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 .
1. Claims 18 – 37 are pending.
Election/Restrictions
2. Applicant's election with traverse of Group I (claims 18 – 24) in the reply filed on 10/31/2025 is acknowledged. The traversal is on the ground(s) that there would be no serious burden on the Office to search and examine all the claims together. This is not found persuasive because the claims are directed to distinct inventions (Groups I, II, III, IV, and V) that lack unity of invention because there is not a special technical feature that makes a contribution over the prior art as set forth in the Office Action dated 09/02/2025. Regarding “would be no serious burden”, the claims are directed to distinct inventions and each would require a different field of search.
The requirement is still deemed proper and is therefore made FINAL.
3. Claims 25 – 37 are withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to a nonelected invention, there being no allowable generic or linking claim. Applicant timely traversed the restriction (election) requirement in the reply filed on 10/31/2025. Claims 18 – 24 are under consideration.
Priority
4. This application claims priority to EP 20192113.7 filed on 08/21/2020.
Information Disclosure Statement
5. The information disclosure statement (IDS) submitted on 02/17/2023 is acknowledged. The submission is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
Drawings
6. Color photographs and color drawings are not accepted in utility applications unless a petition filed under 37 CFR 1.84(a)(2) is granted. Any such petition must be accompanied by the appropriate fee set forth in 37 CFR 1.17(h), one set of color drawings or color photographs, as appropriate, if submitted via the USPTO patent electronic filing system or three sets of color drawings or color photographs, as appropriate, if not submitted via the via USPTO patent electronic filing system, and, unless already present, an amendment to include the following language as the first paragraph of the brief description of the drawings section of the specification:
The patent or application file contains at least one drawing executed in color. Copies of this patent or patent application publication with color drawing(s) will be provided by the Office upon request and payment of the necessary fee.
Color photographs will be accepted if the conditions for accepting color drawings and black and white photographs have been satisfied. See 37 CFR 1.84(b)(2).
Specification
7. The use of the term Abcam, pcDNA, GeneArt, Qiagen, Invtrogen, Akta Pure, NuPage, HiLoad, Amicon, Octet Pellicon, Biomax, Millipore, Maxisorp, Magellan, Microsoft Excel, Tecan, Nunc, which is a trade name or a mark used in commerce, has been noted in this application. The term should be accompanied by the generic terminology; furthermore the term should be capitalized wherever it appears or, where appropriate, include a proper symbol indicating use in commerce such as ™, SM , or ® following the term.
Although the use of trade names and marks used in commerce (i.e., trademarks, service marks, certification marks, and collective marks) are permissible in patent applications, the proprietary nature of the marks should be respected and every effort made to prevent their use in any manner which might adversely affect their validity as commercial marks.
8. The disclosure is objected to because it contains an embedded hyperlink and/or other form of browser-executable code at page 5. Applicant is required to delete the embedded hyperlink and/or other form of browser-executable code; references to websites should be limited to the top-level domain name without any prefix such as http:// or other browser-executable code. See MPEP § 608.01.
Claim Objections
9. Claim 18 is objected to because of the following informalities: in line 2, “linked to a fragment of CD91” should read “linked to a nucleic acid sequence encoding a fragment of CD91” to clarify that the claimed nucleic acid encodes both a signal sequence and a CD91 fragment and not that the nucleic acid encoding a signal sequence is linked to an amino acid that is a fragment of CD91 and to provide antecedent basis for “the encoded fragment” of claims 19 – 21. Appropriate correction is required.
Claim Rejections - 35 USC § 112
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
10. Claims 18 – 24 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
11. Regarding claim 18, the metes and bounds of limitations “(ii)” and “(iii)” are unclear as the claim is drawn to a nucleic acid but the limitations refer to amino acid locations (“N-terminally” and “C-terminally”). Applicant’s specification defines “ligand binding domain” at page 10, lines 12 – 21 and Figure 2 of Applicant’s disclosure shows a cartoon representation of CD91 and each domain with ligand-binding repeats and EGF repeats between domain II and III and III and IV. In Figure 2, domain III has an N-terminal EGF repeat and two C-terminal EGF repeats. Therefore, it is unclear if “does not extend” of claim 18 refers to the ligand-binding repeats, the EGF repeats, or both and what nucleotides are encompassed/excluded by the limitations. Claims 19, 21, 22, 23, and 24 are also rejected as they depend from claim 18 and do not clarify the grounds of rejection.
