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 .
Status of the Claims
Claims 4, 6-7, 9-21 and 24-26 are pending in the instant examination and subject to examination herein.
Information Disclosure Statement
The information disclosure statements (IDS) submitted on 12/17/2024 and 12/23/2024 are in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statements are being considered by the examiner.
Claim Rejections - 35 USC § 112(b)
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 4, 6-7, 9-21 and 24-26 are rejected 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.
Claim 4 is drawn to a method of slowing kidney function decline in a patient suffering from Type 1 diabetes (T1D) while minimizing the risk of diabetic ketoacidosis, the method comprising the following steps:
Identifying a patient suffering from both T1D and chronic kidney disease (CKD);
Administering to the patient a therapeutically effective amount of a sodium-glucose cotransporter 2 (SGLT2) inhibitor.
The term “while minimizing the risk of diabetic ketoacidosis” is indefinite because a person of ordinary skill in the would not know whether the method is being implemented according to the claim. The claim does not require that a patient treated with the claimed method does not experience diabetic ketoacidosis (DKA), or that a patient treated with the claimed method experiences DKA below any given rate (number of occurrences within a given time period) or severity.
The instant Specification defines the term “minimizing the risk of DKA” as meaning “reduces the relative risk [of DKA] versus placebo as compared to the relative risk observed when the SGLT2 inhibitor is administered to a T1D patient without CKD (e.g., a patient with a GFR category of G11 or G22 and a CGA category of A13). Applicant provides, in Table 6 (page 14) evidence that across populations of patients with CKD (525 patients) versus without CKD (76 patients), a lower percentage of patients with CKD experienced DKA compared the percentage of patients without CKD who experienced DKA (2.6% without 3.8%, respectively). However, both populations of patients included patients who experienced DKA. The rates of DKA occurrence across populations does not inform whether any particular patient with CKD is going to have a lower risk The instant Specification does not provide any particular benchmark “risk of DKA” of a “patient without CKD” to be used for comparison of a patient to be treated with the method of claim 4, or any means to holistically assess the “risk of DKA” for a candidate patient with CKD who may be treated with the claimed method or is being or has been treated with the claimed method. Thus, the claim is indefinite because a person of ordinary skill in the art would not know, when selecting a patient to be treated with the method of claim 4, that the intended result of “minimizing the risk of DKA” will be met or has been met.
Claims 6-7, 9-21 and 24-26 are indefinite because these claims depend from claim 4 and do not resolve the indefiniteness of the term “minimizing the risk of DKA”.
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.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claims 4, 6-7, 9, 13 and 15-18 are anticipated by van Raalte.
Claims 4, 6-7, 9, 13 and 15-18 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by van Raalte (van Raalte, D. H., et al.; Diabetes Care, v42, pp1921-1929; 2019)4.
Claim 4 is drawn to a method of slowing kidney function decline in a patient suffering from Type 1 diabetes (T1D) while minimizing the risk of diabetic ketoacidosis, the method comprising the following steps:
Identifying a patient suffering from both T1D and chronic kidney disease (CKD);
Administering to the patient a therapeutically effective amount of a sodium-glucose cotransporter 2 (SGLT2) inhibitor.
The terms “slowing kidney function decline” and “minimizing the risk of ketoacidosis” are not found further limiting on the structure of the claimed method, as these do not impact the manner in which the method is performed, and are therefore considered as intended results of the method.
Van Raalte teaches a review of two clinical trials of adult patients with T1D (inTandem1 and inTandem2), wherein patients were treated with 200 mg/day or 400 mg/day of the SGLT2 inhibitor sotagliflozin in addition to optimized insulin therapy (Abstract, page 1921). Van Raalte teaches the results of treatment for a sub-population of patients with baseline urinary albumin-to-creatinine ratio (UACR) of ≥30 mg/g, a marker of chronic kidney disease (CKD) as indicated by the instant Specification (page 2, lines 12-17): the elevated UACR patients were found to have the UACR reduce by 23.7% or 18.3% (versus placebo) upon treatment with 200 mg/day or 400 mg/day, respectively, of sotagliflozin (Abstract, page 1921).
Thus, claim 4 is anticipated by the teaching of van Raalte.
Claim 6 further limits claim 4 to wherein the SGLT2 inhibitor to be administered is sotagliflozin, and is met by the teaching of van Raalte as discussed above.
