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
Election of Species and Status of the Claims
Applicant’s election of ‘CCB02’ as the single specific centrosome clustering inhibiting agent and ‘subjects with polycystic kidney disease that do not have cancer’ as the single specific patient population receiving administration in the response filed on November 25th 2025 is acknowledged. Claims 29-48 are pending. Claims 31, 33, 40, and 46 (Note that claim 31 is directed towards a subspecies of polycystic kidney disease and not the disease itself). Claims 29-30, 32, 34-39, 41-45, and 47-48 are examined on their merits.
Priority
Receipt is acknowledged of certified copies of papers required by 37 CFR 1.55.
Information Disclosure Statement
The Information Disclosure Statement filed on April 15th 2024 is in compliance with the provisions of 37 CFR 1.97 and has been considered in full. A signed copy of references cited from the IDS is included with this Office Action.
Claim Rejections - 35 USC § 102
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
Claims 29-30, 32, and 36 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Chen (US 2015/0126513 A1 published on May 7th 2015).
Claims 29-30 are directed towards the treatment of polycystic kidney disease via administration of a centrosome clustering inhibiting agent. Chen teaches compounds that act as tankyrase inhibitors (Chen, pg. 13, paragraph [00163]). Chen further teaches that the inhibition of tankyrase results in the inhibition of centrosome clustering (Chen, paragraph [0010]). Chen’s tankyrase inhibitors would therefore be recognized as centrosome clustering inhibitors. Chen additionally teaches the treatment of polycystic kidney disease (Chen pg. 13, paragraph [00164]) with such compounds. Chen thereby anticipates claims 29-30.
Claim 32 requires that, in the method of claim 29, the subject does not have cancer. Chen’s teaches the treatment of polycystic kidney disease (i.e. not polycystic kidney disease in a subject with cancer). Chen thereby anticipates claim 32.
Claim 36 requires that, in the method of claim 29, the centrosome clustering inhibiting agent is administered orally. Chen teaches oral administration (Chen, pg. 12, paragraph [0150]), and anticipates claim 36.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
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 29-30, 32, 34-39, 41-45, and 47-48 are rejected under 35 U.S.C. 103 as being unpatentable over Hadian (WO 2017/097928 A1 published on June 15th 2017) in view of Battini (Battini et al., Loss of polycystin-1 causes centrosome amplification and genomic instability. Hum Mol Genet. 2008 Sep 15;17(18):2819-33) and Levine (Levine et al., Centrosome Amplification Is Sufficient to Promote Spontaneous Tumorigenesis in Mammals, Developmental Cell, Volume 40, Issue 3, 2017, Pages 313-322.e5,).
Applicant’s claims are directed towards the treatment of polycystic kidney disease via administration of centrosome clustering inhibitors.
Polycystic kidney disease is a serious disease of the kidneys characterized by dilation of tubules in the kidney, resulting in enlargement of kidney cysts and ultimately kidney failure. A particular subvariant, autosomal dominant polycystic kidney disease (ADPKD), is known in the art to be caused by a genetic mutation in the PKD1 gene that causes knockdown of the polycystin-1 (PC1) transmembrane protein (Battini, pg. 2819). Within kidney cells where such a mutation is present, this knockdown has been demonstrated to result in centrosome amplification (Battini, pg. 2822, col. 2; Battini, pg. 2828, col. 1). The two conditions (autosomal dominant polycystic kidney disease and centrosome amplification) are therefore interconnected in that the loss of PC1 function (a major identifying factor in ADPKD patients) can be said to cause centrosomal amplification in such patients (Battini, pg. 2830, col. 2). This is a major concern for patients with ADPKD, as centrosome amplification has been demonstrated in the art to be a major risk factor for cancers. In fact, centrosome amplification has been noted to cause spontaneous tumorigenesis (Levine, pg. 317) through abnormal cell division:
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(Levine, graphical abstract).
One of ordinary skill in the art would therefore be highly motivated to prevent such cancers by suppressing centrosomal amplification in patients with autosomal dominant polycystic kidney disease.
