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
Pursuant to the amendment dated 06/05/2026, claims 1, 3, 5, 6, 8-10, 13, 25 and 35 were amended, claims 11, 15, 18-23 and 27-34 were canceled, and claim 36 was newly added. Claims 1-10, 12-14, 16-17, 24-26 and 35-36 are pending in the instant application and are examined on the merits herein.
Priority
The instant application is a National State Application of PCT/US2020/059644, filed on 11/09/2020 and claims benefit of 62/933,138 filed on 11/08/2019.
Withdrawn Rejections
Applicant’s amendment, filed on 06/05/2026, with respect to the rejection of claims 3, 5, 8-11, and 25 under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention, has been fully considered and is persuasive. Applicant has amended claims 3, 5, 8-10, and 25 to remove the phrase “optionally” and cancelled claim 11. The rejection is hereby withdrawn.
Applicant’s amendment, filed on 06/05/2026, with respect to the rejection of claims 6, 8, 10, and 11 under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention, has been fully considered and is persuasive. Applicant has amended claims 6, 8, and 10 to remove the phrase “and/or” and cancelled claim 11. The rejection is hereby withdrawn.
Rejections Necessitated by Amendment
The following are new and/or modified ground(s) necessitated by Applicants' amendment, filed on 06/05/2026, wherein instant independent claims 1, 13 and 35 were amended to alter the breadth and scope of the claims, claim 36 newly added, and wherein the remaining pending claims 2-10, 12, 14, 16, 17, 24-26, and 13-36 depend from said independent claims 1, 13 and 35.
New and/or Modified Rejections
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 1-5, 10, 13, 14, 24, 26, and 35-36 are rejected under 35 U.S.C. 103 as being unpatentable over Loughran (WO 2018/200931 A1, published 11/01/2018, see PTO-892 dated 02/26/2025) and Tan et al. (Expert Opinion on Therapeutic Targets, published 04/19/2017, see PTO-892) as evidenced by Zhang et al. (Blood, published 12/03/2015, see PTO-892).
Loughran drawn to the use of SACLAC as an acid ceramidase (AC) inhibitor for the treatment of acute myeloid leukemia (AML) (abstract). Loughran teaches a pharmaceutical composition comprising a therapeutically effective amount of at least one AC inhibitor and the AC inhibitor may be SACLAC (page 4, lines 24-26). Loughran teaches that the compounds may be administered to a mammalian host (page 27, line 25). Loughran further teaches the composition of SACLAC encapsulated in liposomes which can be comprised of a polyol such as polyethylene glycols (page 29, lines 1-8). Loughran teaches that the SACLAC blocks a common mechanism of ceramide detoxification in AML and is likely to provide therapeutic benefit by facilitating ceramide accumulation and apoptotic death of the proliferative cells (page 35, lines 16-18. Loughran teaches that an additional therapeutic agent may be administered along with SACLAC (page 4, lines 29-30). Loughran teaches the pharmaceutical composition may further comprise one or more additional therapeutic agents (page 25, lines 10-11). Loughran teaches that SACLAC may be administered up to 50 mg/kg body weight (page 36, line 13).
Regarding instant claim 24, Loughran teaches that SACLAC exhibited efficacy in all cell lines testing including drug resistant variants HL60/ABTR, HL60/VCR, KGlA-R and KG1-R. As evidenced by Zhang, KG1-R is a venetoclax-resistant AML cell line.
Loughran does not specify the additional therapeutic agents as recited in instant claim 1.
Tan is drawn to the study of the emergence of acid ceramidase as a therapeutic target for acute myeloid leukemia (title). Tan teaches that AC has emerged as a promising therapeutic target due to its role in neutralizing the pro-death effects of ceramide. Tan teaches that AC inhibitors may prove more effective when combined with other sphingolipid modulators such as exogenous short chain ceramide nanoliposomes (CNL) and that additional studies of AC inhibitors are needed in combination with existing AML therapies (page 588). Tan teaches that DNA hypomethylating agents such as azacitidine and decitabine can increase survival in a fraction of older AML patients (page 583).
