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 .
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 03/16/2026 was filed after the mailing date of the non-final on 11/28/2025. The submission is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
Status of the Claims
Claims 14-17 and 22-28 are pending in this application. Claims 1-13 and 18-21 have been cancelled by applicant.
Claim Rejections - 35 USC § 102
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.
Claims 14-16 and 22-24 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Wang et al. (Biochem. Mol. Bio., doi:10.20944/preprints202004.0315.v1, 12 pages – Not Peer Reviewed Version Published April 19th, 2020 – Final form cited in IDS – previously cited) (“Wang”).
Regarding claim 14, Wang discloses that it is now well accepted that angiotensin-converting enzyme II (ACE2) is the cell receptor of SARS-CoV-2 and the main route for receptor-mediated entry of the virus into the human host. Since ACE2 plays a pivotal role in cellular entry, ACE2 expressing cells serve as critical viral gateways (for viral replication) (page 2, lines 16-20). Wang teaches that high-cannabidiol (CBD) sativa extracts may be used to modulate ACE2 and TMPRSS2, which are disclosed as critical proteins required for SARS-CoV-2 entry into host cells (abstract). Wang discloses dilution of CBD extracts to about 0.01 mg/mL for their experiments, treating different tissue models with their extract solution (page 3, end of para. 1 and section 2.2).
Regarding claims 15 and 22-23, Wang’s disclosure focuses specifically on human host cells, as they mention SARS-CoV-2 uses receptor-mediated entry into the human host via ACE2, expressed in lung tissue, as well as oral and nasal mucosa, kidney, testes, and the
gastrointestinal tract. (abstract, lines 5-8). See also Section 2.2, page 3 and Figure 1, page 6 where different human tissue cells are disclosed.
Regarding claims 16 and 24, Wang discloses their isolated CBD extracts in a DMSO (a carrier and liquid preparation) (page 3, para. 1, lines 9-11).
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.
Claims 17 and 25-28 are rejected under 35 U.S.C. 103 as being unpatentable over Wang et al. (Biochem. Mol. Bio., doi:10.20944/preprints202004.0315.v1, 12 pages – Published April 19th, 2020 – cited in IDS – previously cited) (“Wang”); as applied to claims 14-16 and 22-24; in view of Hava et al. (US 2013/0203715 A1 – previously cited – cited in IDS) (“Hava”); further in view of Rudd et al. (Technology Networks, obtained from technologynetworks.com, [retrieved on Nov. 12th, 2025]<URL: https://www.technologynetworks.com/tn/articles/cbd-vs-thc-what-are-the-main-differences-390017> - previously cited) (“Rudd”).
The teachings of Wang are disclosed in the 102-section above and incorporated herein.
Wang further teaches that extracts with the highest CBD to THC ratios were best at inhibiting ACE2 levels in human cells (see #45 and #10 in Table 1 and their relative effects in downregulating ACE2 in Figures 2B, 3 and 4A-B).
While Wang does not specifically teach: (i) administration wherein CBD is the only active ingredient (claim 17); (ii) wherein the administered composition is a tablet, injection, or spray (claim 25); or (iii) wherein the CBD is administered with another antiviral (simultaneously, sequentially or separately), wherein the other antiviral is selected from those in claim 28 (claims 26-28); the teachings of Hava and Rudd are relied upon for these disclosures.
Hava discloses a method of treating a viral infection, including SARS-CoV (Hava’s claim 5; and [0056] line 8) comprising administration of CBD ([0014], last line of col. 1; and claim 9), thus suggesting a single active ingredient in their formulation. Hava teaches their composition may be in any suitable form, such as a spray ([0077], lines 1-5). Hava discloses their composition further comprising a co-therapeutic agent, such as an anti-viral ([0074], lines 1-6). Hava further discloses co-therapeutic agent may be administered before, after, or concurrently with the CBD ([0074], col. 2, top 3 lines, page 7), and teaches co-therapeutic antiviral agents, such as amantadine [0095].
