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 .
Priority
This Application is a 371 of PCT/US2020/051212, filed September 17, 2020 and claims priority to U.S. Provisional Application No. 62901616, filed September 17, 2019.
Claim Status
Claims 1-2, 5-12, and 19-21 are currently pending. Claims 10-11 are withdrawn as being drawn to a non-elected invention. Claims 1-2, 5-9, 12 and 19-21 are active and subject to examination.
Claim Objections- Withdrawn- Overcome by amendment
The objection to claims 6 and 20 is withdrawn. The minor informality was obviated by the Applicant’s amendment.
Claim Rejections- Overcome by Amendment
The rejection of claims 3-7 and 19-21 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or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention is withdrawn.
The rejection of claims 1-4 and 7-9 under 35 U.S.C. 102(a)(1) as being anticipated by Wang et al. (Journal of Pharmacological Sciences, Vol. 133, Issue 4, April 2017, p. 203-213) is withdrawn.
The rejection of claims 1-9, 12-15 and 19-21 under 35 U.S.C. 102(a)(1) as being anticipated by Sugiyama (US 20070281985 A1) citing to Kitase et al. (Cell Reports, Vol. 22, Issue 6, 6 February 2018, p. 1531-1544) is withdrawn.
The above rejections were overcome by the Applicant’s amendments to the claims.
Claim Rejections - 35 USC § 112(b)- New Grounds of Rejection Necessitated by Amendment
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 1-2, 5-9, 12 and 19-21 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.
Claims 1 and 12 recite: “and reducing serum Pi levels below a threshold level of at least 4.5 mg/dL Pi in the subject”. One of ordinary skill in the art cannot determine the metes and bounds of the claim because it is unclear how reducing the serum Pi levels below a threshold level is further limiting to the method steps or the composition administered to the subject. This is merely a result to be achieved and does not appear to impose any further limitations on the method. The same can be said of the whereby limitation in claim 1. "A ‘whereby clause in a method claim is not given weight when it simply expresses the intended result of a process step positively recited.’" Id. (quoting Minton v. Nat’l Ass’n of Securities Dealers, Inc., 336 F.3d 1373, 1381, 67 USPQ2d 1614, 1620 (Fed. Cir. 2003)).” (MPEP 2111.04). Claims 2, 5-9 and 19-21 depend from claims 1 and 12, respectively but do not resolve this ambiguity and are therefore also indefinite.
This rejection was previously recited for claims 3-4, but and the Applicant argued that the rejection was moot because claims 3 and 4 were cancelled. While the Applicant cancelled claims 3-4, the limitations of these claims were then incorporated into the independent claims and no further rationale was given to obviate the rejection.
Claim Rejections - 35 USC § 103- Previously Presented
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.
The rejection of claim(s) 1-2, 5-9, 12 and 19-21 under 35 U.S.C. 103 as being unpatentable over Wang et al. (Journal of Pharmacological Sciences, Vol. 133, Issue 4, April 2017, p. 203-213), and further in view of Hou et al. (Nephrology, Vol. 23, Suppl. 4, p. 88-94) and Kitase et al. (Cell Reports, Vol. 22, Issue 6, 6 February 2018, p. 1531-1544) is maintained.
The rejection of claim(s) 1-2, 5-9, 12 and 19-21 under 35 U.S.C. 103 as being unpatentable over Wang et al. (Journal of Pharmacological Sciences, Vol. 133, Issue 4, April 2017, p. 203-213), in view of Hou et al. (Nephrology, Vol. 23, Suppl. 4, p. 88-94) and Kitase et al. (Cell Reports, Vol. 22, Issue 6, 6 February 2018, p. 1531-1544), as applied to claims 1-2 and 5-9 above, and further in view of Fromenty (US 2006/0167098 A1) is maintained.
Response to Arguments
The Applicant argues that Wang is not concerned with reducing serum phosphate levels at all, but rather with treating kidney fibrosis (Remarks, p. 7); there is no motivation for a skilled artisan to use 95% enantiopure L-BAIBA; and there is no motivation to reduce serum phosphate concentration below 4.5 mg/dL (p. 8). The Applicant argues that Kitase is focused on bone mass bone viability and muscle function, not in reducing serum phosphate levels (Remarks, p. 8-9). These arguments were fully considered but are not persuasive.
