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 Election Upon further consideration and a search of the prior art , the restriction and species elections are withdrawn. All claims and species are hereby examined. Election/Restrictions During the course of investigation, Examiner determined that a search burden did not exist. Both the restriction and requirement for election of species have been withdrawn. All claims and species hereby examined. Information Disclosure Statement The listing of references in the specification is not a proper information disclosure statement. 37 CFR 1.98(b) requires a list of all patents, publications, or other information submitted for consideration by the Office, and MPEP § 609.04(a) states, "the list may not be incorporated into the specification but must be submitted in a separate paper." Therefore, unless the reference has by cited by the examiner on form PTO-892, they have not been considered. Claim Rejections - 35 USC § 112(b) 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 appl icant regards as his invention. Claim 8 is rejected as indefinite for “CD47 positive and/or CD47 overexpression.” I t is not clear whether any expression of CD47 would meet the claim limitation , or if a certain threshold of expression must be reached before the limitation is fulfilled. This threshold is in and of itself indefinite as the specification has not provided a quantifiable measure for when this threshold is met. Therefore, PHOSTIA would not be able to reasonably ascertain the metes and bounds of the claim. Claim Rejections - 35 USC § 112(a) 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. Claim s 1 -14 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 enablement requirement. The specification is enabling for treating cancer and inflammatory conditions that exhibit CD47 overexpression and for amelioration using SIRPα and SIRPγ expressing extracellular vesicles . However, the specification does not reasonably provide enablement for the prevention of cancer/inflammatory conditions, the treatment of any cancer/inflammatory condition, nor for amelioration via all SIRP proteins or variants/fragments thereof . The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims. MPEP § 2164.01(a) states that there are many factors to be considered when determining whether there is sufficient evidence to support a determination that a disclosure does not satisfy the enablement requirement and whether any necessary experimentation is “undue”. These factors include, but are not limited to: A) The breadth of the claims; (B) The nature of the invention; (C) The state of the prior art; (D) The level of one of ordinary skill; (E) The level of predictability in the art; (F) The amount of direction provided by the inventor; (G) The existence of working examples; and (H) The quantity of experimentation needed to make or use the invention based on the content of the disclosure. In re Wands, 8 USPQ2d, 1400 (CAFC 1988) and MPEP 2164.01. Claim 1 recites: “ A method for preventing or treating cancer or inflammatory disease, condition, or symptom, the method comprising administering to a subject in need thereof a prophylactically or therapeutically effective amount of stem cell-derived extracellular vesicles (EV) that comprise a signal regulatory protein (SIRP), a fragment of the SIRP, a variant of the SIRP, a fragment of the variant, or a variant of the fragment . ” The specification does not provide enablement for ameliorating every cancer o r inflammatory condition, disease, or symptom. CD47 is a protein expressed on the surface of cells that acts as the “don’t-eat-me” signal by binding to SIRP proteins on the surface of macrophages, which prevents them from inducing phagocytosis. Certain conditions like cancer exploit this mechanism by overexpressing CD47 to evade recognition . The external supply of SIRP from SIRP expressing exosomes of the instant invention serves as a CD47 blockade, leaving endogenous macrophages free to recognize and induce phagocytosis of those cells; therefore, it is helpful in those conditions that overexpress CD47. Indeed, the state of the art teaches that a variety of conditions overexpress CD47 for which the specification is enabled for. For example, overexpression has been demonstrated in both solid tumor cancers (Huang et al. pg. 2, left side, second paragraph) and hematopoietic malignancies (Eladl et al., abstract). In addition, a variety of inflammatory conditions exhibit CD47 overexpression: the specification discloses CD47 overexpression in acute liver failure (Fig. 2); the state of the art at the time of filing discloses overexpression in acute kidney failure ( El-Rashid et al., abstract) and at least one kind of bone marrow failure syndrome (Fattizzo et al., pg. 10 line 11 of paragraph). Indeed, Cham et al., teaches that one of ordinary skill in the art would expect CD47 blockade therapies to be applicable to a wide variety of conditions, because its