodies lacks adequate written description because there does not appear to be any correlation between the structure of the claimed VHH antibodies and the function of binding to transferrin receptor. Thus, one of ordinary skill in the art would reasonably conclude that the applicant was not in possession of the full breadth of the claimed genus of anti- TfR VHH antibodies at the time the instant application was filed. Scope of Enablement Claims 1 , 7, 9- 20 , and 22 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 VHH molecules with compatible CDRs derived from their respective parental clones (or variants thereof) and therapeutic compounds/vehicles comprising said therapeutic compounds suitable for CNS treatment, does not reasonably provide enablement VHH molecules formed by interchanging CDRs from different VHH clones or conjugates comprising any therapeutic compound including those not suitable for treating CNS disease. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make or use the invention commensurate in scope with these claims. The nature of the invention relates to VHH (single-domain antibody) molecules that bind both human and non-human transferrin receptor ( TfR ) and undergo receptor-mediated transcytosis to deliver conjugated drugs or imaging agents across the blood brain barrier (BBB) into the central nervous system (CNS) in vivo, thereby providing a platform for CNS-targeted therapies (see Summary of Invention, Page 3 of Specification). Claim 1 is broadly drawn to a conjugate compound comprising one or more VHH molecules and at least one therapeutic compound or vehicle comprising such a therapeutic compound, wherein the CDR from multiple structurally distinct VHH clones can be interchanged. Thus, the claim encompasses numerous possible CDR combinations beyond the specific parental clones and variants disclosed in the specification. The specification describes the generation of VHH antibodies through extensive screening and optimization. A llama-derived VHH library was constructed and more than 2,000 clones were screened for TfR binding, with approximately 450 clones selected for further sequencing and comparison. Additional variants were generated through site-directed mutagenesis, CDR substitutions, humanization strategies, and deep mutational scanning, followed by further rounds of screening. With additional library screening rounds , hundreds of more clones were evaluated to identify antibodies with suitable binding and functional properties (Example III). While the specification discloses numerous sequences of different VHH clones and variants thereof that target transferrin receptor, the specification does not demonstrate or provide evidence that CDRs from different VHH clones can be interchanged with each other without substantially impacting the ability of the resulting VHH antibody to bind to transferrin receptor as it does not appear that each clone are variants/mutants of a single starting clone. Nor does the specification provide any guidance for predicting which CDR combinations from different VHH clones would retain binding activity across the claim scope. It is well-known in the art that the CDR regions of a VHH antibody are primarily responsible for antigen binding and function together to form the binding site ( Hoey et al, 2 nd paragraph of Introduction) . The p rior ar t, however, did not establish that CDRs from structurally distinct VHH clones could be freely interchanged while retaining antigen binding in the absence of additional experimental testing to confirm that such modified antibodies r etained functional activity. Indeed, amino acid variation s in the CDRs of an antigen binding region can negatively impact binding activity (Piche-Nicholas et al, see in particular, Abstract) . As such, artisans would not be able to readily predict which CDRs of structurally distinct VHH clones can be interchanged such that the resulting VHH antibody retains the ability to bind to transferrin receptor. A person of ordinary skill in the art at the time of filing would have had experience in antibody engineering , including library construction, mutagenesis, and screening techniques . Even at this high level of skill, however, the effect of combining CDRs from different VHH clones on antigen binding could not have been readily predicted without additional testing . In Amgen Inc. v. Sanofi, Aventisub LLC, 987 F.3d 1080 (Fed. Cir. 2021), which the Supreme Court affirmed, the Federal Circuit relied on evidence showing that the scope of the claims encompassed millions of antibodies and that it was necessary to screen each candidate antibody in order to determine whether it met the functional limitations of the claim. Id. at 1088. Consequently, the Federal Circuit concluded that there was a lack of enablement (MPEP 2164.06). Thus, the level of skill does not obviate the need for substantial