Prosecution Insights
Last updated: April 19, 2026
Application No. 19/202,402

MYOCARDITIS-TARGETED RADIONUCLIDE MOLECULAR PROBE, PREPARATION METHOD THEREFOR, AND APPLICATION THEREOF

Non-Final OA §103
Filed
May 08, 2025
Examiner
PERREIRA, MELISSA JEAN
Art Unit
1618
Tech Center
1600 — Biotechnology & Organic Chemistry
Assignee
Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology
OA Round
2 (Non-Final)
52%
Grant Probability
Moderate
2-3
OA Rounds
3y 7m
To Grant
78%
With Interview

Examiner Intelligence

Grants 52% of resolved cases
52%
Career Allow Rate
428 granted / 824 resolved
-8.1% vs TC avg
Strong +26% interview lift
Without
With
+25.7%
Interview Lift
resolved cases with interview
Typical timeline
3y 7m
Avg Prosecution
41 currently pending
Career history
865
Total Applications
across all art units

Statute-Specific Performance

§101
1.0%
-39.0% vs TC avg
§103
53.8%
+13.8% vs TC avg
§102
14.9%
-25.1% vs TC avg
§112
16.6%
-23.4% vs TC avg
Black line = Tech Center average estimate • Based on career data from 824 resolved cases