12. Regarding claim 19, it is unclear how the nucleic acid sequence encoding a fragment of CD91 of claim 18 can consist of amino acids since nucleic acids contain nucleotides that encode amino acids but do not contain amino acids.
13. Regarding claim 20, it is unclear how the nucleic acid sequence encoding a fragment of CD91 of claim 18 can consist of amino acids since nucleic acids contain nucleotides that encode amino acids but do not contain amino acids.
14. Regarding claim 21, it is unclear how the nucleic acid sequence encoding a fragment of CD91 of claim 18 can consist of amino acids since nucleic acids contain nucleotides that encode amino acids but do not contain amino acids.
15. Regarding claim 22, it is unclear how the nucleic acid sequence encoding the signal sequence of claim 18 can consist of amino acids since nucleic acids contain nucleotides that encode amino acids but do not contain amino acids.
16. Regarding claim 23, it is unclear how the nucleic acid sequence encoding the signal sequence of claim 18 can consist of amino acids since nucleic acids contain nucleotides that encode amino acids but do not contain amino acids.
Claim Rejections - 35 USC § 112
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.
17. Claim 19 is 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 18 recites “does not extend N-terminally into ligand binding domain II of CD91” and “does not extend C-terminally into ligand binding domain IV of CD91”, while claim 19 recites “consists of amino acids 1184-3292 of CD91”. Therefore, claim 19 does not further limit claim 18 and instead broadens the claim to include residues in other domains. Applicant’s specification discloses that domain III corresponds to amino acids 2481 – 2942 (page 8, lines 31 – 34) 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.
Claim Interpretation
18. For the purpose of applying prior art, claim 18 and 19 are interpreted as a nucleic acid comprising a sequence encoding a signal sequence for secretion of a CD91 polypeptide linked to a nucleic acid sequence encoding a fragment of CD91 wherein the sequence encoding the fragment of CD91 comprises ligand binding domain III of CD91 (which is known as cluster III in the art) and does not comprise ligand binding repeats of domains I, II, or IV.
19. For the purpose of applying prior art, claim 20 is interpreted as the nucleic acid of claim 18 wherein the nucleic acid sequence encoding the fragment of CD91 consists of nucleotides encoding amino acids 2481 – 2942 of SEQ ID NO: 1.
20. For the purpose of applying prior art, claim 21 is interpreted as the nucleic acid of claim 18 wherein the nucleic acid sequence encoding the fragment of CD91 consists of nucleotides encoding SEQ ID NO: 2 or having at least 85% identity to SEQ ID NO: 2.
21. For the purpose of applying prior art, claim 22 is interpreted as the nucleic acid of claim 18 wherein the nucleic acid sequence encoding the signal sequence consists of nucleotides encoding amino acids 1 – 19 of SEQ ID NO: 1.
22. For the purpose of applying prior art, claim 23 is interpreted as the nucleic acid of claim 18 wherein the nucleic acid sequence encoding the signal sequence is linked to the nucleic acid sequence encoding the fragment of CD91 by a nucleic acid sequence encoding a linker comprising a nucleic acid sequence encoding the amino acid sequence of SEQ ID NO: 5.
23. For the purpose of applying prior art, claim 24 is interpreted as the nucleic acid of claim 18 wherein the nucleic acid sequence encoding the signal sequence is linked to the nucleic acid sequence encoding the fragment of CD91 by (i) a nucleic acid sequence encoding a linker and (ii) a nucleic acid sequence encoding a tag for polypeptide purification.
Claim Rejections - 35 USC § 102
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 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.
24. Claim(s) 18, 19, and 21 is/are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Kurasawa (Kurasawa, James H., et al. Biochemistry 54.2 (2015): 481-489.), hereinafter Kurasawa.