Claim 7 further limits claim 4 to wherein the patient is on insulin therapy, and is met by the teaching of van Raalte as discussed above.
Claim 9 further limits claim 4 to wherein the patient has an estimated glomerular flow rate (eGFR) of <60 mL/min/1.73 m2. Van Raalte provides baseline characteristics of the trial patients in Table 1 (page 1923), and includes that 4-5% of patients in each arm of the trials (placebo/200mg/400mg) had eGFR <60 mL/min/1.73 m2.
Claim 13 further limits claim 4 to wherein the patient has UACR ≥30 mg/g, and is met by the teaching of van Raalte as discussed above.
Claim 15 further limits claim 4 to wherein the patient has an eGFR<60 mL/min/1.73 m2 and UACR≥30 mg/g. A person of ordinary skill in the art would at once envisage that these sub-groups, which are shown in van Raalte’s Table 1 (page 1923) to represent 4-5% and 12-14% of the populations of each arm of the studies, would overlap, and van Raalte does not teach any exclusion of participants having both of these attributes, thus patients having both of these attributes would be expected to be present in the study.
Claim 16 further limits claim 4 to wherein the patient has a BMI ≥27 kg/m2. Van Raalte shows in Table 1 (page 1923) that the average BMI in each arm of the studies was >28 kg/m2, thereby indicating that some patients with BMI ≥27 kg/m2 were included.
Claim 17 further limits claim 4 to wherein the patient satisfies at least one criteria from a Markush group of criteria that includes that the patient is an adult, and is met by the teaching of van Raalte as discussed above.
Claim 18 further limits claim 17 to wherein the patient is an adult, and is met by the teaching of van Raalte as discussed above.
Thus, claims 6-7, 9, 13 and 15-18 are anticipated by the teaching of van Raalte.
Claims 4, 7, 9-10, 12-13, 15, 17-18 and 24-26 are anticipated by Hironaka.
Claims 4, 7, 9-10, 12-13, 15, 17-18 and 24-26 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Hironaka (Hironaka, J., et al; Diabetes Research and Clinical Practice, v202, article 110794, pp1-6; 20235,6).
The limitations of claims 4, 7, 9, 13, 15 and 17-18 are discussed in the rejection above and hereby incorporated into the instant rejection.
Hironaka teaches a study in the effects of the SGLT2 inhibitor dapagliflozin on renal function in T1D patients (Abstract). Hironaka shows the characteristics of the study participants in Table 1 (page 3, right hand side), including that the dapagliflozin treatment group included 22% patients with eGFR < 60 mL/min/1.73 m2, 6% patients with eGFR <45 mL/min/1.73 m2 and 26% of patients with UACR ≥30 mg/g.7 Hironaka teaches that during the course of the study, overall decline in eGFR was less in the dapagliflozin treatment group compared to the placebo group (Abstract and Figure 2, page 4). Regarding diabetic ketoacidosis (DKA), Hironaka teaches that although the treatment group included 2 cases of DKA compared to the 1 case of DKA in the placebo group, one of the DKA cases in the treatment group was attributed to insulin pump failure and that the DKA incidence between treatment/placebo group is considered to be equivalent (page 5, right hand side, first full paragraph).
Thus, claim 4 is anticipated by the teaching of Hironaka.
Regarding claim 7, while Hironaka teaches that patients took insulin along with dapagliflozin, as evidenced by Hironaka’s stating that the dose of daily insulin of the study participants is one of the secondary outcomes of the study (page 2, right column, section 3.2) and as Hironaka provides the total daily insulin dose as an attribute of the study population in Table 1 (page 3, right hand side), and also informs that 12% of the dapagliflozin group included patients specifically receiving insulin via an insulin pump (page 3, Table 1, right hand side).
Regarding claim 9, Hironaka teaches the treatment of patients with eGFR < 60 mL/min/1.73 m2, as discussed above.
Regarding claim 10, Hironaka teaches the treatment of patients with eGFR <45 mL/min/1.73m2, as discussed above.