experimentation across the full scope of the claimed genus. Indeed, the inventor’s own disclosure demonstrates that identifying functional VHH antibodies required extensive screening and optimizat i on. In the absence of guidance regarding the interchangeability of CDRs across structurally distinct VHH clones, artisans would necessarily have to engage in undue trial-and-error experimentation to generate and test numerous CDR combinations encompassed by the claim scope to determine which retain binding to transferrin receptor. Claims 7, 9- 20 , and 22 incorporate limitations of claim 1 but do not cure the deficiencies of claim 1 and thus are also rejected. Claim 19 further recites a method of treating a CNS disease in a mammalian subject comprising administering the conjugate of claim 1. The conjugate of claim 1 encompass any therapeutic compound, including those that may have no relevance to treatment of a CNS disease. The specification describes the generation of several anti- TfR VHH-based conjugates to enhance BBB crossing and CNS delivery of therapeutic compounds. For example, anti- TfR VHH-13C3 antibody conjugates led to increased uptake of the murine monoclonal antibody 13C3, which targets amyloid-beta plaques ( Goure et al, see “ SAR228810 ” subsection on Page 9) (Example XIX). VHH-neurotensin (NT(8-13)) fusion proteins enabled CNS entry of the neuropeptide and induced pharmacologic hypothermia, confirming functional brain delivery (Example XXI). VHH-oligonucleotide conjugates also mediated TfR -dependent uptake, broad CNS biodistribution, and strong target gene (e.g. superoxide dismutase, SOD1) knockdown after administration (Examples XXIII – XXXI) . However, the specification does not demonstrate or provide guidance that conjugation of the recited VHH molecules to any therapeutic compound – particular those having no relevance to CNS disease—will result in a conjugate suitable for treating a CNS disorder. The prior art teaches numerous therapeutic compounds suitable for the treatment of CNS disorders, including monoclonal antibodies and protein-based therapies under investigation for brain cancer, lysosomal storage disorders, Alzheimer’s disease and other neurodegenerative disease (see, e.g. Zhao et al, in particular, “T argeting brain disorders by protein- and antibody-based therapeutics ” section and Table 1). Additionally, antisense oligonucleotides are promising therapeutics for various neurological disorders , resulting in RNA knockdown ( e.g. Bennett et al, see entire document, in particular Abstract). However, the prior art does not establish that merely attaching any therapeutic compound to an anti- TfR antibody guarantees therapeutic efficacy in treating a CNS disease. In particular, the art does not teach that compounds lacking relevance to CNS disease will treat a CNS disorder simply by conjugation to a n anti- TfR antibody . For example, artisans would not reasonably expect an anti-respiratory syncytial (RSV) antibody designed to prevent severe lower respiratory tract disease (Jones et al, see Summary) to be therapeutically beneficial in the treatment of a CNS disorder absent of any evidence provided by the specification or scientific literature. Given the diversity of possible therapeutic compounds encompassed by the claim –including compounds with no established CNS relevance –it is highly unpredictable whether such compounds would treat a CNS disorder upon conjugation , especially if not known in the art for doing so. A person of ordinary skill in the art at the time of filing would have had experience in the art of biologics and CNS drug deliver y . Even at this high level of skill, however, determining whether a given therapeutic compound – especially one not known in the art to be relevant to CNS disorders – can function to treat a CNS disease when targeted for delivery across the BBB would require extensive screening . Thus, without further guidance, artisans would have to engage in undue trial-and-error experimentation to determine which therapeutic compounds encompassed by the claim scope can be used to effectively treat a CNS disorder in a subject. Claim 20, which depends from claim 19, does not cure the deficiencies of claim 1 and is thus also rejected. Therefore, the specification is not enabling over the full scope of the claims. The following is a quotation of 35 U.S.C. 112(d): (d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers. The following is a quotation of pre-AIA 35 U.S.C. 112, fourth paragraph: Subject to the following paragraph [i.e., the fifth paragraph of pre-AIA 35 U.S.C. 112], a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers. Claim s 3- 6 and 8 are rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends. Claim 1 (independent claim) recites VHH chain(s) comprising three CDRs and expressly excludes VHH chains comprising specific CDR combinations (e.g. SEQ ID NOs: 1, 2, and 3 or SEQ ID NOs: 5, 6, and 7). C laims 3- 6 and 8 depend from claim 1 and recite full-length VHH amino acid sequences; however some of the full-length VHH sequences recited comprise the excluded CDR combinations. For example, the amino acid sequences of SEQ ID NOs: 273, 276-280, 423, 425, 430, 441, 443, 445, 447, 449, and 451 comprise the prohibited CDR combination of SEQ ID NOs: 5, 6, and 7. The amino acid sequences of SEQ ID NOs: 130-149, 250, and 252-271 comprise the prohibited CDR combination of SEQ ID NOs: 1, 2, and 3. The amino acid sequence of SEQ ID NOs: 250 and 274 comprise the prohibited CDR combination of SEQ ID NOs: 17, 73, and 3. Additionally, the VHH chain of SEQ ID NO: 275 as recited in claim 8 comprise the CDR combination of SEQ ID NOs: 1, 2, and 79; however, claim 1 does not recite that the VHH chain can possess a CDR3 having the amino acid sequence of SEQ ID NO: 79. As such, claims 3- 6 and 8 encompass embodiments that do not incorporate the limitations of claim 1. Accordingly, claims 3 -6 and 8 fail to further limit claim 1, but rather broadens the claim scope. Applicant is advised to review that all dependent claims directed to full-length VHH sequences to ensure they incorporate all limitations of their respective independent claims . While specific deficiencies have been noted, Applicant should verify the proper dependency of all claims. Applicant may cancel the claim(s), amend the claim(s) to place the claim(s) in proper dependent form, rewrite the claim(s) in independent form, or present a sufficient showing that the dependent claim(s) complies with the statutory requirements. Double Patenting The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg , 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman , 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi , 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum , 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel , 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington , 418 F.2d 528, 163 USPQ 644 (CCPA 1969). A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA. A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b). The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13. The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA/25, or PTO/AIA/26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer . Claims 1 -20 and 22 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 16-3 5 of copending Application No. 19495916 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because the co-pending claims either anticipate or are obvious variants over the instant claims. This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented. The co-pending claims recite a conjugate comprising ( i ) one or more VHH molecule(s) of formula FR1-CDR1-FR2-CDR2-FR3-CDR3-FR4, and (ii) at least one therapeutic compound or vehicle comprising said therapeutic compound, wherein said VHH molecule binds at the surface of a cell of the nervous system (e.g. a brain or spinal cord cell) with an affinity of 0.1 nM to 2500 nM and comprises the CDR combinations recited in instant claims 1 and 2 (co-pending claims 16, 24, 25, and 26). A conjugate compound would necessarily comprise a covalent/noncovalent bond or linker between the components of the conjugate. The VHH molecule can comprise i ) an amino acid sequence selected from SEQ ID NOs: 678, 682, 694, 703, 273, 276-284, 412, 415, 418, 421, 423, 425, 428, 430, 433, 436, 439, 441,443,445, 447,449,451,454, 457, 677, 702 (corresponding to respective SEQ ID NOs: recited in instant claim 3) (co-pending claim 17); ii) an amino acid sequence selected from SEQ ID NOs: 242-271, 274, 275, 675, 676, and 701 (corresponding to respective SEQ ID NOs in instant claim 4) (co-pending claim 18); iii) an amino acid sequence selected from SEQ ID NOs: 285-299 (corresponding to SEQ ID NOs of instant claim 5) (co-pending claim 19); iv) an amino acid sequence selected from SEQ ID NOs: 613-615 (corresponding to respective SEQ ID NOs: recited in instant claim 6) (co-pending claim 20); or v) an amino acid sequence selected from SEQ ID NOs: 252-271, and 273-275 (corresponding to respective SEQ ID NOs recited in instant claim 8 (co-pending claims 17 and 18). The VHH molecule further comprises a tag and/or linker (co-pending claim 21). The VHH molecule can be humanized (co-pending claim 22) and bind to human, non-human, and/or rodent transferrin receptor ( TfR ) (co-pending claim 23). The therapeutic compound can be a peptide, polypeptide, protein, antibody, or nucleic acid (co-pending claim 27). The nucleic acid is mRNA, a ribozyme, or an oligonucleotide selected from single stranded/double stranded siRNA, saRNA , gapmer , antisense oligonucleotide, shRNA, miRNA, aptamer RNA, or bridged nucleic acid (co-pending claim 28). The conjugate can further comprise at least one additional compound