Claim 18 is drawn to a nucleic acid comprising a sequence encoding a signal sequence for secretion of a CD91 polypeptide linked to a fragment of CD91, wherein the fragment:
(i) comprises ligand binding domain III of CD91,
(ii) does not extend N-terminally into ligand binding domain II of CD91, and
(iii) does not extend C-terminally into ligand binding domain IV of CD91.
Regarding claim 18 and 19, Kurasawa teaches a nucleic acid encoding a secretion signal (“signal sequence” of claim 18) linked to a nucleic acid sequence encoding cluster III of LRP (“fragment of CD91” of claim 19) consisting of amino acids 2522 – 2941 of SEQ ID NO: 1 (claim 19) (page 483, left col. para. 3; Figure 1 and S1).
Regarding claim 21, Kurasawa teaches the nucleic acid sequence encodes amino acids 2522 – 2941 of SEQ ID NO: 1 which has at least 85% identity to SEQ ID NO: 2 as shown below:
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662
629
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749
634
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Therefore, Kurasawa anticipates claims 18, 19, and 21.
25. Claim(s) 18, 19, and 21 – 24 is/are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Bu (Bu, Guojun, et. al. Journal of Biological Chemistry 271.36 (1996): 22218-22224.), hereinafter Bu which is cited on the IDS filed 02/17/2023 as evidenced by Takayama (Takayama, Yoshiharu, et al. Journal of Biological Chemistry 280.18 (2005): 18504-18510.), hereinafter Takayama.
Claim 18 is drawn to a nucleic acid comprising a sequence encoding a signal sequence for secretion of a CD91 polypeptide linked to a fragment of CD91, wherein the fragment:
(i) comprises ligand binding domain III of CD91,
(ii) does not extend N-terminally into ligand binding domain II of CD91, and
(iii) does not extend C-terminally into ligand binding domain IV of CD91.
Regarding claim 18 and 19, Bu teaches a nucleic acid comprising a nucleic acid sequence encoding a signal sequence for low density lipoprotein receptor-related protein (LRP) secretion (“signal sequence” of claim 18) and a nucleic acid sequence encoding amino acids 2462 – 3004 of LRP (sLRP3) (“ligand binding domain III of CD91” of claim 18 and 19) (page 22219, left col. para. 3 and right col. last para.; Figure 1; page 22220, left col. para. 1).
Regarding claim 21, Bu teaches the nucleic acid sequence encodes amino acids 2462 – 3004 of LRP1 which has at least 85% identity to SEQ ID NO: 2 as shown in the sequence alignment below:
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776
661
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647
653
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Regarding claim 22, Bu teaches the signal sequence encoded by the nucleic acid encodes the LRP signal peptide consisting of amino acids 1 – 19 of SEQ ID NO: 1 (page 22219, left col. para. 3 and right col. last para.; Figure 1B) as evidenced by Takayama (page 18505, right col. para. 5).
Regarding claim 23, Bu teaches the nucleic acid comprises a sequence encoding amino acids AIDAP (“SEQ ID NO: 5”) between the signal peptide nucleic acid sequence and the sequence encoding SLRP3 in Figure 1B (page 22219, left col. para. 3).
Regarding claim 24, Bu teaches the nucleic acid sequence encoding the signal sequence is linked to the nucleic acid sequence encoding SLRP3 by a linker and an HA epitope (“a first tag”) in Figure 1B (page 22219, left col. para. 3; page 2220, left col. para. 1).
Therefore, Bu anticipates claims 18, 19, and 21 – 24.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
26. Claim(s) 18 – 24 is/are rejected under 35 U.S.C. 103 as being unpatentable over Bu (Bu, Guojun, et. al. Journal of Biological Chemistry 271.36 (1996): 22218-22224.), hereinafter Bu which is cited on the IDS filed 02/17/2023 as evidenced by Takayama (Takayama, Yoshiharu, et al. Journal of Biological Chemistry 280.18 (2005): 18504-18510.), hereinafter Takayama in view of Croy (Croy JE, et. al. Biochemistry. 2003 Nov 11;42(44):13049-57), hereinafter Croy which is cited on the IDS filed 02/17/2023 in view of Lillis (Lillis AP et. al. Physiol Rev. 2008 Jul;88(3):887-918), hereinafter Lillis which is cited on the IDS filed 08/17/2023.