Claim 12 further limits claim 4 to wherein the patient has eGFR >15 mL/min/1.73 m2. Hironaka teaches that patients on dialysis were excluded from the study (page 2, right column, section 3.1). A person of ordinary skill in the art would at once recognize that the attribute of being on dialysis includes an eGFR of ≤ 15 mL/min/1.73 m2, because critically low eGFR is inherently associated with dialysis treatment and this inherent attribute was known in the art, as evidenced by Vadakedath (Vadakedath, S. and Kandi, V.; Cureus, v9, article e1603, pp1-6; 2017). Vadakedath teaches a review of the mechanisms underlying complications in the management of chronic renal failure (Abstract, page 1). Vadakedath teaches that there are 5 stages of chronic renal failure, and stage 5 is characterized by GFR < 15 mL/min/1.73 m2 (Abstract) and further teaches that dialysis is done when GFR fall below 15 mL/min/1.73 m2 (page 1, section “Introduction and Background”).
Regarding claim 13, Hironaka teaches that patients with UACR ≥30 mg/g are included in the dapagliflozin treatment group, as discussed above.
Regarding claim 15, while Hironaka does not specifically highlight the overlap of sub-populations of patients identified with eGFR <60 mL/min/1.73 m2 and patients identified with UACR ≥30 mg/g, no exclusion of participants having both of these attributes is taught by Hironaka, and so a person of ordinary skill in the art would at once envisage that these sub-groups, which are shown in Hironaka’s Table 1 to represent 17% and 24% of the populations of the dapagliflozin treatment group, respectively, would overlap, and thus patients having both of these attributes would be expected to be present in the study.
Regarding claims 17 and 18, Hironaka teaches that the average age in the dapagliflozin treatment group was 55, thus adults were included in the study (Table 1, page 3).
Claim 24 further limits the method of claim 4 to wherein the patient is monitored for DKA or the risk of DKA. Claim 25 further limits claim 24 to wherein the monitoring for DKA is done by testing the patient’s blood glucose, arterial pH, and/or serum bicarbonate levels. Hironaka teaches that DKA, which was detected in the study, was defined as acidosis, pH<7.3, with elevated blood and urine ketones and decreased bicarbonate (<18 mEq/L), independent of blood glucose levels (page 2, right column, top paragraph).
Claim 26 further limits the method of claim 4 to wherein the patient is monitored for hypoglycemia or an increased risk of hypoglycemia. Hironaka teaches that hospitalization for hypoglycemia is a secondary outcome of the study (page 2, right column, section 3.2), and that there was no hospitalization due to hypoglycemia in the dapagliflozin group while two hospitalizations for hypoglycemia occurred in the non-use (i.e., placebo, or insulin-only) group (page 4, right column, last paragraph of section 4). Thus, a person of ordinary skill in the art would at once recognize that Hironaka’s method included monitoring for hypoglycemia.
Thus, claims 7, 9-10, 12-13, 15, 17-18 and 24-26 are anticipated by the teaching of Hironaka.
Claims 4, 9-11 and 13-18 are anticipated by Herrington.
Claims 4, 9-11, and 13-18 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Herrington (Herrington, W. G., et al; The New England Journal of Medicine, v388, pp117-127; 2022)8.
Herrington teaches a clinical trial in the treatment of patients with chronic kidney disease with the administration of the SGLT2 inhibitor empagliflozin (Abstract, page 117). With regard to qualification of patients as having chronic kidney disease, Herrington teaches that the study enrolled patients having eGFR of at least 20 but less than 45 mL/min/1.73 m2 (Abstract, page 117). Herrington provides baseline characteristics of the patients in Table 1 (page 122), wherein it is shown that a cohort of patients with Type 1 diabetes were included in the trial (34 out of 3304 total patients treated with emplagliflozin). Herrington teaches that empagliflozin therapy led to a lower risk of progression of kidney disease than placebo.
Thus, claim 4 is anticipated by the teaching of Herrington.
Regarding claims 9-10, as discussed above, 100% patients enrolled in the study had eGFR below 45 mL/min/1.73 m2. Thus 100% of the patient cohort having Type 1 diabetes also had eGFR <45 mL/min/1.73 m2.
Regarding claim 11, Herrington teaches in Table 1 (pages 122-123) that 34% of the patients treated with empagliflozin had eGFR < 30 mL/min/1.73 m2; a person of ordinary skill in the art would at once envisage that this sub-group would overlap with the sub-group of patients having T1D, and thus patients having both of these attributes would be expected to be present in the study. No exclusion of participants having both of these attributes is taught by Herrington.
