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 .
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
This action is in response to the papers filed on September 10, 2025.
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 09/10/2025 has been entered.
Claims 1-9, 11-13, 18-20 and 24-37 are currently pending. Claims 1, 6, 18, 24, 32 and 33 are independent. No new claims are added, amended or canceled.
Therefore, claims 1-9, 11-13, 18-20, and 24-37 are examined on the merits.
The examiner acknowledges receiving an executed Declaration under 37 C.F.R. § 1.132 executed by Dr. Takanori Takebe on September 10, 2025 (“Takebe Declaration ”), and filed on 09/10/2025.
Response to arguments
Maintained objections/ Rejections in response to Applicants’ arguments or amendments
Claim Rejections - 35 USC § 112(a)
Claims 1-5, 20, 25-29 and 32-37 remain rejected under 35 U.S.C. 112, first paragraph, because the specification, while being enabling for
a method of producing liver organoid cells from PSCs via FGF signaling and inhibition of GSK3 signaling for a first period of time, and then incubating the produced foregut spheroids in the presence of retinoic acid at a concentration of 2uM for 1-5 days,
does not reasonably provide enablement for the method of producing liver organoids from PSCs utilizing any concentration of RA for any amount of time which would predictably have the functional property of producing the claimed liver organoids. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to practice the invention commensurate in scope with these claims.
While determining whether a specification is enabling, one considers whether the claimed invention provides sufficient guidance to make and use the claimed invention. If not, whether an artisan would have required undue experimentation to make and use the claimed invention and whether working examples have been provided. When determining whether a specification meets the enablement requirements, some of the factors that need to be analyzed are: the breadth of the claims, the nature of the invention, the state of the prior art, the level of one of ordinary skill, the level of predictability in the art, the amount of direction provided by the inventor, the existence of working examples, and whether the quantity of any necessary experimentation to make or use the invention based on the content of the disclosure is “undue” (In re Wands, 858 F.2d 731, 737, 8 USPQ2ds 1400, 1404 (Fed. Cir. 1988)). Furthermore, USPTO does not have laboratory facilities to test if an invention will function as claimed when working examples are not disclosed in the specification. Therefore, enablement issues are raised and discussed based on the state of knowledge pertinent to an art at the time of the invention. And thus, skepticism raised in the enablement rejections are those raised in the art by artisans of expertise.
Applicant’s working Example only discloses methods involving a method of producing liver organoids from PSCs comprising steps of obtaining definitive endoderm utilizing Activin A, BMP4, B27, FGF4 (FGF activator), N2 and CHIR99021(GSK3 inhibitor) (para. 00067, 00101). Then differentiating said definitive endoderm to posterior foregut spheroids and then culturing via three different methods which utilized retinoic acid at a concentration of 2uM RA for 1-5 days [00104] or 2uM RA for 4 days [00105] to result in the claimed liver organoid.
Applicant has failed to disclose any other culture duration times or concentrations of retinoic acid which would be expected to result in the claimed liver organoids.
Regarding the state of the prior art, Ng2 (US20180258400; IDS Reference) discloses retinoic acid utilized in amounts such as “0.2 μM to 5 μM” in methods of differentiation.
Regarding the level of predictability, Applicant’s own arguments state that the invention is characterized as “the unpredictable arts such as chemistry and biology” and even point to Ng2 to state that PSC generation of organoids is complex and requires differentiation across multiple intermediate states to generate specific somatic types, thus there is a great uncertainty how such cells may react (p. 2, last paragraph). Furthermore, based on the disclosure of Ang (WO2016/056999; cited by Applicant), utilizing retinoic acid at certain time periods is detrimental to the liver organoid formation. Therefore, without guidance from the specification, the formation of the organoids is unpredictable and would require undue experimentation.
Therefore, the specification fails to reasonably inform the ordinary artisan how to make and use the claimed liver organoids via specific culture steps with specific incubation periods which result in having the disclosed and recited biological and functional properties.
In conclusion, the specification fails to provide any guidance as to how an artisan would have dealt with the art-recognized limitations of the claimed method commensurate with the scope of the claimed invention and therefore, limiting the claimed invention to a method of culturing posterior foregut spheroids in the presence of 2uM RA for 1-5 days, thereby producing the liver organoids of the present invention.
Dependent claims are included in the basis of the rejection because they do not correct the primary deficiencies of the independent claim(s).