Bu anticipates claims 18, 19, and 21 – 24 as set forth above. Bu teaches a nucleic acid sequence encoding amino acids 2462 – 3004 of LRP (sLRP3) inclusive of SEQ ID NO: 2 but does not teach a nucleic acid sequence consisting of nucleotides encoding amino acids 2481 – 2942 of claim 20. However, Bu teaches sLRP3 is flanked by EGF repeats in Figure 1A. Bu teaches little or no secretion was observed for sLRP3 unless RAP was coexpressed (Abstract). Bu teaches the nucleic acid encodes the putative ligand binding domain III of LRP as a soluble minireceptor (Abstract). Bu teaches LRP is a multifunctional receptor that can bind and endocytose several structurally and functionally distinct ligands (page 22218, right col. para. 1). Bu teaches such diversity in ligands underscores the important role of LRP1 in various physiological processes (page 22218, right col. last para.). Bu teaches upon binding to LRP, RAP inhibits the binding and/or endocytosis of all the ligands by the receptors on the cell surface and this unique feature of RAP has allowed its extensive use in biological studies of LRP and other receptors including identifying novel receptor ligands (page 22218, right col. para. 1).
Croy teaches the nucleic acid sequence of sLRP3 of Bu (containing all of the ligand-binding complement type repeat clusters of cluster III) encodes a fragment consisting of the N-terminal sequence of LSPCRINNGGCQDLC, where the first amino acid (L) corresponds to amino acid 2479 of SEQ ID NO: 1 (Table 1; page 13052, right col. para. 1 – 2; Figure 1A). Croy does not teach the nucleic acid sequence encoding sLRP3 ends at amino acid 2942 of SEQ ID NO: 1. However, Croy teaches the sLRP3 nucleic acid allows for expression and purification of sLRP3 in a properly folded form in large quantities so the ligand-binding domains could be purified and characterized in solution (page 13050, left col. para. 2). Croy teaches the purified sLRP3 allowed for the measure of binding of ligands to sLRP3 where thrombin-protease nexin 1 bound to sLRP3 and RAP competed for binding of sLRP3 (page 13051, left col.; page 13054, left col. para. 2; page 13056, left col. para. 2). Croy teaches apoE-enriched β-VLDL particles and lactoferrin bound to sLRP3 (page 13055, left col. para. 1). One would have been motivated to combine the teachings of Bu and Croy because both use nucleic acids of sLRP3 to express soluble minireceptors to investigate ligand binding to cluster III of LRP.
Kurasawa teaches nucleic acid sequences encoding fragments of cluster III of LRP which correspond to amino acids 2522 – 2941 of SEQ ID NO: 1 and nucleic acid sequences encoding fragments of cluster III (Figure 1; page 483, left col. para. 3; Figure S1). Kurasawa teaches the sequence of the first CR of cluster III, CR-11, encodes amino acids 2522 – 2561 of SEQ ID NO: 1 and the sequence of last CR of cluster III, CR-20, encodes amino acids 2902 – 2941 of SEQ ID NO: 1 in Figure S1. Kurasawa teaches the ligand binding moiety of LRP is found in complement-type repeats (CRs) and the nucleic acid sequences encoding fragments of cluster III encode overlapping CR doublets as shown in Figure 1 (page 481, left col. para. 1; page 483, left col. para. 3). Kurasawa teaches in Figure 1 that EGF-like repeats flank cluster III . Kurasawa teaches activated FVIII (FVIIIa) binds to cluster III (Abstract). Kurasawa teaches through the expression of fragments of CR’s of cluster III, the binding site of FVIIIa was found to be reside in CR 14 – 19 (Abstract; page 483, left col. para. 3 – 4; Figure 4 – 6; page 486, left col. para. 2). Kurasawa teaches LRP internalizes FVIII from circulation and deficiency of FVIII results in hemophilia A (page 481, right col. para. 2). Kurasawa teaches the need for reducing the frequency of injections calls for generation of longer-lasting therapeutic FVIII, which requires a better understanding of the mechanisms of FVIII clearance (page 481, right col. para. 2). One would have been motivated to combine the teachings of Bu, Croy, and Kurasawa because all three use nucleic acids of sLRP3 to express soluble minireceptors to investigate ligand binding to cluster III of LRP.