selected from a half-life extending moiety, stabilizing group, or scaffold (co-pending claim 2 9 ). The half-life extending moiety, stabilizing group, or scaffold is an antibody, VHH molecule, PEG, serum albumin protein, serum albumin binding moiety, Fc fragment, or Fc heterodimer comprising a modified Fc having the sequence of SEQ ID NO: 664 on the knob arm, or a modified Fc having a sequence of SEQ ID NO: 665 on the hole arm (co-pending claim 30). The amino acid sequences of SEQ ID NOs: 664 and 665 correspond to SEQ ID NOs 664 and 665 of the instant claims . Further recited is a pharmaceutical composition comprising the conjugate compound and a pharmaceutically acceptable support, carrier, or excipient (co-pending claim 31 ) as well as a method for treating a nervous system disease, including those specifically recited in instant claim 22 (co-pending claims 31, 32, 34, and 35). Thus, the co-pending claims meet the limitations of instant claims 1-20 and 22. Claim s 1-20, and 22 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 16-34 of copending Application No. 19495834 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because the co-pending claims either anticipate or are obvious variants over the instant claims. This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented. The co-pending claims recite a conjugate comprising ( i ) one or more VHH molecule(s) of formula FR1-CDR1-FR2-CDR2-FR3-CDR3-FR4, and (ii) one or more oligonucleotide(s), wherein said VHH molecule binds human, non-human, and/or rodent transferrin receptor ( TfR ) at the surface of a muscle cell and comprises the CDR combinations recited in instant claim s 1 and 2 (co-pending claim s 16 and 23 ) . The minimal structure required for the VHH chains to bind to a cell of the CNS (e.g. brain or spinal cord cell) with an affinity of 0.1 nM to 2500 nM are the CDR recited in the instant claims. Thus, the VHH chains of the co-pending claims having the same structure (i.e. CDRs) also possess these functional properties. Further, a conjugate compound would necessarily comprise a covalent/noncovalent bond or linker between the components of the conjugate. The VHH molecule can comprise i ) an amino acid sequence selected from SEQ ID NOs : 678, 682, 694, 703, 273, 276-284, 412, 415, 418, 421, 423, 425, 428, 430, 433, 436, 439, 441,443,445, 447,449,451,454, 457, 677, 702 (corresponding to respective SEQ ID NOs: recited in instant claim 3) (co-pending claim 17); ii) an amino acid sequence selected from SEQ ID NOs: 242-271, 274, 275, 675, 676, and 701 (corresponding to respective SEQ ID NOs in instant claim 4) (co-pending claim 18) ; iii) an amino acid sequence selected from SEQ ID NOs: 285-299 (corresponding to SEQ ID NOs of instant claim 5) (co-pending claim 19) ; iv) an amino acid sequence selected from SEQ ID NOs: 613-615 (corresponding to respective SEQ ID NOs: recited in instant claim 6) (co-pending claim 20) ; or v) an amino acid sequence selected from SEQ ID NOs : 252-271, and 273-275 (corresponding to respective SEQ ID NOs recited in instant claim 8 (co-pending claims 17 and 18). The VHH molecule further comprises a tag and/or linker (co-pending claim 21). The VHH molecule can be humanized (co-pending claim 22). The oligonucleotide is selected from a siRNA, saRNA , gapmer , antisense oligonucleotide (ASO), shRNA, miRNA, aptamer RNA, and bridged nucleic acid (BNA) (co-pending claim 24). The conjugate can further comprise at least one additional compound selected from a half-life extending moiety, stabilizing group, or scaffold (co-pending claim s 26 and 27 ). The half-life extending moiety, stabilizing group, or scaffold is an antibody, VHH molecule, PEG, serum albumin protein, serum albumin binding moiety, Fc fragment, or Fc heterodimer comprising a modified Fc having the sequence of SEQ ID NO: 664 on the knob arm, or a modified Fc having a sequence of SEQ ID NO: 665 on the hole arm. The amino acid sequences of SEQ ID NOs: 664 and 665 correspond to SEQ ID NOs 664 and 665 of the instant claims (co-pending claim 28). Further recited is a pharmaceutical composition comprising the conjugate compound and a pharmaceutically acceptable support, carrier, or excipient (co-pending claim 29) as well as a method for treating a muscular dystrophy such as ALS in a subject (co-pending claims 30, 33, and 34). Thus, the co-pending claims meet the limitations of instant claims 1 - 20, and 22. Conclusion No claims are allowable. Any inquiry concerning this communication or earlier communications from the examiner should be directed to FILLIN "Examiner name" \* MERGEFORMAT LIA TAYLOR whose telephone number is FILLIN "Phone number" \* MERGEFORMAT (571)272-6336 . The examiner can normally be reached FILLIN "Work Schedule?" \* MERGEFORMAT 8:30 - 5:00 M-F . Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. 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