Response to Applicant’s arguments against the Enablement Rejection of claims 1-5, 20, 25-29 and 32-37
Applicant’s arguments and amendments filed 09/10/2025 are considered, however they are not persuasive. Applicant argues that in the Takebe Declaration it is shown that different concentrations and durations of retinoic acid can be utilized to make liver organoids as shown in item 3 and that a person of skill in the art would understand the concentration.
Examiner disagrees. First, Applicant’s working Example only discloses methods involving a method of producing liver organoids from PSCs comprising steps of obtaining definitive endoderm utilizing Activin A, BMP4, B27, FGF4, N2 and CHIR99021 (para. 00101). Then differentiating said definitive endoderm to posterior foregut spheroids and then culturing via three different methods which utilized retinoic acid at a concentration of 2uM RA for 1-5 days [00104] or 2uM RA for 4 days [00105] to result in the claimed liver organoid. Second, as detailed in the previous office action filed 10/31/2024, Applicant’s own arguments state that the invention is characterized as “the unpredictable arts such as chemistry and biology” and even point to Ng2 to state that PSC generation of organoids is complex and requires differentiation across multiple intermediate states to generate specific somatic types, thus there is a great uncertainty how such cells may react (p. 2, last paragraph). Furthermore, based on the disclosure of Ang (WO2016/056999; cited by Applicant), utilizing retinoic acid at certain time periods is detrimental to the liver organoid formation.
Third, the Takebe Declaration has been considered, however, this is not persuasive for any amount of retinoic acid to form organoids. The Takebe Declaration does show concentrations other than what is claimed, specifically a reduction to 0.5uM from the beginning 2uM but it does not provide a scope beyond that of the retinoic acid at 2uM.
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The main argument of the scope of enablement is not concerning that less retinoic acid may be possible, but that retinoic acid at certain dosages at certain points of development is detrimental. Ng2 (US20180258400; IDS Reference) discloses retinoic acid utilized in amounts such as “0.2 μM to 5 μM” in methods of differentiation and therefore, the range shown in Appendix A was already shown to be enabled and discussed in the above Enablement rejection. While scientists might be able to adjust the concentration, there is still a specific time point and duration utilized in Appendix A not claimed in the invention.
Therefore, the utilization of RA without proper scope of when to add the component and for how long would result in undue experimentation.
Claim Rejections - 35 USC § 103
Claim 6, 11 and 13 remain rejected under 35 U.S.C. 103 as being unpatentable over Sato (US20120196312) in view of Gissen et al. (2015. J Hepatol 63(4): 1023–103).
This rejection has been modified as necessitated by the Applicant’s response filed 09/10/2025.
Sato et al. teaches an in vitro liver organoid derived from epithelial stem cells which comprises or consists of a cystic structure with on the outside a layer of cells with buds and a central lumen as depicted in FIG. 55. Sato further teaches that this liver organoid may demonstrate a function inherent to healthy liver tissue, have an elongated shape, with 2 defined domains, i.e., a single layered epithelial domain where highly polarized cells are detected and keratin markers are expressed (this domain resembles the bile duct domain) and the other domain constitutes the main body of the organoid and is formed by a multilayered epithelia with non-polarized cells wherein albumin expression may be detected (Figure 55 A-B, para. 0286-278, 0383). Therefore it is interpreted that Sato teaches polarized cells around a lumen in a liver organoid.
However, Sato et al. does not teach microvilli and mesenchymal cells comprising the luminal structure nor does it explicitly state that the polarized cells are hepatocytes.
Gissen et al. teaches the structural and functional polarity of hepatocytes which are uniquely organized with a basal membrane facing liver sinusoidal endothelial cells (Abstract). Establishment and maintenance of hepatocyte polarity is essential for many functions of hepatocytes and the hepatocytes give rise to the bile canaliculus which has microvilli (p. 1023). These microvilli dramatically increase the surface area of the bile canaliculus for absorption and a lack of microvilli can result in liver disease and malabsorption (p. 1023, 1028, 1030).
It would be obvious to one of ordinary skill in the art that a liver organoid with a lumen surrounded by polarized cells as taught by Sato et al. would form microvilli in the lumen as taught by Gissen et al. with a reasonable expectation of success as it is known in the art that microvilli are formed through the polarity of the hepatocytes in the liver (Gissen et al., Abstract, p. 1023). An artisan would be motivated to modify the luminal structure with microvilli in their liver organoid as they are part of the liver’s functionality through their ability to increase absorption (Gissen et al.; p. 1028, 1030). Sato additionally teaches that epithelial cells which lose polarity due to illness, become mesenchymal cells (p. 1033), therefore, if these liver organoids are utilized in drug testing and modeling liver disease (Sato, para. 0301), an artisan would have mesenchymal cells present at any point within testing with a reasonable expectation of success. While Sato states that it is preferred the organoid is in a non-mesenchymal matrix (para. 0188), this indicates that in the broader embodiments, mesenchymal matrices are included.