Regarding instant claims 1-5, 13 and 14, it would have been prima facie obvious to combine the teachings of Loughran and Tan before the effective filing date of the claimed invention by selecting CNL as the additional therapeutic agent as taught by Tan in the method of treating AML with SACLAC as taught by Loughran to arrive at the claimed invention. It would have been prima facie obvious for one of ordinary skill in the art to combine SACLAC with an additional therapeutic agent such as CNL because Tan teaches that AC inhibitors may be more effective when combined with CNL and Laughran teaches that SACLAC is an AC inhibitor that may be combined with other therapeutic agents. One of ordinary skill in the art would have a reasonable expectation of success because Tan teaches that AC inhibitors may be more effective when combined with CNL and Laughran teaches that SACLAC is an AC inhibitor that may be combined with other therapeutic agents.
Regarding instant claim 10, it would have been prima facie obvious to combine the teachings of Loughran and Tan before the effective filing date of the claimed invention by selecting either decitabine or azacitidine as the additional therapeutic agent as taught by Tan in the method of treating AML with SACLAC as taught by Loughran to arrive at the claimed invention. It would have been prima facie obvious for one of ordinary skill in the art to combine SACLAC with an additional therapeutic agent such as CNL because Tan teaches that studies with AC inhibitors are needed in combination with existing AML therapies and that azacitidine and decitabine are existing AML therapies and Laughran teaches that SACLAC is an AC inhibitor that may be combined with other therapeutic agents. One of ordinary skill in the art would have a reasonable expectation of success because Tan teaches that studies with AC inhibitors are needed in combination with existing AML therapies and that azacitidine and decitabine are existing AML therapies and Laughran teaches that SACLAC is an AC inhibitor that may be combined with other therapeutic agents.
The combined teachings of Loughlin and Tan is silent "wherein said administration alters sphingolipid metabolism and induces alternative splicing of MCL-1 mRNA to favor a pro-apoptotic isoform," as recited by amended independent claim I and "wherein the composition [is configured] to alter sphingolipid metabolism and induces alternative splicing ofMCL-1 mRNA to favor a pro-apoptotic isoform induces apoptosis in AML cells," as recited in amended independent claims 13 and 35. Since the combined teachings of Loughlin and Tan is administering the same active ingredients, SACLAC and 6-CNL, in the same amounts of the instant specification (instant specification page 49, example 7, 5 mg/kg SACLAC), to the same patient population having a cancer that is a venetoclax-resistant AML, the composition taught by the combined teachings of Loughlin and Tan must also be able to achieve the limitation of altering sphingolipids metabolism and induces alternative splicing of MCL-1 mRNA to favor a pro-apoptotic solution. The instantly claimed results are merely a mechanism of action resulting from the administration step. MPEP 2112(II) makes clear that there is no requirement that a person of ordinary skill in the art would have recognized the inherent disclosure at the relevant time, but only that the subject matter is in fact inherent in the prior art reference. Furthermore, MPEP 2145 states that mere recognition of latent properties in the prior art does not render nonobvious an otherwise known invention. Applicant’s recitation of a new mechanism of action for the prior art method would not, by itself, distinguish the instant claims over the prior art teaching the same or nearly the same method steps.
