Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
DETAILED ACTION
This office action is in response to Applicant’s Arguments/Remarks filed 04 August 2026 for application 18/561,881 filed 09 May 2024. Claim 1 is amended. Currently, claims 1-4 and 6-7 are pending.
REJECTIONS WITHDRAWN
The status for each rejection and/or objection in the previous office action is set out below.
35 U.S.C. 102, 103 and Double Patenting
Applicant’s amendments to claim 1, incorporating the limitations of claim 5 into claim 1, were sufficient to overcome the prior 103 rejection.
REJECTIONS – NEW & MAINTAINED
Claim Rejections - 35 USC § 103
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
(New) Claims 1-4 and 7 are rejected under 35 U.S.C. 103 as being unpatentable over Yong et al. (Expanding bone marrow-derived immune regulatory cells and immune regulatory B cells by activating GPCR19 pathway in vivo or in vitro, KR101494275B1, 2013) in view of Sette et al. (Adaptive immunity to SARS-CoV-2 and COVID-19, Cell 2021, 184, 861-881) and Tavares et al. (Blame the signaling: role of cAMP for the resolution of inflammation, Pharmacological Research 2020, 159, 105030).
Yong discloses the use of sodium taurodeoxycholate, HY2191, acting as a GPCR19 agonist and amplifying both Myeloid-derived suppressor cells (MDSC) and immunoregulatory B cells with accompanying anti-inflammatory activities, for the purpose of treating GPCR19-associated diseases including coronaviruses (para. 0009 - pg. 2 & pg. 4). This is achieved as GPCR19 activation increases the concentration of cAMP in bound cells, resulting in an increase in production of both MDSC and immunoregulatory B cells (para. 0009 - pg. 6 & 7).
Sette strengthens this strategy in their discussion on the role of B cells and antibodies during SARS-CoV-2 infections, where they teach that neutralizing antibodies, produced primarily by naïve B cells, develop rapidly in most SARS-CoV-2 infected people. Sette also teaches that generally higher antigen loads drive higher antibody titers and that neutralizing antibody titers are positively correlated with COVID-19 severity in large cohort studies (pg. 865-866 - Antibodies and B cells).
Tavares further reinforces these results by teaching that cAMP, regulator of numerous biological processes including cell migration, activation, proliferation and survival (pg. 2) is a known inducer of anti-inflammatory responses as it modulates the activities of innate immune cells including monocytes, macrophages, and neutrophils and work as a negative regulator to inflammation. During the onset of inflammatory responses, cellular levels of cAMP decrease as the levels of cyclic nucleotide phosphodiesterases (PDEs), enzymes that catalyze hydrolysis of cAMP, increases. Notably, cAMP, through protein kinase A (PKA) can reduce the expression of NF-kB and in turn reduce cytokine levels associated with including TNF-α, IL-1, IL-8, and IL-6.
While there is no prior art that reads upon the recited mechanism of action of inhibiting activation of NLRP3 inflammasome by inhibiting a function of P2X7 before the effective filing date, regardless of what the prior art recognized, as the mechanism the Applicant identified utilizes the same administering method step that administers the same active ingredient to the same population, thus, the newly recited mechanism would necessarily have to occur upon practicing the method fairly suggested by the cited prior art.
As such, it would have been prima facie obvious, to a person of ordinary skill in the art, before the effective filing date, to consider the use of sodium taurodeoxycholate as a GPCR19 agonist in stimulating the growth of B cells in the interest of antibody production for treating diseases such as a respiratory viral infection caused by SARS-CoV-2, whose disease progression correlates strongly on the production of naïve B cells and their antibodies. This mechanism-of-action is underpinned by several mechanisms, some known in the prior art and some cited by the instant application, but are necessarily inherent when treating the same disease and population as the prior art.
(New/Maintained) Regarding the limitation of claim 2, wherein the taurodeoxycholic acid is a compound represented by chemical formula 2, is met as sodium taurodeoxycholate is the sodium salt of taurodeoxycholic acid.
(New/Maintained) Concerning the limitation of claim 3, wherein the salt is a sodium salt, is met as the disclosed compound is sodium taurodeoxycholate.
Pertaining to the limitations of claim 4 are met as Yong also exemplifies that TNF-α, IFN-v, MCP1, IL-6 and IL-1b cytokines were significantly reduced after the administration of HY2191 in the case of a murine model with LPS and CLP induced inflammation (para. 0160 & 163). Tavares further reinforces these results by teaching that cAMP, regulator of numerous biological processes including cell migration, activation, proliferation and survival (pg. 2) is a known inducer of anti-inflammatory responses as it modulates the activities of innate immune cells including monocytes, macrophages, and neutrophils and work as a negative regulator to inflammation. During the onset of inflammatory responses, cellular levels of cAMP decrease as the levels of cyclic nucleotide phosphodiesterases (PDEs), enzymes that catalyze hydrolysis of cAMP, increases. Notably, cAMP, through protein kinase A (PKA) can reduce the expression of NF-kB and in turn reduce cytokine levels associated with including TNF-α, IL-1, IL-8, and IL-6.
With respect to the limitations of claim 7, wherein the coronavirus is one or more selected from the group consisting of Middle East respiratory syndrome coronavirus (MERS-CoV), severe acute respiratory syndrome coronavirus (SARS-CoV), and novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), are met as Sette teaches adaptive immunity to SARS-CoV-2 (abstract).
(New/Maintained) Claim 6 is rejected under 35 U.S.C. 103 as being unpatentable over Yong, Sette and Tavares as applied to claim 1-4 and 7 above, and further in view of CDC (Symptoms of COVID-19, CDC, cdc.gov/covid/signs-symptoms/index.html).
The teachings of Yong, Sette and Tavares are incorporated as reference herein.
They do not, however, specify the symptoms of a lower respiratory tract infection caused by coronavirus including fever, cough, phlegm, body aches, sore throat, diarrhea, conjunctivitis, headache, skin rash, difficulty in breathing, acute bronchitis, pneumonia, pulmonary suppuration, renal failure, renal dysfunction, septic shock, sepsis, and cytokine release syndrome.
The CDC website rectifies this by teaching that infection by the SARS-CoV-2, which caused the COVID-19 pandemic, can cause an infected person to experience a non-exhaustive list of symptoms including fever or chills, cough, shortness of breath or difficulty breathing, sore throat, congestion or runny nose, new loss of taste or smell, fatigue, muscle or body aches, headache, nausea or vomiting, or diarrhea.
These symptoms, while varying in patient populations or from patient-to-patient, are widely observed and experienced before and since the COVID-19 pandemic began. As such, it would be prima facie obvious, to a person of ordinary skill in the art, to have considered the symptoms inherent to persons infected with coronavirus as described by the CDC.
Response to Arguments
Applicant’s arguments, see pgs. 4-5, Rejections Under 35 U.S.C. § 103, filed 04 August 2026, with respect to claims 1-4 and 6-7 have been fully considered and are persuasive. Therefore, rejections of claims 1-4 and 6-7 have been withdrawn. However, upon further consideration, a new ground of rejection is made in view of a different interpretation of the previously applied references.
Conclusion
No claims are allowed.
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/ALLEN CHAO/Examiner, Art Unit 1622
/JAMES H ALSTRUM-ACEVEDO/Supervisory Patent Examiner, Art Unit 1622
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