IP Library Granted Patent US 12,533,353
Granted Patent B2
US 12,533,353 · App. 17/275,732 · Granted Jan 27, 2026

Methods of treatment of cancer comprising CDC7 inhibitors

Inventors: Christian Andrew Hassig (San Diego, CA); Ryan James Hansen (San Diego, CA); Snezana Milutinovic (San Diego, CA); Bryan William Strouse (Ann Arbor, MI)
Assignee: CARNA BIOSCIENCES, INC.
A61K31/496A61K31/519A61K31/5377A61K31/675A61K45/06A61P35/00A61P35/02A61P35/04C07D471/04A61K9/0019
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Quick Facts
Patent No.
US 12,533,353
App. No.
17/275,732
Granted
Jan 27, 2026
Kind
B2
Abstract

Herein disclosed are methods of treatment administering SRA141 as a monotherapy or in a combination therapy useful for inhibiting the growth of tumors such as those in patients with cancer.

Claims (60)

1 . A method of treating a cancer, the method comprising:

administering to a human subject with the cancer a therapeutically effective amount of a compound of formula (I-D) or a pharmaceutically acceptable salt thereof:

wherein the therapeutically effective amount is 100, 160, or 200 mg/day, and half of the therapeutically effective amount is administered twice a day (BID), and wherein the cancer is acute myeloid leukemia, bladder cancer, colon cancer, cecum cancer, renal cancer, head-and-neck cancer, melanoma, gastric cancer, colorectal cancer, hematologic cancer, breast cancer, or cervical cancer.

2 . The method of claim 1 , wherein the subject is identified as having one or more of the inclusion criteria disclosed in the table below:

Laboratory Test

Value required

Hemoglobin

≥90 g/L

Absolute neutrophil count

≥1.5 × 10 9 /L

Platelet count

≥120 × 10 9 /L

Bilirubin

≤1.5 × upper limit of normal (ULN)

unless due to Gilbert's syndrome in

which case up to 3 × ULN is

permissible

Alanine aminotransferase

≤2.5 × ULN

(ALT), aspartate

For the Expansion stage,

aminotransferase (AST)

up to 5 × ULN is permissible

and alkaline

if the increase is due to tumor.

phosphatase (ALP)

Serum creatinine

≤1.5 × ULN

or

or

Calculated creatinine

≥60 mL/min using

clearance

Cockcroft-Gault formula.

3 . The method of claim 1 , wherein the subject has not previously had Cdc7 inhibitor therapy.

4 . The method of claim 1 , wherein either

(i) the compound is administered for at least 5 consecutive days; or

(ii) the compound is administered following a dosing schedule selected from the group consisting of: 5 days of dosing followed by 2 days of non-dosing each week; 1 week of daily dosing followed by 1, 2, or 3 weeks of non-dosing; 2 or 3 weeks of daily dosing followed by 1, or 2 weeks of non-dosing; and dosing on days 2 and 3 of a weekly cycle.

5 . The method of claim 1 ,

wherein the hematologic cancer is selected from the group consisting of: acute myeloid leukemia (AML), chronic myelogenous leukemia (CML), chronic eosinophilic leukemia, and diffuse large B-cell lymphoma (DLBCL).

6 . The method of claim 5 , wherein the cancer is diffuse large B-cell lymphoma (DLBCL).

7 . The method of claim 1 , wherein the cancer is not categorized as having a high microsatellite instability (MSI-H) status, or wherein the cancer is categorized as having a microsatellite stability stable (MSS) status.

8 . The method of claim 1 , wherein a tumor associated with the cancer comprises a phenotype selected from the group consisting of: chromosome instability (CIN), a spindle checkpoint assembly defect, a mitosis defect, a G1/S checkpoint defect, and combinations thereof.

9 . The method of claim 1 ,

wherein a tumor associated with the cancer comprises a Wnt signaling pathway mutation; wherein the Wnt signaling pathway mutation is selected from the group consisting of: an Adenomatous polyposis coli (APC) gene mutation, a FAT1 mutation, a FAT4 mutation, and combinations thereof.