Regarding instant claim 36, the combined teachings of Loughlin and Tan is silent to “wherein the SACLAC or the pharmaceutically acceptable salt thereof induced a 10-fold upregulation of Mel-1S isoform relative to a β-actin loading control and a 3-fold increase in the ratio of pro-apoptotic Mcl-1S to prosurvival Mcl-1L.” Since the combined teachings of Loughlin and Tan is administering the same active ingredients, SACLAC and 6-CNL, in the same amounts of the instant specification (instant specification page 49, example 7, 5 mg/kg SACLAC), to the same patient population having a cancer that is a venetoclax-resistant AML, the composition taught by the combined teachings of Loughlin and Tan must also be able to achieve the limitation of inducing a 10-fold upregulation of Mel-1S isoform relative to a β-actin loading control and a 3-fold increase in the ratio of pro-apoptotic Mcl-1S to prosurvival Mcl-1L. The instantly claimed results are merely a mechanism of action resulting from the administration step. MPEP 2112(II) makes clear that there is no requirement that a person of ordinary skill in the art would have recognized the inherent disclosure at the relevant time, but only that the subject matter is in fact inherent in the prior art reference. Furthermore, MPEP 2145 states that mere recognition of latent properties in the prior art does not render nonobvious an otherwise known invention. Applicant’s recitation of a new mechanism of action for the prior art method would not, by itself, distinguish the instant claims over the prior art teaching the same or nearly the same method steps.
Claim 12 is rejected under 35 U.S.C. 103 as being unpatentable over Loughran (WO 2018/200931 A1, published 11/01/2018, see PTO-892 dated 02/26/2025) and Tan et al. (Expert Opinion on Therapeutic Targets, published 04/19/2017, see PTO-892) as applied to claim 1 above, and further in view of Pereg et al. (US 2019/0046602, published 02/14/2019, see PTO-892).
Claim 1 is rejected as discussed above.
The combined teachings of Loughran and Tan are discussed above.
The combined teachings of Loughran and Tan do not teach that the additional therapeutic agents may be gemtuzumab, ozogamicin or midostaurin.
Pereg is drawn to methods of treating AML (title). Pereg teaches a method of treating AML that includes administering to a subject a therapeutically effective amount of a CXCR4 antagonist and a therapeutically effective amount of a chemotherapeutic agent (abstract).Pereg teaches that the chemotherapeutic acgent may be cytarabine (cytosine arabinoside, Ara-C, Cytosar-U), quizartinib (AC220), sorafenib (BAY 43-9006), lestaurtinib (CEP-701), midostaurin (PKC412), carboplatin, carmustine, chlorambucil, dacarbazine, ifosfamide, lomustine, mechlorethamine, procarbazine, pentostatin, (2′deoxycoformycin), etoposide, teniposide, topotecan, vinblastine, vincristine, paclitaxel, dexamethasone, methylprednisolone, prednisone, all-trans retinoic acid, arsenic trioxide, interferon-alpha, rituximab (Rituxan®), gemtuzumab ozogamicin, imatinib mesylate, Cytosar-U), melphalan, busulfan (Myleran®), thiotepa, bleomycin, platinum (cisplatin), cyclophosphamide, Cytoxan®), daunorubicin, doxorubicin, idarubicin, mitoxantrone, 5-azacytidine, cladribine, fludarabine, hydroxyurea, 6-mercaptopurine, methotrexate, 6-thioguanine, or any combination thereof (paragraph 0152).
Regarding instant claim 12, it would have been prima facie obvious to combine the combined teachings of Loughran and Tan with the teachings of Pereg before the effective filing date of the claimed invention by selecting either gemtuzumab ozogamicin or midostaurin as the additional therapeutic agent as taught by Pereg in the method of treating AML with a with SACLAC as taught by Loughran to arrive at the claimed invention. It would have been prima facie obvious for one of ordinary skill in the art to combine SACLAC with an additional therapeutic agent such as gemtuzumab ozogamicin or midostaurin because Tan teaches that studies should be done with existing AML therapies in combination with AC inhibitors, Loughran teaches the use of the AC inhibitor, SACLAC, for treating AML, and Pereg teaches that gemtuzumab ozogamicin or midostaurin may be used as chemotherapeutics in the treatment of AML. One of ordinary skill in the art would have a reasonable expectation of success because Tan teaches that studies should be done with existing AML therapies in combination with AC inhibitors, Loughran teaches the use of the AC inhibitor, SACLAC, for treating AML, and Pereg teaches that gemtuzumab ozogamicin or midostaurin may be used as chemotherapeutics in the treatment of AML.