mechanism is not specific to the pathogen (pg. 8, left side). Altogether, the specification, given the state of the art , existence of working examples, and knowledge of one of ordinary skill in the art, is enabling for cancer and inflammatory conditions that exhibit CD47 overexpression. However, not every cancer or inflammatory condition is characterized by CD47 overexpression. For example, CD47 overexpression was not found in Fibrolamellar Hepatocellular Carcinoma and the art teaches away from pursuing CD47 inhibition as a therapeutic route (Cooney et al., abstract) . Furthermore, in some inflammatory conditions, CD47 enrichment, rather than a blockade, is therapeutic . For example, Yuan et al., teaches that CD47+ enriched extracellular vesicles (EVs) contributed to the amelioration of hepatic ischemia-reperfusion injury in mice (abstract ). In addition, the specification is not enabled for preventing cancer and inflammatory conditions by administering a prophylactically or therapeutically effective amount of SIRP expressing EVs. There are no working examples or details within the instant disclosure drawn toward prevention of a condition using SIRP expressing EVs. Furthermore, because healthy cells express CD47, it is possible that administration of SIRP expressing EVs prior to the development of a pathological condition could have adverse effects by causing the “don’t eat me” signal of healthy cells to be obstructed. Even in therapeutic scenarios , off-tumor binding of anti-CD47 antibodies is known to have adverse consequences on platelet s (Jiang et al., pg. 15, left side, second paragraph) . There is not sufficient evidence in the disclosure to demonstrate prevention of cancer and inflammatory conditions , through the administration of a prophylactically effective amount of the EVs, would have a reasonable likelihood of success , particularly due to the known adverse events associated with targeting CD47 on healthy cells. The specification is not enabl ing for the extracellular vesicles to comprise all types of SIRP proteins in order to treat cancer/inflammatory conditions. The inventive concept of the claimed invention rests on the SIRP expressing EVs being able to bind to problematic CD47-expressing cells. However, multiple versions of SIRP proteins exist, each with different binding affinities. For example, it was known in the art at the time of filing that SIRPβ 1 does not have a detectable affinity for CD47 ( Seiffert et al., abstract) . However, it was known in the art that SIRPγ does bind to CD47, thereby contributing to tumor evasion from macrophages ( US11319360B2 , Column 4, line 20-21 ). Therefore, while the working examples are only drawn to SIRP α expressing EVs, one of ordinary skill in the art would still be enabled for the claimed invention using SIRPγ expressing EVs with a reasonable expectation of success ; however other types of SIRP , such as SIRPβ 1, are not enabled. Furthermore, t he specification is not enabli ng for “a fragment of the SIRP, a variant of the SIRP, a fragment of the variant or a variant of the fragment” embodiments . The specification defines “a fragment” as a segment of the protein, peptide, or nucleic acids, with no limitations on what percent identity match to the natural SIRP sequence s is required (pg. 12) . The specification defines a variant a s “ a protein, peptide, or nucleic acid having has at least one amino acid or nucleotide which is different from the protein, peptide, or nucleic acid ” (pg. 12). The number of possible variants that could be formed through even a single amino acid change at any residue, not to mention any number of mutations that could occur within the natural SIRP sequences, which are over 300 amino acids in length, is vast and thus the scope of this claim is extremely broad. One of ordinary skill in the art would have known that the binding site of SIRP α was restricted to the N terminus ( Liu et al., pg. 682, left side, 7 lines from top ) and which amino acid residues are essential for successful binding between SIRP α and CD47 (Liu et al., pg. 688, eft side, first paragraph) . Therefore , one of ordinary skill in the art would have known what amino acid residues must be included in order for the fragment and variant embodiments of the present invention to perform as prescribed ; however, this does not elucidate how the changing of any other amino acids at an y other residues might affect the structure and function of the SIRP variant. In fact, it was known in the art that SIRP α has “ unusual sensitivity of the protein specificity to amino acid changes ” ( Hatherley et al., pg. 14567, right side, last paragraph) . Furthermore, the unique structure of SIRP proteins specifically contributes to the sensitivity: “ The use of loops for binding provides a mechanism whereby small chemical differences in side chains can have large effects on the shape of the loops without disrupting the core β fold of the molecule, as exemplified by the