10 . The method of claim 1 , wherein the method results in at least one of:

a plasma C max greater than 600 ng/mL of the compound in the subject after administration;

an AUC last greater than 5800 ng-h/mL of the compound in the subject after administration; and

an intra-tumoral concentration of greater than 500 ng/mL of the compound in the subject after administration.

11 . The method of claim 1 ,

wherein the method results in growth inhibition of a tumor or lesion associated with the cancer; wherein the tumor or lesion growth is inhibited by at least 10% relative to an untreated tumor.

12 . The method of claim 1 , wherein the method results in a regression of a tumor associated with the cancer.

13 . The method of claim 1 , wherein the method further comprises administering to the subject a second therapeutically effective amount of one or more additional treatments, wherein the additional treatments are selected from the group consisting of trametinib, rapamycin, bexarotene, tretinoin, ABT-199, copanlisib, BMB673, KU-60019, barasertib, CF1-402257, erlotinib, gemcitabine, and radiation.

14 . The method of claim 13 , wherein the compound and the one or more additional treatments in combination demonstrate synergistic effects.

15 . The method of claim 1 , wherein the compound is administered orally.

16 . The method of claim 1 , wherein the hematologic cancer is AML.

17 . The method of claim 1 , wherein the subject is administered a bis-hydrochloride salt of the compound of formula (I-D).

18 . The method of claim 1 , wherein the therapeutically effective amount of the compound is 100 mg/day, and half of the therapeutically effective amount is administered twice a day (BID).

19 . The method of claim 1 , wherein the therapeutically effective amount of the compound is 160 mg/day, and half of the therapeutically effective amount is administered twice a day (BID).

20 . The method of claim 1 , wherein the therapeutically effective amount of the compound is 200 mg/day, and half of the therapeutically effective amount is administered twice a day (BID).