Regarding claims 13 and 15, as discussed above, 100% of patients enrolled in the study had eGFR <45 mL/min/1.73 m2, and Herrington teaches in Table 1 (pages 122-123) that a total of 79.9% of empagliflozin-treated patients had UACR of ≥ 30 mg/g (cohorts of UACR 30-300 and >300 combined); a person of ordinary skill of art would at once envisage that these sub-groups would both overlap with the cohort of Type 1 diabetic patients, and thus patients having all of these attributes would be expected to be present in the study.
Regarding claim 14, as discussed above, 100% of patients enrolled in the study had eGFR <45 mL/min/1.73 m2, and Herrington teaches in Table 1 (pages 122-123) that more than half (52%) of empagliflozin-treated patients has UACR >300 mg/g, thus a person of ordinary skill in the art would at once envisage that these sub-groups would overlap, and patients having both of these attributes would be expected to be present in the study.
Regarding claim 16, Herrington teaches in Table 1 (pages 122-123) that the average BMI for empagliflozin-treated patients is 29.7; a person of ordinary skill in the art would at once envisage that a substantial portion of the patient population has a BMI >27, and thus the cohort of patients with BMI >27 and the cohort of T1D patients would overlap, and thus patients having both of these attributes would be expected to be present in the study.
Regarding claims 17-18, Herrington teaches that eligible patients were adults (page 118, right column, section “Patients”).
Thus, claims 9-11, and 13-18 are anticipated by the teaching of Herrington.
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.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 4, 6-7, 9, 13, 15-20 and 24-26 are unpatentable over van Raalte in view of Goldenberg.
Claims 4, 6-7, 9, 13, 15-20 and 24-26 are rejected under 35 U.S.C. 103 as being unpatentable over van Raalte (van Raalte, D. H., et al.; Diabetes Care, v42, pp1921-1929; 2019)9 in view of Goldenberg (Goldenberg, R. M., et al.; Diabetes, Obesity and Metabolism, v21, pp2192-2202; 2019)10.
The limitations of claims 4, 6-7, 9, 13, 15-18, 20 and 24-26 and the teaching of van Raalte are discussed in the rejections above and hereby incorporated into the instant rejection.
Claim 19 further limits claim 17, regarding a Markush group of patient attributes, to wherein the patient to be treated must have all the attributes of the Markush group, which include the following:
Patient is an adult;
Patient is not a pregnant woman;
Patient is using multiple daily injections or subcutaneous insulin infusion for insulin delivery;
Patient has an HbA1C within the range of 7.0-11.0%;
Patient has a b-hydroxybutyrate level of ≤0.6 mmol/L.
Claim 20 further limits claim 4 to wherein sotagliflozin is administered orally.
As discussed in the rejection above, van Raalte teaches a method of treating adult patients suffering from T1D with the SGLT2 inhibitor as performed in particular clinical trials (inTandem1 and inTandem2), wherein the population of patients receiving the treatment included patients with CKD. Van Raalte also teaches that eligible patients for the study had HbA1c in the range of 7.0-11.0% and eGFR >45 mL/min/1.73 m2 (page 1922, center column, “Study Design and Population” section). Van Raalte does not explicitly teach or express a preference for/against the other attributes disclosed in claim 17; however, a person of ordinary skill in the art would have a reasonable expectation of success requiring each of the other criteria listed in claim 17, because each of the criteria are either cautionary to ensure the patient’s adequate treatment with the active agent and/or allow for less complicated and more meaningful assessment and determination of the compound’s safety/efficacy.
Regarding pregnant women, it was known in the art that DKA during pregnancy can be precipitated by additional factors including emesis, a common occurrence in pregnancy, and can increase foetal risk, per the teaching of Goldenberg (page 2197, right column, third paragraph), who teaches these factors in the context of a holistic strategy to mitigate the risk of diabetic ketoacidosis in T1D patients taking SGLT inhibitors, called the “STOP DKA Protocol” (Abstract, page 2192). Goldenberg also teaches that SGLT inhibitors are not approved for administration to pregnant women, and states that SGLT inhibitors should not be prescribed to women of childbearing potential who are pregnant or planning pregnancy, or who are unwilling to use an appropriate family planning method, and that SGLT inhibitors should be discontinued as soon as an unplanned pregnancy is diagnosed (page 2197, right column, third paragraph).