variation observed in the complementarity determining regions of antibodies and TCRs ” (Hatherley et al., pg. 14574, left sight , second paragraph from bottom). Not only that, but in order to successfully use the claimed invention, the SIRP variants need not only to bind to CD47, but do so with sufficient affinity to result in a meaningful effect on a cancerous or inflammatory condition , which would further require in vivo studies . The working examples in the specification are only drawn to SIRP α -ESM embodiment (pg. 33); however, due to the sensitivity described above, this one embodiment is not enabling for the entire breadth of the claim’s scope. Altogether, one of ordinary skill in the art would not be able to use the claimed invention without significant undue experimentation. In conclusion, t he specification is enabling for treating cancer and inflammatory conditions that exhibit CD47 overexpression and for amelioration using SIRPα or SIRPγ expression exosomes . However, the specification does not reasonably provide enablement for the prevention of cancer/inflammatory conditions, the treatment of any cancer/inflammatory condition, nor for amelioration via all SIRP proteins or variants/fragments thereof . Claim 1 is 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. MPEP 2163.05 recites: “The written description requirement for a claimed genus may be satisfied through sufficient description of a representative number of species. A ‘representative number of species’ means that the species which are adequately described are representative of the entire genus. Thus, when there is substantial variation within the genus, one must describe a sufficient variety of species to reflect the variation within the genus.” Claim 1 claims “stem cell derived extracellular vesicles (EV), ” while the disclosure is only directed to extracellular vesicles derived from specific adult stem cells, namely bone marrow mesenchymal stem cells (MSCs). Therefore , the genus of stem cell recited in Claim 1 encompasses stem cells of varying types and properties, for which bone-marrow MSC EVs are not fully representative of. Even within MSCs (i.e. umbilical cord, bone marrow, muscle MSCs) , itself a stem cell subtype, Muthu et al . teaches that some species have enhanced properties over others ( pg. 6, right side, first paragraph) . More dramatically, mesenchymal stem cells differ from pluripotent stem cells in that while the former is known in the art to have regenerative properties, the latter has shown tumorigenicity (Lee et al., pg. 1, second paragraph). Altogether, these sources demonstrate the breadth and variety of properties of stem cells such that possession of an exosome from one parent cell of origin does not demonstrate possession of the genus. Since the disclosed species of the invention do not constitute the genus of all stem cells , Applicant is not in possession of the claimed invention. Claim 1 is further rejected under written description for “ a signal regulatory protein (SIRP) , a fragment of the SIRP, a variant of the SIRP, a fragment of the variant or a variant of the fragment.” The genus of the SIRP protein recited is extremely broad, encompassing any combination of amino acid substitutions at any position for any SIRP protein sequence, as well as changes to overall protein structure. As addressed above, the structure function relationship is highly sensitive in the SIRP proteins such that one embodiment within the genus could not possibly re present the entire breadth claimed . The working examples in the specification are only drawn to SIRP α -ESM embodiment (pg. 33). Since the disclosed species of the invention do not constitute the genus recited , Applicant is not in possession of the claimed invention. Claim Rejections - 35 USC § 103 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. Claim(s) 1-8, and 14 is/are rejected under 35 U.S.C. 103 as being unpatentable over Koh et al., US 20200148746 (hereafter Koh ‘746) in view of Muthu et al., Exosomal therapy—a new frontier in regenerative medicine, Stem Cell Investigation 2021, pgs. 1-14 (hereafter Muthu et al) . The claims recite a method for preventing or treating cancer or inflammatory disease, wherein the condition is related to CD47 overexpression, by administering stem cell-derived extracellular vesicles (EV) that comprise a signal regulatory protein (SIRP), wherein the SIRP protein includes SIRP α and the stem cells include bone marrow stem cells. The claims further recite that the SIRP is linked to at least one EV protein such as the receptor tyrosine kinase is a platelet-derived growth factor receptor (PDGFR) . The claims further limit that the EV comprises an anti-cancer or anti-inflammatory agent. Koh ‘746 teaches a method of treating cancer by administering a recombinant exosome in which a phagocytosis promoting protein is presented on the surface thereof; in one embodiment the phagocytosis presenting protein is SIRP ( pg. 49 of Koh ‘746, right side, Claim 15). It further teaches that the SIRP protein is SIRP α (pg. 49 of Koh ‘746, right side, Claim 5). It further teaches that the tumor treated by SIRP α -exosomes had CD47 overexpression [0082]. I t further teaches that the SIRP linked to an EV protein, namely a receptor tyrosine kinsase including PDGFR (Fig. 1). Lastly, Koh ‘746 teaches that the exosomes comprise an anticancer agent ( pg. 49 of Koh ‘746, left side, Claim 7). Koh ‘746 does not teach that the exosomes are stem-cell derived, but rather that they are derived from HEK293 cells [0064]. Muthu et al. teach es that exosomes, a type of extracellular vesicle , are used in therapeutic treatments for various conditions because they have the characteristics of the parent cell of origin (abstract). Specifically , the surface markers on MSC exosomes are essential in “regeneration…immunoregulation, intracellular communication, and tissue metabolism” ( pg. 6, eft side, last paragraph) that make them useful in treating inflammatory disorders and as anti-cancer therapies (pg. 8, left side, last paragraph) . Muthu et al. specifically teaches key sources of MSC exosomes include bone marrow, adipose tissue, placental cells, umbilical cells (pg. 6, left side, second paragraph from bottom) . Muthu et al. provides motivation to choose stem cells derived EVs, including bone marrow derived exosomes from mesenchymal stem cells (MSCs), in therapeutic applications of exosomes because of their beneficial properties like regeneration and immunoregulation, which are desirable for treating cancer and inflammatory conditions. Furthermore, these sources are in the same field of endeavor, namely extracellular vesicle research. Therefore, it would have been obvious to one of ordinary skill in the art to incorporate the teachings from Muthu into the method of Koh ‘746 to enhance the efficacy of cancer treatment. Claim(s) 9-10 is/are rejected under 35 U.S.C. 103 as being unpatentable over Koh ‘746 and Muthu et al., as applied above, in further view of Fattizzo et al., Mesenchymal Stem Cells in Aplastic Anemia and Myelodysplastic Syndromes: The “Seed and Soil” Crosstalk, 2020, Int. J. Molecular Sciences, pgs. 1-18 (hereafter Fattizzo et al.). Koh ‘746 and Muthu et al. teach the limitations of C laim 1 from which C laim 9 and 10 depend . Koh ‘746 and Muthu et al. don’t teach that the inflammatory disease, condition or symptom to be selected from a group including bone marrow failure. Fattizzo teaches that CD47 is overexpressed in myelodysplastic syndromes, which is a type of bone marrow failure. Given that Koh '746 teaches SIRP expressing exosomes successfully treat a condition characterized by CD47 overexpression , it would have been obvious to one of ordinary skill in the art to apply this method to other conditions overexpressing CD47, like MDS. Claim(s) 11 is/are rejected under 35 U.S.C. 103 as being unpatentable over Koh ‘746 and Muthu et al., as applied above, in further view of Cham et al., Immunotherapeutic Blockade of CD47 Inhibitory Signaling Enhances Innate and Adaptive Immune Responses to Viral Infection, 2020, Cell Reports, pgs. 1-14 (hereafter Cham et al). Koh ‘746 and Muthu et al. teach the limitations of C laim 1 from which claim 11 depend s. Koh ‘746 and Muthu et al. do not teach a method for treating a viral infection including hepatitis virus infection. Cham et al ., teaches that CD47 blockade would be useful for infectious disease (abstract). Cham et al., teaches enhanced viral control follow ing infection from a virus called lymphocytic choriomeningitis (abstract), but also states, “ o ther applications for CD47 blockade include… hepatitis B, and herpes simplex virus 2 ” (pg.7 right side , last sentence, pg. 8 left side first paragraph). Furthermore , it teaches that one of ordinary skill in the art would expect CD47 blockade therapies to be applicable to a wide variety of conditions, because its mechanism is not specific to the pathogen (pg. 8, left side, first paragraph). Based on the promising results from CD47 blockade for treating one type of viral infection, namely lymphocytic choriomeningitis , as well as the explicit motivation to pursue this as a therapeutic option for other viral infections such as hepatitis virus infection, one of ordinary skill in the art would have been motivated to combine the teachings of Koh ‘746 and Muthu et. al with Cham et al. to use a SIRP expressing exosome to treat a hepatitis virus infection . Claim(s) 12 is/are rejected under 35 U.S.C. 103 as being unpatentable over Koh ‘746 and Muthu et al., as applied above, in further view of Lerbs et al., CD47 prevents the elimination of diseased fibroblasts in scleroderma , 2020, JCI Insight, Pgs. 1-18 (hereafter Lerbs et al.) Koh ‘746 and Muthu et al. teach the limitations of C laim 1 from which C laim 12 depend s. Koh ‘746 and Muthu et al. do not teach a method of treating fibrosis including skin fibrosis. Lerbs et al., teaches that increased expression of