Assignments (3)
ASSIGNMENT OF ASSIGNOR'S INTEREST Recorded Jun 11, 2025
From: GLAXOSMITHKLINE LLC
To: CARNA BIOSCIENCES, INC.
Reel/Frame 071543/0742 →
ASSIGNMENT OF ASSIGNOR'S INTEREST Recorded Jul 1, 2024
From: SIERRA ONCOLOGY LLC
To: GLAXOSMITHKLINE LLC
Reel/Frame 067883/0963 →
CHANGE OF NAME Recorded May 26, 2023
From: SIERRA ONCOLOGY, INC.
To: SIERRA ONCOLOGY LLC
Reel/Frame 063790/0568 →
Priority Claims (1)
WO PCT/US2019/019676 · Feb 26, 2019 · international
Continuity (3)
Provisional Application 62760638 · Nov 13, 2018
Provisional Application 62735778 · Sep 24, 2018
Related Publication 20210393620A1 · Dec 23, 2021
References Cited (86)
US 4107288A · Oppenheim et al. · 1978 [cited by applicant]
US 5145684A · Liversidge et al. · 1992 [cited by applicant]
US 8552048B2 · Ammons et al. · 2013 [cited by applicant]
US 8742113B2 · Irie · 2014 [cited by examiner]
US 20110118298A1 · Fritz et al. · 2011 [cited by applicant]
US 20120276093A1 · Ballinari et al. · 2012 [cited by applicant]
US 20140018533A1 · Irie et al. · 2014 [cited by applicant]
US 20150218138A1 · Vanotti et al. · 2015 [cited by applicant]
US 20170065609A1 · Funakoshi · 2017 [cited by examiner]
US 20210393620A1 · Hassig et al. · 2021 [cited by applicant]
CA 3042849 · 2018 [cited by applicant]
JP 2007501825 · 2007 [cited by applicant]
JP 2007501827 · 2007 [cited by applicant]
JP 2009515849 · 2009 [cited by applicant]
JP 2009519919 · 2009 [cited by applicant]
JP 2009534400 · 2009 [cited by applicant]
JP 2010505922 · 2010 [cited by applicant]
JP 2010519324 · 2010 [cited by applicant]
JP 2010527324 · 2010 [cited by applicant]
JP 2011507908 · 2011 [cited by applicant]
JP 2012519653 · 2012 [cited by applicant]
JP 2012533551 · 2012 [cited by applicant]
JP 2012533553 · 2012 [cited by applicant]
JP 2013511487 · 2013 [cited by applicant]
JP 2013522212 · 2013 [cited by applicant]
JP 2013525303 · 2013 [cited by applicant]
JP 2013525304 · 2013 [cited by applicant]
JP 2013525354 · 2013 [cited by applicant]
WO WO2007110344 · 2007 [cited by applicant]
WO WO2010122979 · 2010 [cited by applicant]
WO WO2011102399 · 2011 [cited by applicant]
WO WO2012002568 · 2012 [cited by applicant]
WO WO2012133802 · 2012 [cited by applicant]
WO WO2015115355 · 2015 [cited by applicant]
WO 2019165473 · 2019 [cited by applicant]
Kent, “Absolute Dose”, The Oxford Dictionary of Sports Science and Medicine, 2006, 3 ed. (Year: 2006). [cited by examiner]
Shimizu et al., “First-in-human phase 1 study of TAK-931, an oral cell division cycle 7 (CDC7) inhibitor, in patients with advanced solid tumors”, 2018, Journal of Clinical Oncology, Meeting Abstract (Year: 2018). [cited by examiner]
Takeda, “An Open-Label, Phase 2, Parallel Arm Study to Evaluate the Safety, Tolerability, and Activity of TAK-931 Single Agent in Patients With Metastatic Pancreatic Cancer, Metastatic Colorectal Cancer, and Other Advan… [cited by examiner]
Nowak et al., “The role of chromosomal instability in tumor initiation”, 2002, PNAS, 99, pp. 16226-16231 (Year: 2002). [cited by examiner]
Zhang et al., “Multiple roles of APC and its therapeutic implications in colorectal cancer”, 2017, Journal of the National Cancer Institute, 109, pp. 1-10 (Year: 2017). [cited by examiner]
Zhao et al., “Inhibition of CHK1 enhances cell death induced by the Bcl-2-selective inhibitor ABT-199 in acute myeloid leukemia cells”, 2016, Oncotarget, 7, pp. 34785-34799 (Year: 2016). [cited by examiner]
Sawa et al., “Drug design with Cdc7 kinase: a potential novel cancer therapy target”, 2008, Drug Design, Development and Therapy , 2, pp. 255-264 (Year: 2008). [cited by examiner]
Krawczyk et al., “Increased Activity of the S Phase Kinase Cdc7 is Associated with Poor Outcome in Diffuse Large B Cell Lymphoma (DLBCL)”, 2009, Blood, 114, 2 pgs. (Year: 2009). [cited by examiner]