Rudd teaches CBD is non-psychotropic and does not elicit a “high” while THC is psychotropic (page 4, para. 1).
Therefore, regarding claim 17, it would have been prima facie obvious to one of ordinary skill prior to the effective filing date of the instant application to contact a human cell with a composition comprising CBD as the only pharmaceutically active ingredient to inhibit SARS-CoV-2 replication, via inhibition of viral entry into the cell. One of ordinary skill would have been motivated to do so with a reasonable expectation of success because Wang discloses that high-CBD compositions (with low THC levels) were the most potent at inhibiting ACE2 expression, and that ACE2 is a critical protein required for SARS-CoV-2 entry into host cells; further because Hava suggests that their CBD composition, with no other active ingredients, is capable of treating a SARS-CoV infection in humans; and Rudd discloses that CBD, unlike THC, is not psychotropic and therefore does not illicit a “high,” which may be unpleasant for some subjects.
Regarding claim 25, Hava discloses their CBD composition may be administered in any suitable form, including a spray ([0077], lines 1-5). Therefore, one of ordinary skill would have been motivated to prepare a spray formulation comprising CBD in a carrier in order to spray cells, thus maximizing efficacy of the contacting of cells with CBD in order to inhibit SARS-CoV-2 replication. One of ordinary skill would have had a reasonable expectation of success in view of Wang’s disclosure of a CBD composition in DMSO; and Hava’s disclosure of a CBD composition in spray form.
Regarding claims 26-28, Hava discloses their composition further comprising a co-therapeutic agent, such as an anti-viral like amantadine ([0074], lines 1-6; and [0095]). Hava further discloses co-therapeutic agent may be administered before, after, or concurrently with the CBD ([0074], col. 2, top 3 lines, page 7).
Further comprising claim 27, Applicant is advised that the courts have held that any order of performing process steps is prima facie obvious in the absence of new or unexpected results (In re Gibson, 39 F.2d 975, 5 USPQ 230 (CCPA 1930); Ex Parte Rubin, 128 USPQ 440 (Bd. App. 1959)). See MPEP §2144.04 IV C. Therefore, the claimed order of steps is an obvious variant of the steps of the cited prior art.
Response to Arguments
Claim Rejections - 35 USC § 102
Applicant's arguments filed 03/02/2026 have been fully considered but they are not persuasive.
Applicant argues that Wang is directed to inhibition of viral entry into the cell, not inhibition of viral replication, stating that these are sequential stages in the viral life cycle, and that to inhibit viral replication, viral entry into the cell must have already occurred. Applicant cited Example 1 of the spec., which allegedly demonstrates reduction of viral nucleic acid load of cells infected by SARS-CoV-2.
This is not persuasive. As applicant states, viral replication occurs after viral entry into the cell, therefore, by inhibiting viral entry into the cell, viral replication will also be inhibited. Applicant is advised that the fact that the inventor has recognized another advantage which would flow naturally from following the suggestions of the prior art cannot be the basis for patentability. See Ex parte Obiaya, 227 USPQ 58, 60 (Bd. Pat. App. & Inter. 1985). The claim has been given the broadest reasonable interpretation (In re Hyatt, 211 F.3d1367, 1372, 54 USPQ2d 1664, 1667 (Fed. Cir. 2000) (see MPEP 2111); and Wang anticipates the instant claims.
In response to Applicant’s arguments regarding Example 1 of the spec. (starting page 12 of the specification) – Example 1 discloses infection of Vero E6 cells with SARS-CoV-2, followed by treatment with cannabidiol. It is noted that the features upon which applicant relies are not recited in the rejected claim(s). Although the claims are interpreted in light of the specification, limitations from the specification are not read into the claims. See In re Van Geuns, 988 F.2d 1181, 26 USPQ2d 1057 (Fed. Cir. 1993).
Claim Rejections - 35 USC § 103
Applicant's arguments filed 03/02/2026 have been fully considered but they are not persuasive.