CD47 in Scleroderma, which is a condition that causes skin fibrosis ( abstract ). Furthermore, a combination of CD47 and IL-6 inhibition was able to reverse skin fibrosis ( Fig. 7 ). CD47 inhibition alone eliminates dermal fibroblasts in vivo (Fig. 6 ) , which are drivers of fibrosis progression (pg. 11, fourth paragraph from bottom). Koh ‘746 does not teach a method for treating skin fibrosis. However, simply the teaching from Lerbs et al. that CD47 is overexpressed in skin fibrosis, is itself a motivation to combine Koh ‘746 and Lerbs et al., since the method in Koh ‘746 was able to treat another condition overexpressing CD47, namely cancer. Furthermore, Lerbs et al.’s explicit teachings that CD47 inhibition eliminates a driver of skin fibrosis progression, namely fibroblasts, further indicates that the method taught by Koh ‘746 would have a reasonable expectation of success. Based on the successful results in Lerbs et al., one of ordinary skill in the art would be motivated to apply the known method of CD47 inhibition, namely SIRP-expressing exosomes, to treat skin fibrosis. Claim(s) 1 3 is/are rejected under 35 U.S.C. 103 as being unpatentable over Koh ‘746 and Muthu et al., as applied above, in further view of Huang et al., Regulation of CD47 expression in cancer cells , 2020, Translational Oncology, pgs. 1-7 (hereafter Huang). Koh ‘746 and Muthu et al. teach the limitations of C laim 1 from which C laim 13 depend s. Koh ‘746 further teaches that SIRP expressing exosomes are able to bind to colon cells (Figs. 6 and 7). Huang et al. teaches high expression of CD47 in a variety of cancers including myeloid leukemia (AML), non-Hodgkin lymphoma (NHL), breast cancer, and melanoma (pg. 2, left side, second paragraph). The method of treating cancer as a genus and the ability of SIRP expressing exosomes to bind to cancer cells, taught by Koh ‘746, is itself a motivation to one of ordinary skill in the art to apply the method of Koh ‘746 to various species within the genus of cancer, including colon cancer. To further support this rejection, Huang et al. teaches specific cancer species known in the art to have a high expression of CD47 . Since Koh et al. teaches that the SIRP expressing exosomes successfully treated a CD47 overexpression cancer, as addressed previously, it would have been obvious to one of ordinary skill in the art to apply the method to other cancers overexpressing CD47. 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 . Claim 1 is rejected on the ground of nonstatutory double patenting a s being unpatentable over claim 12 of U.S. Patent No. US11319360 (hereafter Koh ‘360) in view of Muthu et al., Exosomal therapy—a new frontier in regenerative medicine, Stem Cell Investigation 2021, pgs. 1-14 (hereafter Muthu et al). Instant Claim 1 recites a method of treating cancer comprising administering to a subject a therapeutically effective amount of stem-cell derived extracellular vesicles (EV) that comprise a signal regulatory protein (SIRP). Claim 12 of Koh ‘360 recites a method of treating cancer comprising administering to a subject a therapeutically effective amount of a recombinant exosome comprising a SIRP protein. However, Koh ‘360 does not recite that the exosome, which is a type of extracellular vesicle, is stem cell derived. Muthu et al. teaches that stem-cell derived exosomes were known in the art to be used for a variety of therapeutic applications due to their regenerative properties (abstract) . It would have been obvious to one of ordinary skill in the art that the SIRP expressing vesicle could be a stem-cell derived extracellular vesicle. In fact, one would have been motivated to implement this modification because Muthu specifically provides motivation for using MSC stem cells, including bone marrow stem cells, for treating cancer and inflammatory conditions (pg. 8, left side, last paragraph) due to their regenerative and immunomodulatory benefits (pg. 6, eft side, last paragraph) . The specification states that exosomes are a species of extracellular vesicles (pg. 10, line 4). The only difference between instant Claim 1 and Claim 12 of Koh ‘360 is that the instant extracellular vesicles were derived from stem cells, which given the state of the art is not a patentably distinct limitation. Conclusion No claims allowed. Any inquiry concerning this communication or earlier communications from the examiner should be directed to FILLIN "Examiner name" \* MERGEFORMAT MICHELLE C BUCCINI whose telephone number is FILLIN "Phone number" \* MERGEFORMAT (571)272-1352 . The examiner can normally be reached FILLIN "Work Schedule?" \* MERGEFORMAT M-F 7:30-5 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, FILLIN "SPE Name?" \* MERGEFORMAT Jeffrey Stucker can be reached at FILLIN "SPE Phone?" \* MERGEFORMAT 5712720911 . 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. /MICHELLE CALLAHAN BUCCINI/ Examiner, Art Unit 1675 /JEFFREY STUCKER/ Supervisory Patent Examiner, Art Unit 1675