The present application is directed towards a method of treating or ameliorating nephropathy in a subject, comprising administering to the subject a composition comprising a therapeutically effective amount of at least 95% enantiomerically pure L-BAIBA and reducing serum phosphate (Pi) levels below a threshold level of at least 4.5 mg/dL Pi in a subject. In summary, the Applicant argues that it is non-obvious to use 95% enantiomerically pure L-BAIBA and that it is non-obvious to use L-BAIBA to reduce serum Pi levels in a subject to normal levels. These arguments are not persuasive because one of ordinary skill in the art would have a reasonable expectation of success to treat hyperphosphatemia caused by CKD with L-BAIBA because it is well known to treat CKD with BAIBA (which includes L-BAIBA), hyperphosphatemia is a known result of CKD, and enantiomerically pure L-BAIBA is known to increase bone vitality which would lower phosphate levels in patients with CKD.
Wang teaches that BAIBA is produced from the catabolism of valine (L-valine), showing that the BAIBA includes L-BAIBA (Wang, p. 203). A prima facie case of obviousness exists for stereoisomers:
Compounds which are position isomers (compounds having the same radicals in physically different positions on the same nucleus) or homologs (compounds differing regularly by the successive addition of the same chemical group, e.g., by -CH2- groups) are generally of sufficiently close structural similarity that there is a presumed expectation that such compounds possess similar properties. In re Wilder, 563 F.2d 457, 195 USPQ 426 (CCPA 1977). See also In re May, 574 F.2d 1082, 197 USPQ 601 (CCPA 1978) (stereoisomers prima facie obvious); Aventis Pharma Deutschland v. Lupin Ltd., 499 F.3d 1293, 84 USPQ2d 1197 (Fed. Cir. 2007) (5(S) stereoisomer of ramipril obvious over prior art mixture of stereoisomers of ramipril.).
MPEP 2144.09.II.
As shown by Hou, hyperphosphatemia is a natural consequence of nephropathy (CKD). As Wang teaches that BAIBA can treat CKD, one of ordinary skill in the art would reasonably expect that kidney function would increase by administering BAIBA or an enantiomer thereof, and that greater control of serum phosphate concentration could be achieved. Furthermore, Hou teaches that bone mineral metabolism is disrupted in patients with CKD leading to hyperphosphatemia. Kitase teaches that enantiomerically pure L-BAIBA can restore bone vitality and stop bone loss. Therefore, one of ordinary skill in the art would reasonably expect that L-BAIBA would treat hyperphosphatemia associated with CKD.
The Applicant presents nothing unexpected in this invention. The Applicant does not actually show that serum phosphate levels are lowered by administering L-BAIBA. In fact, the Applicant shows that serum phosphate levels were slightly higher in model mice administered L-BAIBA as compared to the control or D-BAIBA:
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(Instant Fig. 5C). BAIBA is well known to treat CKD as demonstrated by Wang. L-BAIBA is also well known to impact bone mineral metabolism which is involved in hyperphosphatemia as demonstrated by Hou and Kitase. The Applicant has not provided a significant inventive contribution over the prior art and has failed to demonstrate anything unexpected.
Reiterated Rejection
Claim(s) 1-2, 5-9, 12 and 19-21 is/are rejected under 35 U.S.C. 103 as being unpatentable over Wang et al. (Journal of Pharmacological Sciences, Vol. 133, Issue 4, April 2017, p. 203-213), as applied to claims 1-4 and 7-9 above, and further in view of Hou et al. (Nephrology, Vol. 23, Suppl. 4, p. 88-94) and Kitase et al. (Cell Reports, Vol. 22, Issue 6, 6 February 2018, p. 1531-1544).
Claim 1 recites:
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Wang teaches that BAIBA (e.g. L-BAIBA) is a treatment for nephropathy, specifically chronic kidney disease (CKD):
Renal fibrosis and dysfunction were clinically presented in CKD patients.40, 41 Inhibition of renal fibrosis may be a good strategy to improve renal function in CKD patients.41, 42 In this study, our results showed that UUO caused dramatic inductions of profibrogenic genes including α-SMA, COL 1 and FN, as well as PCNA protein and mRNA expressions after surgery, whereas BAIBA significantly suppressed α-SMA, COL 1, FN and PCNA protein and mRNA expressions in UUO kidneys. These results demonstrated that BAIBA can reverse the deposition of ECM and renal fibrosis in UUO kidneys. BAIBA may be potentially served as a possible drug in the treatment of renal fibrosis diseases.
Taken together, our data provide the first demonstration that BAIBA significantly alleviated the fibrotic responses and renal functional impairment in the obstructed kidneys. Inhibition of Ang II/IL-17/ROS signaling pathway was responsible for the role of BAIBA in attenuating renal fibrosis. BAIBA may be useful for the treatment of patients with chronic kidney diseases.