Regarding claim 11, the combination of Sato and Gissen make obvious claim 6. Moreover, Sato et al. teaches that the liver organoid can express PROX1 and C3 (para. 0253, 0260, 0263)
Regarding claim 13, the combination of Sato and Gissen make obvious claim 6. Moreover, Sato et al. does not explicitly state that the liver organoid does not comprise inflammatory cells. However, as it does not state that it does comprise any inflammatory cells such as T cells, it is interpreted to be free of inflammatory cells.
Therefore the invention would be obvious to one of ordinary skill in the art at the time of the effective filing date.
Response to Applicant’s arguments against the 103 Rejection of claims 6, 11, and 13, and additionally all dependent claims
Applicant’s arguments and amendments filed 09/10/2025 are considered, however they are not persuasive. Applicant argues that while Gissen may describe microvilli on hepatocytes, it would not be obvious to envision an organoid with internalized microvilli with a reasonable expectation of success as the Takebe Declaration describes it as “counterintuitive” and it had not at that point been reliably engineered in vitro.
Examiner disagrees. As stated in the above 103 rejection It would be obvious to one of ordinary skill in the art that a liver organoid with a lumen surrounded by polarized cells as taught by Sato et al. would form microvilli in the lumen as taught by Gissen et al. with a reasonable expectation of success as it is known in the art that microvilli are formed through the polarity of the hepatocytes in the liver (Gissen et al., Abstract, p. 1023). Therefore such a feature could be formed as a result of organoid formation. Sato additionally teaches that epithelial cells which lose polarity due to illness, become mesenchymal cells (p. 1033), therefore, if these liver organoids are utilized in drug testing and modeling liver disease (Sato, para. 0301), an artisan would have mesenchymal cells present at any point within testing with a reasonable expectation of success. Therefore, such structures would form with a reasonable expectation of success in the claimed liver organoid.
Therefore, Gissen provides teachings and predictability of the structures forming in the production of the organoids claimed.
Claim 8 is rejected under 35 U.S.C. 103 as being unpatentable over Sato (supra) in view of Gissen et al. (supra) as applied to claim 6, above, and in further view of Ramachandran et al. (2015. PLOs One 10(10): 1-12; IDS Reference filed on 09/10/2019).
This rejection has been modified as necessitated by the Applicant’s response filed 09/10/2025.
As discussed in the 103 rejection of claim 6, above, Sato and Gissen et al. render obvious an in vitro liver organoid derived from an epithelial stem cell comprising a luminal structure with polarized hepatocytes and internalized microvilli comprising mesenchymal stem cells.
However, these references do not teach that the organoid comprises Kupffer cells or stellate cells.
Ramachandran et al. teaches liver organoids made from various cell types (Abstract). Furthermore, Ramachandran et al. teaches that ongoing experiments aim at further optimizing the parameters for long term culture and differentiation of liver organoids as well as the integration of liver cell types such as Kupffer cells and stellate cells in order to generate organoids which resemble in vivo conditions (p. 12, last paragraph).
It would have been obvious to one of ordinary skill in the art to include as Kupffer cells and stellate cells as taught by Ramachandran et al. In the liver organoid taught by Sato and Gissen et al. with a reasonable expectation of success. An artisan would be motivated to include Kupffer cells and stellate cells in liver organoids in order to generate organoids which resemble in vivo conditions (Ramachandran et al., p. 12, last paragraph).
Therefore, the invention would be obvious to one of ordinary skill in the art.
Claims 9, 30, and 31 are rejected under 35 U.S.C. 103 as being unpatentable over Sato (supra) in view of Gissen et al. (supra) as applied to claim 6 above, and in further view of Ng2 (US20180258400; IDS Reference).
This rejection has been modified as necessitated by the Applicant’s response filed 09/10/2025.
As discussed in the 103 rejection of claim 6 above, Sato and Gissen et al. render obvious a liver organoid derived from an epithelial stem cell comprising a luminal structure with polarized hepatocytes and internalized microvilli comprising mesenchymal cells.
However, these references do not teach that the organoid is characterized by having bile production capacity or bile transport activity.