Office Action

§103
DETAILED ACTION 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 . Claims and Previous Objections/Rejections Status Claims 1 and 6 are pending in the application. Claims 2-5 are withdrawn from consideration. Any text of the non-elected/withdrawn claims must be present. The withdrawn claims 2-5 are missing the text of the claims. Any non-elected claims that are being canceled must have the status identifier (canceled). Any objections and/or rejections from previous office actions that have not been reiterated in this office action are obviated. Modified Grounds of Rejection 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. Claim(s) 1 and 6 is/are rejected under 35 U.S.C. 103 as being unpatentable over Jaafar-Thiel et al. (US 2024/0173441A1) in view of Low et al. (US 2024/0238458A1). Jaafar-Thiel et al. (US 2024/0173441A1) discloses compounds of formula A PNG media_image1.png 74 126 media_image1.png Greyscale (Formula A) used for radioimaging (abstract; p1, [0011]; p2, [0013]; p7, [0094]; p8, [0119]). The PNG media_image2.png 60 76 media_image2.png Greyscale comprises a chelating moiety (p2, [0014],[0023]; p7, [0089],[0096]; p8, [0120]; p9-13, [0137]). The chelating moiety comprises DOTA, PNG media_image3.png 154 294 media_image3.png Greyscale , PNG media_image4.png 186 318 media_image4.png Greyscale , etc. (p9, [0137-0138]; p15; p40, structure 10; p43, structure 19). The PNG media_image4.png 186 318 media_image4.png Greyscale chelating moiety encompasses the p-SCN-Bn-DOTA chelator of the instant claims. The V moiety comprises a targeting moiety comprising a FAP (Fibroblast activation protein), such as linagliptin, FAPI-02, etc. (p2, [0017]; p7, [0089],[0098]; p8, [0122]; p30, [0258]). The linagliptin encompasses the linagliptin of the instant claims. The L moiety comprises a bond wherein the targeting moiety is bound directly to the chelating moiety (p2, [0016]; p7, [0089],[0097]; p8, [0121]; p20, [0208]). The L moiety bond encompasses covalently bonding the chelator to the Linagliptin of the instant claims. The n is an integer selected from 1 to 10 (p2, [0018]; p7, [0099]; p8, [0123]). The chelating moiety may optionally chelate a copper radionuclide, such as 61Cu, 64Cu, 67Cu (p2, [0015]; p7, [0105]; p8, [0117],[0126]; p57, [0373]). The targeting moiety is known to be suitable for use with 68Ga for use in medical imaging (p24, [0221]). Jaafar-Thiel et al. does not explicitly disclose directly binding the chelating moiety PNG media_image4.png 186 318 media_image4.png Greyscale to the linagliptin via the bond L. Jaafar-Thiel et al. discloses the compound PNG media_image5.png 368 462 media_image5.png Greyscale and that the targeting moieties include those that target HER2, PSMA, SSTR, FAP (p23, [0220]; p24, [0225]; p56, [0355]). It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to substitute the HER2 targeting moiety of Jaafar-Thiel et al. for the linagliptin targeting moiety of Jaafar-Thiel et al. for the advantage of providing site specific targeting of the radioimaging agents to different cell surface receptors, e.g. cells in the tumor microenvironment, inflammatory tissues, sites of a myocardial infarct, etc. Jaafar-Thiel et al. does not explicitly disclose chelating 68Ga to the chelating moiety or myocarditis. Low et al. (US 2024/0238458A1) discloses Fibroblast activation protein (FAP)-targeting compounds for imaging and/or treating an inflammatory disease/disorder (abstract). The inflammatory disease or disorder includes myocarditis, etc. (p129, [0662]). The compounds (e.g. conjugates) comprise the formula (I) PNG media_image6.png 26 64 media_image6.png Greyscale wherein A is a FAPα ligand (targeting moiety), L is a linker and B’ is a radio-imaging agent, etc. (p1, [0013-0017]; p52, [0329]). B’ is a chelating group bound to an isotope (p2, [0047]; p6, [0066]). The chelating group comprises DOTA, PNG media_image7.png 194 368 media_image7.png Greyscale , PNG media_image8.png 206 298 media_image8.png Greyscale , etc. (p7, left column; p9, [0069]; p65, right column; p68, [0451-0453]). The isotope is suitable for PET, SPECT, etc. and comprises 68Ga, 64Cu, 67Cu, etc. (p10, [0071]; p64, [0440],[0443]; p69, [0458-0459]). It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to chelate the 68Ga radionuclide of Low et al. to the chelating moiety PNG media_image4.png 186 318 media_image4.png Greyscale of Jaafar-Thiel et al. as Low et al. teaches that the chelator PNG media_image8.png 206 298 media_image8.png Greyscale chelates 68Ga, 64Cu, 67Cu for the advantage site specific targeting of the compounds to specific cell surface receptors for PET imaging of myocarditis in a subject. The substitution of one known radionuclide, such as copper radionuclides for another known radionuclide, such as 68Ga predictably yields a myocarditis-targeted radionuclide molecular probe/imaging agent for PET. Response to Arguments Applicant's arguments filed 12/22/25 have been fully considered but they are not persuasive. Applicant asserts that the reference of Jaafar-Thiel et al. teaches that L is a linker used to connect the chelating moiety and the targeting moiety V so that the chelating moiety and targeting moiety are not connected directly with each other. The claimed probe has no need for a specialized linker. The reference of Jaafar-Thiel et al. teaches that the L moiety may comprise a bond or a linker. The L moiety comprises a bond wherein the targeting moiety is bound directly to the chelating moiety (p20, [0208]). Applicant asserts that Linagliptin is a small-molecule compound with high target specificity toward DPP4 and is a non-peptidomimetic DPP4-targeting compound with a xanthine structure, which forms a non-covalent bond with groups of an activated an amino group of the DPP4 inhibitor and coordinately bonded to a mete site of DPP4. Linagliptin is a small molecule drug that has been applied clinically for many years and is beyond doubt in pharmacological safety. The amended claim 1 adopts the radioactive metallic radionuclide (68Ga) as a tracer to qualitatively diagnose myocarditis. Thus achieves the purpose of the present invention: improve the specificity and targeting capability of detection probes for myocardial inflammatory cells. The reference of Jaafar-Thiel et al. teaches that stated above and that the targeting moiety of the radioimaging probes comprises Linagliptin which targets inflammatory tissues. The Linagliptin of Jaafar-Thiel et al. encompasses the Linagliptin of the instant claims, has the same properties and is capable of the same functions, such as improving the specificity and targeting capabilities of detection probes and targeting myocardial inflammatory cells. Also, the Applicant concedes that Linagliptin is a known DPP4-targeted small-molecule inhibitor with high target specificity for DPP4. Products of identical chemical composition can not have mutually exclusive properties. A chemical composition and its properties are inseparable. Thus the claiming of a new use, new function or unknown property which is inherently present in the prior art does not necessarily make the claim patentable and does not render the old composition patentably new to the discoverer. In re Best, 562 F.2d 1252, 1254, 195 USPQ 430, 433 (CCPA 1977). Applicant asserts that DPP4 and FAP are completely different targets in the diagnosis and treatment of myocarditis. The three stages of the process are stated in the REMARKS p6. The core pathological feature of myocarditis is the infiltration of inflammatory cells into the myocardial interstitium, accompanied by myocardial cells degeneration and necrosis. DPP4 and FAP both belong to the DPP/POP-like serine peptidase family, but they have significant differences in their expression profiles and biological localizations: DPP4 is primarily located on the surface of immune cells, such as T cells, DC cells, and NK cells, and can be significantly up regulated following immune activation. FAP, on the other hand, is highly expressed in fibroblasts and is often regarded as a marker of “activated fibroblasts” related to tissue remodeling. Based on the differences, it can be inferred that FAP may serve as an important biomarker during the chronic fibrosis stage of myocarditis, but it is unlikely to provide an effective reflection of immune activation in the early stages of fulminant myocarditis. Thus, FAP-targeting probes and DPP4-targeting probes have different clinical implications in terms of disease progression assessment and therapeutic strategies. From pathological mechanisms to clinical applications, there is no substantial overlap between the two. Furthermore, Linagliptin is a DPP4-targetred small-molecule inhibitor rather than a FAP-targeted inhibitor. Its affinity for FAP is much weaker, with rapid dissociation from recombinant human FAP, particularly under physiological pH (7.3), where it exhibits transient binding behavior. The difference in target occupancy between DPP4 and FAP by linagliptin can exceed 200-fold. The instant claims are not drawn to a method of imaging myocarditis with a Linagliptin imaging probe. The reference of Jaafar-Thiel et al. teaches that stated above, the targeting moiety of the radioimaging probes comprises Linagliptin and that the radiolabeled imaging probes target inflammatory tissues via the targeting moiety. Although, Jaafar-Thiel et al. states that Linagliptin is a FAP inhibitor the Linagliptin encompasses the Linagliptin of the instant claims, has the same properties and is capable of the same functions, such as targeting DPP4. Also, the Applicant concedes that Linagliptin is a known DPP4-targeted small-molecule inhibitor with high target specificity for DPP4. Therefore, the Linagliptin bound to a metal chelator will target DPP4, such as located on the surface of immune cells. Products of identical chemical composition can not have mutually exclusive properties. A chemical composition and its properties are inseparable. Thus the claiming of a new use, new function or unknown property which is inherently present in the prior art does not necessarily make the claim patentable and does not render the old composition patentably new to the discoverer. In re Best, 562 F.2d 1252, 1254, 195 USPQ 430, 433 (CCPA 1977). Applicant asserts that when a small-molecule ligand is modified into a “ligand-linker-chelator-metal radionuclide” radioprobe, its targeting ability primarily depends on whether the pharmacophore can still enter and effectively match the binding pocket of the target protein. The length and flexibility of the linker further determine whether the chelating moiety causes steric hinderance at the protein surface or introduces unintended interactions. A linker that is too short or rigid may reduce binding affinity. A moderately extended linker may place the chelator into a solvent-exposed region, thus preserving binding to some degree. However, an excessively long linker can increase conformational entropy loss and non-specific binding risk. The instant claims are not drawn to a method of imaging myocarditis with a Linagliptin imaging probe. The reference of Jaafar-Thiel et al. was not used to teach that L is a linker moiety. The reference of Jaafar-Thiel et al. teaches that the L moiety may comprise a bond or a linker. The L moiety comprising a bond yields an imaging probe wherein the targeting moiety is bound directly to the chelating moiety (p20, [0208]). Therefore, there is no linker and the resulting radioprobe comprises “ligand-chelator-metal radionuclide.” Applicant assert that the chelators, such as DOTA or NOTA, when complexed with metal ions, alter the overall charge, polarity and conformational distribution of the molecule, thereby impacting the crucial pharmacokinetic parameters such as Log D, plasma protein binding, tissue permeability, and renal clearance/hepatic uptake. The chelating moiety PNG media_image4.png 186 318 media_image4.png Greyscale of Jaafar-Thiel et al. encompasses the p-SCN-Bn-DOTA chelator of the instant claims, has the same properties and is capable of the