Lillis teaches LRP1 contains CRs, EGF repeats, β-propeller domains, a transmembrane domain, and a cytoplasmic domain (page 888, right col. last para.). Lillis teaches the β -propeller packs tightly against the C-terminal EGF module and CRs can fold back over the EGF repeats and the β -propeller thus affecting ligand binding and release (page 889, right col. para. 2; Figure 2). Lillis teaches the complexity of LRP1’s role in biology arises from its ability to interact with a variety of ligands thus placing LRP1 in a unique position to impact normal and abnormal mammalian physiology in a variety of ways (page 909, right col. last para.).
It would have been obvious prior to the effective filing date of the invention as claimed for the person of ordinary skill in the art to combine the teachings of Bu regarding a nucleic acid comprising a nucleic acid sequence encoding a signal sequence linked to a nucleic acid sequence sLRP3 with the teachings of Croy regarding the sLRP3 nucleic acid sequence of Bu encodes a fragment starting with amino acid 2479 of SEQ ID NO: 1 with the teachings of Kurasawa regarding a nucleic acid encoding a signal sequence linked to a nucleic acid encoding cluster III of LRP that corresponds to amino acids 2522 – 2941 of SEQ ID NO: 1 with the teachings of Lillis regarding the EGF repeats of LRP1 can affect ligand binding and release to arrive at the claimed nucleic acid sequence where the fragment of CD91 consists of nucleotides encoding amino acids 2481 – 2942 of SEQ ID NO: 1 through routine optimization. One would have been motivated to combine the teachings in a nucleic acid sequence that encodes a soluble CD91 minireceptor to identify ligands that bind to cluster III and the location of the binding as Bu teaches LRP is a multifunctional receptor that can bind and endocytose several structurally and functionally distinct ligands and such diversity in ligands underscores the important role of LRP1 in various physiological processes and Lillis teaches the complexity of LRP1’s role in biology arises from its ability to interact with a variety of ligands thus placing LRP1 in a unique position to impact normal and abnormal mammalian physiology in a variety of ways. A rationale for arriving at the claimed nucleic acid sequence through routine optimization comes from the teachings of Bu, Croy, Kurasawa, and Lillis: Bu teaches little or no secretion was observed for sLRP3 unless RAP was coexpressed and sLRP3 is flanked by EGF repeats; Croy teaches the nucleic acid sequence of sLRP3 encodes a fragment that starts with amino acid 2479 of SEQ ID NO: 1 and that sLRP3 was secreted and purified in a properly folded form in large quantities allowing for the measure of binding of ligands to sLRP3; Kurasawa teaches nucleic acid sequences encoding fragments of cluster III of LRP which correspond to amino acids 2522 – 2941 of SEQ ID NO: 1 and that these nucleic acids allowed for expression and purification of cluster III for determining the binding site of Factor VIIIa; Lillis teaches regions flanking the CRs (EGF repeats and β-propeller) can affecting ligand binding and release. Taken together, Bu, Croy, Kurasawa, and Lillis provide a rationale for one of ordinary skill in the art to arrive at the claimed nucleic acid encoding the claimed amino acids with a reasonable expectation of success because Croy and Kurasawa teach that varying the nucleic acid sequence can result in soluble minireceptors of domain III for measuring ligand binding and identifying the location of ligand binding. One would have a reasonable expectation of success in combining the teachings as Croy teaches the purified sLRP3 allowed for the measure of binding of ligands to sLRP3 where thrombin-protease nexin 1 bound to sLRP3 and RAP competed for binding of sLRP3 and Kurasawa teaches FVIIIa binds to cluster III and through the expression of fragments of CR’s of cluster III, the binding site of FVIIIa was identified.
Conclusion
No claims allowed.
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/Z.M.B./Examiner, Art Unit 1632
/MARCIA S NOBLE/Primary Examiner, Art Unit 1632