Regarding claims 9 and 31, Ng2 teaches liver organoids derived from pluripotent stem cells (Abstract). These organoids contain at least two cell types consisting of hepatocytes, cholangiocytes, liver specific endothelial cells (LSEC), stellate cells, hepatic myofibroblast and hepatoblasts (para. 0008). Furthermore, NgPatent teaches that the liver organoids form bile ducts and the organoids are capable of performing liver functions (para. 0020). The bile canaliculi is also functional as the hepatocyte secreted molecules (CDF) is shown to be transported from the bile canaliculi into bile duct-like cyst structure formed by the cholangiocytes (FIG. 36A-36C). Thus, the liver organoid described herein exhibits organ level functions which could only be achieved by functional interaction of multiple cell types to form tissue structures (para. 0463).
It would be obvious to one of ordinary skill in the art to modify liver organoids as taught by Sato and Gissen et al. to have bile transport activity or production such as the liver organoids of Ng2 with a reasonable expectation of success. As the method steps of McCracken are the same as the present application, the method would yield the same result of liver organoids. Furthermore, one would be motivated to have liver organoids which exhibit bile transport activity or production as these liver organoids would allow investigation into organ level functions in a dish which would be more reflective of human specific liver diseases (Ng2; para. 0463)
Regarding claim 30, the combination of Sato and Gissen make obvious claim 6. Moreover, Sato et al. teaches that the organoids are comprised of hepatocytes, cholangiocytes and stem cell markers which express ALB, HNF4a, and epcam (para. 0247, 0152, 0260, 0272). Additionally the staining of e-cadherin was utilized therefore the organoids express e-cadherein (para. 383) and the organoids in culture conditions genes such as AFP were detected (para 0559). However Sato does not teach that the organoids express RBP4, CK19, HNF6, CYP3A4. Although not explicitly taught, as evidenced by Ng2 teaches that cells such as cholangiocytes, hepatocytes and other liver specific cells in cultured liver organoids express markers of HNF4a, AFP, CK19, ALB, HNF6 and CYP3A4 (para. 0008-0011, 249, claims 84-87), therefore the liver organoid of Sato and Gissen would have a reasonable expectation of success in expressing the claimed markers.
Therefore the invention as a whole would be obvious to one of ordinary skill in the art.
Claim 12 is rejected under 35 U.S.C. 103 as being unpatentable over Sato (supra) in view of Gissen et al. (supra) as applied to claim 6 above, and in further view of Markova et al. (2013. Clin Pharmacol Ther. 94(6):678-86; IDS Reference filed 09/10/2019)
This rejection has been modified as necessitated by the Applicant’s response filed 09/10/2025.
As discussed in the 103 rejection of claim 6 above, Sato and Gissen et al. render obvious a liver organoid derived from an epithelial stem cell comprising a luminal structure with polarized hepatocytes and internalized microvilli comprising mesenchymal cells. Sato further teaches that the liver organoids are useful in regenerative medicine, for example in acute liver failure or disease, and additionally are useful in non-therapeutic studies such as liver embryology, liver cell lineages, and differentiation pathways; gene expression studies including recombinant gene expression; mechanisms involved in liver injury and repair; research of inflammatory and infectious diseases of the liver and studies of pathogenetic mechanisms (para. 0287, 0301). However, these references do not teach that the organoid comprises a drug metabolism cytochrome variant.
Markova et al. teaches that Bosentan (Tracleer) is an endothelin receptor antagonist prescribed for the treatment of pulmonary arterial hypertension (PAH). Its use is limited by drug-induced liver injury (DILI). Morkova et al. found that CY2C9*2 is a potential marker of Bosentan induced liver injury (Abstract). Pharmacogenetic marker might be useful in the identification of patients at increased risk of this serious toxicity and lead to alterations in treatment that would avoid this unnecessary risk if further validated (p. 683).
It would be obvious to one of ordinary skill in the art to modify a liver organoid for the purpose of studying liver disease as taught by Sato et al. and Gissen et al. to comprise a drug metabolism cytochrome variant such as CY2C9*2 as taught by Markova et al. with a reasonable expectation of success. An artisan would be motivated to alter the liver organoid with a drug metabolism cytochrome variant such as CY2C9*2 in order to use it for a known function of studying disease (Sato; para. 0287, 0301) And additionally validating CY2C9*2 as a potential marker of Bosentan induced liver injury (Markova et al.; Abstract, p. 683).
Therefore, the invention would be obvious to one of ordinary skill in the art at the time of the effective filing date.