Applicant argues Wang discloses inhibition of viral entry, not replication – see response to this argument in the section above. Applicant argues that Hava discloses no experimental validation to support efficacy of treatment against SARS-CoV; and that SARS-CoV-2 is a novel coronavirus with different pathogenicity from SARS-CoV; and that a person of ordinary skill in the art (POSITA) would not have expected Hava’s treatment scheme for SARS-CoV could be applied to inhibit viral replication of SARS-CoV-2 without additional research. Applicant argues that Hava and Wang are independent and unrelated, and that a POSITA would not have been motivated to combine the “two completely different mechanisms of action”. Applicant further argues Wang attributes inhibition to the “entourage effect” between CBD and THC, and that “whole plant extracts have more pronounced biological effects that individual cannabinoids”. Applicant argues that Wang’s data fails to establish an actual relationship between CBD content alone and the observed efficacy, citing Figures 2 to 5 – specifically citing extract #130 (2.63% CBD, 1:3 THC:CBD), which allegedly “downregulated ACE2”, while #131 (6.1% CBD, 1:14 THC CBD), with higher CBD content had no significant effect on ACE2 (Figure 2A) – Applicant states that based on Wang, a POSITA would have prioritized multi-component cannabis extracts over compositions comprising CBD of Formula I. Applicant argues that Rudd does not cure the deficiencies of Wang and Hava, only stating that CBD is not psychoactive, while THC is. Applicant further states there is no motivation to combine the art of record to arrive at the instant invention.
In response to applicant's arguments against the references individually, one cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986).
In response to applicant's argument that Hava and Wang are nonanalogous art, it has been held that a prior art reference must either be in the field of the inventor’s endeavor or, if not, then be reasonably pertinent to the particular problem with which the inventor was concerned, in order to be relied upon as a basis for rejection of the claimed invention. See In re Oetiker, 977 F.2d 1443, 24 USPQ2d 1443 (Fed. Cir. 1992).
In this case, Wang relates to administration of cannabidiol (high CBD cannabis extract) may be used to modulate ACE2 expression in COVID-19 target tissues (abstract); and further states “it would also be important to test the effects of C. sativa lines on other receptors involved in SARS-CoV2 entry” (page 10, para. 1, line 8). Hava discloses methods of treating viral infection, including SARS-CoV (a coronavirus related to SARS-CoV-2) comprising administration of CBD (see Hava’s claim 5; [0056], line 8; and [0014]; as well as claim 9). Regardless of Hava’s recitation that CBD functions as a TRP channel agonist, vs an ACE2 modulator in Wang’s disclosure, does not make Wang and Hava “non-analogous art”. A recitation of the intended use must result in a structural difference between the claimed invention and the prior art in order to patentably distinguish the claimed invention from the prior art. If the prior art structure is capable of performing the intended use, then it meets the claim. Note: MPEP 2111.02. Both Wang and Hava relate to the inhibition of a coronavirus cell entry comprising CBD.
In response to Applicant’s argument that Wang attributes inhibition to the “entourage effect” between CBD and THC, and that “whole plant extracts have more pronounced biological effects that individual cannabinoids” – Wang cites the “entourage effect” as a general characteristic of cannabinoids and terpenes, not specifically in the context of viral entry into the cell (see page 10 of Wang, last para.). Wang specifically says “The extracts of our most successful and novel high CBD C. sativa lines, pending further investigation, may become a useful and safe addition to the treatment of COVID-19 as an adjunct therapy” (abstract); and discloses that “less than 0.3% of total THC can be classified as CBD Hemp in Canada and USA” (page 11, lines 1-2).
In response to Applicant’s argument that Wang fails to establish an actual relationship between CBD content alone and the observed efficacy, citing Figures 2 to 5 – specifically citing extract #130 (2.63% CBD, 1:3 THC:CBD), and #131 (6.1% CBD, 1:14 THC CBD) (see Fig. 2A below). While this was the trend observed in EpiOral tissue, in Epilintestinal tissue, extract #45 (1.61% CBD, 1:54 THC:CBD) showed the lowest ACE2 levels across the board (see Fig. 4A-B below) – therefore, one of ordinary skill would have been motivated to use extract #45 (containing only 0.03% THC and a 1:54 THC to CBD ratio). Given Wang’s guidance that “less than 0.3% of total THC can be classified as CBD Hemp in Canada and USA” (page 11, lines 1-2), then Wang reads into the instant claims in view of Hava and Rudd.