Wang, p.212 (emphasis added).
Wang teaches that the BAIBA is supplied in a pharmaceutically acceptable carrier by mouth (water) (Wang, col. 2, p. 206).
While Wang does not teach the treatment of hyperphosphatemia (serum Pi > 4.5 mg/dL) associated with CKD, the method of Wang is inherently assumed to result in the treatment of hyperphosphatemia associated with CKD. It is commonly known in the art that hyperphosphatemia is the result of renal functional impairment. For example, Hou teaches that disturbed mineral metabolism is the result of renal functional impairment in CKD:
At the onset of chronic kidney disease (CKD), the systemic mineral metabolism and bone composition start to change along with glomerular filtration rate (GFR) loss. As the GFR loss aggravates, the disturbed mineral metabolism worsens the bone microstructure and remodelling – scenario that is known as CKD-mineral bone disease (MBD). The Kidney Disease: Improving Global Outcomes (KDIGO) defined CKD-MBD as a broader systemic disorder of mineral and bone metabolism as a result of CKD. 4 CKD-MBD is characterized by the following: (i) abnormal metabolism of calcium, phosphorus, parathyroid hormone (PTH), or vita-min D; (ii) abnormalities in bone turnover, mineralization, volume linear growth or strength; (iii) soft-tissue calcifications, either vascular or extra-osseous.5
CHARACTERISTICS OF MINERAL ANDHORMONAL DISRUPTION IN CKD
As the GFR falls, free serum calcium levels fall and serum phosphorus increases. Because of GFR loss, compensatory production of fibroblast growth factor 23 (FGF-23) decreases levels of sodium-dependent phosphate transport protein (Npt)2a and Npt2c in the kidney, resulting in increased urinary excretion of phosphate.6 In response, the parathyroid glands increase the production of PTH, which decreases the abundance of Npt2a and Npt2c in the proximal tubule, leading to increased urinary Pi excretion that in turn lowers serum Pi levels.7 FGF23 also inhibits the production of 1,25(OH)2D and therefore decreases intestinal Pi absorption, further decreasing serum Pi levels.8 The decreased 1,25(OH)2D induces hypocalcaemia and then stimulated PTH production persists, which ensues secondary hyperparathyroidism(SHPT).9 As GFR continues to fall, however, these compensatory mechanisms fail, leading to hyperphosphatemia, hyperparathyroidism, and higher serum FGF-23 concentration. The SHPT and uremic toxin accumulation accelerate bone turn-over by activating osteoclastogenesis and increased the release of calcium and phosphate from bone.
Hou, p. 88-89 (emphasis added).
Therefore, one of ordinary skill in the art would expect that by treating renal functional impairment, one could treat hyperphosphatemia associated with CKD.
Furthermore, one of ordinary skill in the art would have a reasonable expectation of success to treat hyperphosphatemia associated with CKD by administering L-BAIBA because in patients with CKD-BMD, decreased bone vitality aggravates hyperphosphatemia, and L-BAIBA is also known to improve bone vitality which would improve Pi status. Hou teaches that reduced bone vitality in CKD further increases serum phosphate levels in CKD patients:
Basically, bone cells have less vitality in patients with CKD than in normal persons because of accumulation of uremic toxin and insulin resistance. Thus, low bone turnover is part of the innate character of CKD. 55–57 High PTH serum levels will overcome the indolent bone cells and lead to high turn-over bone disease with the characteristics of relatively higher bone resorption than bone resorption.7 The high turnover status in SHPT can induce increased bone demineralization, which will increase calcium and inorganic phosphate release from bone into circulation. In contrast, overtreatment of CKD patients with Ca-salts, vitamin D receptor analogue (VDRA), or aluminum may cause them to develop low turnover bone disorders and low serum PTH levels. The decreased bone mineralization makes it difficult for calcium and inorganic phosphate to enter into bone, resulting in increased serum calcium and inorganic phos-phate.58 Both high and low bone turnover disorders are characterized by a relatively higher degree of bone resorption than bone formation, which may contribute to the elevated serum calcium and inorganic phosphate levels, and aggravate VC/ossification.
Hou, p. 88-89 (emphasis added).