Altschul et al., “Basic local alignment search tool,” Oct. 1990, J. Mol.Biol. 215:403-410. [cited by applicant]
Eisenhauer, et al., “New response evaluation criteria in solid tumours: revised RECIST guideline (version 1.1),” Jan. 2009, Eur J Cancer, 45(2):228-47. [cited by applicant]
Extended European Search Report in European Application No. 19866944.2, dated May 27, 2022, 8 pages. [cited by applicant]
Foucquier et al., “Analysis of drug combinations: current methodological landscape,” Jun. 2015, Pharmacol. Res. Perspect. 3(3):e00149. [cited by applicant]
Howlader et al., (eds), “SEER Cancer Statistics Review, 1975-2014,” Apr. 2018, National Cancer Institute, retrieved from URL< http://seer.cancer.gov/csr/1975_2014/>, based on Nov. 2016 SEER data submission, posted to th… [cited by applicant]
Irie et al., “Discovery of AS-0141, a Potent and Selective Inhibitor of CDC7 Kinase for the Treatment of Solid Cancers,” Oct. 2021, J Med Chem., 64(19):14153-14164. [cited by applicant]
Masai et al., “Cdc7 kinase complex: a key regulator in the initiation of DNA replication,” Mar. 2002, Journal of Cellular Physiology, 190(3):287-296. [cited by applicant]
Nair et al., “A simple practice guide for dose conversion between animals and human,” Mar. 2016, J. Basic Clin. Pharm, 7(2): 27-31. [cited by applicant]
Needleman et al., “A general method applicable to the search for similarities in the amino acid sequence of two proteins,” Mar. 1970, J Mol Biol. 48:443-53. [cited by applicant]
PCT International Preliminary Report on Patentability in PCT Application No. PCT/US2019/048657, dated Mar. 23, 2021. [cited by applicant]
Pearson et al., “Improved tools for biological sequence comparison,” Apr. 1988, Proc. Nat'l. Acad. Sci. USA 85:2444-8. [cited by applicant]
Smith et al., “Comparison of biosequences,” Dec. 1981, Adv. Appl. Math. 2:482-489. [cited by applicant]
Wang et al., Screening for Microsatellite Instability in Colorectal Cancer and Lynch Syndrome—A Mini Review, Jan. 2016, NA J Med Sci. 2016;9(1);5-11. [cited by applicant]
Zehir et al., “Mutational landscape of metastatic cancer revealed from prospective clinical sequencing of 10,000 patients,” Jun. 2017, Nat Med [Internet]. 2017;23(6). [cited by applicant]
Monga, S. P., et al. “Intratumoral Therapy of Cisplatin/Epinephrine Injectable Gel for Palliation in Patients with Obstructive Esophageal Cancer”, Am. J . Clin. Oncol., 2000, vol. 23, No. 4, pp. 386-392. [cited by applicant]
Tomayko et al., “Determination of subcutaneous tumor size in athymic (nude) mice”, Cancer Chemotherapy and Pharmacology, vol. 24, Issue 3, 1989, pp. 148-154. [cited by applicant]
Richtig et al., “Calculated tumour volume as a prognostic parameter for survival in choroidal melanomas”, Eye, 2004, vol. 18, pp. 619-623. [cited by applicant]
Jensen et al., “Tumor volume in subcutaneous mouse xenografts measured by microCT is more accurate and reproducible than determined by 18F-FDG-microPET or external caliper”, BMC Medical Imaging, 2008, vol. 8, No. 16, 99… [cited by applicant]
Faustino-Rocha et al., “Estimation of rat mammary tumor volume using caliper and ultrasonography measurements”, Lab Animal, Jun. 2013, vol. 42, No. 6, pp. 2017-2224. [cited by applicant]
Bonte et al., “Cdc7-Dbf4 Kinase Overexpression in Multiple Cancers and Tumor Cell Lines is Correlated with p53 Inactivation”, Neoplasia, Sep. 2008, vol. 10, No. 9, pp. 920-931. [cited by applicant]
Cadigan et al., “Wnt signaling: complexity at the surface”, Journal of Cell Science, 2006, vol. 19, No. 3, pp. 395-402. [cited by applicant]
Cheng et al., “Increased Cdc7 expression is a marker of oral squamous cell carcinoma and overexpression of Cdc7 contributes to the resistance to DNA-damaging agents”, Cancer Letters, 2013, vol. 337, No. 2, pp. 218-225. [cited by applicant]