Claims 29-30, 32, and 34-35 are directed towards the treatment of polycystic kidney disease in a patient without cancer via administration of applicant’s elected species of CCB02:
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129
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.
Hadian teaches CCB02 (Hadian, pg. 42, claim 25, compound B) as an inhibitor of centrosome clustering and amplification (Hadian, pg. 30, paragraph [0159]). As one of ordinary would be highly motivated to prevent centrosome amplification in autosomal dominant polycystic kidney disease patients (see the above teachings of Battini and Levine), one of ordinary skill in the art would have a reasonable expectation of success in administering CCB02 to such patients, and claims 29-30, 32, and 34-35 are prima facie obvious.
Claim 36 limits the method of claim 29 to wherein the centrosome clustering inhibiting agent is administered orally. Hadian teaches oral administration (Hadian, pg. 19, paragraph [0076]), and claim 36 is prima facie obvious.
Claim 37 is directed towards a method of reducing kidney cell centrosome amplification in a subject in need thereof via administration of a centrosome clustering inhibiting agent. Regarding centrosomal amplification in the kidneys, Battini teaches that such amplification occurs in ADPKD patients (Battini, abstract). As the administration of centrosome clustering inhibiting agents to such a patient population is obvious (see above), claim 37 is prima facie obvious.
Claim 38 requires that, in the method of claim 37, the subject has an increased number of kidney cells with centrosomal amplification in comparison to a healthy subject. Battini makes such a comparison with the ADPKD population:
“In fact, centrosome amplification was detected in all renal specimens from ADPKD patients (n ¼ 3), but not in cells from control non-cystic human kidneys (n ¼ 5) (Fig. 7A and B). Interestingly, similarly to the animal ADPKD mouse model, centrosomal amplification was also observed in epithelial cells of tubules with seemingly normal histological appearance (Fig. 7C), suggesting that centrosomal amplification may precede rather than follow the cystogenetic process.”
[Battini, pg. 2828]
As the ADPKD patient population would be expected to have such an increase in centrosome amplification the treatment of the ADPKD population is obvious (see above), claim 38 is prima facie obvious.
Claim 39 is directed towards the method of claim 37 wherein the number of kidney cells having centrosome amplification comprise ectopic (i.e. extra) centrosomes. Battini teaches supernumerary centrosomes in the ADPKD patient population (Battini, pg. 2828). As the ADPKD patient population would be expected to have such an increase in centrosome amplification the treatment of the ADPKD population is obvious (see above), claim 38 is prima facie obvious.
Claims 41 and 42 are directed towards the method of claim 37 wherein the centrosome clustering inhibiting agent is CCB02. Claims 41 and 42 are thereby prima facie obvious for the same reasons as claims 35 and 37.
Claim 43 is directed towards a method of inhibiting kidney cell centrosome clustering in a subject in need thereof comprising administration of a centrosome clustering inhibiting agent. As the administration of such an agent to inhibit centrosome clustering in kidneys is obvious (see the above 103 rejection for claim 37), claim 43 is prima facie obvious.
Claim 44 is directed to the method of claim 43 wherein administering the agent results in cell death of kidney cells with more than one centrosome. Hadain teaches that administration of CCB02 results in apoptosis in cells with extra centrosomes (Hadain, pg. 30, paragraph [0160]). Claim 44 is thereby prima facie obvious.
Claim 45 is directed towards the method of claim 43 wherein the agent does not impact normal mitotic spindle formation in single-centrosome kidney cells. Hadian’s compounds are demonstrated to have no impact on mitotic spindle formation in normal cells (Hadian, pg. 28, paragraph [0147]), and claim 45 is prima facie obvious.
Claims 47 and 48 are directed towards the method of claim 43 wherein the centrosome clustering inhibiting agent is CCB02. Claims 47 and 48 are thereby prima facie obvious for the same reasons as claims 35 and 43.
Conclusion
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/A.J.S./Examiner, Art Unit 1629
/JEFFREY S LUNDGREN/Supervisory Patent Examiner, Art Unit 1629