Claim 25 is rejected under 35 U.S.C. 103 as being unpatentable over Loughran (WO 2018/200931 A1, published 11/01/2018, see PTO-892 dated 02/26/2025) and Tan et al. (Expert Opinion on Therapeutic Targets, published 04/19/2017, see PTO-892) as applied to claim 13 above, and further in view of Gunderson (The production and characterization of drug-loaded liposomal and PLGA nanocarriers for targeted treatment of acute myeloid leukemia, published 06/2016, see PTO-892).
Claim 13 is rejected as discussed above.
The combined teachings of Loughran and Tan are discussed above.
Loughran further teaches that SACLAC exhibits low solubility in vehicles for IV drug delivery and suboptimal uptake following i.p. injections (page 36, lines17-19). Drug delivery must be further enhanced in order to achieve additional reduction in leukemic burden and induce remission or cure (page 37, lines 3-5).
The combined teachings of Loughran and Tan do not teach that the AC inhibitor and/or the one or more additional active agents is encapsulated in a polymer nanoparticle, wherein the polymer nanoparticle comprises a biodegradable and biocompatible polymer.
Gunderson is drawn to the study of the production and characterization of drug-loaded liposomal and PLGA nanocarriers for targeted treatment of acute myeloid leukemia (title). Gunderson teaches that the advantages of the use of nanocarrier formulations is the ability to load/encapsulate or bind drugs and therapeutic agents to nanocarriers. Encapsulation enables the use of insoluble drugs by stably incorporating them into hydrophobic microenvironments of nanocarriers. Gunderson teaches that multiple drugs may be loaded onto the same nanocarrier at certain ideal ratios if necessary, as is the case for the daunorubicin-cytarabine loaded liposomal formulation CPX-351, currently in clinical trials for treatment against AM (page 5). Gunderson exemplifies the use of PLGA-PEG nanoparticles for drug encapsulation and release of chlorpromazine (page 27).
It would have been prima facie obvious to combine the combined teachings of Loughran and Tan with the teachings of Gunderson before the effective filing date by encapsulating the AC inhibitor taught by Loughran into the PEG-PGLA nanoparticle taught by Gunderson to arrive at the claimed invention. It would have been prima facie obvious for one of ordinary skill in the art to encapsulate the AC inhibitor, SACLAC, into the PEG-PGLA nanoparticle taught by Gunderson because Loughran teaches that SACLAC has low solubility and Gunderson teaches that PGLA nanocarriers can enable the use of insoluble drugs by incorporating them into hydrophobic microenvironments of nanocarriers. One of ordinary skill in the art would have a reasonable expectation of success because Loughran teaches that SACLAC delivery must be further enhanced in order to achieve additional reduction in leukemic burden and induce remission and Gunderson teaches that PGLA nanocarriers can enable the use of insoluble drugs by incorporating them into hydrophobic microenvironments of nanocarriers.
Claims 1-4, 6, 7, 9, 13, 14, 16, 17, 26 and 36 are rejected under 35 U.S.C. 103 as being unpatentable over Loughran (WO 2018/200931 A1, published 11/01/2018, see PTO-892 dated 02/26/2025) and Lewis (Cell Death Discovery, published 06/28/2018, see PTO-892 dated 02/26/2025).
The teachings of Loughran are discussed above.