While Hou does not teach that L-BAIBA promotes bone vitality and therefore would lower serum phosphate levels, it is commonly known in the art that L-BAIBA promotes bone vitality. For example, Kitase teaches that L-BAIBA prevents bone loss in a mouse model of osteocyte apoptosis:
Exercise has beneficial effects on metabolism and on tissues. The exercise-induced muscle factor β-aminoisobutyric acid (BAIBA) plays a critical role in the browning of white fat and in insulin resistance. Here we show another function for BAIBA, that of a bone-protective factor that prevents osteocyte cell death induced by reactive oxygen species (ROS). l-BAIBA was as or more protective than estrogen or N-acetyl cysteine, signaling through the Mas-Related G Protein-Coupled Receptor Type D (MRGPRD) to prevent the breakdown of mitochondria due to ROS. BAIBA supplied in drinking water prevented bone loss and loss of muscle function in the murine hindlimb unloading model, a model of osteocyte apoptosis.
Kitase, Summary (emphasis added).
Wang teaches that BAIBA is produced from the catabolism of valine (L-valine), showing that the BAIBA includes L-BAIBA (Wang, p. 203). While Wang does not teach enantiomerically pure L-BAIBA, one of ordinary skill in the art would have a reasonable expectation of success to use enantiomerically pure L-BAIBA because Kitase teaches enantiomerically pure L-BAIBA: “The L-isoform was shown to be the more active form compared to the D-isoform (Figure 1A), and L-BAIBA was as or more potent than the well-known anti-apoptotic factors b-estradiol and NAC (Figure 1B).” (Kitase, p. 1532). Kitase uses L-BAIBA which is at least 97% pure (L-BAIBA (Sigma-Aldrich, 51511)). Furthermore, a prima facie case of obviousness exists for stereoisomers:
Compounds which are position isomers (compounds having the same radicals in physically different positions on the same nucleus) or homologs (compounds differing regularly by the successive addition of the same chemical group, e.g., by -CH2- groups) are generally of sufficiently close structural similarity that there is a presumed expectation that such compounds possess similar properties. In re Wilder, 563 F.2d 457, 195 USPQ 426 (CCPA 1977). See also In re May, 574 F.2d 1082, 197 USPQ 601 (CCPA 1978) (stereoisomers prima facie obvious); Aventis Pharma Deutschland v. Lupin Ltd., 499 F.3d 1293, 84 USPQ2d 1197 (Fed. Cir. 2007) (5(S) stereoisomer of ramipril obvious over prior art mixture of stereoisomers of ramipril.).
MPEP 2144.09.II.
As shown above, L-BAIBA is suggested in the art to have a dual mechanism for treating hyperphosphatemia in CKD. One of ordinary skill in the art is well aware that L-BAIBA can both directly improve renal function and improve bone vitality and thus would have a reasonable expectation of success to treat hyperphosphatemia by administering L-BAIBA.
Therefore, claim 1 was prima facie obvious at the time of filing.
Claim 12 is also directed towards the treatment of hyperphosphatemia like claim 1. Claim 12 additionally recites that the hyperphosphatemia is caused by metabolic acidosis. One of ordinary skill in the art would have a reasonable expectation of success to treat hyperphosphatemia cause by metabolic acidosis because metabolic acidosis is a well known cause of bone loss in CKD and hyperphosphatemia. For example, see Hou: “When renal function declined progressively, metabolic acidosis and hyponatremia also result in the bone quantity loss.” (Hou, col. 1, p. 91)
Claim 2 is directed towards the method of claim 1, wherein the nephropathy is CKD. As shown above, Wang teaches the treatment of CKD with L-BAIBA. Therefore, claim 2 was prima facie obvious at the time of filing.
Claims 5 and 19 are directed towards the method of claims 1 and 12, respectively, wherein the composition comprises at least one additional therapeutic compound. Claims 6 and 20 are directed towards the methods of claims 5 and 19, respectively, wherein the additional therapeutic compound is 1,25-dihydroxy vitamin D (calcitriol). While Wang does not teach to additionally administer calcitriol in combination with L-BAIBA, one of ordinary skill in the art would have a reasonable expectation of success to additionally administer calcitriol to CKD patients, particularly those with hyperphosphatemia, because this is a common practice in the art. For example, Hou teaches that it is important to supplement with vitamin D analogues in patients with CKD-BMD because calcitriol levels are decreased in these patients:
FGF23 also inhibits the production of 1,25(OH)2D and therefore decreases intestinal Pi absorption, further decreasing serum Pi levels.8 The decreased 1,25(OH)2D induces hypocalcaemia and then stimulated PTH production persists, which ensues secondary hyperparathyroidism(SHPT).9 As GFR continues to fall, however, these compensatory mechanisms fail, leading to hyperphosphatemia, hyper-parathyroidism, and higher serum FGF-23 concentration. The SHPT and uremic toxin accumulation accelerate bone turn-over by activating osteoclastogenesis and increased the release of calcium and phosphate from bone.10 Under physio-logical condition, FGF-23 decreases the PTH from gland.11 As progressive GFR loss, PTH was resistant to the suppression byFGF-23 and sequential nodular parathyroid hyperplasiaformed.12,13 On the aspect of vascular health, hyperphosphatemia, SHPT, and hypovitaminosis were strongly associated with increased cardiovascular morbidity and mortality and increases the risk of calciphylaxis.14 Therefore, the treatment on SHPT focus on (i) phosphate restriction, (ii) calcimimetics and (iii) vitamin D analogues supplement.