same functions, such as when complexed with metal ions it analogously provides crucial pharmacokinetic parameters. Applicant asserts that moreover, the oxidation state, ionic radius, and coordination geometry of the metal radionuclide further fine-tune the complex’s charge distribution and spatial footprint: more stable and inert metal-chelator combinations are beneficial for maintaining an intact probe in vivo. The reference of Jaafar-Thiel et al. teaches that the chelating moiety may optionally chelate 61Cu, 64Cu, 67Cu and that the targeting moiety is suitable for use with 68Ga. The reference of Low et al. teaches that the chelating moiety PNG media_image8.png 206 298 media_image8.png Greyscale may chelate 68Ga, 64Cu, 67Cu for PET and/or SPECT imaging. It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to chelate the 68Ga radionuclide of Low et al. to the chelating moiety PNG media_image4.png 186 318 media_image4.png Greyscale of Jaafar-Thiel et al. as Low et al. teaches that the chelator PNG media_image8.png 206 298 media_image8.png Greyscale chelates 68Ga, 64Cu, 67Cu for the advantage site specific targeting of the compounds to specific cell surface receptors for PET imaging of myocarditis in a subject. The substitution of one known radionuclide, such as copper radionuclide for another known radionuclide, such as 68Ga predictably yields a myocarditis-targeted radionuclide molecular probe/imaging agent. The 68Ga-chelated PNG media_image4.png 186 318 media_image4.png Greyscale of Jaafar-Thiel et al. encompasses the PNG media_image9.png 216 290 media_image9.png Greyscale moiety of the instant claims, has the same properties and is capable of the same functions, such as providing a stable and inert metal-chelator combination that is beneficial for maintaining an intact probe in vivo. Applicant asserts that in Jaafar-Thiel et al., the use of linagliptin as a probe precursor is limited to a conceptual proposal for FAP targeting. There is no sufficient or reproducible characterization data provided to substantiate the claimed compounds, nor are there in vivo animal data validating their biological behavior, target specificity, or imaging/diagnostic feasibility for DPP4-targeted molecular imaging. The instant claims are not drawn to a method of imaging myocarditis via targeting a Linagliptin imaging probe. The reference of Jaafar-Thiel et al. is stated above. The Linagliptin of Jaafar-Thiel et al. encompasses the Linagliptin of the instant claims, has the same properties and is capable of the same functions, such as targeting DPP4. Also, the Applicant concedes that Linagliptin is a known DPP4-targeted small-molecule inhibitor with high target specificity for DPP4. The chelating moiety PNG media_image4.png 186 318 media_image4.png Greyscale of Jaafar-Thiel et al. encompasses the p-SCN-Bn-DOTA chelator of the instant claims, has the same properties and is capable of the same functions, such as chelate 68Ga. Therefore, the Linagliptin bound to a metal chelator necessarily targets DPP4, has target specificity, and/or imaging/diagnostic feasibility for DPP4-targeted molecular imaging. Products of identical chemical composition can not have mutually exclusive properties. A chemical composition and its properties are inseparable. Thus the claiming of a new use, new function or unknown property which is inherently present in the prior art does not necessarily make the claim patentable and does not render the old composition patentably new to the discoverer. In re Best, 562 F.2d 1252, 1254, 195 USPQ 430, 433 (CCPA 1977). Applicant asserts that the 68Ga-DOTA-compound of the instant claims is an optimized technical systematic experimental pipeline, including candidate structure screening via computational modeling and structure-property analysis; and controllable synthesis of the compounds; and standard chemical and radiochemical characterization to confirm structure, purity and stability; and in vivo pharmacokinetics and biodistributions, yielding key data on organ uptake; and validation in disease animal models, demonstrating application efficacy and reproducibility. The instant claims are not drawn to a method of imaging myocarditis with a Linagliptin imaging probe. The instant claims are not drawn to a method of synthesizing a Linagliptin imaging probe. The references of Jaafar-Thiel et al. and Low et al. are stated above. The Linagliptin of Jaafar-Thiel et al. encompasses the Linagliptin of the instant claims, has the same properties and is capable of the same functions, such as targeting DPP4. The 68Ga-chelated PNG media_image4.png 186 318 media_image4.png Greyscale encompasses the PNG media_image9.png 216 290 media_image9.png Greyscale moiety of the instant claims, has the same properties and is capable of the same functions, such as chelating 68Ga and providing an effective probe for imaging myocarditis in vivo. Conclusion No claims are allowed at this time. Any inquiry concerning this communication or earlier communications from the examiner should be directed to MELISSA JEAN PERREIRA whose telephone number is (571)272-1354. The examiner can normally be reached M9-3, T9-3, W9-3, Th9-2, F9-2. 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, Michael Hartley can be reached at 571-272-0616. 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. /MELISSA J PERREIRA/Examiner, Art Unit 1618
Read full office action

Prosecution Timeline

May 08, 2025
Application Filed
Sep 22, 2025
Non-Final Rejection — §103
Dec 22, 2025
Response Filed
Jan 06, 2026
Non-Final Rejection — §103 (current)

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Study what changed to get past this examiner. Based on 5 most recent grants.

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Prosecution Projections

2-3
Expected OA Rounds
52%
Grant Probability
78%
With Interview (+25.7%)
3y 7m
Median Time to Grant
Moderate
PTA Risk
Based on 824 resolved cases by this examiner. Grant probability derived from career allow rate.

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