Cremolini et al., “First-line chemotherapy for mCRC—a review and evidence-based algorithm”, Nat Rev Clin Oncol, 2015, vol. 12, No. 10, pp. 607-619. [cited by applicant]
Dienstmann et al., “Consensus molecular subtypes and the evolution of precision medicine in colorectal cancer”, Nat Rev Cancer, 2017, vol. 17, pp. 79-92. [cited by applicant]
Ferlay et al., “Cancer incidence and mortality worldwide: Sources, methods and major patterns in GLOBOCAN 2012”, International Journal of Cancer, 2015, vol. 136, pp. E359-E386. [cited by applicant]
Fodde et al., Mutations in the APC tumour suppressor gene cause chromosomal instability, Nature Cell Biology, Apr. 2001, vol. 3, pp. 433-438. [cited by applicant]
Gregory et al., “CDK9 inhibition by dinaciclib potently suppresses Mcl-1 to induce durable apoptotic responses in aggressive MYC-driven B-cell lymphoma in vivo”, Leukemia, 2015, vol. 29, pp. 1437-1441. [cited by applicant]
Guinney et al., The Consensus Molecular Subtypes of Colorectal Cancer, Nat Med., 2016, vol. 21, No. 11, pp. 1350-1356. [cited by applicant]
Hailey et al., “Biliary Proliferative Lesions in the Sprague-Dawley Rat: Adverse/Non-adverse”, 2014, vol. 42, pp. 844-854. [cited by applicant]
Hou et al., “High expression of cell division cycle 7 protein correlates with poor prognosis in patients with diffuse large B-cell lymphoma”, Med Oncol, 2012, vol. 29, pp. 3498-3503. [cited by applicant]
Huggett et al., “Cdc7 is a potent anti-cancer target in pancreatic cancer due to abrogation of the DNA origin activation checkpoint”, Oncotarget, 2016, vol. 7, No. 14, pp. 18495-18507. [cited by applicant]
“ICH Harmonised Tripartite Guideline: Nonclinical Evaluation for Anticancer Pharmaceuticals S9”, International Conference on Harmonisation of Technical Requirements for Registration of Pharmaceuticals for Human Use, 200… [cited by applicant]
Iwai et al., “Phospho-proteomics analysis to determine the signaling pathways affected by a novel CDC7-selective inhibitor TAK-931”, AACR Annual Meeting, 2018, Abstract 2312. [cited by applicant]
Larasati et al., “Mechanisms Governing DDK Regulation of the Initiation of DNA Replication”, Genes, 2017, vol. 8 (1), 3, pp. 1-12. [cited by applicant]
Montagnoli et al., “Cdc7 Inhibition Reveals a p53-Dependent Replication Checkpoint That is Defective in Cancer Cells.”, Cancer Research, 2004, vol. 64, pp. 7110-7116. [cited by applicant]
Rodriguez-Acebes et al., “Targeting DNA Replication before it Starts: Cdc7 as a Therapeutic Target in p53-Mutant Breast Cancers”, The American Journal of Pathology, Oct. 2010, vol. 177, No. 4, pp. 2034-2045. [cited by applicant]
Schukken et al., “CIN and Aneuploidy: Different Concepts, Different Consequences”, BioEssays, 2018, vol. 40, No. 1, pp. 1-9. [cited by applicant]
Swords et al., “Cdc7 kinase—A new target for drug development”, European Journal of Cancer, 2010, vol. 46, pp. 33-40. [cited by applicant]
Therkildsen et al., “The predictive value of KRAS, NRAS, BRAF, PIK3CA and PTEN for anti-EGFR treatment in metastatic colorectal cancer: A systematic review and meta-analysis”, Acta Oncologica, 2014, vol. 53, No. 7, pp. … [cited by applicant]
Xiang et al., “A selective CDC7 inhibitor (LY3177833) impacts chromosome dynamics and has robust and durable activity in PDX tumor models”, AACR Annual Meeting, 2016, Late breaking abstract. [cited by applicant]
Zehir et al., “Mutational landscape of metastatic cancer revealed from prospective clinical sequencing of 10,000 patients”, Nature Medicine, Jun. 2017, vol. 23, No. 6, pp. 706-713. [cited by applicant]
International Search Report issued Nov. 15, 2019 in International (PCT) Application No. PCT/US2019/048657. [cited by applicant]
Chava, S. et al., “Co-targeting of specific epigenetic regulators in combination with CDC7 potently inhibit melanoma growth.” 2022, iScience 25, 104752, 43 pages. [cited by applicant]