Hou, p. 89.
The Applicant has failed to demonstrate any unexpected effects from the combination of L-BAIBA and calcitriol, and only recites these two agents in combination, which are already known in the art for CKD. Therefore, claims 5-6 and 19-20 were prima facie obvious at the time of filing.
Claim 7 is directed towards the method of claim 1, wherein the composition is formulated for oral administration. Wang teaches that BAIBA can be administered orally in a mouse model of CKD:
Male Sprague–Dawley rats were randomly divided into three groups (n = 7 for each group): (1) Sham group, (2) UUO group, (3) UUO plus BAIBA group. All rats were anesthetized by intraperitoneal injection of sodium pentobarbital (50 mg/kg). A middle incision of abdomen was cut to expose ureter, and the left was ligated with 4.0 silk at three points. The sham rats were subjected to same surgery without left ureter ligation. The UUO rats were randomly divided into two groups: UUO with vehicle and UUO with 150 mg/kg/day of BAIBA dissolved in drinking water for 2-week period. At 14 days after UUO, the animals were sacrificed by an overdose of pentobarbital sodium (150 mg/kg, i.v.). The left kidneys were removed for histopathological and molecular biology examinations.22
Wang, p. 206 (emphasis added).
Therefore, claim 7 is anticipated.
Claim 8 is directed towards the method of claim 1, wherein the subject is a mammal, and claim 9 is directed towards the method of claim 1 wherein the mammal is human. Wang teaches the treatment of human patients with L-BAIBA. Therefore, claim 8-9 were prima facie obvious at the time of filing.
Claim(s) 1-2, 5-9 and 19-21 is/are rejected under 35 U.S.C. 103 as being unpatentable over Wang et al. (Journal of Pharmacological Sciences, Vol. 133, Issue 4, April 2017, p. 203-213), in view of Hou et al. (Nephrology, Vol. 23, Suppl. 4, p. 88-94) and Kitase et al. (Cell Reports, Vol. 22, Issue 6, 6 February 2018, p. 1531-1544), as applied to claims 1-4 and 7-9 above and further in view of Fromenty (US 2006/0167098 A1)
The rejection of claims 1-2 and 5-9 above is incorporated herein by reference.
In the election requirement, the applicant elected a salt of L-BAIBA as the form of L-BAIBA. While, Wang and Kitase teach the administration of free L-BAIBA and not a salt of L-BAIBA, one of ordinary skill in the art would have a reasonable expectation of success to substitute L-BAIBA for a salt of L-BAIBA, because salts of L-BAIBA are commonly known in the art. For example, Fromenty teaches “administering to a human or non human animal in need thereof, as therapeutically active agent, an effective amount of β-aminoisobutyric acid, derivative, prodrug, metabolite or complex thereof” (Fromenty, Specification, paragraph 0029), wherein “[t]he term “derivatives” include inorganic or organic salts, esters or amides of β-aminoisobutyric acid” (Fromenty, Specification, paragraph 0029) and wherein salts include:
…not only the addition salts with carboxylic organic acids, like the acetate for example, but also other addition salts such as for example the trifluoroacetate, as well as the addition salts with inorganic acids such as the sulphate, hydrochloride and the like. The derivatives also include the salts resulting from the salivation of the carboxyl group and in particular the salts of alkali metals or alkaline earth metals such as the salts of sodium or of calcium.
Formenty, Specification, paragraph 0044.
Therefore, administering a salt of L-BAIBA was prima facie obvious at the time of filing.
Given the above teachings, the invention as a whole was prima facie obvious at the time of filing.
Conclusion
No claim is found to be allowable.
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 extension fee 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 date of this final action.
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/HEATHER DAHLIN/Examiner, Art Unit 1629
/JEFFREY S LUNDGREN/Supervisory Patent Examiner, Art Unit 1629