Claim 18, 19 and 24 are rejected under 35 U.S.C. 103 as being unpatentable over Sato (supra) in view of Gissen et al. (supra) as applied to claim 6 above, and in further view of Ortega (US2013/0189327; IDS Reference 022 filed on 02/26/2021) and Ortega2 (US2017/0191030, US filing date: May 2015; IDS filed 02/26/2020)
This rejection has been modified as necessitated by the Applicant’s response filed 09/10/2025.
As discussed in the 103 rejection of claim 6, above, Sato and Gissen et al. render obvious a liver organoid derived from an epithelial stem cell comprising a luminal structure with polarized hepatocytes and internalized microvilli comprising mesenchymal cells. However, these references do not teach that the liver organoids are implanted in patients in order to treat liver disease or that the liver organoids are contacted with a candidate compound
Ortega teaches purposes of liver organoids (Abstract). Specifically, Ortega teaches that liver organoids may be used in regenerative medicine to repair the liver, for example the treatment of metabolic liver disease (para. 0233, para. 0237).
It would be obvious to one of ordinary skill in the art to utilize the liver organoids taught by Sato and Gissen for the purpose of repairing the liver in the case of metabolic liver diseases as taught by Ortega with a reasonable expectation of success. An artisan would be motivated to utilize the liver organoids of Sato and Gissen as Ortega teaches that liver organoids are known in the art to be utilized for regenerative medicine and therefore it would be substituting a known liver organoid for another.Regarding claim 24, the combined teachings of Sato and Gissen render obvious claim 6.
However, these references do not teach that the liver organoids are contacted with a candidate compound for drug testing.
Ortega2 teaches contacting liver organoids with candidate compounds for the purpose of drug discovery and toxicology screening. The method involves exposing an organoid to one or a library of candidate molecules and evaluating organoids for any effects to identify the effects as a potential drug or cosmetic (para. 0081, 0306, 0326-0327).
It would be obvious to one of ordinary skill in the art to utilize the liver organoids taught by Sato and Gissen for the purpose of drug screening via contacting with candidate compounds taught by Ortega2 with a reasonable expectation of success. Doing so would be substituting liver organoids known for the same purpose of mimicking the environment of the liver. This would allow the tailoring of treatment according to responsiveness (Ortega2, para. 0322).
Therefore, the invention would be obvious to one of ordinary skill in the art at the time of the effective filing date.
Double Patenting
Claim 1-9, 11-13, 18-20, and 24-37 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claim 1-5, 24-27, and 29-41, of copending Application No. 16/611,998 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of 16/611,998 recite a genus for which the claims in the current application are the species. ‘998 recites a liver organoid made by the same process with the same method steps expressing the same markers which would inherently be the liver organoid of the present application. The singular difference in claim language between Claim 1 and Claim 1 of ‘998 is the presence of a wnt activator, however in Claim 31 of ‘998, GSK3 inhibitors are included in the genus of Wnt signaling pathway activators.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claim 1-9, 11-13, 18-20, and 24-37 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 1-17 of US Patent No. 12428622 (formerly copending Application No. 17/275,169). Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of US Patent No. 12428622 recite a genus for which the claims in the current application are the species. ‘622 recites a liver organoid made by the same process with the same method steps expressing the same markers which would inherently be the in vitro liver organoid of the present application. The difference in claim language between Claim 1 and Claim 1 of ‘622 is the presence of a wnt activator, however, GSK3 inhibitors are included in the genus of Wnt signaling pathway activators. Both the present application and ‘622 produce liver organoids, though ‘622 intends to utilize the liver organoid to produce HSCs.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
In response to Applicant’s arguments against the Double Patenting rejection of claims 1-9, 11-13, 18-20, and 24-37
Applicant’s arguments have been considered, however they are not persuasive. Applicant requests all double patenting rejections be held in abeyance. Examiner denies this request. It is noted that former Application ‘169 is newly patented and is now US12428622 (Patent ‘622)
Therefore, the rejection is maintained.
Conclusion
No claims are allowed.
All claims are identical to or patentably indistinct from, or have unity of invention with claims in the application prior to the entry of the submission under 37 CFR 1.114 (that is, restriction (including a lack of unity of invention) would not be proper) and all claims could have been finally rejected on the grounds and art of record in the next Office action if they had been entered in the application prior to entry under 37 CFR 1.114. Accordingly, THIS ACTION IS MADE FINAL even though it is a first action after the filing of a request for continued examination and the submission under 37 CFR 1.114. See MPEP § 706.07(b). 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.
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/ALEXANDRA F CONNORS/Examiner, Art Unit 1634
/MARIA G LEAVITT/Supervisory Patent Examiner, Art Unit 1634
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