Loughran further teaches that sphingolipid metabolism produces bioactive signaling molecules that regulate cell survival and differentiation. Ceramide, sphingosine, and sphingosine 1-phosphate (S1P) represent the bioactive core of the complex sphingolipid synthetic and inter-conversion pathways. Ceramide can be cleaved by a ceramidase to produce sphingosine, which is subsequently phosphorylated by sphingosine kinase (SK) to produce S1P. Ceramide accumulation induces cell death mechanisms while S1P promotes survival through receptor dependent or independent signaling pathways that play a key role in response to therapy. Ceramide and S1P also exert opposing effects on apoptotic regulators of the Bcl-2 family. Ceramide decreases Mcl-1 but S1P promotes Mcl-1 expression. Mcl-1 is a key survival protein and promising therapeutic target that is able to prevent apoptosis and mediate resistance to Bcl-2 targeting agents (page 2, lines 7-17). Treatment with SACLAC reduces S1P in AML cells (page 4, line 5).
Loughran does not specify the additional therapeutic agents may be a Bcl-2 inhibitor or cytarabine (AraC).
Lewis teaches the administration of venetoclax for treatment of AML. Lewis teaches that ceramides are deacylated by ceramidases to form sphingosine and subsequently, through the action of sphingosine kinases (SPHKs), generate sphingosine-2-phosphate (S1P). Notably, considerable evidence implicates important roles for several of these sphingolipid metabolic enzymes in tumorigenesis and resistance to therapy in hematological malignancies (page 2, column 2). Lewis also teaches that overexpression of AC can reduce the effectiveness and suggests that combining a Bcl-2 inhibitor with another compound for AC inhibition for treatment (column 2, page 6). Lewis teaches that treatment with cytarabine has a synergistic effect when combined with SPHK1 inhibition (page 6, column 2). SPHK1 inhibition is linked with Mcl-1 degradation and Mcl-1 is a marker of resistance to venetoclax. Therefore, it can be inferred that inhibition of SPHK1 with cytarabine could work to overcome venetoclax resistance in AML (page 7, column 1). Lewis further teaches that the targeting of Mcl-1 through AC inhibition warrants further investigation in combination with Bcl-2 inhibitor, Venetoclax (page 6, column 2).
It would have been prima facie obvious to combine the teachings of Loughran and Lewis before the effective filing date of the claimed invention selecting venetoclax as the additional therapeutic agent as taught by Lewis in the method of treating AML with SACLAC as taught by Loughran to arrive at the claimed invention. It would have been prima facie obvious for one of ordinary skill in the art to select venetoclax as the additional therapeutic agent because Lewis teaches combining a Bcl-2 inhibitor such as venetoclax with another compound for AC inhibition for treatment and Loughran teaches the administration of SACLAC, an AC inhibitor, with additional therapeutic agents for treatment of AML. One of ordinary skill in the art would have a reasonable expectation of success Lewis teaches combining a Bcl-2 inhibitor with an AC inhibitor for treating AML.
It would have been prima facie obvious to combine the teachings of Loughran and Lewis before the effective filing date of the claimed invention by selecting AraC as the additional therapeutic agents as taught by Lewis in the method of treating AML with SACLAC as taught by Loughran to arrive at the claimed invention. It would have been prima facie obvious for one of ordinary skill in the art to select AraC as the additional therapeutic agents because Lewis teaches AraC can work synergistically with SPHK1 inhibition and Loughran teaches the administration of SACLAC, an AC inhibitor, with additional therapeutic agents for treatment of AML. One of ordinary skill in the art would have a reasonable expectation of success Lewis teaches inhibition of SPHK1 with cytarabine could work to overcome venetoclax resistance in AML and Loughran teaches that SACLAC reduces S1P in AML cells.