Regarding patients using multiple daily injections or subcutaneous insulin infusion for insulin delivery, it was known in the art that the use of one or the other of these methods for insulin administration constitutes “adhering to an intensive insulin regimen” and reduces complications associated with T1D along with additional factors, including maintaining healthy behavioral habits and comprehensive monitoring of glucose levels, per the teaching of Goldenberg (page 2193, left column, first paragraph).
Regarding patients having a b-hydroxybutyrate level of ≤0.6 mmol/L, it was known in the art that this level of b-hydroxybutyrate represents a risk point for DKA, as taught by Goldenberg. Goldenberg teaches details in the protocols of the inTandem trials, which are the same trials taught by van Raalte as discussed above, and Goldenberg teaches that all participants were provided with urine ketone strips as well as blood b-hydroxybutyrate meters and strips. They received instructions on detecting and treating ketosis and were told to contact their study site immediately if their b-hydroxybutyrate levels were >0.6 mmol/L, regardless of their glucose readings (page 2197, left column, first full paragraph). Additionally, Goldenberg teaches the mechanisms for DKA in T1D and risk associated with SGLT2 inhibition: DKA is frequently caused by an excessive rise in glucagon levels in a milieu of absolute or relative insulin deficiency that in turn stimulates hepatic glycogenolysis. The resultant hyperglycaemic environment and osmotic diuresis promote a volume depleted state that may progress to acute kidney injury. The lack of effective insulin fuels lipolysis, which provides a source of free fatty acids that are shunted through the ketosis pathway and converted into three different ketone bodies: the predominant b-hydroxybutyrate, its oxidized but less stable form acetoacetate, and acetone. The overwhelming build-up of glucose and ketone bodies in the presence of insulin deficiency culminates in elevated anion gap metabolic acidosis, with potentially fatal outcomes if DKA is not diagnosed and treated in a timely fashion (page 2193, right column, section 2 first paragraph). Goldenberg further teaches why DKA should be monitored by ketones in the particular case of patients taking SGLT inhibitors: SGLT2 inhibition within the kidney cm mitigate the marked hyperglycaemia of typical DKA, sometimes resulting in only moderate hyperglycaemia which can cause confusion for patients and healthcare providers, sometimes leading to missed diagnosis due to "euglycaemic" DKA where blood glucose is <14 mmol/L (pages 2193-2194, including Figure 1).
Regarding claim 20, Goldenberg teaches that sotagliflozin is an orally administered SGLT2 inhibitor (Abstract, page 2192).
Regarding claims 24-26, as discussed above Goldenberg teaches that all participants in the inTandem trials were provided with urine ketone strips as well as blood b-hydroxybutyrate meters and strips. They received instructions on detecting and treating ketosis and were told to contact their study site immediately if their b-hydroxybutyrate levels were >0.6 mmol/L, regardless of their glucose readings (page 2197, left column, first full paragraph).
Applicant’s invention is unpatentable over the teaching of van Raalte in view of the teaching of Goldenberg, because a person of ordinary skill in the art would have a reasonable expectation of success in treating T1D patients with CKD using the method of van Raalte of combination therapy of the orally-administered SGLT2 inhibitor sotagliflozin with insulin administration, and limiting the patient population to patients having all the attributes as claimed in claim 17 and monitoring glucose and b-hydroxybutyrate, because van Raalte teaches that patients with CKD can be treated with a combination of sotagliflozin and insulin, and patients for the treatment as implemented in the inTandem1 trial should be adults and have HbA1C in the range of 7.0-11.0%, and because each of the criteria of claim 17 are either cautionary to ensure the patient’s adequate treatment with the active agent and/or allow for less complicated and more meaningful assessment of the compound’s safety/efficacy, and it was known in the art, per the teaching of Goldenberg, that pregnancy introduces additional factors in the occurrence and risk of DKA, and that an intensive insulin regimen based on multiple daily injections or use of an insulin infusion pump reduces the risk of complications in T1D along with monitoring of glucose in T1D patients, and that b-hydroxybutyrate is an important signal for DKA which should be regularly monitored alongside blood glucose, with a b-hydroxybutyrate target of ≤0.6 mmol/L.