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In response to applicant’s argument that there is no teaching, suggestion, or motivation to combine the references, the examiner recognizes that obviousness may be established by combining or modifying the teachings of the prior art to produce the claimed invention where there is some teaching, suggestion, or motivation to do so found either in the references themselves or in the knowledge generally available to one of ordinary skill in the art. See In re Fine, 837 F.2d 1071, 5 USPQ2d 1596 (Fed. Cir. 1988), In re Jones, 958 F.2d 347, 21 USPQ2d 1941 (Fed. Cir. 1992), and KSR International Co. v. Teleflex, Inc., 550 U.S. 398, 82 USPQ2d 1385 (2007).
In this case, Wang discloses that it is now well accepted that angiotensin-converting enzyme II (ACE2) is the cell receptor of SARS-CoV-2 and the main route for receptor-mediated entry of the virus into the human host. Since ACE2 plays a pivotal role in cellular entry, ACE2 expressing cells serve as critical viral gateways (for viral replication) (page 2, lines 16-20). Wang teaches that high-cannabidiol (CBD) sativa extracts may be used to modulate ACE2 and TMPRSS2, which are disclosed as critical proteins required for SARS-CoV-2 entry into host cells (abstract). Wang discloses dilution of CBD extracts to about 0.01 mg/mL for their experiments, treating different tissue models with their extract solution (page 3, end of para. 1 and section 2.2). Wang further teaches that extracts with the highest CBD to THC ratios were best at inhibiting ACE2 levels in human cells (see #45 and #10 in Table 1 and their relative effects in downregulating ACE2 in Figures 2B, 3 and 4A-B).
Hava discloses a method of treating a viral infection, including SARS-CoV (Hava’s claim 5; and [0056] line 8) comprising administration of CBD ([0014], last line of col. 1; and claim 9), thus suggesting a single active ingredient in their formulation. Hava teaches their composition may be in any suitable form, such as a spray ([0077], lines 1-5). Hava discloses their composition further comprising a co-therapeutic agent, such as an anti-viral ([0074], lines 1-6). Hava further discloses co-therapeutic agent may be administered before, after, or concurrently with the CBD ([0074], col. 2, top 3 lines, page 7), and teaches co-therapeutic antiviral agents, such as amantadine [0095].
Rudd teaches CBD is non-psychotropic and does not elicit a “high” while THC is psychotropic (page 4, para. 1).
Therefore, it would have been prima facie obvious to one of ordinary skill prior to the effective filing date of the instant application to contact a human cell with a composition comprising CBD as the only pharmaceutically active ingredient to inhibit SARS-CoV-2 replication, via inhibition of viral entry into the cell. One of ordinary skill would have been motivated to do so with a reasonable expectation of success because Wang discloses that high-CBD compositions (with low THC levels, such as extract #45, at 0.03% THC – considered CBD in the USA and Canada) were the most potent at inhibiting ACE2 expression, and that ACE2 is a critical protein required for SARS-CoV-2 entry into host cells; further because Hava suggests that their CBD composition, with no other active ingredients, is capable of treating a SARS-CoV infection in humans; further because Rudd discloses that CBD, unlike THC, is not psychotropic and therefore does not illicit a “high,” which may be unpleasant for some subjects.
Conclusion
THIS ACTION IS MADE FINAL. Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to JACKSON J HERNANDEZ whose telephone number is (571)272-5382. The examiner can normally be reached Mon - Thurs 7:30 to 5.
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/JACKSON J HERNANDEZ/Examiner, Art Unit 1627
/SARAH PIHONAK/Primary Examiner, Art Unit 1627