The combined teachings of Loughlin and Lewis is silent "wherein said administration alters sphingolipid metabolism and induces alternative splicing of MCL-1 mRNA to favor a pro-apoptotic isoform," as recited by amended independent claim I and "wherein the composition [is configured] to alter sphingolipid metabolism and induces alternative splicing ofMCL-1 mRNA to favor a pro-apoptotic isoform induces apoptosis in AML cells," as recited in amended independent claims 13 and 35. Since the combined teachings of Loughlin and Lewis is administering the same active ingredients, SACLAC and ventoclax, in the same amounts of the instant specification (instant specification page 49, example 7, 5 mg/kg SACLAC), to the same patient population having a cancer that is a venetoclax-resistant AML, the composition taught by the combined teachings of Loughlin and Lewis must also be able to achieve the limitation of altering sphingolipids metabolism and induces alternative splicing of MCL-1 mRNA to favor a pro-apoptotic solution. The instantly claimed results are merely a mechanism of action resulting from the administration step. MPEP 2112(II) makes clear that there is no requirement that a person of ordinary skill in the art would have recognized the inherent disclosure at the relevant time, but only that the subject matter is in fact inherent in the prior art reference. Furthermore, MPEP 2145 states that mere recognition of latent properties in the prior art does not render nonobvious an otherwise known invention. Applicant’s recitation of a new mechanism of action for the prior art method would not, by itself, distinguish the instant claims over the prior art teaching the same or nearly the same method steps.
Regarding instant claim 36, the combined teachings of Loughlin and Lewis is silent to “wherein the SACLAC or the pharmaceutically acceptable salt thereof induced a 10-fold upregulation of Mel-1S isoform relative to a β-actin loading control and a 3-fold increase in the ratio of pro-apoptotic Mcl-1S to prosurvival Mcl-1L.” Since the combined teachings of Loughlin and Lewis is administering the same active ingredients, SACLAC and ventoclax, in the same amounts of the instant specification (instant specification page 49, example 7, 5 mg/kg SACLAC), to the same patient population having a cancer that is a venetoclax-resistant AML, the composition taught by the combined teachings of Loughlin and Lewis must also be able to achieve the limitation of inducing a 10-fold upregulation of Mel-1S isoform relative to a β-actin loading control and a 3-fold increase in the ratio of pro-apoptotic Mcl-1S to prosurvival Mcl-1L. The instantly claimed results are merely a mechanism of action resulting from the administration step. MPEP 2112(II) makes clear that there is no requirement that a person of ordinary skill in the art would have recognized the inherent disclosure at the relevant time, but only that the subject matter is in fact inherent in the prior art reference. Furthermore, MPEP 2145 states that mere recognition of latent properties in the prior art does not render nonobvious an otherwise known invention. Applicant’s recitation of a new mechanism of action for the prior art method would not, by itself, distinguish the instant claims over the prior art teaching the same or nearly the same method steps.
Claim 8 is rejected under 35 U.S.C. 103 as being unpatentable over Loughran (WO 2018/200931 A1, published 11/01/2018, see PTO-892 dated 02/26/2025) and Lewis (Cell Death Discovery, published 06/28/2018, see PTO-892 dated 02/26/2025) as applied to claims 1 and 6 above, and further in view of Wei et al. (J. Clin Oncol, published 03/20/2019, see PTO-892 dated 02/26/2025).
Claims 1 and 6 are rejected as discussed above.
The combined teachings of Loughran and Lewis are discussed above.
The combined teachings of Loughran and Lewis do not teach administration of the combination of the additional active agents venetoclax and cytarabine.
Wei is drawn to the study of venetoclax combined with low-dose cytarabine for patients with AML (title). Wei teaches that cytarabine had demonstrated the ability to down regulate Mcl-1 expression and act synergistically with venetoclax against AML (column 1, page1278).