Thus, the invention was prima facie obvious at the time of filing.
Claims 4, 6-7, 9, 13 and 15-18 and 20-21 are unpatentable over van Raalte in view of Lexicon.
Claims 4, 6-7, 9, 13 and 15-21 are rejected under 35 U.S.C. 103 as being unpatentable over van Raalte (van Raalte, D. H., et al.; Diabetes Care, v42, pp1921-1929; 2019)11 in view of Lexicon (Clinical Trial NCT02384941, “Efficacy, Safety, and Tolerability Study of Sotagliflozin as Adjunct Therapy in Adult Patients With Type 1 Diabetes Mellitus Who Have Inadequate Glycemic
Control With Insulin Therapy (inTandem1),” ClinicalTrials.gov, Record History 10Feb2020, Accessed 14Aug2026)12.
The limitations of claims 4, 6-7, 9, 13, 15-18 and 20 and the teaching of van Raalte are discussed in the rejections above and hereby incorporated into the instant rejection.
Claim 21 further limits claim 21 to wherein the sotagliflozin is administered as a tablet, caplet, or capsule.
Van Raalte does not teach how to administer sotagliflozin, in particular how sotagliflozin was administered in the inTandem1 and/or inTandem2 clinical trials. However a person of ordinary skill in the art would have a reasonable expectation of success in treating a T1D patient with CDK using the method of combination therapy of the SGLT2 inhibitor sotagliflozin with insulin therapy, as taught by van Raalte, and administering sotagliflozin orally in tablet form, because it was known in the art that in the inTandem1 trial, one of the same 2 trials taught by van Raalte, sotagliflozin was administered as 200 mg and/or 400 mg tablets, per the teaching of Lexicon.
Lexicon provides a report of the inTandem1 clinical trial, including the protocols for treatment, and Lexicon teaches that the trial had three cohorts, including a placebo-treated cohort, and two sotagliflozin cohorts, wherein sotagliflozin was administered as either a 200 mg tablet or 400 mg tablet (Arms and Interventions section).
Applicant’s invention is unpatentable over the teaching of van Raalte in view of the teaching of Lexicon, because a person of ordinary skill in the art would have a reasonable expectation of success in treating T1D patients with CKD using the method of van Raalte of combination therapy of the orally-administered SGLT2 inhibitor sotagliflozin with insulin administration, and administering sotagliflozin orally in tablet form, because van Raalte teaches that patients with CKD can be treated with a combination of sotagliflozin and insulin, as evidenced by the inTandem1 and inTandem2 clinical trials, and because it was known in the art that sotagliflozin was administered orally, in tablet form, in the inTandem1 trial, per the teaching of Lexicon.
Thus, the invention was prima facie obvious at the time of filing.
Conclusion
Any inquiry concerning this communication or earlier communications from the examiner should be directed to W. JUSTIN YOUNGBLOOD whose telephone number is (703)756-5979. The examiner can normally be reached on Monday-Thursday from 8am to 5pm. The examiner can also be reached on alternate Fridays.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Jeffrey S. Lundgren, can be reached at telephone number (571) 272-5541. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/W.J.Y./Examiner, Art Unit 1629
/JEFFREY S LUNDGREN/Supervisory Patent Examiner, Art Unit 1629
1 G1 = eGFR ≥90 mL/min/1.73 m2, per instant Specification, page 4, lines 22-23.
2 G2 = eGFR 60-89 mL/min/1.73 m2, per instant Specification, page 4, lines 22-23.
3 A1 = UACR < 30mg/g, per instant Specification, page 4, lines 25-26.
4 Cited in Applicant’s Information Disclosure Statement dated 12/17/2024.
5 Article available online 17June2023.
6 Cited in Applicant’s Information Disclosure Statement dated 12/23/2024.
7 Hironaka reports 74% of patients have UACR < 30 mg/g; thus, the remainder had UACR ≥30 mg/g.
8 Cited in Applicant’s Information Disclosure Statement dated 12/17/2024.
9 Cited in Applicant’s Information Disclosure Statement dated 12/17/2024.
10 Cited in Applicant’s Information Disclosure Statement dated 12/23/2024.
11 Cited in Applicant’s Information Disclosure Statement dated 12/17/2024.
12 https://clinicaltrials.gov/study/NCT02384941
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