It would have been prima facie obvious to combine the combine teachings of Loughran and Lewis with the teachings of Wei before the effective filing date of the claimed invention by selecting the combination of cytarabine and venetoclax as taught by Wei as the additional therapeutic agents with SACLAC for the treatment of AML taught by Loughran to arrive at the claimed invention. It would have been prima facie obvious for a person of ordinary skill in the art to select the combination of cytarabine and venetoclax as additional therapeutic agents in combination with SACLAC for the treatment of AML because Wei teaches that cytarabine and venetoclax work synergistically against AML, Lewis a Bcl-2 inhibitor combined with another compound for AC inhibition for treatments, and Loughran teaches that SACLAC is an AC inhibitor that may be used in combination with other therapeutics for the treatment of AML. One of ordinary skill in the art would have a reasonable expectation of success because Wei teaches that cytarabine and venetoclax work synergistically against AML, Lewis a Bcl-2 inhibitor combined with another compound for AC inhibition for treatments, and Loughran teaches that SACLAC is an AC inhibitor that may be used in combination with other therapeutics for the treatment of AML
Response to Arguments
Applicant's arguments filed 06/05/2026 have been fully considered in so much as they apply to the amended claims but they are not persuasive.
Applicant argues that Loughran, Tan, and Zhang, taken alone or in hypothetical combination, do not appear to disclose "wherein said administration alters sphingolipid metabolism and induces alternative splicing of MCL-1 mRNA to favor a pro-apoptotic isoform," as recited by amended independent claim I and "wherein the composition [is configured] to alter sphingolipid metabolism and induces alternative splicing ofMCL-1 mRNA to favor a pro-apoptotic isoform induces apoptosis in AML cells," as recited in amended independent claims 13 and 35. The argument is unpersuasive. Since the combined teachings of Loughlin and Tan is administering the same active ingredients, SACLAC and 6-CNL, in the same amounts of the instant specification (instant specification page 49, example 7, 5 mg/kg SACLAC), to the same patient population having a cancer that is a venetoclax-resistant AML, the composition taught by the combined teachings of Loughlin and Tan must also be able to achieve the limitation of altering sphingolipids metabolism and induces alternative splicing of MCL-1 mRNA to favor a pro-apoptotic solution. The instantly claimed results are merely a mechanism of action resulting from the administration step. MPEP 2112(II) makes clear that there is no requirement that a person of ordinary skill in the art would have recognized the inherent disclosure at the relevant time, but only that the subject matter is in fact inherent in the prior art reference. Furthermore, MPEP 2145 states that mere recognition of latent properties in the prior art does not render nonobvious an otherwise known invention. Applicant’s recitation of a new mechanism of action for the prior art method would not, by itself, distinguish the instant claims over the prior art teaching the same or nearly the same method steps.
Applicant argues that Loughran and Lewis, taken alone or in hypothetical combination,, do not appear to disclose "wherein said administration alters sphingolipid metabolism and induces alternative splicing of MCL-1 mRNA to favor a pro-apoptotic isoform," as recited by amended independent claim I and "wherein the composition [is configured] to alter sphingolipid metabolism and induces alternative splicing ofMCL-1 mRNA to favor a pro-apoptotic isoform induces apoptosis in AML cells," as recited in amended independent claim 13. The argument is unpersuasive. Since the combined teachings of Loughlin and Lewis is administering the same active ingredients, SACLAC and ventoclax, in the same amounts of the instant specification (instant specification page 49, example 7, 5 mg/kg SACLAC), to the same patient population having a cancer that is a venetoclax-resistant AML, the composition taught by the combined teachings of Loughlin and Lewis must also be able to achieve the limitation of altering sphingolipids metabolism and induces alternative splicing of MCL-1 mRNA to favor a pro-apoptotic solution. The instantly claimed results are merely a mechanism of action resulting from the administration step. MPEP 2112(II) makes clear that there is no requirement that a person of ordinary skill in the art would have recognized the inherent disclosure at the relevant time, but only that the subject matter is in fact inherent in the prior art reference. Furthermore, MPEP 2145 states that mere recognition of latent properties in the prior art does not render nonobvious an otherwise known invention. Applicant’s recitation of a new mechanism of action for the prior art method would not, by itself, distinguish the instant claims over the prior art teaching the same or nearly the same method steps.
Conclusion
No claims are allowed.
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). 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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/S.L.S./Examiner, Art Unit 1693
/SCARLETT Y GOON/Supervisory Patent Examiner, Art Unit 1693
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